Cardiovascular — MCQs

Q: A 33-year-old woman presents to her physician's office for a postpartum check-up. She gave birth to a full-term boy via an uncomplicated vaginal delivery 3 weeks ago and has been exclusively breastfeeding her son. The hormone most responsible for promoting milk let-down during lactation in this new mother would lead to the greatest change in the level of which of the following factors?

IP3. ***IP3*** - The hormone responsible for milk let-down is **oxytocin**, which acts via **Gq protein-coupled receptors**. - Gq protein activation leads to the activation of **phospholipase C**, which hydrolyzes **PIP2** into **IP3** (inositol triphosphate) and DAG (diacylglycerol). IP3 then signals the release of intracellular calcium. *Ras* - **Ras** is a small GTPase involved in signal transduction pathways, typically associated with **receptor tyrosine kinases** and cell growth/differentiation, not primarily with oxytocin signaling for milk let-down. - It plays a role in the **MAP kinase pathway**, distinct from the Gq protein pathway activated by oxytocin. *Phospholipase A* - **Phospholipase A** enzymes (PLA1, PLA2, PLC, PLD) hydrolyze phospholipids, but **phospholipase A2** is primarily known for producing **arachidonic acid**, a precursor to prostaglandins and leukotrienes, which is not the main downstream effector of oxytocin. - While phospholipases are involved in lipid signaling, **phospholipase C** is the specific enzyme activated by oxytocin's Gq pathway leading to IP3 production. *cGMP* - **cGMP** (cyclic guanosine monophosphate) is a second messenger typically produced by **guanylyl cyclases** in response to nitric oxide or natriuretic peptides. - It is involved in processes like **vasodilation** and smooth muscle relaxation, distinct from the oxytocin pathway for milk ejection. *cAMP* - **cAMP** (cyclic adenosine monophosphate) is a common second messenger generated by **adenylyl cyclase** following activation of **Gs protein-coupled receptors**. - While important in many hormonal pathways, it is not the primary signaling molecule downstream of oxytocin's action on its receptors for milk let-down, which predominantly uses the Gq pathway.

Q: A 68-year-old man is brought to the emergency department 30 minutes after collapsing on the street. On arrival, he is obtunded. His pulse is 110/min and blood pressure is 250/120 mm Hg. A CT scan of the head shows an intracerebral hemorrhage involving bilateral thalamic nuclei and the third ventricle. Cortical detection of which of the following types of stimuli is most likely to remain unaffected in this patient?

Olfactory. ***Olfactory*** - The **olfactory pathway** is unique among sensory modalities as it is the only one that **bypasses the thalamus** and projects directly to the **olfactory cortex** (piriform cortex), which is not affected by the thalamic hemorrhage. - While the patient is obtunded, cortical detection of olfactory stimuli itself could theoretically remain intact if the relevant cortical areas are preserved. *Visual* - **Visual pathways** rely heavily on the **lateral geniculate nucleus (LGN)** of the thalamus for relaying information from the retina to the visual cortex. - Damage to the thalamus, especially in a hemorrhage affecting bilateral nuclei, would severely compromise visual processing. *Gustatory* - **Gustatory (taste) pathways** involve a relay in the **ventral posteromedial nucleus (VPM)** of the thalamus before projecting to the gustatory cortex. - A thalamic hemorrhage would therefore impair the transmission of taste information to the cortex. *Facial fine touch* - **Fine touch sensation from the face** is relayed through the **ventral posteromedial nucleus (VPM)** of the thalamus, which processes sensory input from the trigeminal system. - Bilateral thalamic hemorrhage would disrupt this somatosensory pathway, affecting detectable fine touch. *Proprioception* - **Proprioception**, the sense of body position and movement, is relayed primarily through the **ventral posterolateral nucleus (VPL)** of the thalamus. - Damage to the thalamus would significantly impair the transmission of proprioceptive information to the somatosensory cortex.

Q: A medical student volunteers for an experiment in the physiology laboratory. Before starting the experiment, her oral temperature is recorded as 36.9°C (98.4°F). She is then made to dip both her hands in a bowl containing ice cold water. She withdraws her hands out of the water, and finds that they look pale and feel very cold. Her oral temperature is recorded once more and is found to be 36.9°C (98.4°F) even though her hands are found to be 4.5°C (40.0°F). Which of the following mechanisms is responsible for the maintenance of her temperature throughout the experiment?

Cutaneous vasoconstriction. **Cutaneous vasoconstriction** - **Cutaneous vasoconstriction** reduces blood flow to the skin, minimizing heat loss from the core to the periphery and maintaining **core body temperature**. - The pale and cold hands indicate significant vasoconstriction, diverting blood away from the extremities to protect the more vital internal organs. *Shivering* - **Shivering** is a mechanism for generating heat through rapid, involuntary muscle contractions. - While it increases heat production, it would only be activated if the **core body temperature** began to drop, which did not happen in this scenario. *Muscular contraction* - **Muscular contraction** can generate heat, but it is typically a more generalized response to cold or a component of shivering. - In this localized cold exposure, other mechanisms are primarily responsible for maintaining the overall **core temperature**. *Diving reflex* - The **diving reflex** involves bradycardia, peripheral vasoconstriction, and blood redistribution to protect the brain and heart during submersion. - While it includes vasoconstriction, its primary trigger is face immersion in cold water (or apnea), and its systemic effects are more pronounced than what's described in this localized hand immersion. *Endogenous pyrogen release* - **Endogenous pyrogen release** leads to fever by resetting the hypothalamic thermoregulatory set point to a higher level. - This mechanism is associated with infection or inflammation and would cause a systemic increase in body temperature, not the maintenance of a normal temperature in response to localized cold.

Q: A 50-year-old man presents to the emergency department due to altered mental status. His symptoms began approximately two weeks prior to presentation where he complained of increasing fatigue, malaise, loss of appetite, and subjective fever. Vital signs are significant for a temperature of 102.0°F (38.9°C). On physical examination, there is a holosystolic murmur in the tricuspid area, linear non-blanching reddish lesions under the nails, and needle tracks on both antecubital fossa. A transthoracic echocardiogram shows a vegetation on the tricuspid valve. Blood cultures return positive for Staphylococcus aureus. A lumbar puncture is prompted due to altered mental status in the setting of fever; however, there is no bacteria found on cerebral spinal fluid (CSF) culture. Which of the following cell structures prevents the penetration of the bacteria into the CSF from his blood?

Tight junctions. ***Tight junctions*** - **Tight junctions** between endothelial cells of brain capillaries form the **blood-brain barrier**, restricting the passage of bacteria and other large molecules from the bloodstream into the cerebrospinal fluid. - While bacteria are present systemically (causing endocarditis), the integrity of these tight junctions prevents their entry into the central nervous system, explaining the **negative CSF culture**. *Hemidesmosomes* - **Hemidesmosomes** are cell junctions that anchor cells to the **basement membrane**, providing structural integrity to epithelial tissues. - They are not involved in controlling the permeability of the **blood-brain barrier** or preventing bacterial penetration into the CSF. *Capillary fenestrations* - **Capillary fenestrations** are pores in the endothelial cells of certain capillaries (e.g., kidneys, endocrine glands) that allow for rapid exchange of substances. - Brain capillaries, unlike these, are characterized by a **lack of fenestrations** as a key component of the blood-brain barrier, specifically to restrict molecular passage. *Desmosomes* - **Desmosomes** provide strong cell-to-cell adhesion by anchoring to intermediate filaments, commonly found in tissues subject to mechanical stress (e.g., skin, heart muscle). - They do not form a permeability barrier and are not a feature of the **blood-brain barrier** that prevents bacterial invasion. *Gap junctions* - **Gap junctions** are channels that allow direct passage of ions and small molecules between adjacent cells, facilitating intercellular communication. - They are not involved in regulating the passage of large entities like bacteria across a cellular barrier such as the **blood-brain barrier**.

Q: A 70-year-old man comes to the physician for evaluation of worsening nocturia, fatigue, and shortness of breath on exertion. While he used to be able to walk for 15 minutes at a time, he now has to pause every 5 minutes. Recently, he has started using two pillows to avoid waking up short of breath at night. He has a history of hypertension treated with daily amlodipine and prazosin; he has difficulty adhering to his medication regimen. His pulse is 75/min, and blood pressure is 150/90 mm Hg. Physical examination shows a laterally displaced apical heartbeat and 2+ bilateral pitting edema of the lower legs. Auscultation shows an S4 gallop and fine bibasilar rales. Further evaluation is most likely to show which of the following pathophysiologic changes in this patient?

Constriction of efferent renal arterioles. ***Constriction of efferent renal arterioles*** - The patient's symptoms (fatigue, shortness of breath on exertion, orthopnea, pitting edema, laterally displaced apical beat, S4 gallop, bibasilar rales) are consistent with **heart failure** secondary to uncontrolled hypertension. - In heart failure, decreased cardiac output leads to **renal hypoperfusion**, activating the **renin-angiotensin-aldosterone system (RAAS)**, which causes efferent arteriolar constriction to maintain glomerular filtration pressure. *Reduction of alveolar surface tension* - **Pulmonary edema**, indicated by bibasilar rales and orthopnea, leads to **increased alveolar surface tension** due to fluid accumulation diluting surfactant and interfering with its function. - A reduction in alveolar surface tension would make lung expansion easier, which is not the case here. *Increase in urinary bicarbonate excretion* - This patient's heart failure would lead to **decreased renal perfusion** and potential metabolic acidosis due to poor tissue oxygenation and lactic acid buildup. - The kidneys would typically respond by **retaining bicarbonate** to buffer the acidosis, not excreting it. *Retention of potassium* - In heart failure, activation of the RAAS leads to increased **aldosterone secretion**, which promotes sodium reabsorption and **potassium excretion** in the distal tubule. - This typically results in **hypokalemia**, not potassium retention. *Decrease in total peripheral vascular resistance* - In heart failure, the body compensates for reduced cardiac output by **increasing sympathetic tone** and activating the RAAS, both of which lead to **vasoconstriction** and increased total peripheral vascular resistance. - A decrease in total peripheral vascular resistance would worsen hypoperfusion and is not consistent with the elevated blood pressure of 150/90 mm Hg.

Q: A 32-year-old woman presents to the clinic with complaints of insomnia, diarrhea, anxiety, thinning hair, and diffuse muscle weakness. She has a family history of type 1 diabetes mellitus and thyroid cancer. She drinks 1–2 glasses of wine weekly. Her vital signs are unremarkable. On examination, you notice that she also has bilateral exophthalmos. Which of the following results would you expect to see on a thyroid panel?

Low TSH, high T4, high T3. ***Low TSH, high T4, high T3*** - The patient's symptoms (insomnia, diarrhea, anxiety, thinning hair, muscle weakness, and exophthalmos) are classic for **hyperthyroidism**, specifically **Graves' disease**. - In primary hyperthyroidism, the thyroid gland overproduces T4 and T3, leading to high levels of these hormones and a compensatory **suppression of TSH** due to negative feedback. *Low TSH, low T4, low T3* - This pattern is indicative of **central or secondary hypothyroidism**, where a problem with the pituitary gland prevents adequate TSH production, subsequently leading to low T4 and T3. - The patient's symptoms of hyperthyroidism (e.g., exophthalmos, anxiety, diarrhea) contradict this hormonal profile. *High TSH, high T4, high T3* - This combination is rare and suggests **TSH-secreting pituitary adenoma** (secondary hyperthyroidism) or resistance to thyroid hormone. - While it involves elevated thyroid hormones, the elevated TSH is a key differentiator from primary hyperthyroidism like Graves' disease. *High TSH, low T4, low T3* - This is the hallmark of **primary hypothyroidism**, where the thyroid gland is underactive and cannot produce enough T4 and T3, causing the pituitary to release more TSH in an attempt to stimulate it. - The patient's symptoms (e.g., insomnia, anxiety, diarrhea, exophthalmos) are directly opposite to those seen in hypothyroidism. *Normal TSH, high T4, high T3* - While it involves elevated thyroid hormones, a **normal TSH** with high T4/T3 is highly atypical for hyperthyroidism and would prompt suspicion of laboratory error or assay interference. - In true hyperthyroidism, TSH would virtually always be suppressed due to the negative feedback mechanism.

Q: You have been asked to deliver a lecture to medical students about the effects of various body hormones and neurotransmitters on the metabolism of glucose. Which of the following statements best describes the effects of sympathetic stimulation on glucose metabolism?

Epinephrine increases liver glycogenolysis.. ***Epinephrine increases liver glycogenolysis.*** - **Epinephrine**, released during sympathetic stimulation, primarily acts to increase **glucose availability** for immediate energy. - It achieves this by stimulating **glycogenolysis** (breakdown of glycogen into glucose) in the liver via **beta-adrenergic receptors**. *Norepinephrine causes increased glucose absorption within the intestines.* - **Norepinephrine** primarily causes **vasoconstriction** and can *decrease* **intestinal motility** and nutrient absorption due to shunting blood away from the digestive tract during stress. - Glucose absorption is mainly regulated by digestive enzymes and transport proteins, not directly increased by norepinephrine. *Without epinephrine, insulin cannot act on the liver.* - **Insulin** acts on the liver independent of epinephrine to promote **glucose uptake**, **glycogenesis**, and **lipid synthesis**. - Epinephrine and insulin have **antagonistic effects** on liver glucose metabolism; epinephrine increases glucose output, while insulin decreases it. *Peripheral tissues require epinephrine to take up glucose.* - **Insulin** is the primary hormone required for **glucose uptake** by most peripheral tissues, especially **muscle** and **adipose tissue**, via **GLUT4 transporters**. - Epinephrine generally *reduces* glucose uptake by peripheral tissues to preserve glucose for the brain during stress. *Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.* - Sympathetic stimulation, primarily acting through **alpha-2 adrenergic receptors** on pancreatic beta cells, actually **inhibits** **insulin secretion**. - This inhibition helps to increase blood glucose levels by reducing insulin's glucose-lowering effects.

A 33-year-old woman presents to her physician's office for a postpartum check-up. She gave birth to a full-term boy via an uncomplicated vaginal delivery 3 weeks ago and has been exclusively breastfeeding her son. The hormone most responsible for promoting milk let-down during lactation in this new mother would lead to the greatest change in the level of which of the following factors?

A 68-year-old man is brought to the emergency department 30 minutes after collapsing on the street. On arrival, he is obtunded. His pulse is 110/min and blood pressure is 250/120 mm Hg. A CT scan of the head shows an intracerebral hemorrhage involving bilateral thalamic nuclei and the third ventricle. Cortical detection of which of the following types of stimuli is most likely to remain unaffected in this patient?

A medical student volunteers for an experiment in the physiology laboratory. Before starting the experiment, her oral temperature is recorded as 36.9°C (98.4°F). She is then made to dip both her hands in a bowl containing ice cold water. She withdraws her hands out of the water, and finds that they look pale and feel very cold. Her oral temperature is recorded once more and is found to be 36.9°C (98.4°F) even though her hands are found to be 4.5°C (40.0°F). Which of the following mechanisms is responsible for the maintenance of her temperature throughout the experiment?

A previously healthy 35-year-old woman comes to the physician because of palpitations and anxiety for the past 2 months. She has had a 3.1-kg (7-lb) weight loss in this period. Her pulse is 112/min. Cardiac examination shows normal heart sounds with a regular rhythm. Neurologic examination shows a fine resting tremor of the hands; patellar reflexes are 3+ bilaterally with a shortened relaxation phase. Urine pregnancy test is negative. Which of the following sets of laboratory values is most likely on evaluation of blood obtained before treatment? | TSH | Free T4 | Free T3 | Thyroxine-binding globulin |

A 50-year-old man presents to the emergency department due to altered mental status. His symptoms began approximately two weeks prior to presentation where he complained of increasing fatigue, malaise, loss of appetite, and subjective fever. Vital signs are significant for a temperature of 102.0°F (38.9°C). On physical examination, there is a holosystolic murmur in the tricuspid area, linear non-blanching reddish lesions under the nails, and needle tracks on both antecubital fossa. A transthoracic echocardiogram shows a vegetation on the tricuspid valve. Blood cultures return positive for Staphylococcus aureus. A lumbar puncture is prompted due to altered mental status in the setting of fever; however, there is no bacteria found on cerebral spinal fluid (CSF) culture. Which of the following cell structures prevents the penetration of the bacteria into the CSF from his blood?

A 70-year-old man comes to the physician for evaluation of worsening nocturia, fatigue, and shortness of breath on exertion. While he used to be able to walk for 15 minutes at a time, he now has to pause every 5 minutes. Recently, he has started using two pillows to avoid waking up short of breath at night. He has a history of hypertension treated with daily amlodipine and prazosin; he has difficulty adhering to his medication regimen. His pulse is 75/min, and blood pressure is 150/90 mm Hg. Physical examination shows a laterally displaced apical heartbeat and 2+ bilateral pitting edema of the lower legs. Auscultation shows an S4 gallop and fine bibasilar rales. Further evaluation is most likely to show which of the following pathophysiologic changes in this patient?

A 32-year-old woman presents to the clinic with complaints of insomnia, diarrhea, anxiety, thinning hair, and diffuse muscle weakness. She has a family history of type 1 diabetes mellitus and thyroid cancer. She drinks 1–2 glasses of wine weekly. Her vital signs are unremarkable. On examination, you notice that she also has bilateral exophthalmos. Which of the following results would you expect to see on a thyroid panel?

A 60-year-old obese man comes to the emergency department with tightness in his chest and lower extremity edema. He has a history of heart failure that has gotten worse over the last several years. He takes finasteride, lisinopril, and albuterol. He does not use oxygen at home. He has mildly elevated blood pressure, and he is tachycardic and tachypneic. Physical examination shows an overweight man having difficulty speaking with 2+ pitting edema on his lower extremities up to his thighs. The attending asks you to chart out the patient's theoretical cardiac function curve from where it was 5 years ago when he was healthy to where it is right now. What changes occurred in the last several years without compensation?

You have been asked to deliver a lecture to medical students about the effects of various body hormones and neurotransmitters on the metabolism of glucose. Which of the following statements best describes the effects of sympathetic stimulation on glucose metabolism?

Q10

A 12-year-old girl is brought to the emergency department 3 hours after the sudden onset of colicky abdominal pain and vomiting. She also has redness and swelling of the face and lips without pruritus. Her symptoms began following a tooth extraction earlier this morning. She had a similar episode of facial swelling after a bicycle accident 1 year ago which resolved within 48 hours without treatment. Vital signs are within normal limits. Examination shows a nontender facial edema, erythema of the oral mucosa, and an enlarged tongue. The abdomen is soft and there is tenderness to palpation over the lower quadrants. An abdominal ultrasound shows segmental thickening of the intestinal wall. Which of the following is the most likely cause of this patient's condition?

Cardiovascular US Medical PG Practice Questions and MCQs

Question 1: A 33-year-old woman presents to her physician's office for a postpartum check-up. She gave birth to a full-term boy via an uncomplicated vaginal delivery 3 weeks ago and has been exclusively breastfeeding her son. The hormone most responsible for promoting milk let-down during lactation in this new mother would lead to the greatest change in the level of which of the following factors?

A. Ras
B. Phospholipase A
C. cGMP
D. cAMP
E. IP3 (Correct Answer)

Explanation: ***IP3*** - The hormone responsible for milk let-down is **oxytocin**, which acts via **Gq protein-coupled receptors**. - Gq protein activation leads to the activation of **phospholipase C**, which hydrolyzes **PIP2** into **IP3** (inositol triphosphate) and DAG (diacylglycerol). IP3 then signals the release of intracellular calcium. *Ras* - **Ras** is a small GTPase involved in signal transduction pathways, typically associated with **receptor tyrosine kinases** and cell growth/differentiation, not primarily with oxytocin signaling for milk let-down. - It plays a role in the **MAP kinase pathway**, distinct from the Gq protein pathway activated by oxytocin. *Phospholipase A* - **Phospholipase A** enzymes (PLA1, PLA2, PLC, PLD) hydrolyze phospholipids, but **phospholipase A2** is primarily known for producing **arachidonic acid**, a precursor to prostaglandins and leukotrienes, which is not the main downstream effector of oxytocin. - While phospholipases are involved in lipid signaling, **phospholipase C** is the specific enzyme activated by oxytocin's Gq pathway leading to IP3 production. *cGMP* - **cGMP** (cyclic guanosine monophosphate) is a second messenger typically produced by **guanylyl cyclases** in response to nitric oxide or natriuretic peptides. - It is involved in processes like **vasodilation** and smooth muscle relaxation, distinct from the oxytocin pathway for milk ejection. *cAMP* - **cAMP** (cyclic adenosine monophosphate) is a common second messenger generated by **adenylyl cyclase** following activation of **Gs protein-coupled receptors**. - While important in many hormonal pathways, it is not the primary signaling molecule downstream of oxytocin's action on its receptors for milk let-down, which predominantly uses the Gq pathway.

Question 2: A 68-year-old man is brought to the emergency department 30 minutes after collapsing on the street. On arrival, he is obtunded. His pulse is 110/min and blood pressure is 250/120 mm Hg. A CT scan of the head shows an intracerebral hemorrhage involving bilateral thalamic nuclei and the third ventricle. Cortical detection of which of the following types of stimuli is most likely to remain unaffected in this patient?

A. Visual
B. Gustatory
C. Facial fine touch
D. Proprioception
E. Olfactory (Correct Answer)

Explanation: ***Olfactory*** - The **olfactory pathway** is unique among sensory modalities as it is the only one that **bypasses the thalamus** and projects directly to the **olfactory cortex** (piriform cortex), which is not affected by the thalamic hemorrhage. - While the patient is obtunded, cortical detection of olfactory stimuli itself could theoretically remain intact if the relevant cortical areas are preserved. *Visual* - **Visual pathways** rely heavily on the **lateral geniculate nucleus (LGN)** of the thalamus for relaying information from the retina to the visual cortex. - Damage to the thalamus, especially in a hemorrhage affecting bilateral nuclei, would severely compromise visual processing. *Gustatory* - **Gustatory (taste) pathways** involve a relay in the **ventral posteromedial nucleus (VPM)** of the thalamus before projecting to the gustatory cortex. - A thalamic hemorrhage would therefore impair the transmission of taste information to the cortex. *Facial fine touch* - **Fine touch sensation from the face** is relayed through the **ventral posteromedial nucleus (VPM)** of the thalamus, which processes sensory input from the trigeminal system. - Bilateral thalamic hemorrhage would disrupt this somatosensory pathway, affecting detectable fine touch. *Proprioception* - **Proprioception**, the sense of body position and movement, is relayed primarily through the **ventral posterolateral nucleus (VPL)** of the thalamus. - Damage to the thalamus would significantly impair the transmission of proprioceptive information to the somatosensory cortex.

Question 3: A medical student volunteers for an experiment in the physiology laboratory. Before starting the experiment, her oral temperature is recorded as 36.9°C (98.4°F). She is then made to dip both her hands in a bowl containing ice cold water. She withdraws her hands out of the water, and finds that they look pale and feel very cold. Her oral temperature is recorded once more and is found to be 36.9°C (98.4°F) even though her hands are found to be 4.5°C (40.0°F). Which of the following mechanisms is responsible for the maintenance of her temperature throughout the experiment?

A. Shivering
B. Muscular contraction
C. Cutaneous vasoconstriction (Correct Answer)
D. Diving reflex
E. Endogenous pyrogen release

Explanation: **Cutaneous vasoconstriction** - **Cutaneous vasoconstriction** reduces blood flow to the skin, minimizing heat loss from the core to the periphery and maintaining **core body temperature**. - The pale and cold hands indicate significant vasoconstriction, diverting blood away from the extremities to protect the more vital internal organs. *Shivering* - **Shivering** is a mechanism for generating heat through rapid, involuntary muscle contractions. - While it increases heat production, it would only be activated if the **core body temperature** began to drop, which did not happen in this scenario. *Muscular contraction* - **Muscular contraction** can generate heat, but it is typically a more generalized response to cold or a component of shivering. - In this localized cold exposure, other mechanisms are primarily responsible for maintaining the overall **core temperature**. *Diving reflex* - The **diving reflex** involves bradycardia, peripheral vasoconstriction, and blood redistribution to protect the brain and heart during submersion. - While it includes vasoconstriction, its primary trigger is face immersion in cold water (or apnea), and its systemic effects are more pronounced than what's described in this localized hand immersion. *Endogenous pyrogen release* - **Endogenous pyrogen release** leads to fever by resetting the hypothalamic thermoregulatory set point to a higher level. - This mechanism is associated with infection or inflammation and would cause a systemic increase in body temperature, not the maintenance of a normal temperature in response to localized cold.

Question 4: A previously healthy 35-year-old woman comes to the physician because of palpitations and anxiety for the past 2 months. She has had a 3.1-kg (7-lb) weight loss in this period. Her pulse is 112/min. Cardiac examination shows normal heart sounds with a regular rhythm. Neurologic examination shows a fine resting tremor of the hands; patellar reflexes are 3+ bilaterally with a shortened relaxation phase. Urine pregnancy test is negative. Which of the following sets of laboratory values is most likely on evaluation of blood obtained before treatment? | TSH | Free T4 | Free T3 | Thyroxine-binding globulin |

A. ↓ ↑ ↑ normal (Correct Answer)
B. ↑ ↓ ↓ ↓
C. ↓ ↓ ↓ normal
D. ↑ normal normal normal
E. ↓ ↑ normal ↑

Explanation: ***↓ ↑ ↑ normal*** - The patient presents with classic symptoms of **hyperthyroidism**, including palpitations, anxiety, weight loss, tachycardia, and a fine resting tremor. These symptoms are consistent with an **elevated metabolic state** caused by excess thyroid hormones. - In primary hyperthyroidism, the thyroid gland overproduces T4 and T3, leading to **high levels of free T3 and free T4**. This increased feedback inhibits the pituitary, causing a **decreased TSH** level. Thyroxine-binding globulin (TBG) levels are typically normal in uncomplicated hyperthyroidism. *↑ ↓ ↓ ↓* - This pattern of laboratory values (high TSH, low free T4, low free T3) is characteristic of **primary hypothyroidism**, where the thyroid gland is underactive and fails to produce sufficient thyroid hormones. This directly contradicts the patient's hyperthyroid symptoms. - A low TBG level can occur in conditions like severe liver disease or nephrotic syndrome, but it does not align with the patient's clinical presentation of hyperthyroidism. *↓ ↓ ↓ normal* - While a low TSH is consistent with hyperthyroidism, low free T4 and free T3 levels signify **hypothyroidism**. This combination would suggest **secondary or central hypothyroidism**, where the pituitary gland is not stimulating the thyroid sufficiently. - This scenario would present with symptoms of hypometabolism (e.g., fatigue, weight gain, bradycardia), which are antithetical to the patient's symptoms. *↑ normal normal normal* - A high TSH with normal free T4 and free T3 levels suggests **subclinical hypothyroidism**, where the thyroid gland is beginning to fail, but peripheral hormone levels are still within the normal range. - This pattern does not explain the pronounced hyperthyroid symptoms experienced by the patient, which point to significantly elevated thyroid hormone levels. *↓ ↑ normal ↑* - This option presents a low TSH and high free T4, which is consistent with hyperthyroidism. However, a **normal free T3** would be unusual in overt hyperthyroidism, as both T3 and T4 are typically elevated. - An elevated **TBG** is often seen in conditions like pregnancy or estrogen therapy, which would increase total T4 but usually result in normal free T4. This pattern does not fully align with the patient's clinical picture of active hyperthyroidism.

Question 5: A 50-year-old man presents to the emergency department due to altered mental status. His symptoms began approximately two weeks prior to presentation where he complained of increasing fatigue, malaise, loss of appetite, and subjective fever. Vital signs are significant for a temperature of 102.0°F (38.9°C). On physical examination, there is a holosystolic murmur in the tricuspid area, linear non-blanching reddish lesions under the nails, and needle tracks on both antecubital fossa. A transthoracic echocardiogram shows a vegetation on the tricuspid valve. Blood cultures return positive for Staphylococcus aureus. A lumbar puncture is prompted due to altered mental status in the setting of fever; however, there is no bacteria found on cerebral spinal fluid (CSF) culture. Which of the following cell structures prevents the penetration of the bacteria into the CSF from his blood?

A. Hemidesmosomes
B. Capillary fenestrations
C. Tight junctions (Correct Answer)
D. Desmosomes
E. Gap junctions

Explanation: ***Tight junctions*** - **Tight junctions** between endothelial cells of brain capillaries form the **blood-brain barrier**, restricting the passage of bacteria and other large molecules from the bloodstream into the cerebrospinal fluid. - While bacteria are present systemically (causing endocarditis), the integrity of these tight junctions prevents their entry into the central nervous system, explaining the **negative CSF culture**. *Hemidesmosomes* - **Hemidesmosomes** are cell junctions that anchor cells to the **basement membrane**, providing structural integrity to epithelial tissues. - They are not involved in controlling the permeability of the **blood-brain barrier** or preventing bacterial penetration into the CSF. *Capillary fenestrations* - **Capillary fenestrations** are pores in the endothelial cells of certain capillaries (e.g., kidneys, endocrine glands) that allow for rapid exchange of substances. - Brain capillaries, unlike these, are characterized by a **lack of fenestrations** as a key component of the blood-brain barrier, specifically to restrict molecular passage. *Desmosomes* - **Desmosomes** provide strong cell-to-cell adhesion by anchoring to intermediate filaments, commonly found in tissues subject to mechanical stress (e.g., skin, heart muscle). - They do not form a permeability barrier and are not a feature of the **blood-brain barrier** that prevents bacterial invasion. *Gap junctions* - **Gap junctions** are channels that allow direct passage of ions and small molecules between adjacent cells, facilitating intercellular communication. - They are not involved in regulating the passage of large entities like bacteria across a cellular barrier such as the **blood-brain barrier**.

Question 6: A 70-year-old man comes to the physician for evaluation of worsening nocturia, fatigue, and shortness of breath on exertion. While he used to be able to walk for 15 minutes at a time, he now has to pause every 5 minutes. Recently, he has started using two pillows to avoid waking up short of breath at night. He has a history of hypertension treated with daily amlodipine and prazosin; he has difficulty adhering to his medication regimen. His pulse is 75/min, and blood pressure is 150/90 mm Hg. Physical examination shows a laterally displaced apical heartbeat and 2+ bilateral pitting edema of the lower legs. Auscultation shows an S4 gallop and fine bibasilar rales. Further evaluation is most likely to show which of the following pathophysiologic changes in this patient?

A. Reduction of alveolar surface tension
B. Constriction of efferent renal arterioles (Correct Answer)
C. Increase in urinary bicarbonate excretion
D. Retention of potassium
E. Decrease in total peripheral vascular resistance

Explanation: ***Constriction of efferent renal arterioles*** - The patient's symptoms (fatigue, shortness of breath on exertion, orthopnea, pitting edema, laterally displaced apical beat, S4 gallop, bibasilar rales) are consistent with **heart failure** secondary to uncontrolled hypertension. - In heart failure, decreased cardiac output leads to **renal hypoperfusion**, activating the **renin-angiotensin-aldosterone system (RAAS)**, which causes efferent arteriolar constriction to maintain glomerular filtration pressure. *Reduction of alveolar surface tension* - **Pulmonary edema**, indicated by bibasilar rales and orthopnea, leads to **increased alveolar surface tension** due to fluid accumulation diluting surfactant and interfering with its function. - A reduction in alveolar surface tension would make lung expansion easier, which is not the case here. *Increase in urinary bicarbonate excretion* - This patient's heart failure would lead to **decreased renal perfusion** and potential metabolic acidosis due to poor tissue oxygenation and lactic acid buildup. - The kidneys would typically respond by **retaining bicarbonate** to buffer the acidosis, not excreting it. *Retention of potassium* - In heart failure, activation of the RAAS leads to increased **aldosterone secretion**, which promotes sodium reabsorption and **potassium excretion** in the distal tubule. - This typically results in **hypokalemia**, not potassium retention. *Decrease in total peripheral vascular resistance* - In heart failure, the body compensates for reduced cardiac output by **increasing sympathetic tone** and activating the RAAS, both of which lead to **vasoconstriction** and increased total peripheral vascular resistance. - A decrease in total peripheral vascular resistance would worsen hypoperfusion and is not consistent with the elevated blood pressure of 150/90 mm Hg.

Question 7: A 32-year-old woman presents to the clinic with complaints of insomnia, diarrhea, anxiety, thinning hair, and diffuse muscle weakness. She has a family history of type 1 diabetes mellitus and thyroid cancer. She drinks 1–2 glasses of wine weekly. Her vital signs are unremarkable. On examination, you notice that she also has bilateral exophthalmos. Which of the following results would you expect to see on a thyroid panel?

A. Low TSH, low T4, low T3
B. High TSH, high T4, high T3
C. Low TSH, high T4, high T3 (Correct Answer)
D. High TSH, low T4, low T3
E. Normal TSH, high T4, high T3

Explanation: ***Low TSH, high T4, high T3*** - The patient's symptoms (insomnia, diarrhea, anxiety, thinning hair, muscle weakness, and exophthalmos) are classic for **hyperthyroidism**, specifically **Graves' disease**. - In primary hyperthyroidism, the thyroid gland overproduces T4 and T3, leading to high levels of these hormones and a compensatory **suppression of TSH** due to negative feedback. *Low TSH, low T4, low T3* - This pattern is indicative of **central or secondary hypothyroidism**, where a problem with the pituitary gland prevents adequate TSH production, subsequently leading to low T4 and T3. - The patient's symptoms of hyperthyroidism (e.g., exophthalmos, anxiety, diarrhea) contradict this hormonal profile. *High TSH, high T4, high T3* - This combination is rare and suggests **TSH-secreting pituitary adenoma** (secondary hyperthyroidism) or resistance to thyroid hormone. - While it involves elevated thyroid hormones, the elevated TSH is a key differentiator from primary hyperthyroidism like Graves' disease. *High TSH, low T4, low T3* - This is the hallmark of **primary hypothyroidism**, where the thyroid gland is underactive and cannot produce enough T4 and T3, causing the pituitary to release more TSH in an attempt to stimulate it. - The patient's symptoms (e.g., insomnia, anxiety, diarrhea, exophthalmos) are directly opposite to those seen in hypothyroidism. *Normal TSH, high T4, high T3* - While it involves elevated thyroid hormones, a **normal TSH** with high T4/T3 is highly atypical for hyperthyroidism and would prompt suspicion of laboratory error or assay interference. - In true hyperthyroidism, TSH would virtually always be suppressed due to the negative feedback mechanism.

Question 8: A 60-year-old obese man comes to the emergency department with tightness in his chest and lower extremity edema. He has a history of heart failure that has gotten worse over the last several years. He takes finasteride, lisinopril, and albuterol. He does not use oxygen at home. He has mildly elevated blood pressure, and he is tachycardic and tachypneic. Physical examination shows an overweight man having difficulty speaking with 2+ pitting edema on his lower extremities up to his thighs. The attending asks you to chart out the patient's theoretical cardiac function curve from where it was 5 years ago when he was healthy to where it is right now. What changes occurred in the last several years without compensation?

A. Cardiac output went up, and right atrial pressure went down
B. Cardiac output went down, and right atrial pressure went down
C. Cardiac output went up, and right atrial pressure went up
D. Cardiac output went down, and right atrial pressure went up (Correct Answer)
E. Both cardiac output and right atrial pressures are unchanged

Explanation: ***Cardiac output went down, and right atrial pressure went up*** - In **uncompensated heart failure**, the heart's pumping efficiency decreases, leading to a **reduced cardiac output** as the cardiac function curve shifts downward. - The inability to pump blood forward effectively causes blood to back up in the venous system, increasing **venous pressure** and, consequently, **right atrial pressure**, shifting the curve to the right. - This represents the **Frank-Starling relationship without compensatory mechanisms** such as sympathetic activation, fluid retention, or cardiac remodeling. *Cardiac output went up, and right atrial pressure went down* - An **increased cardiac output** with a **decreased right atrial pressure** would suggest improved cardiac function, which is contrary to the patient's worsening heart failure symptoms. - This scenario would typically be seen in states of increased demand with good cardiac reserve, not decompensated heart failure. *Cardiac output went down, and right atrial pressure went down* - While **cardiac output decreases** in heart failure, **right atrial pressure typically increases** due to backward pressure from circulatory congestion. - A decrease in both would be unusual in this context and might suggest conditions like **hypovolemia**, which is not indicated by the patient's significant edema. *Cardiac output went up, and right atrial pressure went up* - An **increased cardiac output** is inconsistent with the progression of **heart failure**, which is characterized by a decline in the heart's ability to pump. - While right atrial pressure would be elevated, the upward trend in cardiac output would indicate a different physiological state, perhaps a high-output heart failure, but the overall clinical picture suggests a low-output state. *Both cardiac output and right atrial pressures are unchanged* - The patient's presentation with worsening chest tightness and lower extremity edema clearly indicates a **deterioration in cardiac function**, meaning changes in cardiac output and right atrial pressure must have occurred. - Unchanged parameters would imply a stable condition, which is not the case for this patient with progressive heart failure.

Question 9: You have been asked to deliver a lecture to medical students about the effects of various body hormones and neurotransmitters on the metabolism of glucose. Which of the following statements best describes the effects of sympathetic stimulation on glucose metabolism?

A. Norepinephrine causes increased glucose absorption within the intestines.
B. Without epinephrine, insulin cannot act on the liver.
C. Peripheral tissues require epinephrine to take up glucose.
D. Epinephrine increases liver glycogenolysis. (Correct Answer)
E. Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.

Explanation: ***Epinephrine increases liver glycogenolysis.*** - **Epinephrine**, released during sympathetic stimulation, primarily acts to increase **glucose availability** for immediate energy. - It achieves this by stimulating **glycogenolysis** (breakdown of glycogen into glucose) in the liver via **beta-adrenergic receptors**. *Norepinephrine causes increased glucose absorption within the intestines.* - **Norepinephrine** primarily causes **vasoconstriction** and can *decrease* **intestinal motility** and nutrient absorption due to shunting blood away from the digestive tract during stress. - Glucose absorption is mainly regulated by digestive enzymes and transport proteins, not directly increased by norepinephrine. *Without epinephrine, insulin cannot act on the liver.* - **Insulin** acts on the liver independent of epinephrine to promote **glucose uptake**, **glycogenesis**, and **lipid synthesis**. - Epinephrine and insulin have **antagonistic effects** on liver glucose metabolism; epinephrine increases glucose output, while insulin decreases it. *Peripheral tissues require epinephrine to take up glucose.* - **Insulin** is the primary hormone required for **glucose uptake** by most peripheral tissues, especially **muscle** and **adipose tissue**, via **GLUT4 transporters**. - Epinephrine generally *reduces* glucose uptake by peripheral tissues to preserve glucose for the brain during stress. *Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.* - Sympathetic stimulation, primarily acting through **alpha-2 adrenergic receptors** on pancreatic beta cells, actually **inhibits** **insulin secretion**. - This inhibition helps to increase blood glucose levels by reducing insulin's glucose-lowering effects.

Question 10: A 12-year-old girl is brought to the emergency department 3 hours after the sudden onset of colicky abdominal pain and vomiting. She also has redness and swelling of the face and lips without pruritus. Her symptoms began following a tooth extraction earlier this morning. She had a similar episode of facial swelling after a bicycle accident 1 year ago which resolved within 48 hours without treatment. Vital signs are within normal limits. Examination shows a nontender facial edema, erythema of the oral mucosa, and an enlarged tongue. The abdomen is soft and there is tenderness to palpation over the lower quadrants. An abdominal ultrasound shows segmental thickening of the intestinal wall. Which of the following is the most likely cause of this patient's condition?

A. T-cell mediated immune reaction
B. Drug-induced bradykinin excess
C. Leukotriene overproduction
D. Immune-complex deposition
E. Complement inhibitor deficiency (Correct Answer)

Explanation: ***Complement inhibitor deficiency*** - This patient's presentation with recurrent episodes of **angioedema** (face and lip swelling, enlarged tongue, intestinal wall thickening causing abdominal pain), particularly triggered by **trauma** (tooth extraction, bicycle accident), strongly suggests **hereditary angioedema (HAE)**. HAE is caused by a deficiency or dysfunction of **C1 esterase inhibitor**, a key complement inhibitor. - A deficiency in C1 esterase inhibitor leads to uncontrolled activation of both the **complement cascade** and the **kallikrein-bradykinin pathway**, resulting in excessive **bradykinin production**, which causes increased vascular permeability and localized edema without urticaria or pruritus. *T-cell mediated immune reaction* - **T-cell mediated reactions** are typically associated with **delayed-type hypersensitivity reactions** (e.g., contact dermatitis, graft rejection) and **autoimmune disorders**, which do not fit the acute, recurrent, non-pruritic angioedema seen here. - These reactions primarily involve cell-mediated cytotoxicity or cytokine release, rather than rapid fluid extravasation due to bradykinin excess. *Drug-induced bradykinin excess* - While drug-induced angioedema (e.g., from **ACE inhibitors**) can also cause bradykinin excess, this patient's history of episodes since childhood (after a bicycle accident) and the current exacerbation after a tooth extraction, makes a **hereditary predisposition** much more likely than an isolated drug reaction in a 12-year-old. - The triggers (trauma, dental procedure) are classic for HAE, which involves an intrinsic defect in bradykinin regulation, not merely an external pharmaceutical cause. *Leukotriene overproduction* - **Leukotrienes** are potent mediators involved in **allergic reactions** and **asthma**, contributing to bronchoconstriction, vascular permeability, and inflammation. - Conditions involving leukotriene overproduction, such as aspirin-exacerbated respiratory disease, typically present with bronchospasm, rhinitis, or urticaria, which are not the primary features here. *Immune-complex deposition* - **Immune-complex deposition** is characteristic of conditions like **serum sickness**, **lupus nephritis**, or **vasculitis**, leading to inflammation, fever, rash, and organ damage. - These conditions do not typically present with isolated, recurrent, non-pruritic angioedema and do not involve the specific mechanism of bradykinin overproduction seen in this patient.

Question 11: A 49-year-old male complains of heartburn, epigastric pain, and diarrhea. He has a past medical history significant for heartburn that is nonresponsive to omeprazole. He denies any alcohol intake, and has not been taking any nonsteroidal anti-inflammatory drugs. An endoscopy is performed, which shows two ulcers in the proximal duodenum, and one in the distal third of the duodenum. Which of the following is most likely true about this patient’s current condition?

A. Chronic atrophic gastritis would decrease the suspected hormone level
B. Secretin administration would suppress the release of the suspected hormone in this patient
C. Parietal cell hypertrophy is likely present (Correct Answer)
D. The suspected hormone acts via a receptor tyrosine kinase signaling pathway
E. Increasing omeprazole dose will likely decrease the suspected hormone level

Explanation: ***Parietal cell hypertrophy is likely present*** - The patient's symptoms (refractory heartburn, epigastric pain, diarrhea, and multiple duodenal ulcers, including distal ones) are highly suggestive of **Zollinger-Ellison syndrome (ZES)**, caused by a gastrinoma. - **Gastrinomas** overproduce gastrin, which leads to **parietal cell hyperplasia and hypertrophy** due to its trophic effects and excessive acid secretion. This results in the observed multiple, refractory ulcers. *Chronic atrophic gastritis would decrease the suspected hormone level* - **Chronic atrophic gastritis** typically causes a *decrease* in gastric acid production due to glandular atrophy and loss of parietal cells. - This reduction in acid secretion would lead to an *increase* in gastrin release as a feedback mechanism, trying to stimulate acid production, not a decrease. *Secretin administration would suppress the release of the suspected hormone in this patient* - In healthy individuals, **secretin** *inhibits* gastrin release from G cells, but in patients with **gastrinomas**, secretin paradoxically *stimulates* gastrin release. - A positive secretin stimulation test (rise in gastrin levels after secretin administration) is a diagnostic hallmark for gastrinoma. *The suspected hormone acts via a receptor tyrosine kinase signaling pathway* - The suspected hormone, **gastrin**, exerts its effects primarily by binding to the **cholecystokinin B (CCK2) receptor**, which is a **G protein-coupled receptor (GPCR)**. - Activation of this GPCR leads to increased intracellular calcium and protein kinase C activity, not a receptor tyrosine kinase pathway. *Increasing omeprazole dose will likely decrease the suspected hormone level* - While omeprazole *reduces acid secretion* and may alleviate symptoms, it does so by inhibiting the proton pump in parietal cells. - Reducing acid output through omeprazole would *increase* gastrin release via a feedback loop, as the body tries to compensate for the perceived lack of acid, rather than decreasing gastrin levels in ZES patients.

Question 12: Twenty minutes after delivery of a newborn infant, a 22-year-old woman starts breastfeeding. Initially, the expressed milk is thick and yellowish. Three days later, the mother's breasts swell and the expressed milk becomes thinner and whiter. A decrease in maternal serum concentration of which of the following is most likely responsible for the observed changes in milk production?

A. Human chorionic gonadotropin
B. Oxytocin
C. Thyroxine
D. Progesterone (Correct Answer)
E. Estrogen

Explanation: ***Progesterone*** - The drop in **progesterone** levels after birth removes its inhibitory effect on **milk production**, allowing for the transition from **colostrum** to **mature milk**. - High levels of **progesterone** during pregnancy inhibit the full effects of **prolactin** on the mammary glands, preventing lactation (lactogenesis II). - After placental delivery, the dramatic fall in progesterone allows prolactin to stimulate copious milk secretion, typically occurring around day 3-5 postpartum. *Human chorionic gonadotropin* - **hCG** maintains the corpus luteum during early pregnancy but is not directly involved in the regulation of postpartum milk production. - Its levels decrease significantly after delivery, but this decrease is not the primary driver of milk changes. *Oxytocin* - **Oxytocin** is responsible for **milk ejection (let-down)**, not milk production or changes in milk composition. - Its levels tend to increase during breastfeeding due to suckling, rather than decrease. *Thyroxine* - **Thyroxine** (thyroid hormones) is essential for overall metabolism and can affect milk supply, but a decrease in its levels is not primarily responsible for the switch from colostrum to mature milk. - Decreased thyroxine would more likely lead to *reduced* milk production or broader metabolic disturbances. *Estrogen* - **Estrogen** levels decrease significantly after delivery, similar to progesterone, but progesterone's inhibitory effect on lactation is more direct and critical for the transition in milk type. - While high estrogen during pregnancy also inhibits lactation, the removal of progesterone's block is the key trigger for copious milk secretion.

Question 13: A 55-year-old woman has a total thyroidectomy for papillary thyroid carcinoma. She complains of tingling around the mouth 11 hours after the operation. Her condition rapidly deteriorates with difficulty breathing and chest tightness. Which of the following best represent the signaling pathway of the deficient hormone responsible for this patient’s symptoms?

A. Cyclic guanosine monophosphate (cGMP)
B. Cyclic adenosine monophosphate (cAMP) (Correct Answer)
C. Intracellular receptors
D. Receptor tyrosine kinase
E. Inositol trisphosphate (IP3)

Explanation: ***Cyclic adenosine monophosphate (cAMP)*** - The patient's symptoms of perioral tingling, difficulty breathing, and chest tightness after total thyroidectomy suggest **hypocalcemia**, likely due to accidental removal or damage to the **parathyroid glands** during surgery. - The deficient **parathyroid hormone (PTH)** acts primarily through the **cAMP second messenger system** to increase serum calcium levels. *Cyclic guanosine monophosphate (cGMP)* - **cGMP** is a second messenger system primarily involved in mediating the effects of hormones like **atrial natriuretic peptide (ANP)** and **nitric oxide**, which are unrelated to calcium homeostasis and parathyroid function. - This pathway is not the primary mechanism of action for **PTH**. *Intracellular receptors* - **Intracellular receptors** are typically used by **steroid hormones** (e.g., cortisol, estrogen) and **thyroid hormones**, which are lipid-soluble and can cross the cell membrane. - **PTH** is a peptide hormone and acts on cell surface receptors. *Receptor tyrosine kinase* - **Receptor tyrosine kinases (RTKs)** are transmembrane receptors involved in signaling pathways for hormones like **insulin** and **growth factors**, promoting cell growth, differentiation, and metabolism. - This is not the primary signaling pathway for **PTH**. *Inositol trisphosphate (IP3)* - The **IP3/DAG (diacylglycerol)** pathway is another common second messenger system used by various hormones (e.g., **vasopressin, oxytocin, TRH**), leading to the release of intracellular calcium. - While it involves calcium signaling, it is not the primary or most characteristic pathway for **PTH** action, which predominantly utilizes **cAMP**.

Question 14: A 28-year-old female comes to the emergency department complaining of heart palpitations. She has had multiple episodes of these in the past few months. She has found that if she wears tight clothing then sometimes these episodes will stop spontaneously. On presentation to the ED, she feels like her heart is pounding and reports feeling nauseous. She appears mildly diaphoretic. Her blood pressure is 125/75 mmHg, pulse is 180/min, and respirations are 22/min with an O2 saturation of 99% on room air. A neck maneuver is performed and her pulse returns to 90/min with improvement of her symptoms. Stimulation of afferent fibers from which nerve are most responsible for the resolution of her symptoms?

A. Facial
B. Hypoglossal
C. Glossopharyngeal (Correct Answer)
D. Trigeminal
E. Vagus

Explanation: ***Glossopharyngeal*** - The question specifically asks about **afferent fibers** responsible for the resolution of symptoms during the neck maneuver (carotid sinus massage). - The **glossopharyngeal nerve (cranial nerve IX)** provides the **afferent (sensory) limb** of the baroreflex by carrying signals from **baroreceptors in the carotid sinus** to the nucleus tractus solitarius in the medulla. - When the carotid sinus is massaged, baroreceptors are stimulated → afferent signals travel via **CN IX** → medullary cardiovascular centers → efferent vagal output → heart rate slows. - This is the afferent pathway that initiates the reflex response to terminate **supraventricular tachycardia (SVT)**. *Vagus* - The **vagus nerve (cranial nerve X)** is crucial for treating SVT, but it provides the **efferent (motor) limb** of the baroreflex, not the afferent limb. - After afferent signals from CN IX reach the medulla, the vagus nerve carries parasympathetic output to the SA node to slow the heart rate. - If the question asked about efferent fibers, vagus would be correct, but it asks specifically about **afferent fibers**. *Facial* - The **facial nerve (cranial nerve VII)** primarily controls **facial expressions**, carries taste sensation from the anterior two-thirds of the tongue, and innervates salivary glands. - It has no role in the baroreflex or cardiac rhythm regulation via neck maneuvers. *Hypoglossal* - The **hypoglossal nerve (cranial nerve XII)** is responsible for **tongue movement**. - It has no involvement in cardiac rhythm regulation or the afferent pathways of the baroreflex. *Trigeminal* - The **trigeminal nerve (cranial nerve V)** mediates sensation from the face and controls the muscles of **mastication (chewing)**. - While trigeminal stimulation via the **diving reflex** (cold water on face) can cause bradycardia, this is not the mechanism involved in carotid sinus massage for SVT treatment.

Question 15: A researcher is studying the effects of hormones on different cells within the ovarian follicle. She adds follicle stimulating hormone (FSH) to a culture of ovarian follicle cells. She then measures the activity levels of different enzymes within the cells. Which enzyme and ovarian cell type would be expected to be stimulated by the addition of FSH?

A. Desmolase; theca interna cell
B. Aromatase; theca externa cell
C. Aromatase; granulosa cell (Correct Answer)
D. Desmolase; granulosa cell
E. Aromatase; theca interna cell

Explanation: ***Aromatase; granulosa cell*** - **FSH** acts directly on **granulosa cells** to stimulate their proliferation and differentiation. - One of the key functions of stimulated granulosa cells is the production of **aromatase**, an enzyme responsible for converting **androgens** (produced by theca cells) into **estrogens**. *Desmolase; theca interna cell* - **Desmolase** (specifically cholesterol desmolase, or CYP11A1) is found in **theca interna cells** and is responsible for converting cholesterol into **androgens**. - Theca interna cell activity, including desmolase, is primarily stimulated by **LH**, not FSH. *Aromatase; theca externa cell* - The **theca externa cells** are primarily connective tissue and lack significant endocrine function, including aromatase activity. - **Aromatase** is predominantly present in the granulosa cells. *Desmolase; granulosa cell* - While granulosa cells are crucial for estrogen synthesis via aromatase, they do not produce **desmolase**. - **Desmolase** is the key enzyme in theca interna cells for androgen synthesis. *Aromatase; theca interna cell* - **Theca interna cells** produce **androgens** under the influence of **LH** and do not express **aromatase**. - **Aromatase** is exclusively expressed in the **granulosa cells** and converts these androgens into estrogens.

Question 16: A 29-year-old woman presents to a physician for evaluation of palpitations, increased sweating, and unintentional weight loss despite a good appetite. She also reports difficulty swallowing and voice changes. All of the symptoms have developed over the past 6 months. The patient has no concurrent illnesses and takes no medications. The vital signs include the following: blood pressure 125/80 mm Hg, heart rate 106/min, respiratory rate 15/min, and temperature 37.0℃ (98.6℉). The physical examination was significant for increased perspiration, fine digital tremors, and a small mass on the posterior aspect of the tongue, which moves with movements of the tongue. There is no neck swelling. The thyroid profile is as follows: Triiodothyronine (T3) 191 ng/dL (2.93 nmol/L) Thyroxine (T4), total 22 µg/dL (283.1 nmol/L) Thyroid-stimulating hormone (TSH) 0.2 µU/mL (0.2 mU/L) A radioiodine thyroid scan reveals hyper-functional thyroid tissue at the base of the patient’s tongue. Which of the following statements is correct?

A. This patient is at increased risk of thyroid carcinoma development.
B. There is a male predilection for this condition.
C. This condition results from a failure of caudal migration of thyroid tissue. (Correct Answer)
D. Most often in such a condition, there is an additional thyroid tissue elsewhere in the neck.
E. Ectopic thyroid tissue is most commonly found in the mediastinum.

Explanation: ***This condition results from a failure of caudal migration of thyroid tissue.*** - This patient's symptoms (palpitations, sweating, weight loss with good appetite, dysphagia, voice changes, and a mass at the base of the tongue, along with **hyperthyroidism** on labs) are highly suggestive of a **lingual thyroid**. - **Lingual thyroid** occurs when the thyroid gland fails to descend from its embryological origin at the **foramen cecum** at the base of the tongue to its normal position in the neck during embryological development. *This patient is at increased risk of thyroid carcinoma development.* - While thyroid carcinoma can occur in lingual thyroids, the risk is generally **low**, ranging from 1-3%. The primary concern is often the obstructive symptoms and hyperthyroidism. - The most significant association with increased risk of thyroid carcinoma is usually with **radiation exposure** or certain genetic syndromes, which are not mentioned here. *There is a male predilection for this condition.* - **Lingual thyroid** is more common in **females**, with a female-to-male ratio of approximately 4:1 to 7:1. - This condition is also more often diagnosed during periods of **increased physiological demand for thyroid hormones**, such as puberty, pregnancy, or menopause. *Most often in such a condition, there is an additional thyroid tissue elsewhere in the neck.* - In over 70% of cases, the lingual thyroid is the **ONLY functioning thyroid tissue** present in the patient. - This is why surgical removal of a lingual thyroid requires careful consideration of potential **post-operative hypothyroidism** and lifelong hormone replacement. *Ectopic thyroid tissue is most commonly found in the mediastinum.* - The **base of the tongue (lingual thyroid)** is the **most common site** of ectopic thyroid tissue, accounting for approximately 90% of cases. - Other less common locations for ectopic thyroid include sublingual, subhyoid, mediastinal, and very rarely intracardiac or intrasplenic areas.

Question 17: A 42-year-old man is referred for an endocrinology consult because of decreased triiodothyronine (T3) hormone levels. He presented to the emergency department 1 week prior to this consultation with pneumonia and was admitted to a medicine service for management of his infection. He has since recovered from his infection after intravenous antibiotic administration. He currently has no symptoms and denies feeling cold or lethargic. A panel of laboratory tests are obtained with the following results: Thyroid-stimulating hormone: 4.7 µU/mL Thyroxine (T4): 6 µg/dL Triiodothyronine (T3): 68 ng/dL Which of the following additional findings would most likely also be seen in this patient?

A. Increased free T3 concentration
B. Increased reverse T3 concentration (Correct Answer)
C. Decreased free T3 concentration
D. Normal free and reverse T3 concentration
E. Decreased reverse T3 concentration

Explanation: ***Increased reverse T3 concentration*** - The patient's presentation including recent severe illness (pneumonia), normal TSH, slightly low T4, and low T3, with no symptoms of hypothyroidism, is classic for **euthyroid sick syndrome** (also known as non-thyroidal illness syndrome). - In euthyroid sick syndrome, there is a characteristic increase in the peripheral conversion of T4 to **inactive reverse T3 (rT3)** rather than to active T3, due to altered deiodinase activity (decreased type 1 deiodinase and increased type 3 deiodinase). - **Elevated rT3 is the most specific finding** that distinguishes euthyroid sick syndrome from primary hypothyroidism. *Increased free T3 concentration* - This would contradict the initial finding of **decreased total T3** and the typical pattern of euthyroid sick syndrome, where free T3 is usually decreased or low-normal. - An increased free T3 level would suggest **hyperthyroidism**, which is inconsistent with the patient's clinical picture and other lab values. *Decreased free T3 concentration* - While free T3 would indeed be decreased in euthyroid sick syndrome along with total T3, this finding is **less specific** than elevated reverse T3. - Decreased free T3 can be seen in **primary hypothyroidism, central hypothyroidism, and euthyroid sick syndrome**, making it less diagnostically useful. - The question asks for the "most likely" additional finding, and **elevated reverse T3 is the hallmark biochemical marker** that best characterizes euthyroid sick syndrome and differentiates it from true hypothyroidism. *Normal free and reverse T3 concentration* - This would be inconsistent with the primary finding of **decreased T3** and the clinical context of recent severe illness, which almost invariably alters thyroid hormone metabolism. - Normal levels would imply that the initial T3 finding was an anomaly or that the patient does not have euthyroid sick syndrome. *Decreased reverse T3 concentration* - A decreased reverse T3 concentration is typically seen in conditions like **hyperthyroidism** or during recovery phases of severe illness, not during the acute phase where rT3 is elevated. - This finding would contradict the metabolic adaptations seen in **euthyroid sick syndrome**, where T4 is preferentially converted to rT3 (via type 3 deiodinase) to conserve energy during critical illness.

Question 18: A 15-year-old boy is brought to the emergency department by his father 10 minutes after falling into a frozen lake during ice fishing. He was in the water for less than 1 minute before his father managed to pull him out. On arrival, his clothes are still wet and he appears scared. His body temperature is 36.2°C (97.1°F), pulse is 102/min, blood pressure is 133/88 mm Hg. Which of the following mechanisms contributes most to maintaining this patient's core body temperature?

A. Inhibition of the thyroid axis
B. Involuntary muscular contractions (Correct Answer)
C. Activation of thermogenin
D. Increase in hypothalamic set point
E. Contraction of arrector pili muscles

Explanation: ***Involuntary muscular contractions*** - **Shivering** is the body's primary mechanism for increasing heat production in response to cold stress, involving rapid, involuntary muscle contractions to generate heat. - This process significantly increases the **metabolic rate** and heat output, crucial for maintaining core body temperature when exposed to cold environments. *Inhibition of the thyroid axis* - The **thyroid axis** is generally activated in response to chronic cold exposure to increase basal metabolic rate, not inhibited. - Inhibition of thyroid hormones would lead to a decrease in metabolism and heat production, worsening hypothermia. *Activation of thermogenin* - **Thermogenin** (uncoupling protein 1) is found primarily in **brown adipose tissue** and its activation leads to non-shivering thermogenesis. - While present in infants and some adults, shivering is a much more significant and rapid response to acute cold in a 15-year-old. *Increase in hypothalamic set point* - An increase in the **hypothalamic set point** is characteristic of **fever**, where the body aims to achieve a higher temperature. - In this scenario, the body is trying to maintain its normal set point despite cold exposure, not raise it. *Contraction of arrector pili muscles* - **Contraction of arrector pili muscles** causes **piloerection** (goosebumps), which traps a layer of air close to the skin. - While contributing to insulation, this mechanism is relatively minor in humans compared to the heat generated by shivering.

Question 19: A 43-year-old woman comes to the physician because of a 3-month history of tremor, diarrhea, and a 5-kg (11-lb) weight loss. Her pulse is 110/min. Examination shows protrusion of the eyeball when looking forward. A bruit is heard over the anterior neck on auscultation. Serum studies show autoantibodies to the thyroid-stimulating hormone receptor. The patient decides to undergo definitive treatment for her condition with a radioactive tracer. The success of this treatment directly depends on the activity of which of the following?

A. Anion-oxidizing enzyme
B. Transmembrane carrier (Correct Answer)
C. Lysosomal protease
D. Binding globulin
E. Hormone-activating enzyme

Explanation: ***Transmembrane carrier*** - Radioactive iodine treatment relies on the uptake of iodine by thyroid follicular cells via the **sodium-iodide symporter (NIS)**, a **transmembrane carrier protein**. - NIS actively transports iodide into thyroid cells, allowing the radioactive iodine to concentrate in the thyroid and destroy overactive tissue. *Anion-oxidizing enzyme* - This refers to **thyroid peroxidase (TPO)**, an enzyme that oxidizes iodide to iodine, incorporates iodine into thyroglobulin, and couples iodinated tyrosines. - While essential for thyroid hormone synthesis, TPO's activity does not directly determine the success of **radioactive iodine uptake** for treatment. *Lysosomal protease* - **Lysosomal proteases** are involved in the breakdown of thyroglobulin to release thyroid hormones (T3 and T4) into circulation. - They are important for the *release* of hormones but not for the *uptake* of iodine for radioactive treatment. *Binding globulin* - **Thyroxine-binding globulin (TBG)** is a plasma protein that transports thyroid hormones in the blood, maintaining a reservoir of T3 and T4. - TBG's activity affects the availability of free thyroid hormones but has no direct role in the cellular uptake of radioactive iodine by the thyroid gland. *Hormone-activating enzyme* - This typically refers to deiodinases, enzymes that convert T4 (prohormone) into the more active T3 in peripheral tissues. - These enzymes act *outside* the thyroid gland to activate hormones, and their activity does not directly influence the uptake of radioactive iodine.

Question 20: A scientist is studying patients with neuromuscular weakness and discovers a mutation in a plasma membrane ion channel. She thinks that this mutation may have an effect on the dynamics of action potentials so she investigates its effect in an isolated neuronal membrane. She finds that the ion channel has no effect when potassium, sodium, and calcium are placed at physiological concentrations on both sides of the membrane; however, when some additional potassium is placed inside the membrane, the channel rapidly allows for sodium to enter the membrane. She continues to examine the mutant channel and finds that it is more rapidly inactivated compared with the wildtype channel. Which of the following effects would this mutant channel most likely have on the electrical profile of neurons in these patients?

A. Decreased hyperpolarization potential
B. Increased threshold for action potential activation
C. Increased action potential refractory period
D. Decreased resting membrane potential
E. Decreased action potential amplitude (Correct Answer)

Explanation: ***Decreased action potential amplitude*** - The mutant channel opens when intracellular potassium is elevated, allowing **sodium influx**. This suggests it's a **sodium channel** that is sensitive to potassium. - Its **rapid inactivation** means that less sodium will enter the cell during an action potential, leading to a smaller depolarization and thus a **decreased amplitude**. *Decreased hyperpolarization potential* - **Hyperpolarization** is primarily mediated by the efflux of potassium ions, moving the membrane potential further from 0 mV. - The described channel's activity (sodium influx rather than potassium efflux) would not directly cause a decrease in hyperpolarization. *Increased threshold for action potential activation* - The threshold for action potential activation depends on the number of sodium channels needed to open to reach the **threshold potential**. - While rapid inactivation might affect the *success* of an action potential once triggered, it doesn't inherently increase the initial voltage threshold required to open sufficient channels. *Increased action potential refractory period* - The **refractory period** is largely determined by the inactivation state of voltage-gated sodium channels and the activity of potassium channels. - While the mutant channel inactivates rapidly, this would more likely lead to a *shorter* phase of excitability, not necessarily an increased absolute or relative refractory period. *Decreased resting membrane potential* - The **resting membrane potential** is primarily set by the leak channels, particularly potassium leak channels, and the **Na+/K+ ATPase pump**. - The described channel's activity as a sodium channel would not significantly alter the resting potential, as it requires a specific condition (elevated intracellular potassium) to open, which is not characteristic of the resting state.

Question 21: A researcher is studying the effect of hypothalamic lesions on rat behavior and development. She has developed a novel genetic engineering technology that allows her to induce specific mutations in rat embryos that interfere with rat CNS development. She creates several lines of rats with mutations in only one region of the pituitary gland and hypothalamus. She then monitors their growth and development over six weeks. One line of rats has a mean body mass index (BMI) that is significantly lower than that of control rats. Food intake decreased by 40% in these rats compared to controls. These rats likely have a lesion in which of the following locations?

A. Lateral hypothalamus (Correct Answer)
B. Suprachiasmatic nucleus
C. Ventromedial area
D. Paraventricular nucleus
E. Posterior hypothalamus

Explanation: ***Lateral hypothalamus*** - The **lateral hypothalamus** is known as the **"hunger center"**. Lesions in this area lead to **aphagia** (decreased food intake) and **weight loss**. - Decreased food intake by 40% and significantly lower BMI are consistent with a lesion affecting the lateral hypothalamus. *Suprachiasmatic nucleus* - The **suprachiasmatic nucleus** is the primary regulator of **circadian rhythms** and sleep-wake cycles. - Lesions here would primarily affect sleep patterns and daily physiological rhythms, not directly cause severe reductions in food intake or BMI. *Ventromedial area* - The **ventromedial hypothalamus** is considered the **"satiety center"**. Lesions in this region typically lead to **hyperphagia** (increased food intake) and **obesity**. - This effect is the opposite of what is observed in the rat line described in the question. *Paraventricular nucleus* - The **paraventricular nucleus** plays a role in various functions, including stress response, metabolism, and **feeding behavior**, but its lesion mostly causes increased feeding specifically of carbohydrates. - While it's involved in feeding, severe aphagia and dramatic weight loss are more classically associated with lateral hypothalamic lesions. *Posterior hypothalamus* - The **posterior hypothalamus** is involved in temperature regulation and arousal. - Lesions in this area can cause problems with **thermoregulation** and can lead to somnolence, but are not directly associated with a primary reduction in food intake and BMI.

Question 22: In an experimental model, a compound is centrally administered to mice. Following administration, the mice display increased desire for food and increased appetite. The administered compound is most likely similar to which of the following?

A. Leptin
B. Neuropeptide-Y (Correct Answer)
C. Cholecystokinin
D. Glucagon-like peptide 1
E. Peptide YY

Explanation: ***Neuropeptide-Y*** - **Neuropeptide Y (NPY)** is a potent **orexigenic peptide** that, when centrally administered, stimulates appetite and increases food intake. - Its actions primarily occur within the **hypothalamus**, where it promotes a state of positive energy balance. *Leptin* - **Leptin** is an **anorexigenic hormone** produced by adipose tissue that signals satiety to the brain, thereby *reducing* appetite and food intake. - Administration of leptin would lead to *decreased* desire for food, directly opposite to the scenario described. *Cholecystokinin* - **Cholecystokinin (CCK)** is a **satiety hormone** released in response to nutrient presence in the small intestine, acting to *reduce* food intake. - It slows gastric emptying and sends signals of fullness to the brain, thus *decreasing* appetite. *Glucagon-like peptide 1* - **Glucagon-like peptide 1 (GLP-1)** is an **incretin hormone** that *reduces* appetite and promotes satiety by slowing gastric emptying and increasing insulin secretion. - Its central administration would lead to *decreased* food desire, not increased. *Peptide YY* - **Peptide YY (PYY)** is an **anorexigenic hormone** released post-prandially from the gastrointestinal tract, signaling satiety and *reducing* appetite. - Central administration of PYY would result in a *decrease* in food intake and desire.

Question 23: A 62-year-old man is found unconscious in the park on a bench, early in the morning in January. The temperature outside is -4.0°C (25°F). He is barefoot and is wearing nothing more than sweatpants, a tee-shirt, and a light coat. Upon arrival at the emergency department, his vitals include: heart rate 45/min, blood pressure 100/70 mm Hg, and respiratory rate 10/min. His core body temperature is 30.0°C (85.5°F). His feet and palms are covered with clear blisters, the skin is yellow with a waxy appearance, and the tissues are edematous. The patient is unresponsive to auditory stimuli. Which of the following cold-associated injuries does the patient have?

A. Trench foot
B. Pernio
C. Frostbite (Correct Answer)
D. Frostnip
E. Immersion foot

Explanation: ***Frostbite*** - The presence of **clear blisters**, **yellow, waxy skin**, and **edema** in a severely cold and underdressed patient at -4.0°C (25°F) is highly indicative of frostbite. Frostbite is a tissue injury caused by **freezing of tissue** at or below 0°C (32°F). - The patient's core body temperature of 30.0°C (85.5°F) indicates **hypothermia**, which often co-occurs with frostbite due to prolonged cold exposure. *Trench foot* - **Trench foot** (or non-freezing cold injury) occurs from prolonged exposure to **wet and cold** (but not freezing) conditions, typically between 0°C and 15°C (32°F-60°F). - While it can cause blistering and tissue damage, the characteristic **waxy appearance** and exposure to sub-freezing temperatures make frostbite a more accurate diagnosis. *Pernio* - **Pernio**, also known as **chilblains**, are small, itchy, painful, red, or purple skin swellings that occur on the skin surface due to **repeated exposure to cold but non-freezing temperatures**. - This condition is typically less severe than frostbite and does not involve the deep tissue changes or extensive blistering described. *Frostnip* - **Frostnip** is a mild, superficial cold injury that involves the **freezing of the outer layers of skin** but does not cause permanent tissue damage. - Symptoms include numbness, tingling, and pale skin, but it typically does not involve **blister formation** or the waxy appearance seen in more severe cold injuries like frostbite. *Immersion foot* - **Immersion foot** is essentially the same condition as **trench foot**, resulting from prolonged exposure to wet and cold conditions (above freezing), leading to nerve and tissue damage. - The patient's exposure to **sub-freezing temperatures** and the specific skin changes point away from immersion foot and toward freezing-related injury.

Question 24: In large neurons the nucleus can be found a large distance away from the terminal end of its axon. The body has a complex system of intracellular transporters that are able to carry essential proteins from the nucleus to the distal edge of the cell and back. Which of the following proteins are essential for this function?

A. Kinesin, Troponin
B. Myosin, Kinesin
C. Actin, Dynein
D. Dynein, Kinesin (Correct Answer)
E. Glucose, Actin

Explanation: ***Dynein, Kinesin*** - **Kinesin** is primarily responsible for **anterograde transport** (from the cell body to the axon terminal) along microtubules, carrying vesicles and organelles. - **Dynein** handles **retrograde transport** (from the axon terminal back to the cell body), essential for recycling components and signaling. *Kinesin, Troponin* - While **Kinesin** is involved in axonal transport, **Troponin** is a protein found in muscle tissue that regulates muscle contraction, not intracellular transport in neurons. - Troponin binds **calcium ions** and influences the interaction between actin and myosin. *Myosin, Kinesin* - **Kinesin** is involved in microtubule-based transport, but **Myosin** is primarily associated with **actin filaments** for muscle contraction and intracellular movement, not long-distance axonal transport. - Myosin functions as a **motor protein** that converts chemical energy in ATP into mechanical force. *Actin, Dynein* - **Dynein** is crucial for retrograde axonal transport, but **Actin** is a structural protein forming microfilaments that are involved in cell shape, motility, and some short-distance transport, not the major long-distance axonal transport mechanism. - Actin filaments serve as tracks for **myosin motors**, primarily in the cell cortex. *Glucose, Actin* - **Glucose** is a sugar molecule, the primary energy source for cells, and not a transport protein. - **Actin** forms microfilaments for cell structure and short-range movement, not long-distance axonal transport as described.

Question 25: A 17-year-old previously healthy, athletic male suddenly falls unconscious while playing soccer. His athletic trainer comes to his aid and notes that he is pulseless. He begins performing CPR on the patient until the ambulance arrives but the teenager is pronounced dead when the paramedics arrived. Upon investigation of his primary care physician's office notes, it was found that the child had a recognized murmur that was ruled to be "benign." Which of the following conditions would have increased the intensity of the murmur?

A. Inspiration
B. Placing the patient in a squatting position
C. Valsalva (Correct Answer)
D. Passive leg raise
E. Handgrip

Explanation: ***Valsalva*** - The patient's sudden death after collapsing during soccer, coupled with a previously noted "benign" murmur, strongly suggests **hypertrophic obstructive cardiomyopathy (HOCM)**, which is a common cause of sudden cardiac death in young athletes. The **Valsalva maneuver** decreases preload and left ventricular volume, thereby **increasing the left ventricular outflow tract (LVOT) obstruction** and hence the intensity of the HOCM murmur. - This maneuver reduces venous return to the heart, leading to reduced ventricular filling and decreased stroke volume. This exacerbates the obstruction in HOCM, making the murmur louder. *Inspiration* - **Inspiration** typically **increases venous return to the right side of the heart**, which would generally intensify right-sided murmurs (e.g., tricuspid regurgitation). - It would have **minimal effect or slightly decrease** the intensity of a left-sided obstructive murmur like that in HOCM, as it does not directly increase the LVOT obstruction. *Placing the patient in a squatting position* - Squatting increases both **preload** and **afterload** by increasing systemic vascular resistance and venous return. - This increase in ventricular volume would **reduce the outflow tract obstruction** in HOCM, thereby **decreasing the intensity of the murmur**. *Passive leg raise* - A **passive leg raise** increases **venous return** and thus **preload**, leading to increased ventricular filling. - Similar to squatting, this increased left ventricular volume would **reduce the left ventricular outflow tract obstruction** associated with HOCM, thereby **decreasing the murmur's intensity**. *Handgrip* - The **handgrip maneuver** primarily **increases afterload** and, to some extent, preload by increasing systemic vascular resistance. - While it can increase the intensity of murmurs like mitral regurgitation and ventricular septal defect, it would generally **decrease or have no significant effect** on the murmur of HOCM due to the increased ventricular volume reducing the outflow obstruction.

Question 26: One day after undergoing surgery for a traumatic right pelvic fracture, a 73-year-old man has pain over his buttocks and scrotum and urinary incontinence. Physical examination shows right-sided perineal hypesthesia and absence of anal sphincter contraction when the skin around the anus is touched. This patient is most likely to have which of the following additional neurological deficits?

A. Impaired hip flexion
B. Paralysis of hip adductors
C. Absent cremasteric reflex
D. Impaired psychogenic erection
E. Absent reflex erection (Correct Answer)

Explanation: ***Absent reflex erection*** - The patient's symptoms (buttock/scrotal pain, perineal hypesthesia, urinary incontinence, absent anal sphincter contraction) suggest **damage to the sacral plexus and pudendal nerve**, consistent with a **cauda equina syndrome**. - **Reflex erections** are primarily mediated by the **sacral parasympathetic outflow (S2-S4)**, which are likely compromised given the other sacral nerve deficits. *Impaired hip flexion* - **Hip flexion** is primarily controlled by the **L1-L3 nerve roots** (e.g., iliopsoas muscle), and while a severe pelvic fracture could cause widespread nerve damage, the current symptoms localize more strongly to the sacral region. - The described symptoms are more indicative of **sacral nerve involvement** rather than higher lumbar segments that govern hip flexion. *Paralysis of hip adductors* - **Hip adduction** is mainly innervated by the **obturator nerve (L2-L4)**. - The patient's symptoms point to **S2-S4 nerve dysfunction** (perineal sensation, anal sphincter, bladder), which are distinct from the obturator nerve's primary innervations. *Absent cremasteric reflex* - The **cremasteric reflex** is mediated by the **genitofemoral nerve (L1-L2)**. - The symptoms presented are more consistent with **sacral nerve damage**, specifically S2-S4, rather than the higher lumbar segments responsible for the cremasteric reflex. *Impaired psychogenic erection* - **Psychogenic erections** are initiated by **supraspinal input** descending through the thoracolumbar spinal cord (T10-L2) to activate sympathetic pathways. - While sacral nerve damage can affect the final efferent pathway for all erections, the direct impairment of psychogenic initiation is linked to higher centers and **thoracolumbar sympathetic outflow**, not purely sacral damage.

Question 27: A 56-year-old woman presents to the emergency department after falling in the shower 2 days ago. At that time, she was complaining of severe back pain that she treated with over the counter acetaminophen. Since the fall, she has had increasing stomach pain and difficulty walking. She has not urinated or had a bowel movement since the incident. She has no significant past medical history and takes a multivitamin regularly. No significant family history. Her vitals include: blood pressure 137/82 mm Hg, pulse 78/min, respiratory rate 16/min, temperature 37.0°C (98.6°F). On physical examination, she is alert and oriented but in great discomfort. There is focal, non-radiating midline pain with palpation of the L1 vertebrae. On pinprick sensory testing, she reveals decreased sensations below the level of the knees bilaterally. Muscle strength is 4/5 in both lower extremities. Which of the following additional findings would most likely be present in this patient?

A. Decreased deep tendon reflexes (Correct Answer)
B. Intentional tremors
C. Increased deep tendon reflexes
D. Decreased muscle strength in upper extremities
E. Difficulty in swallowing

Explanation: ***Decreased deep tendon reflexes*** - The patient's presentation with **severe back pain at L1**, **bowel and bladder dysfunction**, **sensory deficits below the knees**, and **difficulty walking** points to a **conus medullaris syndrome** or **cauda equina syndrome**. - The **spinal cord terminates at approximately L1-L2** (conus medullaris), below which are the nerve roots of the cauda equina. - Lesions at or below L1 affect the **lower motor neurons (LMN)** directly, producing **hyporeflexia or areflexia** (decreased or absent deep tendon reflexes). - The **early bowel and bladder dysfunction** combined with **bilateral sensory loss** is characteristic of **conus medullaris syndrome**, which presents with predominantly **LMN signs** including decreased reflexes. *Increased deep tendon reflexes* - **Hyperreflexia** is a hallmark of **upper motor neuron (UMN) lesions** affecting the spinal cord above the level of L1-L2. - At the L1 vertebral level, the spinal cord is terminating (conus medullaris), so compression here affects lower motor neurons, not upper motor neurons. - UMN signs would only be expected if the lesion were at a higher thoracic or cervical level. *Intentional tremors* - **Intention tremors** are associated with **cerebellar dysfunction**, characterized by tremor that worsens with goal-directed movement. - The patient's symptoms localize to the spinal cord/nerve roots at L1, not the cerebellum. *Decreased muscle strength in upper extremities* - The patient's lesion is at **L1 level**, which is far below the **cervical spinal cord segments** (C5-T1) that innervate the upper extremities. - Upper extremity weakness would only occur with cervical or high thoracic cord lesions. *Difficulty in swallowing* - **Dysphagia** results from dysfunction of **cranial nerves IX, X, and XII** or lesions affecting the **brainstem** or **cortical swallowing centers**. - A spinal lesion at L1 cannot cause swallowing difficulties.

Question 28: A 48-year-old woman is brought to the emergency department by her family at her psychiatrist's recommendation. According to her family, she has been more restless than her baseline over the past week. The patient herself complains that she feels her mind is racing. Her past medical history is significant for bipolar disorder on lithium and type 1 diabetes mellitus. The family and the patient both assert that the patient has been taking her medications. She denies any recent illness or sick contacts. The patient's temperature is 100°F (37.8°C), blood pressure is 100/60 mmHg, pulse is 130/min, and respirations are 20/min. She appears diaphoretic, and her cardiac exam is notable for an irregularly irregular rhythm with a 2/6 early systolic murmur. Blood counts and metabolic panel are within normal limits. The patient's lithium level is within therapeutic range. Which of the following laboratory tests would be the most useful to include in the evaluation of this patient?

A. Thyroglobulin level
B. Thyroid stimulating hormone and total thyroxine levels
C. Thyrotropin-releasing hormone stimulation test
D. Triiodothyronine and thyroxine levels
E. Thyroid stimulating hormone and free thyroxine levels (Correct Answer)

Explanation: ***Thyroid stimulating hormone and free thyroxine levels*** - This patient presents with symptoms highly suggestive of **hyperthyroidism**, including **restlessness**, **tachycardia** (pulse 130/min), **diaphoresis**, and a **racing mind**. These symptoms, particularly in a patient on lithium (which can induce thyroid dysfunction), necessitate a thorough thyroid evaluation. - While total T4 can be influenced by protein binding, **free T4** is the active form of the hormone and provides a more accurate assessment of thyroid status, along with **TSH** as the primary screening test. *Thyroglobulin level* - **Thyroglobulin** is primarily used as a tumor marker in the follow-up of patients treated for differentiated thyroid cancer to detect recurrence. - It is not a primary diagnostic test for hyperthyroidism and would not be the most useful initial test in this scenario. *Thyroid stimulating hormone and total thyroxine levels* - While TSH and total T4 are used, **total T4** levels can be affected by changes in **thyroid-binding globulin (TBG)**, which can be altered by various conditions or medications (e.g., estrogen, liver disease). - Therefore, **free thyroxine** provides a more accurate reflection of thyroid function than total thyroxine. *Thyrotropin-releasing hormone stimulation test* - A **TRH stimulation test** is primarily used to investigate subtle abnormalities in the hypothalamic-pituitary-thyroid axis, often when other thyroid function tests are equivocal. - It is not a first-line diagnostic test for overt hyperthyroidism and would be overly complex for initial evaluation of this patient's symptoms. *Triiodothyronine and thyroxine levels* - While T3 and T4 levels are part of thyroid function assessment, specifying **free thyroxine** versus total thyroxine is crucial for accuracy. - **Free T4** levels, along with TSH, are generally the most informative initial tests for diagnosing conditions like hyperthyroidism.

Question 29: An investigator is studying the crossbridge cycle of muscle contraction. Tissue from the biceps brachii muscle is obtained at the autopsy of an 87-year-old man. Investigation of the muscle tissue shows myosin heads attached to actin filaments. Binding of myosin heads to which of the following elements would most likely cause detachment of myosin from actin filaments?

A. ATP (Correct Answer)
B. Troponin C
C. Tropomyosin
D. ADP
E. cGMP

Explanation: ***ATP*** - The binding of **ATP** to the **myosin head** causes a conformational change that reduces its affinity for actin, leading to detachment. - This step is crucial for the muscle to relax and for the subsequent power stroke to occur. *Troponin C* - **Troponin C** is a regulatory protein that binds calcium, which then causes a conformational change in the troponin-tropomyosin complex, revealing the **actin binding sites** for myosin. - It does not directly cause myosin detachment; instead, it facilitates the binding of myosin to actin. *Tropomyosin* - **Tropomyosin** is a long, fibrous protein that covers the **myosin-binding sites** on actin in a relaxed muscle, preventing cross-bridge formation. - Its movement, regulated by troponin, allows myosin to bind, but it does not directly cause detachment. *ADP* - **ADP** is released from the myosin head during the power stroke, but its binding does not cause detachment; rather, it is present during the strongly bound state before **ATP** binds. - The presence of **ADP** and inorganic phosphate (Pi) often promotes the strong binding of myosin to actin. *cGMP* - **cGMP** (cyclic guanosine monophosphate) is a second messenger involved in various cellular processes, including smooth muscle relaxation, but it is not directly involved in the cross-bridge cycle and detachment of **myosin from actin** in skeletal muscle. - Its primary role in muscle physiology is often linked to nitric oxide signaling and vasodilation.

Question 30: An investigator is working with a mutant strain of mice that lack a consistent density of sarcolemmal transverse tubules in the skeletal muscle cells. Which of the following is the most likely associated finding as a result of this abnormality?

A. Impaired binding of acetylcholine to nicotinic acetylcholine receptors
B. Decreased entry of calcium at the presynaptic membrane
C. Impaired synchronization of cross-bridge formation (Correct Answer)
D. Increased activation of myosin-light-chain phosphatase
E. Decreased expression of sarcolemmal Na+/K+ ATPase

Explanation: ***Impaired synchronization of cross-bridge formation*** - **Transverse tubules (T-tubules)** are crucial for rapidly propagating the **action potential** from the sarcolemma deep into the muscle fiber, ensuring a uniform and synchronized release of calcium from the sarcoplasmic reticulum. - A lack of consistent T-tubule density would lead to **desynchronized calcium release** and thus uncoordinated activation of **myosin-actin cross-bridges**, resulting in inefficient and impaired muscle contraction. *Impaired binding of acetylcholine to nicotinic acetylcholine receptors* - The binding of **acetylcholine (ACh)** to **nicotinic ACh receptors** occurs at the **neuromuscular junction** on the surface of the sarcolemma, prior to the generation of the action potential that travels down the T-tubules. - T-tubule abnormalities primarily affect the propagation of the electrical signal *after* it has been initiated on the sarcolemma, not the initial binding of neurotransmitters. *Decreased entry of calcium at the presynaptic membrane* - **Calcium entry at the presynaptic membrane** is vital for the release of **acetylcholine** into the synaptic cleft. - This process is upstream of muscle cell excitation and T-tubule function; T-tubule abnormalities in the muscle cell would not affect calcium entry into the **neuron's presynaptic terminal**. *Increased activation of myosin-light-chain phosphatase* - **Myosin light chain phosphatase (MLCP)** plays a significant role in **smooth muscle relaxation** by dephosphorylating myosin light chains, leading to detachment of cross-bridges. - In **skeletal muscle**, calcium binding to **troponin C** initiates contraction by shifting tropomyosin, allowing myosin to bind to actin; MLCP is not the primary regulator of contraction/relaxation in skeletal muscle. *Decreased expression of sarcolemmal Na+/K+ ATPase* - The **Na+/K+-ATPase** is essential for maintaining the **resting membrane potential** of the muscle cell and restoring ion gradients after an action potential. - While important for muscle function, its expression would not be directly or primarily affected by a structural defect in the **T-tubule system**, which is mainly involved in action potential propagation and calcium release.

Question 31: In the coronary steal phenomenon, vessel dilation is paradoxically harmful because blood is diverted from ischemic areas of the myocardium. Which of the following is responsible for the coronary steal phenomenon?

A. Venodilation
B. Microvessel dilation (Correct Answer)
C. Dilation of the large coronary arteries
D. Systemic arterial dilation
E. Volume loss of fluid in the periphery

Explanation: ***Microvessel dilation*** - The coronary steal phenomenon occurs when **vasodilators** are administered, causing dilation of **healthy coronary microvessels** and a decrease in resistance. - This preferentially diverts blood flow away from already **ischemic areas** with maximally dilated intrinsic microvessels, worsening myocardial ischemia. *Venodilation* - **Venodilation** primarily reduces **preload** by increasing venous capacitance, not by directly altering coronary microcirculatory blood flow distribution in a way that causes "steal." - While some vasodilators have venodilatory effects, this specific effect is not the mechanism behind coronary steal. *Dilation of the large coronary arteries* - Dilation of large coronary arteries alone doesn't cause the "steal" but rather improves overall blood flow. The critical issue is the differential response of **collateral** and **non-collateral microvessels**. - **Stenoses** in large coronary arteries are the underlying pathology, but the steal phenomenon itself results from changes in **downstream microvascular resistance**. *Systemic arterial dilation* - **Systemic arterial dilation** primarily reduces afterload and can lower blood pressure, but it does not specifically explain the redistribution of coronary blood flow to the detriment of ischemic zones within the myocardium. - The key to coronary steal is the **heterogeneity of response** at the microvascular level within the coronary circulation. *Volume loss of fluid in the periphery* - **Volume loss** in the periphery would influence overall circulatory dynamics and cardiac output but is not directly responsible for the **localized myocardial blood flow redistribution** characteristic of the coronary steal phenomenon. - Coronary steal is a physiological process related to **vasoreactivity** and not hypovolemia.

Question 32: A 36-year-old woman is admitted to the hospital for the evaluation of progressive breathlessness. She has no history of major medical illness. Her temperature is 37°C (98.6°F), pulse is 110/min, and respirations are 22/min. Pulse oximetry on room air shows an oxygen saturation of 99%. Cardiac examination shows a loud S1 and S2. There is a grade 2/6 early systolic murmur best heard in the 2nd right intercostal space. Cardiac catheterization shows a mixed venous oxygen saturation of 55% (N= 65–70%). Which of the following is the most likely cause of this patient's breathlessness?

A. Increased peripheral shunting
B. Decreased hemoglobin concentration
C. Increased carbon dioxide retention
D. Increased pulmonary vascular resistance
E. Decreased left ventricular ejection fraction (Correct Answer)

Explanation: ***Decreased left ventricular ejection fraction*** - The key finding is a **mixed venous oxygen saturation of 55% (normal 65-70%)** with **normal arterial oxygen saturation (99%)**, which indicates **increased tissue oxygen extraction** - Increased oxygen extraction occurs when **cardiac output is reduced** → tissues must extract more oxygen from each pass of blood to meet metabolic demands - This is the classic physiologic compensation in **heart failure with reduced ejection fraction** - The cardiac findings (loud heart sounds, systolic murmur) suggest underlying cardiac pathology causing reduced cardiac output and progressive breathlessness *Increased peripheral shunting* - Peripheral shunting (e.g., arteriovenous malformations) would cause **venous blood to bypass capillary beds**, resulting in **decreased oxygen extraction** and **higher mixed venous O2 saturation**, not lower - Would typically cause **hypoxemia** with reduced pulse oximetry, but this patient has 99% oxygen saturation *Decreased hemoglobin concentration* - Anemia reduces oxygen-carrying capacity but would not explain the **low mixed venous oxygen saturation** to this degree - The **pulse oximetry of 99%** indicates adequate oxygen saturation of available hemoglobin - Anemia typically causes **high cardiac output** (compensatory) rather than the low cardiac output state indicated by the low mixed venous O2 saturation *Increased carbon dioxide retention* - **Hypercapnia** results from **hypoventilation** and impaired gas exchange, typically causing **respiratory acidosis** - Would present with altered mental status, drowsiness, or signs of respiratory failure - Does not explain the **low mixed venous oxygen saturation** with normal arterial oxygen saturation - The cardiac findings point to a primary cardiac rather than respiratory problem *Increased pulmonary vascular resistance* - **Pulmonary hypertension** causes **right ventricular dysfunction** and can present with breathlessness and a loud P2 component of S2 - However, isolated pulmonary hypertension would not cause the same degree of **systemic oxygen extraction** increase - The low mixed venous O2 saturation indicates **reduced systemic cardiac output**, which primarily reflects **left ventricular dysfunction** rather than isolated right-sided pathology

Question 33: An investigator is studying the electrophysical properties of gastrointestinal smooth muscle cells using microelectrodes. He measures the resting membrane potential of a cell to be -70 mV. The equilibrium potentials of different ions involved in generating the membrane potential are shown. ENa+ +65 mV EK -85 mV ECa2+ +120 mV EMg2+ +10 mV ECl- -85 mV Which of the following is the most important contributor to the difference between the resting membrane potential and the equilibrium potential of potassium?

A. Influx of Ca2+ ions
B. Influx of Cl- ions
C. Influx of Mg2+ ions
D. Influx of Na+ ions (Correct Answer)
E. Electrogenic effect of Na+/K+-ATPase

Explanation: ***Influx of Na+ ions*** - The resting membrane potential (-70 mV) is **more positive** than the potassium equilibrium potential (-85 mV) by approximately 15 mV. This difference exists because the membrane is **not exclusively permeable to K+**. - At rest, there is a small but significant **Na+ permeability**, creating a continuous **Na+ leak** into the cell driven by both the concentration gradient and the electrical gradient (ENa = +65 mV is far more positive than RMP). - This **depolarizing Na+ influx** pulls the resting membrane potential toward ENa, making it less negative than it would be if only K+ channels were open. This is the **primary contributor** to why RMP (-70 mV) is more positive than EK (-85 mV). - The **Goldman-Hodgkin-Katz equation** demonstrates that RMP depends on the relative permeabilities and concentrations of all permeable ions, with Na+ leak being the key factor preventing RMP from equaling EK. *Electrogenic effect of Na+/K+-ATPase* - The **Na+/K+-ATPase** actively pumps **3 Na+ out** and **2 K+ in** per cycle, creating a net efflux of one positive charge with a small **hyperpolarizing effect** (approximately -3 to -5 mV). - This would actually make the membrane potential **more negative**, moving it closer to or slightly below EK, not explaining why RMP is more positive than EK. - While the pump is essential for maintaining ion gradients, its direct electrogenic contribution is small and acts in the opposite direction from what the question asks. *Influx of Ca2+ ions* - Influx of **Ca2+ ions** (ECa2+ = +120 mV) would cause **depolarization**, but Ca2+ permeability at rest is extremely low in most cells. - While Ca2+ influx occurs during excitation in smooth muscle, it is not a significant contributor to the resting membrane potential difference from EK. *Influx of Cl- ions* - The equilibrium potential of **Cl- (-85 mV)** is essentially equal to EK. Chloride influx would tend to **stabilize** the membrane potential near -85 mV, not explain why it is more positive at -70 mV. - In many smooth muscle cells, Cl- is near equilibrium at rest and does not significantly contribute to moving RMP away from EK. *Influx of Mg2+ ions* - The equilibrium potential of **Mg2+ (+10 mV)** is positive, but **Mg2+ permeability** at rest is negligible in most cell membranes. - Mg2+ is primarily an intracellular ion that acts as a cofactor for enzymes and does not significantly contribute to resting membrane potential through membrane flux.

Question 34: A 27-year-old woman presents to her doctor complaining of pain in her neck that radiates to her left ear. The pain has been more or less constant for the last 3 weeks and increases when she chews and swallows. She was in her normal state of health before the pain started. She also mentions that she has been experiencing palpitations, muscle weakness, and increased sweating for the last 2 weeks. Past medical history is significant for a flu-like illness 2 months ago. She currently takes no medication and neither consumes alcohol nor smokes cigarettes. Her pulse is 104/min and irregular with a blood pressure of 140/80 mm Hg. On examination, the physician notices that the patient is restless. There is a presence of fine tremors in both hands. The anterior neck is swollen, warm to the touch, and markedly tender on palpation. Thyroid function tests and a biopsy are ordered. Which of the following deviations from the normal is expected to be seen in her thyroid function tests?

A. Normal Serum TSH, ↑ Total T4, Normal Free T4, Normal I131 Uptake
B. ↓ Serum TSH, ↑ Total T4, ↑ Free T4, ↑ I131 Uptake
C. Normal Serum TSH, ↓ Total T4, Normal Free T4, Normal I131 Uptake
D. ↑ Serum TSH, ↑ Total T4, ↑ Free T4, ↑ I 131 Uptake
E. ↓ Serum TSH, ↑ Total T4, ↑ Free T4, ↓ I131 Uptake (Correct Answer)

Explanation: ***↓ Serum TSH, ↑ Total T4, ↑ Free T4, ↓ I131 Uptake*** - This pattern is characteristic of **thyrotoxicosis** (increased thyroid hormone levels) combined with decreased thyroid gland activity, which is typical for conditions like **subacute thyroiditis** (as suggested by the flu-like illness and painful, tender thyroid). - The elevated **T3/T4** (Total and Free) results from the release of preformed hormones from the inflamed thyroid, while the **low TSH** is due to negative feedback. The **decreased I-131 uptake** indicates that the thyroid gland is not actively synthesizing new hormones. *Normal Serum TSH, ↑ Total T4, Normal Free T4, Normal I131 Uptake* - This combination is inconsistent with the patient's symptoms of hyperthyroidism (palpitations, sweating, tremors) and a **tender, swollen thyroid**. - **Normal Free T4** and **Normal TSH** would suggest euthyroid status, which is not what the clinical presentation indicates. *↓ Serum TSH, ↑ Total T4, ↑ Free T4, ↑ I131 Uptake* - This pattern suggests a hyperthyroid state where the thyroid gland is actively overproducing hormones, as seen in **Graves' disease** or toxic nodular goiter. - However, subacute thyroiditis is characterized by **low I-131 uptake** because the thyroid gland is damaged and releases preformed hormones rather than actively synthesizing new ones. *Normal Serum TSH, ↓ Total T4, Normal Free T4, Normal I131 Uptake* - This combination is not indicative of the patient's hyperthyroid symptoms (- **palpitations, muscle weakness, increased sweating**). - **Normal Free T4** and **Normal TSH** would suggest euthyroid status, which is inconsistent with the clinical picture. *↑ Serum TSH, ↑ Total T4, ↑ Free T4, ↑ I 131 Uptake* - An **elevated TSH** would indicate **primary hypothyroidism**, where the thyroid gland is underactive, and the pituitary tries to stimulate it. - This contradicts the patient's clinical signs of **hyperthyroidism** (palpitations, sweating, tremors) and the elevated Total and Free T4.

Question 35: A researcher measures action potential propagation velocity in various regions of the heart in a 42-year-old Caucasian female. Which of the following set of measurements corresponds to the velocities found in the atrial muscle, AV Node, Purkinje system, and ventricular muscle, respectively?

A. 0.05 m/s, 1.1 m/s, 2.2 m/s, 3.3 m/s
B. 2.2 m/s, 0.3 m/s, 0.05 m/s, 1.1 m/s
C. 0.3 m/s, 2.2 m/s, 0.05 m/s, 1.1 m/s
D. 0.5 m/s, 1.1 m/s, 2.2 m/s, 3 m/s
E. 1.1 m/s, 0.05 m/s, 2.2 m/s, 0.3 m/s (Correct Answer)

Explanation: ***1.1 m/s, 0.05 m/s, 2.2 m/s, 0.3 m/s*** - This option correctly lists the approximate conduction velocities for the **atrial muscle (1.1 m/s)**, **AV node (0.05 m/s)**, **Purkinje system (2.2 m/s)**, and **ventricular muscle (0.3 m/s)**, respectively. - The **AV node has the slowest conduction velocity (~0.05 m/s)**, which is crucial for delaying ventricular contraction and allowing complete ventricular filling. - The **Purkinje system has the fastest conduction velocity (~2-4 m/s)**, ensuring rapid and coordinated ventricular depolarization. - **Atrial muscle (~1 m/s)** and **ventricular muscle (~0.3-0.5 m/s)** have intermediate velocities. *0.05 m/s, 1.1 m/s, 2.2 m/s, 3.3 m/s* - This sequence is incorrect because it places the **AV node's velocity (0.05 m/s)** first (as atrial muscle) and significantly overestimates ventricular muscle velocity (3.3 m/s). - Atrial muscle conducts faster than 0.05 m/s, and ventricular muscle velocity should be approximately 0.3-0.5 m/s, not 3.3 m/s. *2.2 m/s, 0.3 m/s, 0.05 m/s, 1.1 m/s* - This option incorrectly assigns the **highest velocity (2.2 m/s)** to atrial muscle, which is characteristic of the Purkinje system, and misplaces the **slowest velocity (0.05 m/s)** in the Purkinje system instead of the AV node. - The values do not align with known physiological conduction speeds across cardiac tissues. *0.3 m/s, 2.2 m/s, 0.05 m/s, 1.1 m/s* - This sequence incorrectly places the **slowest velocity (0.05 m/s)** in the Purkinje system, which is known for the most rapid conduction, and assigns an unrealistically high velocity (2.2 m/s) to the AV node. - The arrangement directly contradicts the physiological function and relative speeds within the cardiac conduction system. *0.5 m/s, 1.1 m/s, 2.2 m/s, 3 m/s* - This option underestimates the **atrial muscle velocity** (0.5 m/s instead of ~1 m/s) and significantly overestimates the **ventricular muscle velocity** (3 m/s instead of ~0.3-0.5 m/s). - The provided values do not accurately represent the typical ranges of conduction velocities for each specified cardiac region.

Question 36: A 27-year-old man is running on the treadmill at his gym. His blood pressure prior to beginning his workout was 110/72. Which of the following changes in his cardiovascular system may be seen in this man now that he is exercising?

A. Decreased blood pressure
B. Decreased systemic vascular resistance (Correct Answer)
C. Increased systemic vascular resistance
D. Decreased stroke volume
E. Decreased heart rate

Explanation: ***Decreased systemic vascular resistance*** - During dynamic exercise, metabolic vasodilation in exercising muscles leads to a substantial **decrease in systemic vascular resistance (SVR)** to accommodate increased blood flow. - This vasodilation overrides the systemic vasoconstriction driven by the sympathetic nervous system, resulting in a net decrease in overall SVR. *Decreased blood pressure* - While SVR decreases, **systolic blood pressure typically increases** during exercise due to increased cardiac output. - **Diastolic blood pressure** usually remains stable or may slightly decrease, but overall blood pressure, specifically the mean arterial pressure, is generally maintained or elevated. *Increased systemic vascular resistance* - This is incorrect as **vasodilation in active muscles** causes a significant decrease in overall systemic vascular resistance. - An increase in SVR would typically hinder blood flow to working muscles and is not a characteristic cardiovascular response to dynamic exercise. *Decreased stroke volume* - Stroke volume generally **increases significantly** during exercise due to enhanced venous return, increased contractility, and reduced afterload (from decreased SVR). - A decreased stroke volume would limit cardiac output and exercise performance. *Decreased heart rate* - Heart rate **increases proportionally with exercise intensity** to boost cardiac output and oxygen delivery to active muscles. - A decreased heart rate would counteract the body's physiological demand for increased blood flow during physical activity.

Question 37: A group of investigators is performing a phase I trial of a novel drug among patients with chronic right upper quadrant pain. Iminodiacetic acid labeled with technetium 99m is administered intravenously and subjects are subsequently imaged with a gamma camera. It is found that administration of the experimental drug increases the amount of iminodiacetic acid in the intestines. The effect of this novel drug is most similar to that of a substance secreted by which of the following cells?

A. Pancreatic D cells
B. Antral G cells
C. Jejunal I cells (Correct Answer)
D. Duodenal S cells
E. Duodenal K cells

Explanation: ***Jejunal I cells*** - The imaging study with **iminodiacetic acid (HIDA)** scan assesses **gallbladder function** and bile flow; increased intestinal HIDA suggests increased bile secretion into the duodenum. - **I cells** in the jejunum secrete **cholecystokinin (CCK)**, which stimulates gallbladder contraction and the release of bile into the intestines, mimicking the drug's effect. *Pancreatic D cells* - **Pancreatic D cells** secrete **somatostatin**, a hormone that generally inhibits digestive processes, including bile secretion and gallbladder contraction. - This effect is opposite to the experimental drug's action of increasing bile flow into the intestines. *Antral G cells* - **Antral G cells** secrete **gastrin**, which primarily stimulates gastric acid secretion by parietal cells and promotes gastric motility. - Gastrin has a minimal direct effect on bile secretion or gallbladder contraction. *Duodenal S cells* - **S cells** in the duodenum secrete **secretin**, which primarily stimulates bicarbonate and water secretion from the pancreas and bile ducts, without a direct effect on gallbladder contraction or bile acid secretion. - Secretin's main role is to neutralize gastric acid in the duodenum. *Duodenal K cells* - **K cells** in the duodenum and jejunum secrete **gastric inhibitory polypeptide (GIP)**, which primarily stimulates insulin release from pancreatic beta cells in response to glucose and inhibits gastric acid secretion. - GIP does not directly stimulate bile flow or gallbladder contraction.

Question 38: A 34-year-old woman comes to the emergency department because of decreased appetite, nausea, vomiting, and episodic abdominal pain for the past two months. The pain is sharp, colicky, and lasts about an hour after meals. Her stools are light in appearance and difficult to flush. Physical examination shows tenderness in the right upper quadrant. Without treatment, this patient is at greatest risk for developing which of the following?

A. Steatohepatitis
B. Megaloblastic anemia
C. Delayed wound healing
D. Low bone mineral density (Correct Answer)
E. Glossitis

Explanation: ***Low bone mineral density*** - This patient presents with symptoms highly suggestive of **gallstones** (cholelithiasis) leading to **biliary obstruction** or **cholestasis**, evidenced by episodic postprandial colicky pain, nausea, vomiting, and light-colored, difficult-to-flush stools (steatorrhea due to **fat malabsorption**). - Chronic fat malabsorption inhibits the absorption of **fat-soluble vitamins** (A, D, E, K). A deficiency in **vitamin D** is a significant risk factor for **low bone mineral density** and **osteoporosis** over time. *Steatohepatitis* - **Steatohepatitis** (fatty liver inflammation) is typically associated with **metabolic syndrome**, chronic alcohol use, or rapid weight loss, which are not directly indicated here. - While gallstones can be linked to obesity, they do not directly cause steatohepatitis in the way described by the patient's acute symptoms. *Megaloblastic anemia* - **Megaloblastic anemia** is primarily caused by deficiencies in **vitamin B12** or **folate**. - While malabsorption can lead to B12 deficiency (e.g., in pancreatic insufficiency affecting intrinsic factor activity), biliary obstruction directly impacts fat-soluble vitamin absorption, not primarily B12 or folate. *Delayed wound healing* - **Delayed wound healing** can be a symptom of **vitamin C** or **zinc deficiency**, or overall malnutrition. - Although chronic malabsorption can lead to general malnutrition, vitamin D deficiency and its impact on bone health are a more specific and immediate long-term risk associated with the described symptoms. *Glossitis* - **Glossitis** (inflammation of the tongue) is typically associated with deficiencies in **vitamin B group** vitamins (e.g., B12, folate, niacin, riboflavin) or **iron deficiency**. - While this patient might eventually develop general nutritional deficiencies, biliary obstruction leading to fat malabsorption does not directly or primarily cause these specific B vitamin deficiencies.

Question 39: A 48-year-old female visits your office complaining that she has trouble swallowing solids and liquids, has persistent bad breath, and sometimes wakes up with food on her pillow. Manometry studies show an absence of functional peristalsis and a failure of the lower esophageal sphincter to relax upon swallowing. The patient's disorder is associated with damage to which of the following?

A. Submucosal (Meissner’s) plexus
B. Muscularis mucosa
C. Myenteric (Auerbach’s) plexus (Correct Answer)
D. Lamina propria
E. Submucosa

Explanation: ***Myenteric (Auerbach’s) plexus*** - The clinical presentation, including **dysphagia for solids and liquids**, **regurgitation**, bad breath, and findings from manometry (absence of functional peristalsis, failure of LES relaxation), is classic for **achalasia**. - Achalasia is characterized by the degeneration of ganglion cells in the **myenteric (Auerbach's) plexus** of the esophageal wall, leading to impaired esophageal motility and LES dysfunction. *Submucosal (Meissner’s) plexus* - The submucosal plexus is primarily involved in regulating **secretions and local blood flow** within the gastrointestinal tract. - While important for GI function, damage to this plexus is not the primary cause of the severe motility disorders seen in achalasia. *Muscularis mucosa* - The muscularis mucosa is a thin layer of smooth muscle within the mucosa that causes **local movements of the mucosal folds**. - It does not control the major peristaltic contractions of the esophagus or the relaxation of the lower esophageal sphincter. *Lamina propria* - The lamina propria is a layer of connective tissue within the mucosa, rich in **lymphoid tissue, blood vessels, and nerves**, providing structural support and immune function. - It does not play a direct role in regulating esophageal peristalsis or LES function. *Submucosa* - The submucosa is a layer of connective tissue that contains the **submucosal plexus, blood vessels, and lymphatic vessels**. - While it houses the submucosal plexus, the primary pathology in achalasia involves the myenteric plexus, which controls the muscularis propria responsible for peristalsis.

Question 40: A neurophysiology expert is teaching his students the physiology of the neuromuscular junction. While describing the sequence of events that takes place at the neuromuscular junction, he mentions that as the action potential travels down the motor neuron, it causes depolarization of the presynaptic membrane. This results in the opening of voltage-gated calcium channels, which leads to an influx of calcium into the synapse of the motor neuron. Consequently, the cytosolic concentration of Ca2+ ions increases. Which of the following occurs at the neuromuscular junction as a result of this increase in cytosolic Ca2+?

A. Generation of an end plate potential
B. Exocytosis of acetylcholine from the synaptic vesicles (Correct Answer)
C. Increased Na+ and K+ conductance of the motor end plate
D. Binding of Ca2+ ions to NM receptors
E. Release of Ca2+ ions into the synaptic cleft

Explanation: ***Exocytosis of acetylcholine from the synaptic vesicles*** - The increase in **cytosolic Ca2+** within the presynaptic terminal is the primary trigger for the fusion of **synaptic vesicles** filled with **acetylcholine (ACh)** with the presynaptic membrane. - This fusion process, known as **exocytosis**, releases ACh into the **synaptic cleft**, initiating synaptic transmission. *Generation of an end plate potential* - The **end plate potential (EPP)** is generated *after* acetylcholine (ACh) is released into the synaptic cleft and binds to receptors on the motor end plate. - This event occurs *following* the Ca2+-induced release of neurotransmitter, not as a direct result of the Ca2+ increase itself. *Increased Na+ and K+ conductance of the motor end plate* - Increased **Na+ and K+ conductance** across the motor end plate membrane is a direct consequence of acetylcholine binding to its receptors, which are **ligand-gated ion channels**. - This change in conductance *generates the end plate potential*, occurring after ACh release. *Binding of Ca2+ ions to NM receptors* - **NM receptors** (nicotinic muscle receptors) are located on the **postsynaptic membrane** (motor end plate) and bind to **acetylcholine (ACh)**, not Ca2+ ions. - Calcium's primary role in this context is presynaptic: triggering ACh release. *Release of Ca2+ ions into the synaptic cleft* - Calcium ions enter the **presynaptic terminal** from the synaptic cleft, and their increased cytosolic concentration within the presynaptic terminal drives neurotransmitter release. - Calcium itself is not released *into* the synaptic cleft in this process; rather, it enters the presynaptic neuron from the cleft.

Question 41: An investigator is studying muscle contraction in tissue obtained from the thigh muscle of an experimental animal. After injection of radiolabeled ATP, the tissue is stimulated with electrical impulses. Radioassay of these muscle cells is most likely to show greatest activity in which of the following structures?

A. H zone
B. M line
C. A band (Correct Answer)
D. Z line
E. I band

Explanation: ***A band*** - The **A band** contains the entire length of the **thick myosin filaments** along with the **overlap zone** where myosin and actin interact. Myosin has **ATPase activity**, meaning it binds and hydrolyzes **ATP** to power muscle contraction through cross-bridge cycling. - Therefore, the greatest accumulation of **radiolabeled ATP** and its breakdown products would be found where **myosin heads** are located throughout the A band. - The A band represents the most complete answer as it encompasses all regions containing myosin ATPase activity. *H zone* - The **H zone** is the central part of the **A band** where only **thick myosin filaments** are present, with no overlap with thin actin filaments. - While myosin heads with ATPase activity are present here and would show radiolabeled ATP, the **H zone** is only a **subset** of the A band. The **A band** is the more comprehensive answer as it includes both the H zone and the overlap regions where most cross-bridge cycling occurs. *M line* - The **M line** is the very center of the **H zone** and anchors the **thick filaments**. - It consists of structural proteins like **myomesin** and **creatine kinase**. While creatine kinase can phosphorylate ADP to regenerate ATP, it does not directly hydrolyze ATP for muscle contraction the way myosin ATPase does. *Z line* - The **Z line** (or Z disc) marks the boundaries of a **sarcomere** and anchors the **thin actin filaments**. - It contains proteins like **alpha-actinin** and **desmin** but does not directly consume ATP for muscle contraction. *I band* - The **I band** contains only **thin actin filaments** and extends from the edge of the A band to the Z line. - While actin is crucial for contraction, it does not possess **ATPase activity**; ATP hydrolysis primarily occurs at the **myosin heads** located in the A band.

Question 42: A 40-year-old Caucasian male presents to the emergency room after being shot in the arm in a hunting accident. His shirt is soaked through with blood. He has a blood pressure of 65/40, a heart rate of 122, and his skin is pale, cool to the touch, and moist. This patient is most likely experiencing all of the following EXCEPT:

A. Decreased sarcomere length in the myocardium
B. Increased stroke volume (Correct Answer)
C. Confusion and irritability
D. Decreased preload
E. Increased thromboxane A2

Explanation: ***Increased stroke volume*** - The patient is experiencing **hypovolemic shock** due to significant blood loss, meaning their **cardiac output** is severely compromised. - In shock, the heart attempts to compensate by increasing **heart rate**, but **stroke volume** is typically decreased due to reduced **preload**. *Decreased sarcomere length in the myocardium* - In situations of significant blood loss and **decreased preload**, there is less venous return to the heart, leading to reduced end-diastolic volume. - According to the **Frank-Starling law**, reduced end-diastolic volume results in shorter initial sarcomere length, which reduces the force of contraction and thus, **stroke volume**. *Confusion and irritability* - **Hypovolemic shock** leads to widespread **tissue hypoperfusion**, especially to vital organs like the brain. - Reduced cerebral blood flow results in impaired brain function, manifesting as **confusion, irritability**, and altered mental status. *Decreased preload* - Significant blood loss leads to a reduction in the **total circulating blood volume**. - This reduction directly decreases the venous return to the heart, thus lowering the **end-diastolic volume** and subsequently, the **preload**. *Increased thromboxane A2* - In response to **vascular injury and bleeding**, the body initiates hemostasis, a critical component of which is platelet aggregation. - **Thromboxane A2** is a potent vasoconstrictor and platelet aggregator released by activated platelets to form a **platelet plug** and help stop bleeding.

Question 43: A 56-year-old woman is admitted to the hospital for progressive bilateral lower extremity weakness and absent deep tendon reflexes. Cerebrospinal fluid analysis shows an elevated protein concentration and a normal cell count. Treatment with plasmapheresis is initiated, after which her symptoms start to improve. Four weeks after her initial presentation, physical examination shows normal muscle strength in the bilateral lower extremities and 2+ deep tendon reflexes. Which of the following changes in neuronal properties is the most likely explanation for the improvement in her neurological examination?

A. Increase in length constant (Correct Answer)
B. Decrease in action potential amplitude
C. Decrease in transmembrane resistance
D. Increase in axial resistance
E. Increase in axonal capacitance

Explanation: ***Increase in length constant*** - The clinical picture of **Guillain-Barré Syndrome (GBS)** involves **demyelination**, leading to a *decrease* in the **length constant**, which impairs action potential propagation. - **Plasmapheresis** in GBS helps remove autoantibodies, allowing for remyelination or repair, thereby *increasing* the **length constant** and improving nerve conduction. *Decrease in action potential amplitude* - A decrease in action potential amplitude would indicate *worsening* nerve function, not improvement, as it suggests the nerve is less able to generate strong electrical signals. - The amplitude of an action potential is primarily determined by the **number and conductance of voltage-gated sodium channels**, not directly affected in a way that would reflect recovery by a *decrease*. *Decrease in transmembrane resistance* - A *decrease* in **transmembrane resistance** (resistance to current flow across the membrane) would allow more current to leak out, *reducing* the length constant and *impairing* conduction. - In GBS, demyelination already causes a *decrease* in transmembrane resistance; recovery would involve an *increase* in resistance due to remyelination. *Increase in axial resistance* - An *increase* in **axial resistance** (resistance to current flow along the axon) would *impede* the spread of depolarization and *slow* conduction velocity. - Factors such as **axon diameter** affect axial resistance, and an *increase* would lead to *worsening* of neurological function, not improvement. *Increase in axonal capacitance* - An *increase* in **axonal capacitance** would mean the axon requires more charge to change its voltage, thus *slowing down* the rate of depolarization and *impairing* conduction velocity. - **Myelination** *reduces* capacitance, which is crucial for rapid signal propagation; an *increase* would be detrimental to nerve function.

Question 44: A 45-year-old man comes to the physician because of persistent reddening of the face for the past 3 months. During this period he also had difficulty concentrating at work and experienced generalized fatigue. He has fallen asleep multiple times during important meetings. His mother has rheumatoid arthritis. He has hypertension and asthma. He has smoked one pack of cigarettes daily for 28 years and drinks one alcoholic beverage per day. Medications include labetalol and a salbutamol inhaler. He is 170 cm (5 ft 7 in) tall and weighs 88 kg (194 lb); BMI is 30.4 kg/m2. His temperature is 37.1°C (98.8°F), pulse is 88/min, respirations are 14/min, and blood pressure is 145/85 mm Hg. Physical examination shows erythema of the face that is especially pronounced around the cheeks, nose, and ears. His neck appears short and wide. The remainder of the examination shows no abnormalities. Which of the following is the most likely cause of this patient's facial discoloration?

A. Increased cortisol levels
B. Delayed-type hypersensitivity
C. Antibody-mediated vasculopathy
D. Increased serotonin levels
E. Increased EPO production (Correct Answer)

Explanation: ***Increased EPO production*** - The patient's **facial redness (plethora)**, **fatigue**, **difficulty concentrating**, and **sleepiness** are characteristic symptoms of **polycythemia**, which can be caused by increased **erythropoietin (EPO)** production. - His chronic smoking (**28 pack-years**) and obesity (**BMI 30.4 kg/m²**) put him at high risk for **chronic hypoxemia** (e.g., from **COPD** or **sleep apnea**), which can trigger a compensatory increase in EPO and subsequent **secondary polycythemia**. *Increased cortisol levels* - Increased cortisol (e.g., in **Cushing's syndrome**) can cause **facial plethora** and fatigue, but it is typically associated with features like **central obesity**, **striae**, muscle weakness, and new-onset diabetes, which are not described. - While he has hypertension and obesity, the primary complaint of prominent facial redness and hypersomnia points more specifically to a red blood cell disorder. *Delayed-type hypersensitivity* - This mechanism is associated with **allergic contact dermatitis** or other inflammatory skin conditions, typically characterized by **itching**, **blistering**, or **eczematous changes**. - It does not explain the generalized symptoms of fatigue, difficulty concentrating, or the specific appearance of uniform facial redness (plethora). *Antibody-mediated vasculopathy* - Conditions like **lupus** or **vasculitis** can cause skin manifestations, but these usually present as specific lesions (e.g., **rashes**, **ulcers**, **purpura**) or systemic symptoms of inflammation, rather than just generalized facial redness. - The patient's symptoms are more consistent with a volume-related issue rather than an immune-mediated vascular inflammation. *Increased serotonin levels* - Elevated serotonin, such as in **carcinoid syndrome**, can cause episodic **flushing** and fatigue. - However, carcinoid syndrome is also typically associated with **diarrhea**, **bronchospasm**, and **cardiac valvular lesions**, none of which are mentioned in this patient's presentation.

Question 45: A 26-year-old male engineer presents to a reproductive specialist due to the inability to conceive after 2 years of trying with his 28-year-old wife. He reports that he is healthy without any significant medical history, surgeries, or medications. He was adopted at 17 years-old. On exam, he is well appearing without dysmorphic features. He has a high pitched voice, absent facial hair, is 5 feet 8 inches tall, and has a BMI of 19 kg/m^2. On genitourinary exam, his testicles are descended bilaterally without varicoceles, and testicular volume is 8cc bilaterally. He has a stretched penile length of 6cm. He has labwork from his primary care physician that is significant for low LH, FSH, and testosterone. What is the most likely cause of his infertility?

A. Primary Hypogonadism
B. Fragile X Syndrome
C. Kleinfelter Syndrome
D. Prader-Willi Syndrome
E. Kallman Syndrome (Correct Answer)

Explanation: ***Kallman Syndrome*** - The patient presents with **hypogonadotropic hypogonadism** (low LH, FSH, and testosterone) and associated features like **absent facial hair**, **high-pitched voice**, and **micropenis** (stretched penile length of 6cm). While not explicitly stated, **anosmia** or **hyposmia** is a hallmark of Kallman syndrome, differentiating it from other causes of hypogonadotropic hypogonadism. - The patient's presentation with **infertility** and signs of **incomplete pubertal development** (absent facial hair, high-pitched voice, reduced testicular volume of 8cc) in the context of low gonadotropins points to a central defect in gonadotropin-releasing hormone secretion, characteristic of Kallman syndrome. *Primary Hypogonadism* - This condition is characterized by **elevated LH and FSH** with low testosterone, due to a problem with testicular function, which is contrary to the patient's lab results of low LH and FSH. - While it causes **infertility** and **low testosterone**, it does not typically present with the specific constellation of symptoms like micropenis and absent facial hair in the presence of low gonadotropins. *Fragile X Syndrome* - This syndrome is associated with **intellectual disability**, **macroorchidism** (large testes), and distinctive facial features, none of which are described in the patient. - While it can cause infertility, it is not typically associated with **hypogonadotropic hypogonadism** or the specific phenotypic features presented. *Kleinfelter Syndrome* - This is a form of **primary hypogonadism** (47,XXY karyotype) characterized by **small, firm testes**, gynecomastia, and typically **elevated FSH and LH** due to testicular failure. - The patient's lab results show **low LH and FSH**, and the testicular volume, while small, is not described as "firm," making Klinefelter syndrome less likely. *Prader-Willi Syndrome* - This syndrome is characterized by **obesity**, **intellectual disability**, and **hypotonia**, alongside hypogonadism, which are not consistent with the patient's presentation (BMI 19, no intellectual disability mentioned). - The hypogonadism in Prader-Willi syndrome is **hypogonadotropic**, but the absence of other defining features makes this diagnosis less probable.

Question 46: A recently deceased 92-year-old woman with a history of arrhythmia was discovered to have amyloid deposition in her atria upon autopsy. Upon further examination, there was no amyloid found in any other organs. The peptide at fault was identified and characterized by the pathologist performing the autopsy. Before its eventual deposition in the cardiac atria, which of the following functions was associated with the peptide?

A. Antigen recognition
B. Reduction of blood calcium concentration
C. Stimulation of lactation
D. Vasodilation (Correct Answer)
E. Slowing of gastric emptying

Explanation: ***Vasodilation*** - The description of amyloid deposition confined to the atria in an elderly patient points to **isolated atrial amyloidosis**, which involves the deposition of **atrial natriuretic peptide (ANP)**. - Before deposition, ANP's primary function is to promote **vasodilation** and natriuresis, contributing to blood pressure regulation. *Antigen recognition* - **Antigen recognition** is a function of proteins like immunoglobulins and T-cell receptors, which are not typically involved in isolated atrial amyloidosis. - Amyloid associated with antigen recognition is usually **AL amyloidosis (light-chain amyloidosis)**, which is systemic and affects multiple organs, unlike the localized deposition described. *Reduction of blood calcium concentration* - The reduction of blood calcium concentration is primarily mediated by **calcitonin**, a hormone secreted by the thyroid gland. - This function is unrelated to the atrial amyloidosis described, which involves a peptide from cardiac myocytes. *Stimulation of lactation* - **Lactation** is stimulated by hormones like **prolactin** and oxytocin, which are produced in the pituitary gland and hypothalamus, respectively. - This process is entirely unconnected to the peptide responsible for amyloid deposition in the heart. *Slowing of gastric emptying* - **Slowing of gastric emptying** can be influenced by various hormones, such as **peptide YY** or **glucagon-like peptide-1 (GLP-1)**, which are primarily secreted in the gastrointestinal tract. - This physiological process is not linked to the function of ANP or the pathology of atrial amyloidosis.

Question 47: A researcher is studying physiologic and hormonal changes that occur during pregnancy. Specifically, they examine the behavior of progesterone over the course of the menstrual cycle and find that it normally decreases over time; however, during pregnancy this decrease does not occur in the usual time frame. The researcher identifies a circulating factor that appears to be responsible for this difference in progesterone behavior. In order to further examine this factor, the researcher denatures the circulating factor and examines the sizes of its components on a western blot as compared to several other hormones. One of the bands the researcher identifies in this circulating factor is identical to that of another known hormone with which of the following sites of action?

A. Thyroid gland (Correct Answer)
B. Adrenal gland
C. Adipocytes
D. Bones
E. Kidney tubules

Explanation: ***Correct: Thyroid gland*** - The circulating factor described is **human chorionic gonadotropin (hCG)**, which maintains the corpus luteum and progesterone production during early pregnancy - hCG is a **glycoprotein hormone** composed of an **α subunit** and a **β subunit** - The **α subunit of hCG is identical** to the α subunits of **TSH (thyroid-stimulating hormone)**, **LH (luteinizing hormone)**, and **FSH (follicle-stimulating hormone)** - When denatured and examined on Western blot, one of the bands (the α subunit) would be identical to that of **TSH** - **TSH acts on the thyroid gland** to stimulate thyroid hormone synthesis and release - This structural similarity explains why very high levels of hCG (as in molar pregnancy or hyperemesis gravidarum) can sometimes cause **thyrotoxicosis** due to cross-reactivity with TSH receptors *Incorrect: Adrenal gland* - **ACTH (adrenocorticotropic hormone)** acts on the adrenal cortex to stimulate cortisol production - ACTH is a **peptide hormone** derived from POMC (pro-opiomelanocortin) and does **NOT share any structural components** with hCG - There is no identical band between hCG and ACTH on Western blot *Incorrect: Adipocytes* - Adipocytes are regulated by hormones like **insulin** and **leptin** - Neither of these hormones share structural components with hCG *Incorrect: Bones* - Bones are primarily regulated by **PTH (parathyroid hormone)**, **calcitonin**, and **vitamin D** - None of these hormones share structural components with hCG *Incorrect: Kidney tubules* - Kidney tubules are regulated by **ADH (antidiuretic hormone/vasopressin)** and **aldosterone** - Neither shares structural components with hCG

Question 48: A group of scientists discovered a neurotoxin that prevents neurons from releasing neurotransmitters. They performed a series of experiments to determine the protein that the neurotoxin affected. They used a fluorescent molecule that localizes to synaptic vesicles. In the control experiment, they observed the movement of vesicles from the cell body down the axon and finally to the synapse, and they saw movement from the synapse back to the cell body. When the neurotoxin was applied, the vesicles stopped moving down the axon, but movement back to the cell body still occurred. They also applied tetanospasmin and botulinum toxin to see if these toxins exhibited similar behavior but they did not. Which of the following proteins is most likely affected by this neurotoxin?

A. SNAP-25
B. Kinesin (Correct Answer)
C. Dynein
D. Synaptobrevin
E. Alpha/Beta tubulin

Explanation: ***Kinesin*** - Kinesin is a **motor protein** responsible for **anterograde transport** (movement away from the cell body) of vesicles along microtubules in axons. - The neurotoxin stopping vesicles from moving down the axon indicates interference with anterograde transport, which is primarily mediated by kinesin. *SNAP-25* - **SNAP-25** is a component of the **SNARE complex** involved in the fusion of synaptic vesicles with the presynaptic membrane, leading to neurotransmitter release. - Tetanospasmin and botulinum toxin, which affect neurotransmitter release, specifically cleave SNARE proteins like SNAP-25, but the described toxin's effect on vesicle *movement* rather than *fusion* differentiates it. *Dynein* - Dynein is a **motor protein** responsible for **retrograde transport** (movement towards the cell body) of vesicles along microtubules. - The observation that movement back to the cell body (retrograde transport) still occurred after neurotoxin application rules out dynein as the affected protein. *Synaptobrevin* - **Synaptobrevin** (also known as VAMP) is another component of the **SNARE complex**, located on the vesicle membrane, crucial for neurotransmitter release. - Its disruption would primarily impair vesicle fusion and neurotransmitter release, similar to SNAP-25, but would not directly stop the *downstream movement* of vesicles. *Alpha/Beta tubulin* - **Alpha/beta tubulin dimers** are the building blocks of **microtubules**, which serve as tracks for both anterograde and retrograde transport. - While microtubules are essential for vesicle movement, if tubulin itself were directly affected, both anterograde and retrograde transport would likely be impaired, which contradicts the observation that retrograde movement continued.

Question 49: A 20-year-old man is brought to the emergency room for evaluation of a back injury sustained while at work. A CT scan of the lumbar spine shows an incidental 2-cm mass adjacent to the inferior vena cava. Histologic examination of a biopsy specimen of the mass shows clusters of chromaffin cells. This mass is most likely to secrete which of the following substances?

A. Aldosterone
B. Dehydroepiandrosterone
C. Norepinephrine (Correct Answer)
D. Cortisol
E. Estrogen

Explanation: **Norepinephrine** - The description of a mass with **clusters of chromaffin cells** is characteristic of a **pheochromocytoma**, a tumor typically arising from the **adrenal medulla**. - **Pheochromocytomas** are known to secrete catecholamines, primarily **norepinephrine** and epinephrine. *Aldosterone* - **Aldosterone** is secreted by the **zona glomerulosa** of the **adrenal cortex** and is involved in blood pressure regulation. - Tumors secreting aldosterone are usually **aldosteronomas** (Conn's syndrome) and do not arise from chromaffin cells. *Dehydroepiandrosterone* - **Dehydroepiandrosterone (DHEA)** is an **adrenal androgen** secreted by the **zona reticularis** of the adrenal cortex. - Its secretion is associated with cortical tumors or hyperplasia, not chromaffin cell tumors. *Cortisol* - **Cortisol** is a glucocorticoid produced by the **zona fasciculata** of the **adrenal cortex**. - Elevated cortisol levels are usually due to **Cushing's syndrome**, often caused by adrenal adenomas or hyperplasia, not chromaffin cell tumors. *Estrogen* - While small amounts of **estrogen** can be produced by the adrenal glands, the primary sites of estrogen synthesis are the **ovaries** and **placenta**. - A tumor composed of **chromaffin cells** is not typically associated with significant estrogen secretion.

Question 50: A 65-year-old man comes to his primary care physician for a routine health maintenance examination. He takes no medications. Physical examination and laboratory studies show no abnormalities. Compared to a healthy adolescent, this patient is most likely to have which of the following changes in immune function?

A. Decreased responsiveness to vaccines (Correct Answer)
B. Increased number of circulating B cells
C. Decreased number of neutrophil precursors
D. Increased complement protein production
E. Decreased autoimmunity

Explanation: ***Decreased responsiveness to vaccines*** - With aging, the immune system undergoes **immunosenescence**, leading to a decline in both humoral and cell-mediated immunity. This includes reduced ability to produce a robust and lasting immune response to new antigens, such as those introduced by **vaccines**. - Specifically, there is a decrease in the number and function of naive B and T cells, impairing the body's capacity to generate optimal primary and secondary antibody responses, making older adults less responsive to immunization. *Increased number of circulating B cells* - The total number of circulating **B cells** generally remains stable or slightly decreases with age, but their functional capacity often declines. - While some specific B cell subsets might increase, overall B cell production and their ability to produce high-affinity antibodies is usually impaired in the elderly. *Decreased number of neutrophil precursors* - The production of **neutrophils** and their precursors in the bone marrow is generally maintained or even increased in older adults, though their functional efficiency (e.g., phagocytosis, chemotaxis) may be slightly reduced. - Significant decreases in neutrophil precursors are not a typical feature of normal aging but rather indicative of bone marrow suppression or specific hematologic conditions. *Increased complement protein production* - **Complement protein production** generally remains stable or shows minor changes with aging, with some components potentially increasing, but a significant and widespread increase is not characteristic. - The overall function of the complement system may be marginally altered, but elderly individuals do not typically exhibit globally increased complement protein synthesis. *Decreased autoimmunity* - Autoimmunity often **increases with age**, not decreases. This is due to a decline in immune tolerance, impaired clearance of apoptotic cells, and cumulative exposure to various environmental triggers. - The incidence of many **autoimmune diseases**, such as giant cell arteritis and polymyalgia rheumatica, is higher in older adults.

Question 51: A 44-year-old female with a 3-year history of biliary colic presents with acute cholecystitis. After further evaluation, she undergoes a laparoscopic cholecystectomy without complication. Which of the following is true following this procedure?

A. Lipid absorption is increased
B. Lipid absorption is unaffected
C. Lipid absorption is decreased
D. The overall amount of bile acids is reduced
E. The composition of the bile acid pool is altered (Correct Answer)

Explanation: ***The composition of the bile acid pool is altered*** - While major changes in overall lipid absorption are uncommon after cholecystectomy, the removal of the gallbladder eliminates its role in **concentrating and storing bile**. This can lead to a more continuous, albeit less concentrated, flow of bile into the duodenum, subtly altering the **bile acid composition** to favor primary bile acids over secondary bile acids. - The liver continuously produces bile, and without the gallbladder to modify and store it, the enterohepatic circulation's dynamics change, impacting the ratios of various bile acids. *Lipid absorption is increased* - This is generally false; the gallbladder's primary role is to store and concentrate bile for fat digestion, but its removal does not typically lead to an overall increase in lipid absorption. - While prompt bile delivery might improve absorption in some specific scenarios, it's not a general outcome. *Lipid absorption is unaffected* - Although the majority of patients tolerate cholecystectomy without significant malabsorption, some subtle changes in digestion can occur. - The absence of concentrated bile release can alter the efficiency of fat emulsification, meaning it's not entirely unaffected, though often not clinically significant. *Lipid absorption is decreased* - Significant **lipid malabsorption with steatorrhea** is rare after cholecystectomy in patients with normal liver and pancreatic function. - While the *regulation* of bile delivery changes, the overall capacity for lipid digestion and absorption is usually maintained due to continuous bile production by the liver. *The overall amount of bile acids is reduced* - The liver continues to produce bile acids, and these are still recycled via the **enterohepatic circulation**. - While the *concentration* of bile released at any one time may be lower, the overall daily production and circulation of bile acids are generally maintained.

Question 52: A 33-year-old pilot is transported to the emergency department after she was involved in a cargo plane crash during a military training exercise in South Korea. She is conscious but confused. She has no history of serious illness and takes no medications. Physical examination shows numerous lacerations and ecchymoses over the face, trunk, and upper extremities. The lower extremities are cool to the touch. There is continued bleeding despite the application of firm pressure to the sites of injury. The first physiologic response to develop in this patient was most likely which of the following?

A. Increased respiratory rate
B. Increased capillary refill time
C. Decreased systolic blood pressure
D. Decreased urine output
E. Increased heart rate (Correct Answer)

Explanation: ***Increased heart rate*** - **Tachycardia** is often the first physiological response to **hypovolemia** (due to hemorrhage, such as that stemming from multiple lacerations). The heart attempts to compensate for reduced circulating blood volume by increasing its pumping rate. - This sympathetic nervous system response aims to maintain **cardiac output** and tissue perfusion as **blood pressure** and **venous return** start to fall. *Increased respiratory rate* - An increased respiratory rate, or **tachypnea**, typically occurs later as the body attempts to compensate for decreased oxygen delivery and metabolic acidosis that can result from sustained hypoperfusion and shock. - While significant, it usually follows the initial hemodynamic adjustments of the heart. *Increased capillary refill time* - **Increased capillary refill time** indicates impaired peripheral perfusion and is a sign of more significant **hypovolemic shock**, often occurring after initial compensatory mechanisms have been activated. - This reflects **peripheral vasoconstriction**, a later compensatory mechanism, rather than the very first physiological response. *Decreased systolic blood pressure* - **Decreased systolic blood pressure** (hypotension) is a later sign of shock and indicates a failure of the body's compensatory mechanisms to maintain adequate blood volume and perfusion, often reflecting a loss of more than 30-40% of blood volume. - The body initially tries to maintain blood pressure through increased heart rate and vasoconstriction before it drops. *Decreased urine output* - **Decreased urine output** (oliguria) is a renal compensatory mechanism in response to reduced renal perfusion and increased antidiuretic hormone (ADH) release, aiming to conserve fluid. - This response takes time to manifest and is not typically the very first physiological change after acute blood loss.

Question 53: A 35-year-old woman presents with exertional dyspnea and fatigue for the past 3 weeks. She says there has been an acute worsening of her dyspnea in the past 5 days. On physical examination, the mucous membranes show pallor. Cardiac exam is significant for the presence of a mid-systolic murmur loudest in the 2nd left intercostal space. A CBC and peripheral blood smear show evidence of microcytic, hypochromic anemia. Which of the following parts of the GI tract is responsible for the absorption of the nutrient whose deficiency is most likely responsible for this patient’s condition?

A. Duodenum (Correct Answer)
B. Jejunum
C. Terminal ileum
D. Body of the stomach
E. Antrum of the stomach

Explanation: ***Duodenum*** - The patient's presentation with **exertional dyspnea**, **fatigue**, **pallor**, and **microcytic, hypochromic anemia** strongly indicates **iron deficiency anemia**. - The **duodenum** is the primary site for **iron absorption** in the gastrointestinal tract, specifically in its acidic environment. *Jejunum* - The jejunum is primarily responsible for the absorption of most **nutrients** like carbohydrates, proteins, and fats. - While some minimal iron absorption can occur here, it is not the main site for **dietary iron uptake**. *Terminal ileum* - The **terminal ileum** is the key site for the absorption of **vitamin B12** (cobalamin) and **bile salts**. - Deficiency in vitamin B12 leads to **macrocytic anemia**, which is not consistent with this patient's microcytic anemia. *Body of the stomach* - The body of the stomach produces **hydrochloric acid** and **intrinsic factor** from parietal cells. - While HCl is crucial for releasing iron from food, the stomach itself is not a primary site for **iron absorption**. *Antrum of the stomach* - The antrum of the stomach is mainly involved in **grinding food** and initiating digestion, as well as producing **gastrin**. - It plays no direct role in the absorption of **iron** or other micronutrients responsible for the patient's anemic symptoms.

Question 54: A 30-year-old gravida 1 woman comes to the office for a prenatal visit. She is at 20 weeks gestation with no complaints. She is taking her prenatal vitamins but stopped the prescribed ferrous sulfate because it was making her constipated. Urinalysis shows trace protein. Uterine fundus is the expected size for a 20-week gestation. Just before leaving the examination room, she stops the physician and admits to eating laundry detergent. She is embarrassed and fears she is going crazy. Which of the following is the most likely diagnosis?

A. Normal pregnancy
B. Iron deficiency anemia (Correct Answer)
C. Plummer-Vinson syndrome
D. Brief psychotic disorder
E. Pre-eclampsia

Explanation: ***Iron deficiency anemia*** - The patient exhibits **pica** (craving and eating non-food substances such as laundry detergent), which is a common manifestation of **iron deficiency anemia** in pregnant women. - She also stopped taking **ferrous sulfate** due to constipation, indicating a potential ongoing iron deficiency that is now symptomatic. - Pica in pregnancy is strongly associated with iron deficiency and typically resolves with iron supplementation. *Normal pregnancy* - While trace protein in urine can be normal in pregnancy, **pica** (eating non-food items) is not a normal physiological finding and suggests an underlying nutritional deficiency. - The patient's admission of shame and fear of "going crazy" further indicates this is a pathological behavior requiring evaluation. *Plummer-Vinson syndrome* - This syndrome is characterized by **iron deficiency anemia**, **dysphagia** (due to esophageal webs), and **glossitis**. - Although the patient likely has iron deficiency, dysphagia and glossitis are not mentioned, making this specific syndrome diagnosis less likely without the classic triad. *Brief psychotic disorder* - This disorder involves a sudden onset of **psychotic symptoms** such as delusions, hallucinations, or disorganized speech, lasting less than a month. - Pica, while unusual behavior, is not a primary psychotic symptom and is specifically linked to nutritional deficiencies (particularly iron) rather than a thought disorder. *Pre-eclampsia* - Pre-eclampsia is characterized by **new-onset hypertension** (blood pressure ≥140/90 mmHg) and **proteinuria** after 20 weeks of gestation. - The patient's blood pressure is not mentioned, and while she has trace proteinuria, there is no indication of hypertension or other classic symptoms like severe headaches, visual disturbances, or right upper quadrant pain.

Question 55: A 53-year-old man comes to the physician because of fatigue, recurrent diarrhea, and an 8-kg (17.6-lb) weight loss over the past 6 months. He has a 4-month history of recurrent blistering rashes on different parts of his body that grow and develop into pruritic, crusty lesions before resolving spontaneously. Physical examination shows scaly lesions in different phases of healing with central, bronze-colored induration around the mouth, perineum, and lower extremities. Laboratory studies show: Hemoglobin 10.1 mg/dL Mean corpuscular volume 85 μm3 Mean corpuscular hemoglobin 30.0 pg/cell Serum Glucose 236 mg/dL Abdominal ultrasonography shows a 3-cm, solid mass located in the upper abdomen. This patient's mass is most likely derived from which of the following types of cells?

A. Gastrointestinal enterochromaffin cells
B. Pancreatic β-cells
C. Pancreatic δ-cells
D. Pancreatic α-cells (Correct Answer)
E. Gastric G-cells

Explanation: ***Pancreatic α-cells*** - The patient's symptoms of **fatigue, recurrent diarrhea, weight loss, blistering rash (necrolytic migratory erythema)**, and **hyperglycemia** are classic features of a **glucagonoma**. - A **glucagonoma** is a tumor of the pancreatic α-cells that **secretes excessive glucagon**, leading to these characteristic signs and symptoms, supported by the presence of an **upper abdominal mass**. *Gastrointestinal enterochromaffin cells* - Tumors of gastrointestinal enterochromaffin cells (carcinoid tumors) typically produce **serotonin** and present with flushing, diarrhea, bronchospasm, and valvular heart disease, not the skin rash or hyperglycemia seen here. - While carcinoid tumors can cause diarrhea, the additional symptoms of **necrolytic migratory erythema** and **diabetes** are not characteristic. *Pancreatic β-cells* - Tumors of pancreatic β-cells (**insulinomas**) produce excessive insulin, leading to **hypoglycemia**, not the hyperglycemia observed in this patient. - Insulinomas cause symptoms like sweating, tremors, confusion, and palpitations, which are inconsistent with the patient's presentation. *Pancreatic δ-cells* - Pancreatic δ-cell tumors (**somatostatinomas**) secrete **somatostatin**, which can cause **diabetes mellitus**, steatorrhea, and gallstones. - While diabetes is present, the characteristic **necrolytic migratory erythema** and severe diarrhea are less common with somatostatinomas. *Gastric G-cells* - Tumors of gastric G-cells (**gastrinomas**) secrete **gastrin**, leading to **Zollinger-Ellison syndrome**, characterized by severe peptic ulcers, abdominal pain, and chronic diarrhea. - Gastrinomas do not typically cause **necrolytic migratory erythema** or significant hyperglycemia.

Question 56: A 25-year-old patient is brought into the emergency department after he was found down by the police in 5 degree celsius weather. The police state the patient is a heroin-user and is homeless. The patient's vitals are T 95.3 HR 80 and regular BP 150/90 RR 10. After warming the patient, you notice his left lower leg is now much larger than his right leg. On exam, the patient has a loss of sensation on his left lower extremity. There is a faint palpable dorsalis pedal pulse, but no posterior tibial pulse. The patient is unresponsive to normal commands, but shrieks in pain upon passive stretch of his left lower leg. What is the most probable cause of this patient's condition?

A. Diabetes
B. Cellulitis
C. Embolized clot
D. Reperfusion associated edema (Correct Answer)
E. Necrotizing fasciitis

Explanation: ***Reperfusion associated edema*** - The patient's history of being found in cold weather, along with signs of **hypothermia** (T 95.3), suggests a period of **ischemia** followed by reperfusion. The sudden swelling, pain on passive stretch, and sensory loss in the left lower leg are classic signs of **compartment syndrome**, which can be triggered by reperfusion injury and edema. - While a faint dorsalis pedis pulse is present, the absence of a posterior tibial pulse indicates significant compromised blood flow, and the severe pain on passive stretch is a hallmark of increased pressure within a muscle compartment. *Diabetes* - While diabetes can cause neuropathy and vascular complications, it does not typically present with acute, severe localized swelling and pain on passive stretch in a previously healthy 25-year-old. - The acute nature of the symptoms following exposure to cold and subsequent warming points away from chronic diabetic complications. *Cellulitis* - Cellulitis is a bacterial skin infection that would typically present with **erythema**, **warmth**, and spreading tenderness, but not the severe, deep, and acute pain on passive stretch or the profound sensory deficit seen here. - It does not explain the initial period of cold exposure followed by reperfusion. *Embolized clot* - An embolized clot would cause acute limb ischemia, characterized by the "6 Ps" (**pain, pallor, pulselessness, paresthesias, paralysis, poikilothermia**). While the patient has some of these, the dramatic swelling *after warming* and the pain on passive stretch are more indicative of compartment syndrome due to reperfusion. - The presence of a faint dorsalis pedal pulse makes complete arterial occlusion less likely, though significant compromise is present. *Necrotizing fasciitis* - Necrotizing fasciitis presents with rapidly progressing pain out of proportion to exam, skin changes (e.g., **bullae, crepitus, discoloration**), and systemic toxicity. While serious, it does not fit the context of acute swelling and pain primarily triggered by reperfusion after cold exposure. - The primary presentation here is related to pressure-induced injury from edema, not primarily an aggressive bacterial infection of the fascia.

Question 57: A 35-year-old man presents to the physician’s clinic due to episodic chest pain over the last couple of months. He is currently pain-free. His chest pain occurs soon after he starts to exercise, and it is rapidly relieved by rest. He recently started training for a marathon after a decade of a fairly sedentary lifestyle. He was a competitive runner during his college years, but he has only had occasional exercise since then. He is concerned that he might be developing some heart disease. He has no prior medical issues and takes no medications. The family history is significant for hypertension and myocardial infarction in his father. His vital signs include: pulse 74/min, respirations 10/min, and blood pressure 120/74 mm Hg. The ECG test is normal. The physician orders an exercise tolerance test that has to be stopped after 5 minutes due to the onset of chest pain. Which of the following contributes most to the decreasing cardiac perfusion in this patient's heart?

A. Ventricular blood volume
B. Force of myocardial contraction
C. Duration of diastole (Correct Answer)
D. Coronary vasoconstriction
E. Diastolic aortic pressure

Explanation: ***Duration of diastole*** - As heart rate increases during exercise, the **duration of diastole** decreases significantly because systole duration is relatively fixed. - The majority of **coronary artery blood flow** to the left ventricle occurs during diastole, so a shortened diastole reduces the time available for myocardial perfusion, especially when oxygen demand is high. *Ventricular blood volume* - **Ventricular blood volume** (preload) generally increases with exercise due to enhanced venous return, which would typically increase stroke volume and cardiac output, not directly decrease cardiac perfusion in the coronary arteries. - While extreme volume overload can stress the heart, it is not the primary factor limiting perfusion in a patient with exercise-induced chest pain indicative of ischemia. *Force of myocardial contraction* - An increased **force of myocardial contraction** (contractility) during exercise raises the heart's oxygen demand because the heart has to work harder. - While increased contractility contributes to higher oxygen demand, it does not directly *decrease* the supply of blood (perfusion) to the heart muscle itself; rather, it highlights the inadequacy of existing perfusion. *Coronary vasoconstriction* - While **coronary vasoconstriction** can reduce blood flow, in this patient with exercise-induced chest pain, the primary issue is likely **fixed atherosclerotic plaques** that prevent adequate vasodilation with increased demand. - *Primary* coronary vasoconstriction is characteristic of conditions like **Prinzmetal angina**, which typically presents with chest pain at rest, not exertion. *Diastolic aortic pressure* - **Diastolic aortic pressure** is the main driving force for coronary blood flow; if it is too low, perfusion can suffer. - While a severely low diastolic pressure would impair perfusion, this patient's blood pressure is normal, and it's less likely the primary factor compared to the reduced time for filling during stress.

Question 58: A 33-year-old man is evaluated by paramedics after being found unconscious outside of his home. He has no palpable pulses. Physical examination shows erythematous marks in a fern-leaf pattern on his lower extremities. An ECG shows ventricular fibrillation. Which of the following is the most likely cause of this patient's findings?

A. Infective endocarditis
B. Lightning strike (Correct Answer)
C. Opioid overdose
D. Hypothermia
E. Cholesterol emboli

Explanation: ***Lightning strike*** - The **fern-leaf pattern** on the skin, known as **Lichtenberg figures**, is pathognomonic for a lightning strike. - **Ventricular fibrillation** is a common and often fatal cardiac arrhythmia caused by the massive electrical discharge from lightning. *Infective endocarditis* - While it can cause cardiac arrhythmias or collapse due to **embolism**, it does not produce **Lichtenberg figures**. - Typical signs include **fever**, **murmurs**, and **Osler's nodes** or **Janeway lesions**, which are not mentioned here. *Opioid overdose* - Leads to **respiratory depression**, **miosis (pinpoint pupils)**, and potentially **bradycardia**, but not ventricular fibrillation or fern-leaf skin patterns. - The patient would typically present with a **depressed level of consciousness** but usually has palpable pulses initially. *Hypothermia* - Can cause cardiac arrhythmias, including **ventricular fibrillation** in severe cases, but would not produce **Lichtenberg figures**. - The patient's skin would typically be **cold to the touch**, and there might be **J-waves** on the ECG. *Cholesterol emboli* - Typically results in widespread **ischemic symptoms** in various organs and can cause skin manifestations like **livedo reticularis** or **"trash foot"**. - It does not cause **ventricular fibrillation** or the characteristic **fern-leaf pattern** seen in lightning strike victims.

Question 59: A medical student is studying human physiology. She learns that there is a membrane potential across cell membranes in excitable cells. The differential distribution of anions and cations both inside and outside the cells significantly contributes to the genesis of the membrane potential. Which of the following distributions of anions and cations best explains the above phenomenon?

A. High concentration of K+ outside the cell and low concentration of K+ inside the cell
B. High concentration of Na+ outside the cell and high concentration of K+ inside the cell (Correct Answer)
C. High concentration of Ca2+ outside the cell and high concentration of Cl- inside the cell
D. Low concentration of K+ outside the cell and high concentration of Ca2+ inside the cell
E. Low concentration of Cl- outside the cell and high concentration of Cl- inside the cell

Explanation: ***High concentration of Na+ outside the cell and high concentration of K+ inside the cell*** - This distribution is maintained by the **Na+/K+ ATPase pump**, which actively transports **3 Na+ ions out of the cell** and **2 K+ ions into the cell**, against their concentration gradients. - This differential concentration of **sodium** and **potassium** ions is critical for establishing the negative **resting membrane potential** as K+ channels allow K+ to leak out, making the inside more negative. *High concentration of K+ outside the cell and low concentration of K+ inside the cell* - This statement is incorrect as the normal physiological state is characterized by a **high concentration of K+ inside the cell** and a low concentration outside. - An increase in extracellular K+ concentration (hyperkalemia) would **depolarize** the cell, affecting excitability. *High concentration of Ca2+ outside the cell and high concentration of Cl- inside the cell* - While Ca2+ is indeed in higher concentration outside the cell, Cl- is typically in **higher concentration outside the cell** compared to inside, which contributes to the membrane potential through its electrochemical gradient. - An elevated intracellular Cl- concentration would make the cell more negative if Cl- channels were open but is not the primary determinant. *Low concentration of K+ outside the cell and high concentration of Ca2+ inside the cell* - The first part is correct—low K+ outside is normal—but a **high concentration of Ca2+ inside the cell** is generally an indicator of cellular pathology or specific physiological events like muscle contraction or neurotransmitter release, not a steady-state condition contributing to resting potential. - Normal intracellular Ca2+ is kept very low due to active pumps. *Low concentration of Cl- outside the cell and high concentration of Cl- inside the cell* - This statement is incorrect as **chloride ions** are typically in a **higher concentration outside the cell** than inside. - The influx of Cl- into the cell, when channels are open, usually hyperpolarizes the membrane, contributing to inhibition, but its gradient is opposite to what is described.

Question 60: A newborn infant with karyotype 46, XY has male internal and external reproductive structures. The lack of a uterus in this infant can be attributed to the actions of which of the following cell types?

A. Granulosa
B. Theca
C. Leydig
D. Reticularis
E. Sertoli (Correct Answer)

Explanation: ***Sertoli*** - **Sertoli cells** in the fetal testis produce **Anti-Müllerian Hormone (AMH)**, which is crucial for the regression of the **Müllerian ducts**. - The **Müllerian ducts** (also called paramesonephric ducts) would otherwise develop into the uterus, fallopian tubes, and upper vagina in the female fetus. In a male fetus, AMH from Sertoli cells causes these structures to degenerate, leading to the absence of a uterus. *Granulosa* - **Granulosa cells** are found in the ovarian follicles of females and are involved in **estrogen synthesis** and support of oocyte development. - They do not play a role in Müllerian duct regression; in fact, the absence of AMH in female fetuses allows the Müllerian ducts to develop. *Theca* - **Theca cells** are also found in the ovarian follicles and are responsible for producing **androgens** (which are then converted to estrogen by granulosa cells). - Like granulosa cells, theca cells are involved in ovarian function and estrogen production, not in the regression of Müllerian ducts. *Leydig* - **Leydig cells** are located in the interstitium of the testes and are responsible for producing **androgens** (primarily testosterone) in response to luteinizing hormone (LH). - Testosterone from Leydig cells promotes the development of the **Wolffian ducts** (which form male internal reproductive structures like the epididymis, vas deferens, and seminal vesicles), but it does not directly cause the regression of the Müllerian ducts. *Reticularis* - The **zona reticularis** is the innermost layer of the adrenal cortex and produces **adrenal androgens**. - While adrenal androgens play a role in puberty and certain endocrine conditions, they are not involved in the differentiation of fetal reproductive tracts or the regression of Müllerian ducts.

Question 61: A 45-year-old man presents to the physician with complaints of burning pain in both feet and lower legs for 3 months. He reports that the pain is especially severe at night. He has a history of diabetes mellitus for the past 5 years, and he frequently skips his oral antidiabetic medications. His temperature is 36.9°C (98.4°F), heart rate is 80/min, respiratory rate is 15/min, and blood pressure is 120/80 mm Hg. His weight is 70 kg (154.3 lb) and height is 165 cm (approx. 5 ft 5 in). The neurologic examination reveals loss of sensations of pain and temperature over the dorsal and ventral sides of the feet and over the distal one-third of both legs. Proprioception is normal; knee jerks and ankle reflexes are also normal. The tone and strength in all muscles are normal. The hemoglobin A1C is 7.8%. Involvement of what type of nerve fibers is the most likely cause of the patient’s symptoms?

A. Aδ & C fibers (Correct Answer)
B. Aα & Aβ fibers
C. Aγ & B fibers
D. Aγ & C fibers
E. Aβ & Aγ fibers

Explanation: ***Aδ & C fibers*** - The patient's symptoms of **burning pain** and loss of **pain and temperature sensations** are characteristic of small fiber neuropathy, which primarily involves **Aδ and C fibers**. - These are **unmyelinated or thinly myelinated** fibers responsible for transmitting pain (nociception) and thermal sensations, and they are frequently affected in **diabetic neuropathy**. *Aα & Aβ fibers* - **Aα fibers** are large, myelinated fibers involved in **proprioception** and motor function; **Aβ fibers** transmit touch and pressure sensations. - The patient's **normal proprioception** and motor strength indicate that these fibers are largely spared. *Aγ & B fibers* - **Aγ fibers** innervate muscle spindles and are involved in **motor control** and stretch reflexes. - **B fibers** are preganglionic autonomic fibers; neither is directly responsible for pain and temperature sensation. *Aγ & C fibers* - While **C fibers** are involved in pain and temperature, **Aγ fibers** are primarily motor, controlling muscle spindle sensitivity. - The combination does not accurately represent the sensory deficits observed in this patient. *Aβ & Aγ fibers* - **Aβ fibers** are involved in touch and pressure, and **Aγ fibers** are motor. - The patient's primary complaint is burning pain and loss of temperature sensation, not deficits related to these fiber types.

Question 62: A 44-year-old man is brought to the emergency department 45 minutes after being involved in a high-speed motor vehicle collision in which he was the restrained driver. On arrival, he has left hip and left leg pain. His pulse is 135/min, respirations are 28/min, and blood pressure is 90/40 mm Hg. Examination shows an open left tibial fracture with active bleeding. The left lower extremity appears shortened, flexed, and internally rotated. Femoral and pedal pulses are decreased bilaterally. Massive transfusion protocol is initiated. An x-ray of the pelvis shows an open pelvis fracture and an open left tibial mid-shaft fracture. A CT scan of the head shows no abnormalities. Laboratory studies show: Hemoglobin 10.2 g/dL Leukocyte count 10,000/mm3 Platelet count <250,000/mm3 Prothrombin time 12 sec Partial thromboplastin time 30 sec Serum Na+ 125 mEq/L K+ 4.5 mEq/L Cl- 98 mEq/L HCO3- 25 mEq/L Urea nitrogen 18 mg/dL Creatinine 1.2 mg/dL The patient is taken emergently to interventional radiology for exploratory angiography and arterial embolization. Which of the following is the most likely explanation for this patient's hyponatremia?

A. Pathologic aldosterone secretion
B. Physiologic aldosterone secretion
C. Adrenal crisis
D. Pathologic ADH (vasopressin) secretion
E. Physiologic ADH (vasopressin) secretion (Correct Answer)

Explanation: ***Physiologic ADH (vasopressin) secretion*** - The patient has significant **hypovolemia** due to massive bleeding from an open pelvic fracture and an open tibial fracture, leading to **hypotension** (BP 90/40 mmHg) and **tachycardia** (HR 135/min). This severe hypovolemia is a potent non-osmotic stimulus for ADH release. - **Physiologic ADH secretion** in response to hypovolemia acts to conserve water, but in the context of ongoing fluid resuscitation with hypotonic fluids (like normal saline after initial blood loss), it leads to **dilutional hyponatremia** as water is retained disproportionately to sodium. *Pathologic aldosterone secretion* - **Pathologic aldosterone secretion** (e.g., from an adrenal adenoma) causes primary hyperaldosteronism, which typically results in **hypertension**, **hypokalemia**, and **metabolic alkalosis**, none of which are seen in this patient. - While aldosterone does contribute to sodium reabsorption, its primary role in this acute, hypovolemic state is to defend circulating volume, and pathologic excess would not explain the observed hyponatremia. *Physiologic aldosterone secretion* - **Physiologic aldosterone secretion** would be appropriately elevated in response to hypovolemia to promote **sodium and water reabsorption** and **potassium excretion** to maintain circulating volume. - While aldosterone conserves sodium, it does not directly cause hyponatremia; rather, it would tend to increase serum sodium by retaining it, as long as ADH is not excessively retaining free water. *Adrenal crisis* - **Adrenal crisis** (acute adrenal insufficiency) would present with severe hypotension, but it is also characterized by **hyponatremia**, **hyperkalemia**, and often **hypoglycemia** due to cortisol deficiency. - Although hyponatremia is present, the patient's potassium is normal (4.5 mEq/L), making adrenal crisis less likely given the absence of hyperkalemia. *Pathologic ADH (vasopressin) secretion* - **Pathologic ADH secretion** (e.g., Syndrome of Inappropriate Antidiuretic Hormone secretion - SIADH) typically occurs in **euvolemic or mildly hypervolemic** states, often associated with malignancies, CNS disorders, or certain drugs. - In SIADH, patients are typically euvolemic (not hypovolemic as seen here), urine osmolality is inappropriately high, and urine sodium is usually elevated (>20 mEq/L), which contradicts the patient's clinical picture of severe hypovolemia.

Question 63: An investigator is developing a drug for muscle spasms. The drug inactivates muscular contraction by blocking the site where calcium ions bind to regulate actin-myosin interaction. Which of the following is the most likely site of action of this drug?

A. Troponin C (Correct Answer)
B. Myosin-binding site
C. Acetylcholine receptor
D. Ryanodine receptor
E. Myosin head

Explanation: ***Troponin C*** - **Calcium ions** bind to **Troponin C**, initiating a conformational change in the troponin-tropomyosin complex, which exposes the **myosin-binding sites on actin**. - Blocking this site directly prevents the **calcium-mediated regulation** of muscle contraction, thus inactivating it. *Myosin-binding site* - The **myosin-binding site** is located on the **actin filament** and is where the **myosin head** attaches to form cross-bridges. - While essential for contraction, this site doesn't directly bind calcium ions to initiate the process. *Acetylcholine receptor* - The **acetylcholine receptor** is located on the **neuromuscular junction** and mediates the transmission of a nerve impulse to the muscle fiber. - Blocking this receptor would prevent muscle depolarization, but it's not the direct site where calcium ions regulate actin-myosin interaction. *Ryanodine receptor* - The **ryanodine receptor** is located on the **sarcoplasmic reticulum** and controls the release of calcium ions into the sarcoplasm. - While it's involved in calcium signaling, it doesn't represent the site where calcium binds to *regulate* the actin-myosin interaction itself. *Myosin head* - The **myosin head** contains the **ATPase activity** and binds to actin to form cross-bridges, enabling muscle contraction. - It does not directly bind **calcium ions** to regulate the initiation of contraction; instead, its binding to actin is regulated by the troponin-tropomyosin complex.

Question 64: A 21-year-old woman presents to the clinic complaining of fatigue for the past 2 weeks. She reports that it is difficult for her to do strenuous tasks such as lifting heavy boxes at the bar she works at. She denies any precipitating factors, weight changes, nail changes, dry skin, chest pain, abdominal pain, or urinary changes. She is currently trying out a vegetarian diet for weight loss and overall wellness. Besides heavier than usual periods, the patient is otherwise healthy with no significant medical history. A physical examination demonstrates conjunctival pallor. Where in the gastrointestinal system is the most likely mineral that is deficient in the patient absorbed?

A. Large intestine
B. Ileum
C. Jejunum
D. Stomach
E. Duodenum (Correct Answer)

Explanation: ***Duodenum*** - The patient's symptoms (fatigue, conjunctival pallor, heavy periods, vegetarian diet) are highly suggestive of **iron deficiency anemia**. The **duodenum** is the primary site for the absorption of dietary iron. - Iron absorption is tightly regulated here to maintain iron homeostasis, and conditions like a vegetarian diet can reduce bioavailable iron, leading to deficiency. *Large intestine* - The large intestine is primarily involved in **water and electrolyte absorption** and the formation of stool. - It does not play a significant role in the absorption of essential minerals like iron. *Ileum* - The ileum is the main site for the absorption of **bile salts** and **vitamin B12**. - While it absorbs some nutrients, it is not the primary site for iron absorption. *Jejunum* - The jejunum is the main site for the absorption of most **nutrients**, including carbohydrates, proteins, and fats. - While some iron absorption can occur here, the **duodenum** is the specialized and most significant site for this process. *Stomach* - The stomach's main roles include **digestion** of proteins and production of **intrinsic factor** for vitamin B12 absorption. - While **acidic pH** in the stomach aids in converting ferric iron (Fe3+) to ferrous iron (Fe2+), which is more readily absorbed, direct iron absorption in the stomach lining is minimal.

Question 65: A 65-year-old man comes to the physician for the evaluation of a 2-month history of worsening fatigue and shortness of breath on exertion. While he used to be able to walk 4–5 blocks at a time, he now has to pause every 2 blocks. He also reports waking up from having to urinate at least once every night for the past 5 months. Recently, he has started using 2 pillows to avoid waking up coughing with acute shortness of breath at night. He has a history of hypertension and benign prostatic hyperplasia. His medications include daily amlodipine and prazosin, but he reports having trouble adhering to his medication regimen. His pulse is 72/min, blood pressure is 145/90 mm Hg, and respiratory rate is 20/min. Physical examination shows 2+ bilateral pitting edema of the lower legs. Auscultation shows an S4 gallop and fine bibasilar rales. Further evaluation is most likely to show which of the following pathophysiologic changes in this patient?

A. Increased left ventricular compliance
B. Decreased alveolar surface tension
C. Increased potassium retention
D. Increased tone of efferent renal arterioles (Correct Answer)
E. Decreased systemic vascular resistance

Explanation: ***Increased tone of efferent renal arterioles*** - The patient's symptoms (fatigue, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, bilateral pitting edema, S4 gallop, rales, hypertension) are highly suggestive of **heart failure**, primarily left-sided due to his history of **uncontrolled hypertension**. - In response to decreased cardiac output and renal perfusion in heart failure, the **renin-angiotensin-aldosterone system (RAAS)** is activated. This activation leads to **angiotensin II** production, which constricts **efferent renal arterioles**, increasing the glomerular filtration rate and maintaining renal perfusion pressure to sustain function. *Increased left ventricular compliance* - This patient's findings, particularly the **S4 gallop** and history of uncontrolled hypertension, indicate **diastolic dysfunction**, which is characterized by a **stiff, non-compliant left ventricle**. - The S4 gallop is produced by the atria contracting against a **stiff ventricle**, reflecting reduced ventricular compliance. *Decreased alveolar surface tension* - **Decreased alveolar surface tension** (due to surfactant) is a normal physiological state that prevents alveolar collapse and facilitates gas exchange. - In heart failure, the presence of **bibasilar rales** indicates **pulmonary edema** (fluid accumulation in the alveoli and interstitial spaces), which would *increase* the work of breathing and impair gas exchange, but does not directly relate to decreased surface tension. *Increased potassium retention* - Activation of the **renin-angiotensin-aldosterone system (RAAS)** leads to increased **aldosterone** secretion. Aldosterone promotes **sodium reabsorption** and **potassium excretion** in the renal collecting ducts. - Therefore, chronic RAAS activation in heart failure typically leads to **potassium wasting**, not retention. *Decreased systemic vascular resistance* - In heart failure, especially due to chronic hypertension, the body attempts to compensate by activating the **sympathetic nervous system** and **RAAS**, leading to **vasoconstriction** and an *increase* in systemic vascular resistance to maintain blood pressure and perfusion to vital organs. - **Decreased systemic vascular resistance** would typically worsen the low cardiac output state, and is not a compensatory mechanism in this context.

Question 66: A 16-year-old girl is brought to the emergency room with hyperextension of the cervical spine caused by a trampoline injury. After ruling out the possibility of hemorrhagic shock, she is diagnosed with quadriplegia with neurogenic shock. The physical examination is most likely to reveal which of the following constellation of findings?

A. Pulse: 110/min; blood pressure: 88/50 mm Hg; respirations: 26/min; normal rectal tone on digital rectal examination (DRE); normal muscle power and sensations in the limbs
B. Pulse: 116/min; blood pressure: 80/40 mm Hg; respirations: 16/min; loss of rectal tone on DRE; reduced muscle power and absence of sensations in the limbs
C. Pulse: 54/min; blood pressure: 88/44 mm Hg; respirations: 26/min; increased rectal tone on DRE; normal muscle power and sensations in the limbs
D. Pulse: 99/min; blood pressure: 188/90 mm Hg; respirations: 33/min; loss of rectal tone on DRE; reduced muscle power and absence of sensations in the limbs
E. Pulse: 56/min; blood pressure: 88/40 mm Hg; respirations: 22/min; loss of rectal tone on DRE; reduced muscle power and absence of sensations in the limbs (Correct Answer)

Explanation: **Pulse: 56/min; blood pressure: 88/40 mm Hg; respirations: 22/min; loss of rectal tone on DRE; reduced muscle power and absence of sensations in the limbs** - **Neurogenic shock** is characterized by **bradycardia** and **hypotension** due to the loss of sympathetic tone below the level of the injury, so a pulse of 56/min and blood pressure of 88/40 mm Hg are consistent findings. - **Quadriplegia** indicates significant neurological dysfunction with **loss of muscle power and sensation** in all four limbs, and loss of **rectal tone** is a key indicator of spinal cord injury. *Pulse: 110/min; blood pressure: 88/50 mm Hg; respirations: 26/min; normal rectal tone on digital rectal examination (DRE); normal muscle power and sensations in the limbs* - This option presents **tachycardia** (pulse 110/min), which is inconsistent with the **bradycardia** expected in neurogenic shock. - **Normal rectal tone**, muscle power, and sensation are directly contradictory to a diagnosis of quadriplegia and spinal cord injury. *Pulse: 116/min; blood pressure: 80/40 mm Hg; respirations: 16/min; loss of rectal tone on DRE; reduced muscle power and absence of sensations in the limbs* - The **tachycardia** (pulse 116/min) in this option is not characteristic of **neurogenic shock**, which presents with bradycardia. - While loss of rectal tone, reduced muscle power, and absence of sensations are consistent with quadriplegia, the vital signs do not fully align with neurogenic shock. *Pulse: 54/min; blood pressure: 88/44 mm Hg; respirations: 26/min; increased rectal tone on DRE; normal muscle power and sensations in the limbs* - **Increased rectal tone** and normal muscle power/sensations are inconsistent with **quadriplegia** and spinal cord injury, where loss of function is expected. - While bradycardia and hypotension are present, these neurological findings contradict the core diagnosis. *Pulse: 99/min; blood pressure: 188/90 mm Hg; respirations: 33/min; loss of rectal tone on DRE; reduced muscle power and absence of sensations in the limbs* - This option describes **hypertension** (188/90 mmHg), which is not characteristic of **neurogenic shock**, where **hypotension** is a prominent feature. - **Tachycardia** (pulse 99/min) is also inconsistent with the bradycardia seen in neurogenic shock.

Question 67: A 54-year-old man presents to the emergency department complaining of shortness of breath and fatigue for 1 day. He reports feeling increasingly tired. The medical records show a long history of intravenous drug abuse, and a past hospitalization for infective endocarditis 2 years ago. The echocardiography performed at that time showed vegetations on the tricuspid valve. The patient has not regularly attended his follow-up appointments. The visual inspection of the neck shows distension of the neck veins. What finding would you expect to see on this patient’s jugular venous pulse tracing?

A. Obliterated x descent
B. Absent a waves
C. Large a waves
D. Decreased c waves
E. Prominent y descent (Correct Answer)

Explanation: ***Prominent y descent*** - A prominent y descent in the **jugular venous pulse (JVP)** tracing is characteristic of **tricuspid regurgitation**, which is highly probable given the patient's history of **intravenous drug abuse** and previous **infective endocarditis** affecting the tricuspid valve. - The **y descent** reflects the rapid emptying of the right atrium into the right ventricle during early diastole; in tricuspid regurgitation, the increased right atrial volume due to regurgitant flow leads to a more rapid and pronounced fall in right atrial pressure once the tricuspid valve opens. *Obliterated x descent* - An obliterated or absent **x descent** is more typically seen in conditions like **cardiac tamponade** or severe **right ventricular failure**, where there's impaired right atrial filling during ventricular systole. - While the patient has heart issues, the clinical picture strongly points to tricuspid regurgitation, which would not typically cause an obliterated x descent. *Absent a waves* - **Absent a waves** in the JVP tracing most commonly suggest **atrial fibrillation**, where there is no organized atrial contraction. - The case description does not provide information to suggest atrial fibrillation as the primary issue. *Large a waves* - **Large a waves** (cannon a waves) are indicative of conditions where there is increased resistance to right atrial emptying during atrial contraction, such as **tricuspid stenosis**, **pulmonary hypertension**, or certain types of **atrial-ventricular dissociation**. - While the history of endocarditis could theoretically lead to tricuspid stenosis, tricuspid regurgitation is a more common sequela in IV drug users and better fits the overall clinical picture, and stenosis would not cause a prominent y descent. *Decreased c waves* - The **c wave** in the JVP is caused by the bulging of the tricuspid valve into the right atrium during early ventricular systole. - A decreased c wave is not a typical finding in the context of tricuspid regurgitation; rather, a more prominent c-v wave is expected due to the regurgitant flow.

Question 68: A 62-year-old man with gastroesophageal reflux disease and osteoarthritis is brought to the emergency department because of a 1-hour history of severe, stabbing epigastric pain. For the last 6 months, he has had progressively worsening right knee pain, for which he takes ibuprofen several times a day. He has smoked half a pack of cigarettes daily for 25 years. The lungs are clear to auscultation. An ECG shows sinus tachycardia without ST-segment elevations or depressions. This patient is most likely to have referred pain in which of the following locations?

A. Left shoulder
B. Umbilicus
C. Right groin
D. Right scapula (Correct Answer)
E. Left jaw

Explanation: ***Right scapula*** - The patient's presentation with **severe, stabbing epigastric pain** and a history of **NSAID use** (ibuprofen for osteoarthritis) strongly suggests a **perforated peptic ulcer**. - A perforated peptic ulcer, especially in the duodenum, can cause irritation of the diaphragm, leading to **referred pain** to the **right shoulder** or **scapula** via the phrenic nerve. *Left shoulder* - **Left shoulder pain** is more typically associated with conditions affecting the **spleen** (e.g., splenic rupture) or, less commonly, **cardiac ischemia**, which is ruled out by the ECG. - While referred pain patterns can be variable, a perforating ulcer is less likely to cause isolated left shoulder pain. *Umbilicus* - Pain referred to the **umbilical region** often originates from structures in the **midgut**, such as the small intestine or appendix (early appendicitis). - While a perforated ulcer is an abdominal condition, the characteristic diaphragmatic irritation leading to referred pain is usually felt superiorly. *Right groin* - Pain in the **right groin** is commonly associated with conditions affecting the **ureters** (e.g., renal stones), **hip joint**, or **inguinal hernia**. - It is not a typical site for referred pain from a perforated peptic ulcer. *Left jaw* - **Left jaw pain** is a classic symptom of **myocardial ischemia** or **angina**, which has been largely ruled out by the normal ECG in this patient. - **Referred pain** from a perforated ulcer does not typically manifest in the jaw.

Question 69: An investigator is studying membranous transport proteins in striated muscle fibers of an experimental animal. An electrode is inserted into the gluteus maximus muscle and a low voltage current is applied. In response to this, calcium is released from the sarcoplasmic reticulum of the muscle fibers and binds to troponin C, which results in a conformational change of tropomyosin and unblocking of the myosin-binding site. The membranous transport mechanism underlying the release of calcium into the cytosol most resembles which of the following processes?

A. Opening of acetylcholine receptors at neuromuscular junction
B. Reabsorption of glucose by renal tubular cells
C. Secretion of doxorubicin from dysplastic colonic cells
D. Uptake of fructose by small intestinal enterocytes (Correct Answer)
E. Removal of calcium from cardiac myocytes

Explanation: **Uptake of fructose by small intestinal enterocytes** - The release of calcium from the sarcoplasmic reticulum into the cytosol in muscle contraction is primarily mediated by **ryanodine receptors**, which are a type of **facilitated diffusion channel**. - **Fructose uptake** in the small intestine occurs via **GLUT5 transporters**, which also utilize **facilitated diffusion**, moving fructose down its concentration gradient without direct energy expenditure. *Opening of acetylcholine receptors at neuromuscular junction* - The opening of **acetylcholine receptors** is a form of **ligand-gated ion channel** activity, specific to the binding of acetylcholine. - While it involves channel opening, it's initiated by a chemical signal, whereas sarcoplasmic reticulum calcium release is often voltage-gated or mechanically coupled to voltage sensors. *Reabsorption of glucose by renal tubular cells* - Glucose reabsorption in renal tubules primarily involves **secondary active transport** via **SGLT transporters**, which co-transport glucose with sodium. - This process requires energy indirectly, unlike the facilitated diffusion of calcium from the sarcoplasmic reticulum. *Secretion of doxorubicin from dysplastic colonic cells* - The secretion of doxorubicin, an anticancer drug, from cells often involves **ATP-binding cassette (ABC) transporters** (e.g., MDR1), which utilize **primary active transport** to pump substances against their concentration gradient using ATP. - This is an energy-dependent process, distinct from facilitated diffusion. *Removal of calcium from cardiac myocytes* - The removal of calcium from cardiac myocytes occurs primarily via the **SERCA pump** (an **ATP-dependent active transporter**) back into the sarcoplasmic reticulum and the **Na+/Ca2+ exchanger** (a **secondary active transporter**) out of the cell. - Both mechanisms require energy, either directly or indirectly, to move calcium against its electrochemical gradient.

Question 70: A 47-year-old woman comes to the physician because of fatigue, difficulty falling asleep, and night sweats for the past 6 months. Over the past year, her menstrual cycle has become irregular and her last menstrual period was 2 months ago. She quit smoking 2 years ago. Pelvic exam shows vulvovaginal atrophy. A pregnancy test is negative. Which of the following changes is most likely to occur in this patient's condition?

A. Decreased gonadotropin-releasing hormone
B. Increased inhibin B
C. Decreased luteinizing hormone
D. Increased estrogen
E. Increased follicle-stimulating hormone (Correct Answer)

Explanation: ***Increased follicle-stimulating hormone*** - The patient's symptoms (fatigue, insomnia, night sweats, irregular menses, 2 months amenorrhea, vulvovaginal atrophy) at age 47 are classic for **menopause**. - During menopause, declining **ovarian function** leads to decreased estrogen and inhibin, which in turn causes the pituitary to release more **FSH** and LH via a feedback loop. *Decreased gonadotropin-releasing hormone* - **GnRH** levels are typically increased in menopause due to the lack of negative feedback from ovarian hormones, stimulating the pituitary. - A decrease in GnRH would reduce pituitary gonadotropin secretion, which is contrary to what is observed in menopause. *Increased inhibin B* - **Inhibin B** is produced by ovarian granulosa cells and typically **decreases** significantly during the menopausal transition due to the reduced number of ovarian follicles. - Decreased inhibin B contributes to the rise in FSH levels during menopause. *Decreased luteinizing hormone* - In menopause, both **LH** and FSH levels are **elevated** due to the loss of negative feedback from declining ovarian hormones like estrogen and inhibin. - While FSH rises earlier and more dramatically, LH also increases. *Increased estrogen* - In menopause, the ovaries produce **significantly less estrogen**, leading to the classic symptoms like hot flashes and vaginal atrophy. - The decline in estrogen is a primary hormonal change driving the menopausal transition.

Question 71: An 18-year-old female presents to the clinic complaining of acute abdominal pain for the past couple of hours. The pain is concentrated at the right lower quadrant (RLQ) with no clear precipitating factor and is worse with movement. Acetaminophen seems to help a little but she is concerned as the pain has occurred monthly for the past 3 months. She denies any headache, chest pain, weight changes, diarrhea, nausea/vomiting, fever, or sexual activity. The patient reports a regular menstruation cycle with her last period being 2 weeks ago. A physical examination demonstrates a RLQ that is tender to palpation with a negative psoas sign. A urine beta-hCG test is negative. An ultrasound of the abdomen is unremarkable. What is the main function of the hormone that is primarily responsible for this patient’s symptoms?

A. Inhibition of the anterior pituitary to decrease secretion of FSH and LH
B. Increases the activity of aromatase to synthesize 17-beta-estradiol
C. Increases the activity of cholesterol desmolase to synthesize progesterone (Correct Answer)
D. Induction of pulsatile release of follicle stimulating hormone (FSH) and luteinizing hormone (LH)
E. Inhibition of the hypothalamus to decrease secretion of gonadotrophin releasing hormone (GnRH)

Explanation: ***Increases the activity of cholesterol desmolase to synthesize progesterone*** - The patient's symptoms of recurrent unilateral lower abdominal pain corresponding with her menstrual cycle (2 weeks after her last period, consistent with mid-cycle), negative beta-hCG, and unremarkable ultrasound are highly suggestive of **mittelschmerz** (ovulation pain). - **Luteinizing hormone (LH)** surge is the primary trigger for ovulation. LH acts on ovarian theca and luteal cells to increase the activity of **cholesterol desmolase (CYP11A1/P450scc)**, the rate-limiting enzyme that converts cholesterol to pregnenolone, the precursor for all steroid hormones including **progesterone**. - The mid-cycle LH surge triggers ovulation and subsequent formation of the corpus luteum, which produces progesterone. This steroidogenic action of LH is the most relevant to the ovulation process causing her symptoms. *Inhibition of the anterior pituitary to decrease secretion of FSH and LH* - This describes the **negative feedback** mechanism exerted by **estrogen** and **progesterone** on the anterior pituitary, not the primary function of LH. - While important for menstrual cycle regulation, this mechanism does not trigger ovulation or directly cause mittelschmerz. *Increases the activity of aromatase to synthesize 17-beta-estradiol* - This is the primary function of **FSH (follicle-stimulating hormone)** on **granulosa cells** within the ovarian follicle. - FSH stimulates **aromatase**, which converts androgens (produced by theca cells under LH stimulation) into **estrogen**, primarily **17-beta-estradiol**. - While crucial for follicle maturation, FSH is not the hormone directly responsible for the ovulation event that causes this patient's pain. *Induction of pulsatile release of follicle stimulating hormone (FSH) and luteinizing hormone (LH)* - This is the primary function of **gonadotropin-releasing hormone (GnRH)**, secreted by the hypothalamus. - GnRH's pulsatile release is essential for the menstrual cycle, but GnRH itself is not the direct mediator of ovulation or the associated symptoms. *Inhibition of the hypothalamus to decrease secretion of gonadotrophin releasing hormone (GnRH)* - This represents a **negative feedback** mechanism exerted primarily by **estrogen** and **progesterone** on the hypothalamus. - This feedback loop helps regulate the menstrual cycle but is not the direct mechanism for ovulation or mittelschmerz pain.

Question 72: An investigator is studying gastric secretions in human volunteers. Measurements of gastric activity are recorded after electrical stimulation of the vagus nerve. Which of the following sets of changes is most likely to occur after vagus nerve stimulation? $$$ Somatostatin secretion %%% Gastrin secretion %%% Gastric pH $$$

A. ↓ ↓ ↓
B. ↑ ↓ ↑
C. ↓ ↑ ↓ (Correct Answer)
D. ↑ ↑ ↑
E. ↑ ↑ ↓

Explanation: ***↓ ↑ ↓*** - Vagal stimulation directly promotes **gastrin release** from G cells, which in turn stimulates **acid secretion**. - Increased acid secretion **decreases gastric pH** and a lower pH **inhibits somatostatin secretion** in a negative feedback loop. *↓ ↓ ↓* - This option incorrectly suggests that vagal stimulation would **decrease gastrin secretion**. Vagal stimulation is a primary stimulant for gastrin release. - A decrease in gastrin would lead to less acid, resulting in a **higher gastric pH**, not a lower one. *↑ ↓ ↑* - This suggests an **increase in somatostatin** and a **decrease in gastrin** which is contrary to the direct effects of vagal stimulation. - Furthermore, a decreased gastrin would lead to **higher pH**, not lower, unless acid secretion was independently inhibited, which is not the case here. *↑ ↑ ↑* - This option correctly indicates an **increase in gastrin secretion** but incorrectly suggests an **increase in somatostatin** and an **increase in gastric pH**. - Increased gastrin leads to **increased acid** and thus a **decreased pH**, while high acid levels inhibit somatostatin. *↑ ↑ ↓* - This sequence correctly shows an **increase in gastrin** and a **decrease in pH**, but incorrectly suggests an **increase in somatostatin**. - Somatostatin secretion would be **inhibited** by the increased acid levels resulting from vagal stimulation and gastrin release.

Question 73: A 20-year-old woman reports to student health complaining of 5 days of viral symptoms including sneezing and a runny nose. She started coughing 2 days ago and is seeking cough medication. She additionally mentions that she developed a fever 2 days ago, but this has resolved. On exam, her temperature is 99.0°F (37.2°C), blood pressure is 118/76 mmHg, pulse is 86/min, and respirations are 12/min. Changes in the activity of warm-sensitive neurons in which part of her hypothalamus likely contributed to the development and resolution of her fever?

A. Anterior hypothalamus (Correct Answer)
B. Paraventricular nucleus
C. Suprachiasmatic nucleus
D. Lateral area
E. Posterior hypothalamus

Explanation: ***Anterior hypothalamus*** - The **anterior hypothalamus** contains warm-sensitive neurons that detect increases in body temperature and activate mechanisms for heat dissipation, such as sweating and vasodilation. - In fever, **prostaglandins** increase the set point in the anterior hypothalamus, causing the body to retain heat and increase heat production until the new set point is reached; resolution of fever involves resetting this set point back to normal. *Paraventricular nucleus* - The **paraventricular nucleus** is primarily involved in neuroendocrine functions, stress response, and the regulation of appetite and autonomic nervous system. - It plays a significant role in releasing hormones like **corticotropin-releasing hormone (CRH)** and **oxytocin**, not direct temperature regulation. *Suprachiasmatic nucleus* - The **suprachiasmatic nucleus (SCN)** is the body's main biological clock, regulating **circadian rhythms** including the sleep-wake cycle and daily fluctuations in body temperature. - While it influences the normal diurnal variation in body temperature, it is not directly responsible for the acute regulation of fever. *Lateral area* - The **lateral hypothalamus** primarily functions as the "hunger center," stimulating foraging and feeding behavior. - Damage to this area can lead to **anorexia** and reduced food intake, not impairments in fever response. *Posterior hypothalamus* - The **posterior hypothalamus** is primarily involved in heat conservation and production mechanisms, such as shivering and vasoconstriction, in response to cold. - It contains cold-sensitive neurons and functions to raise body temperature if it falls below the set point, but it is not where the set point itself is regulated in response to pyrogens.

Question 74: You are conducting a lab experiment on skeletal muscle tissue to examine force in different settings. The skeletal muscle tissue is hanging down from a hook. The experiment has 3 different phases. In the first phase, you compress the muscle tissue upwards, making it shorter. In the second phase, you attach a weight of 2.3 kg (5 lb) to its lower vertical end. In the third phase, you do not manipulate the muscle length at all. At the end of the study, you see that the tension is higher in the second phase than in the first one. What is the mechanism underlying this result?

A. The tension in phase 1 is only active, while in phase 2 it is both active and passive.
B. Shortening the muscle in phase 1 pulls the actin and myosin filaments apart.
C. Lengthening of the muscle in phase 2 increases passive tension. (Correct Answer)
D. There are more actin-myosin cross-bridges attached in phase 2 than in phase 1.
E. Shortening of the muscle in phase 1 uses up ATP stores.

Explanation: ***Lengthening of the muscle in phase 2 increases passive tension.*** - Attaching a weight of 2.3 kg (5 lb) in phase 2 **stretches** the muscle, increasing the **passive tension** generated by elastic components like **titin**. - This added passive tension, combined with any active tension, results in a **higher total tension** compared to the shortened state in phase 1 where passive tension is minimal. *The tension in phase 1 is only active, while in phase 2 it is both active and passive.* - While passive tension is more significant in phase 2 due to stretching, the muscle in phase 1, even when compressed, can still generate some **active tension** if stimulated. - The key difference contributing to higher tension in phase 2 is the additional **passive component** from stretching, not necessarily the exclusive presence of active tension in one phase. *Shortening the muscle in phase 1 pulls the actin and myosin filaments apart.* - Shortening the muscle too much, beyond its optimal resting length, leads to **overlap of actin filaments** and **crumpling of myosin filaments**, reducing the number of available cross-bridge binding sites. - This **decreases active tension** rather than pulling filaments apart, which would require excessive stretching. *There are more actin-myofibril cross-bridges attached in phase 2 than in phase 1.* - Shortening the muscle in phase 1 beyond optimal length **reduces the number of cross-bridges** that can form due to actin filament overlap. - While lengthening in phase 2 might bring the muscle closer to an **optimal length** for cross-bridge formation (increasing active tension), the primary reason for the higher tension in phase 2 as described is the increase in **passive tension** from stretching, rather than solely increased active cross-bridge formation. *Shortening of the muscle in phase 1 uses up ATP stores.* - Muscle contraction, whether shortening or lengthening, requires **ATP hydrolysis** for cross-bridge cycling. - The act of shortening itself doesn't uniquely "use up" ATP stores more significantly than other contractile actions to explain the observed tension difference; ATP is continuously consumed and regenerated during muscle activity.

Question 75: A 56-year-old woman visits her family physician accompanied by her son. She has recently immigrated to Canada and does not speak English. Her son tells the physician that he is worried that his mother gets a lot of sugar in her diet and does not often monitor her glucose levels. Her previous lab work shows a HbA1c value of 8.7%. On examination, her blood pressure is 130/87 mm Hg and weight is 102 kg (224.9 lb). Which of the following is the correct location of where the glucose transport is most likely affected in this patient?

A. Skeletal muscle (Correct Answer)
B. Red blood cells
C. Pancreas
D. Brain
E. Liver

Explanation: ***Skeletal muscle*** - This patient presents with an HbA1c of 8.7% and obesity, indicative of **Type 2 Diabetes Mellitus**, where **insulin resistance** is a key feature. - **Skeletal muscle** is a primary site of **glucose uptake** stimulated by insulin and is therefore most significantly affected by insulin resistance. *Red blood cells* - **Red blood cells** take up glucose via **insulin-independent** GLUT1 transporters. - Their glucose transport is generally **not affected** in Type 2 Diabetes, although high glucose levels can lead to glycation of hemoglobin (HbA1c). *Pancreas* - The **pancreas** (specifically beta cells) produces insulin, and in Type 2 Diabetes, there can be a **progressive decline in beta cell function** over time. - However, the initial and primary defect in glucose utilization is **insulin resistance** in peripheral tissues, not impaired glucose transport into pancreatic cells for metabolic regulation. *Brain* - The **brain** primarily utilizes glucose for energy via **insulin-independent** GLUT1 and GLUT3 transporters at the blood-brain barrier and neurons, respectively. - Glucose uptake into the brain is generally **preserved** in Type 2 Diabetes, even in severe insulin resistance. *Liver* - The **liver** is involved in both glucose production (gluconeogenesis, glycogenolysis) and uptake (glycogenesis). In Type 2 Diabetes, the liver exhibits **increased glucose output** due to insulin resistance and impaired suppression of endogenous glucose production. - While **hepatic insulin resistance** is present, the question asks about the primary site where **glucose transport is most likely affected**, and skeletal muscle's role in glucose disposal makes it a more direct answer for impaired glucose transport.

Question 76: A 15-year-old boy is undergoing the bodily changes associated with puberty. He is concerned that he easily develops a foul skin odor, even with mild exercise. Which of the following glandular structures is the causative agent for this foul skin odor?

A. Sebaceous gland
B. Serous gland
C. Apocrine gland (Correct Answer)
D. Mucous gland
E. Eccrine gland

Explanation: ***Apocrine gland*** - **Apocrine glands** become active during puberty and are primarily located in the **axillary** and **genital regions**, secreting a milky, odorless fluid that bacteria on the skin break down, producing a characteristic foul odor. - The onset of this type of body odor during puberty, exacerbated by exercise, is a hallmark of apocrine gland activity. *Sebaceous gland* - **Sebaceous glands** produce **sebum**, an oily substance that lubricates the skin and hair, and its overactivity can contribute to acne. - While sebaceous glands are associated with puberty, their secretions themselves do not typically produce the characteristic foul body odor, although they can make the skin feel greasy. *Serous gland* - **Serous glands** primarily secrete **watery fluids rich in enzymes** or proteins, such as those found in salivary glands (parotid) or the serous membranes (pleura, peritoneum). - These glands are not typically associated with body odor in the skin. *Mucous gland* - **Mucous glands** produce **mucus**, a thick, viscous substance that lubricates and protects surfaces in the respiratory, digestive, and reproductive tracts. - They are not located in the skin in a way that would cause widespread body odor. *Eccrine gland* - **Eccrine glands** are a type of **sweat gland** that are widely distributed over most of the body surface and primarily secrete a **watery sweat** for thermoregulation. - While their sweat contributes to dampness, their secretions are generally odorless and do not directly cause the foul body odor described in the question, unless mixed with other factors.

Question 77: Three days after admission to the intensive care unit for septic shock and bacteremia from a urinary tract infection, a 34-year-old woman has persistent hypotension. Her blood cultures were positive for Escherichia coli, for which she has been receiving appropriate antibiotics since admission. She has no history of serious illness. She does not use illicit drugs. Current medications include norepinephrine, ceftriaxone, and acetaminophen. She appears well. Her temperature is 37.5°C (99.5°F), heart rate 96/min, and blood pressure is 85/55 mm Hg. Examination of the back shows costovertebral tenderness bilaterally. Examination of the thyroid gland shows no abnormalities. Laboratory studies show: Hospital day 1 Hospital day 3 Leukocyte count 18,500/mm3 10,300/mm3 Hemoglobin 14.1 g/dL 13.4 g/dL Serum Creatinine 1.4 mg/dL 0.9 mg/dL Fasting glucose 95 mg/dL 100 mg/dL TSH 1.8 μU/mL T3, free 0.1 ng/dL (N: 0.3–0.7 ng/dL) T4, free 0.9 ng/dL (N: 0.5–1.8 ng/dL) Repeat blood cultures are negative. An x-ray of the chest shows no abnormalities. Which of the following is the most likely underlying mechanism of this patient's laboratory abnormalities?

A. Sick euthyroid syndrome (Correct Answer)
B. Subclinical hypothyroidism
C. Pituitary apoplexy
D. Medication toxicity
E. Fibrous thyroiditis

Explanation: ***Sick euthyroid syndrome*** - The patient's **low free T3** and **normal TSH** in the setting of severe illness (septic shock) are characteristic of **sick euthyroid syndrome**, a common response to acute stress. - Despite the **abnormal thyroid hormone levels**, this condition typically does not require thyroid hormone replacement as it is an adaptive response to conserve energy during critical illness. *Subclinical hypothyroidism* - **Subclinical hypothyroidism** is characterized by an **elevated TSH** with normal free T4 levels, which is not seen here as TSH is normal. - While it can manifest as fatigue or subtle symptoms, it is less likely given the acute, severe presentation with normal TSH. *Pituitary apoplexy* - **Pituitary apoplexy** is a sudden hemorrhage or infarction of the pituitary gland, typically presenting with severe headache, visual disturbances, and signs of hypopituitarism (e.g., adrenal insufficiency, central hypothyroidism). - The patient's presentation does not include headache or visual changes, and her TSH is normal, making pituitary apoplexy less likely. *Medication toxicity* - While some medications (e.g., amiodarone, lithium) can affect thyroid function, these are not among her current medications. - The thyroid abnormalities are directly tied to her critical illness, rather than a drug side effect. *Fibrous thyroiditis* - **Fibrous thyroiditis** (**Riedel's thyroiditis**) is a rare condition involving extensive fibrosis of the thyroid gland, typically presenting as a hard, fixed, painless goiter, and can lead to hypothyroidism. - The patient's thyroid examination is normal, and the acute onset of her thyroid abnormalities is inconsistent with this chronic fibrosing process.

Question 78: A previously healthy 39-year-old woman comes to the physician because of a slowly enlarging, painless neck mass that she first noticed 3 months ago. During this period, she has also experienced intermittent palpitations, hair loss, and a weight loss of 4.5 kg (10 lb). There is no personal or family history of serious illness. She appears anxious and fidgety. Her temperature is 37.1°C (98.8°F), pulse is 101/min and irregular, respirations are 16/min, and blood pressure is 140/90 mm Hg. Physical examination shows a firm, nontender left anterior cervical nodule that moves with swallowing. Laboratory studies show: TSH 0.4 μU/mL T4 13.2 μg/dL T3 196 ng/dL Ultrasonography confirms the presence of a 3-cm solid left thyroid nodule. A thyroid 123I radionuclide scintigraphy scan shows increased uptake in a nodule in the left lobe of the thyroid gland with suppression of the remainder of the thyroid tissue. Which of the following is the most likely underlying mechanism of this patient's condition?

A. Gain-of-function mutations of the TSH receptor (Correct Answer)
B. Thyroglobulin antibody production
C. Activation of oncogenes promoting cell division
D. Persistent TSH stimulation and heterogeneous thyroid tissue hyperplasia
E. Thyroid peroxidase autoantibody-mediated destruction of thyroid tissue

Explanation: ***Gain-of-function mutations of the TSH receptor*** - The patient's symptoms (palpitations, weight loss, anxiety, irregular pulse) and lab results (low TSH, high T3/T4) indicate **hyperthyroidism**. The **hot nodule** on scintigraphy with suppressed surrounding tissue points to a **toxic adenoma**. - **Gain-of-function mutations** in the TSH receptor gene (e.g., *TSHR* gene) cause constitutive activation of the receptor, leading to autonomous thyroid hormone production independent of TSH. *Thyroglobulin antibody production* - **Antithyroglobulin antibodies** are typically associated with autoimmune thyroid diseases like **Hashimoto's thyroiditis** (hypothyroidism) or occasionally Graves' disease (hyperthyroidism), but the specific presentation here points to a functional nodule. - While they can be present in Graves' disease, the scintigraphy showing a **single hot nodule** with suppressed surrounding tissue is not characteristic of Graves' disease, which typically shows diffuse uptake. *Activation of oncogenes promoting cell division* - While thyroid nodules can be malignant and involve **oncogene activation** (e.g., *BRAF, RET/PTC*), this mechanism primarily relates to uncontrolled cell growth and **cancer**, not necessarily hyperfunction and excessive hormone production (toxic nodule). - Malignant nodules are typically "cold" on scintigraphy, meaning they do not take up iodine, unlike the **"hot" nodule** described in this patient. *Persistent TSH stimulation and heterogeneous thyroid tissue hyperplasia* - This description is characteristic of a **multinodular goiter** or **diffuse hyperplasia**, often seen in conditions of **chronic TSH stimulation** (e.g., iodine deficiency leading to hypothyroidism and compensatory TSH rise). - The patient has **suppressed TSH** and a **single hyperfunctioning nodule**, not diffuse hyperplasia or chronic TSH stimulation. *Thyroid peroxidase autoantibody-mediated destruction of thyroid tissue* - **Thyroid peroxidase (TPO) antibodies** are involved in **Hashimoto's thyroiditis**, an autoimmune condition leading to gradual **destruction of thyroid tissue** and **hypothyroidism**. - This patient presents with **hyperthyroidism** and a hyperfunctioning nodule, which is the opposite of the clinical picture seen with TPO antibody-mediated destruction.

Question 79: A 28-year-old man presents to his primary care physician for a general checkup. The patient is a healthy young man with no significant past medical history. He is a MD/PhD student and lives in New York City. He exercises frequently and is doing very well in school. He is currently sexually active with multiple female partners and does not use protection. His temperature is 98.9°F (37.2°C), blood pressure is 147/98 mmHg, pulse is 90/min, respirations are 14/min, and oxygen saturation is 99% on room air. Physical exam is notable for a very muscular young man. The patient has comedonal acne and palpable breast tissue. Testicular exam reveals small and symmetrical testicles. Which of the following laboratory changes is most likely to be found in this patient?

A. Elevated hematocrit
B. Elevated liver enzymes (AST/ALT)
C. Decreased endogenous testosterone
D. Increased estradiol
E. Decreased LH and FSH (Correct Answer)

Explanation: ***Decreased LH and FSH*** - This patient exhibits symptoms (e.g., **comedonal acne**, **palpable breast tissue**, **small and symmetrical testicles**, and **hypertension**) suggestive of **anabolic steroid abuse**. Exogenous anabolic steroids suppress the hypothalamic-pituitary-gonadal (HPG) axis, leading to decreased production of **Luteinizing Hormone (LH)** and **Follicle-Stimulating Hormone (FSH)**. - This is the **most direct and consistent laboratory finding** in anabolic steroid abuse. The suppression of LH and FSH is the primary mechanism that leads to **testicular atrophy** (as seen in this patient) and subsequent suppression of endogenous testosterone production. - LH and FSH will be **measurably low** in virtually all cases of anabolic steroid abuse, making this the most reliable laboratory marker. *Decreased endogenous testosterone* - Anabolic steroid abuse suppresses the HPG axis, leading to decreased **endogenous testosterone production** (due to lack of LH stimulation). However, because patients are administering **exogenous testosterone or testosterone derivatives**, the **total testosterone level** measured in the laboratory may actually be normal, elevated, or vary widely depending on timing of administration and the specific steroid used. - This makes total testosterone an **unreliable marker** compared to LH/FSH, which will be consistently suppressed. Additionally, distinguishing endogenous from exogenous testosterone requires specialized testing not typically done in routine workup. *Elevated hematocrit* - While anabolic steroids stimulate erythropoiesis, leading to **elevated hematocrit** (polycythemia) in many users, this is not as **universally present** or as directly reflective of the HPG axis suppression that causes the testicular atrophy observed clinically. - Elevated hematocrit increases the risk of **thrombotic events** but is a secondary effect rather than the primary hormonal disruption. *Elevated liver enzymes (AST/ALT)* - Oral anabolic steroids, particularly **17-alpha-alkylated compounds**, are **hepatotoxic** and can cause elevated liver enzymes. However, not all anabolic steroids are equally hepatotoxic (injectable forms are less so), and the clinical presentation here more directly points to the **HPG axis suppression** evidenced by testicular atrophy. - Liver enzyme elevation is **variable** depending on the type and route of steroid administration. *Increased estradiol* - Many anabolic steroids are **aromatized to estrogen** (estradiol), which causes **gynecomastia** (as seen in this patient). However, while increased estradiol explains the breast tissue, the **most consistent and diagnostically specific** laboratory finding that explains the testicular atrophy is the suppression of LH and FSH. - Increased estradiol is a contributing factor to some clinical signs but is not as universally present or as directly related to the testicular findings as LH/FSH suppression.

Question 80: An 11-year-old boy presents with a 2-day history of uncontrollable shivering. During admission, the patient’s vital signs are within normal limits, except for a fluctuating body temperature registering as low as 35.0°C (95.0°F) and as high as 40.0°C (104.0°F), requiring alternating use of cooling and warming blankets. A complete blood count (CBC) is normal, and a chest radiograph is negative for consolidations and infiltrates. An MRI of the brain reveals a space-occupying lesion infiltrating the posterior hypothalamus and extending laterally. Which of the following additional findings are most likely, based on this patient’s physical examination?

A. Polyuria
B. Hyperphagia
C. Galactorrhea
D. Sleep disturbances
E. Anorexia (Correct Answer)

Explanation: **Anorexia** - **Hypothalamic lesions**, particularly those affecting the **lateral hypothalamus**, often lead to **anorexia** and **weight loss** due to the role of this region in stimulating appetite. - The patient's presentation with **uncontrollable shivering** and **deregulated body temperature** further points to hypothalamic dysfunction, which can also disrupt feeding centers. *Polyuria* - **Polyuria** is typically associated with damage to the **posterior pituitary gland** or its connections to the hypothalamus, leading to **diabetes insipidus** (lack of ADH). - While a hypothalamic lesion can affect ADH production, the primary symptom constellation in this case more strongly suggests disruption of other hypothalamic functions. *Hyperphagia* - **Hyperphagia** (increased appetite) and **obesity** are most commonly linked to damage to the **ventromedial hypothalamus**, which is considered the satiety center. - The presented lesion is described as infiltrating the posterior hypothalamus and extending laterally, making hyperphagia less likely than anorexia. *Galactorrhea* - **Galactorrhea** is often caused by **hyperprolactinemia**, which can result from lesions compressing the **pituitary stalk** or interfering with **dopamine's inhibitory effect** on prolactin release in the anterior pituitary. - While a large hypothalamic lesion could theoretically impact pituitary function secondarily, galactorrhea is not a direct or most likely consequence of a posterior and lateral hypothalamic lesion. *Sleep disturbances* - While the **hypothalamus** plays a critical role in **sleep-wake cycles** (e.g., the **suprachiasmatic nucleus**), **uncontrollable shivering** and **poikilothermia** point more directly to acute disruption of temperature regulation rather than sleep disturbances as the most prominent likely additional finding. - Many types of brain lesions can cause sleep disturbances, but the specific presentation here suggests a more particular set of hypothalamic dysfunctions.

Question 81: A 25-year-old woman presents to her primary care physician for her yearly physical exam. She has no past medical history and says that she does not currently have any health concerns. On physical exam, she is found to have hyperactive patellar reflexes but says that she has had this finding since she was a child. She asks her physician why this might be the case. Her physician explains that there are certain cells that are responsible for detecting muscle stretch and responding to restore the length of the muscle. Which of the following is most likely a characteristic of these structures?

A. They inhibit the activity of alpha-motoneurons
B. They activate inhibitory interneurons
C. They are in parallel with extrafusal skeletal muscle fibers (Correct Answer)
D. They are in series with extrafusal skeletal muscle fibers
E. They are innervated by group Ib afferent neurons

Explanation: ***They are in parallel with extrafusal skeletal muscle fibers*** - The structures described are **muscle spindles**, which are **stretch receptors** located within the muscle belly and arranged in parallel with **extrafusal muscle fibers**. - This parallel arrangement allows them to detect changes in **muscle length** and the rate of change of length, initiating the **stretch reflex**. *They inhibit the activity of alpha-motoneurons* - Muscle spindles, primarily through their **Ia afferent fibers**, **excite** alpha-motoneurons, leading to muscle contraction and opposing the stretch. - **Inhibition** of alpha-motoneurons is typically associated with structures like **Golgi tendon organs**, which respond to muscle tension. *They activate inhibitory interneurons* - While muscle spindles do excite **excitatory interneurons** that activate synergistic muscles, their primary action in the monosynaptic stretch reflex is direct excitation of **alpha-motoneurons**. - **Inhibitory interneurons** are typically involved in mediating **reciprocal inhibition** of antagonistic muscles in response to muscle spindle activation. *They are in series with extrafusal skeletal muscle fibers* - Structures arranged in **series** with extrafusal muscle fibers are **Golgi tendon organs**, which are tension receptors. - Muscle spindles are oriented **in parallel** to detect changes in muscle length. *They are innervated by group Ib afferent neurons* - Muscle spindles are primarily innervated by **group Ia (primary) afferent neurons** and **group II (secondary) afferent neurons**, which detect muscle length and rate of change of length. - **Group Ib afferent neurons** innervate **Golgi tendon organs**, which are sensitive to muscle tension.

Question 82: A 71-year-old man comes to the physician because of decreased sexual performance for the past 2 years. He reports that it takes longer for his penis to become erect, and he cannot maintain an erection for as long as before. His ejaculations have become less forceful. Once he has achieved an orgasm, he requires several hours before he can have another orgasm. He has been happily married for 40 years and he has no marital conflicts. His only medication is esomeprazole for gastroesophageal reflux disease. Examination shows coarse dark pubic and axillary hair. The skin of his lower extremity is warm to the touch; pedal pulses and sensation are intact. Rectal examination shows a symmetrically enlarged prostate with no masses. His fasting serum glucose is 96 mg/dL and his prostate-specific antigen is 3.9 ng/mL (N < 4). Which of the following etiologies is the most likely cause of the patient's symptoms?

A. Physiologic (Correct Answer)
B. Psychogenic
C. Neoplastic
D. Vascular
E. Neurogenic

Explanation: ***Physiologic*** - The patient's symptoms, including **longer erection time**, inability to **maintain an erection**, less forceful ejaculations, and a prolonged **refractory period**, are all common age-related changes in male sexual function. - Absence of specific underlying medical conditions (normal glucose, intact sensation and pulses) and marital conflicts further supports a **physiologic aging process**. *Psychogenic* - This is less likely as the patient reports a **happy marriage** and no marital conflicts, ruling out a common psychogenic cause for sexual dysfunction. - Psychogenic erectile dysfunction typically presents with sudden onset, situational dysfunction, and often preserves **nocturnal erections**, which are not mentioned here. *Neoplastic* - While an enlarged prostate is noted, the **PSA is within normal limits** for his age (< 4 ng/mL), and the examination reveals no masses, making prostate cancer an unlikely cause of the sexual dysfunction. - Sexual dysfunction as a primary symptom of prostate cancer is rare unless advanced disease causes significant hormonal changes or nerve involvement. *Vascular* - The presence of **warm skin** to the touch and **intact pedal pulses** and sensation in the lower extremities makes significant vascular compromise an unlikely cause of erectile dysfunction. - Vascular erectile dysfunction typically presents with a more sudden onset and may be associated with risk factors like **diabetes, hypertension, or hyperlipidemia**, which are not clearly evident here. *Neurogenic* - **Intact sensation** in the lower extremities makes a broad neurogenic cause for erectile dysfunction less likely. - Neurogenic causes often present with other neurological deficits or are associated with conditions like **diabetes (neuropathy)**, **spinal cord injury**, or **multiple sclerosis**, which are not indicated.

Question 83: A 56-year-old woman presents to the emergency department with an episode of nausea and severe unrelenting right upper abdominal pain. She had a cholecystectomy for gallstones a year earlier and has since experienced frequent recurrences of abdominal pain, most often after a meal. Her past medical history is otherwise unremarkable and she only takes medications for her pain when it becomes intolerable. Her physical exam is normal except for an intense abdominal pain upon deep palpation of her right upper quadrant. Her laboratory values are unremarkable with the exception of a mildly elevated alkaline phosphatase, amylase, and lipase. Her abdominal ultrasound shows a slightly enlarged common bile duct at 8 mm in diameter (N = up to 6 mm) and a normal pancreatic duct. The patient is referred to a gastroenterology service for an ERCP (endoscopic retrograde cholangiopancreatography) to stent her common bile duct. During the procedure the sphincter at the entrance to the duct is constricted. Which statement best describes the regulation of the function of the sphincter which is hampering the cannulation of the pancreatic duct in this patient?

A. The sphincter is contracted between meals.
B. A hormone released by duodenal cells that stimulates gastrointestinal motility is the most effective cause of relaxation.
C. Regulation of function of the sphincter of Oddi does not involve neural inputs.
D. A hormone released by the I cells of the duodenum in the presence of fatty acids is the most effective cause of relaxation. (Correct Answer)
E. Sphincter relaxation is enhanced via stimulation of opioid receptors.

Explanation: ***A hormone released by the I cells of the duodenum in the presence of fatty acids is the most effective cause of relaxation.*** - The **sphincter of Oddi** relaxes primarily in response to **cholecystokinin (CCK)**, which is released by **I cells** in the duodenum when **fatty acids** and amino acids enter the small intestine. This relaxation allows bile and pancreatic enzymes to flow into the duodenum to aid digestion. - The patient's symptoms of post-cholecystectomy pain and dilated common bile duct suggest **sphincter of Oddi dysfunction**, where the sphincter fails to relax properly, hindering bile flow. *The sphincter is contracted between meals.* - While the sphincter of Oddi does maintain a **tonic contraction** between meals to prevent bile reflux and store bile in the gallbladder, this statement doesn't describe the primary mechanism for its **relaxation during digestion**. - The problem in this patient is the failure of the sphincter to relax, rather than its normal contracted state. *A hormone released by duodenal cells that stimulates gastrointestinal motility is the most effective cause of relaxation.* - This likely refers to **motilin**, which is released by enterochromaffin cells (Mo cells) in the duodenum and primarily regulates gastrointestinal motility, particularly the migrating motor complex. - Motilin does not directly or most effectively cause relaxation of the sphincter of Oddi; **CCK** from I cells is the primary hormonal mechanism. *Regulation of function of the sphincter of Oddi does not involve neural inputs.* - The function of the sphincter of Oddi is under **complex neural and hormonal control**. - Both **parasympathetic (vagal)** and **sympathetic** nervous inputs modulate its activity, often working in conjunction with CCK to coordinate bile and pancreatic juice release. *Sphincter relaxation is enhanced via stimulation of opioid receptors.* - **Opioid receptors** in the sphincter of Oddi, when stimulated, can actually cause **contraction** or spasm of the sphincter. - This is a well-known side effect that can worsen or induce biliary colic, not enhance relaxation.

Question 84: A 34-year-old woman comes to the physician because she has not had her period for 4 months. Menses had previously occurred at regular 28-day intervals with moderate flow. A home pregnancy test was negative. She also reports recurrent headaches and has noticed that when she goes to the movies she cannot see the outer edges of the screen without turning her head to each side. This patient's symptoms are most likely caused by abnormal growth of which of the following?

A. Adenohypophysis (Correct Answer)
B. Astrocytes
C. Schwann cells
D. Pineal gland
E. Arachnoid cap cells

Explanation: ***Adenohypophysis*** - The patient's symptoms of **amenorrhea**, recurrent headaches, and **bitemporal hemianopsia** (cannot see the outer edges of the screen) strongly suggest a **pituitary adenoma**. - Pituitary adenomas typically arise from the **adenohypophysis** and can cause hormonal imbalances (leading to amenorrhea) and compress the **optic chiasm** (leading to visual field defects). *Astrocytes* - **Astrocytes** are glial cells that support neurons and form the **blood-brain barrier**; their abnormal growth typically leads to **gliomas**, which present with different symptoms like seizures, focal neurological deficits, or increased intracranial pressure, rather than specific endocrine dysfunction and bitemporal hemianopsia. - While gliomas can cause headaches and visual field defects, the combination with **amenorrhea** points away from this diagnosis. *Schwann cells* - **Schwann cells** produce myelin in the peripheral nervous system; abnormal growth usually results in **schwannomas**, which present with symptoms related to cranial nerve or spinal nerve compression (e.g., hearing loss in acoustic neuroma), not typically bitemporal hemianopsia or amenorrhea. - Schwannomas are derived from the myelin sheaths of peripheral nerves and would not explain the endocrine disturbances seen here. *Pineal gland* - Lesions of the **pineal gland** often cause **Parinaud syndrome** (failure of upward gaze, pupillary abnormalities) due to compression of the superior colliculi, and can also lead to **hydrocephalus** or precocious puberty. - While headaches can occur, **bitemporal hemianopsia** and **amenorrhea** are not characteristic presentations of pineal gland tumors. *Arachnoid cap cells* - Abnormal growth of **arachnoid cap cells** leads to **meningiomas**, which are typically slow-growing tumors arising from the meninges. - Meningiomas can cause headaches and focal neurological deficits depending on their location, but they do **not typically cause bitemporal hemianopsia** or **endocrine dysfunction** like amenorrhea, as they are usually external to the brain tissue.

Question 85: A 60-year-old male engineer who complains of shortness of breath when walking a few blocks undergoes a cardiac stress test because of concern for coronary artery disease. During the test he asks his cardiologist about what variables are usually used to quantify the functioning of the heart. He learns that one of these variables is stroke volume. Which of the following scenarios would be most likely to lead to a decrease in stroke volume?

A. Anxiety
B. Heart failure (Correct Answer)
C. Exercise
D. Pregnancy
E. Digitalis

Explanation: ***Heart failure*** - In **heart failure**, the heart's pumping ability is impaired, leading to a reduced **ejection fraction** and thus a decreased **stroke volume**. - The weakened myocardium cannot effectively contract to expel the normal volume of blood, resulting in lower blood output per beat. *Anxiety* - **Anxiety** typically causes an increase in **sympathetic nervous system** activity, leading to increased heart rate and myocardial contractility. - This often results in a temporary **increase in stroke volume** due to enhanced cardiac performance, not a decrease. *Exercise* - During **exercise**, there is a significant **increase in venous return** and sympathetic stimulation, leading to increased **end-diastolic volume** and contractility. - This physiological response causes a substantial **increase in stroke volume** to meet the body's higher oxygen demands. *Pregnancy* - **Pregnancy** leads to significant **physiological adaptations** to accommodate the growing fetus, including a substantial increase in **blood volume**. - This increased blood volume and cardiac output result in an **increase in stroke volume** to maintain adequate perfusion for both mother and fetus. *Digitalis* - **Digitalis** is a cardiac glycoside that **increases intracellular calcium** in myocardial cells, enhancing the **force of contraction**. - This positive inotropic effect leads to an **increased stroke volume** by improving the heart's pumping efficiency.

Question 86: A 25-year-old man is admitted to the hospital after a severe motor vehicle accident as an unrestrained front-seat passenger. Appropriate life-saving measures are given, and the patient is now hemodynamically stable. Physical examination shows a complete loss of consciousness. There are no motor or ocular movements with painful stimuli. The patient has bilaterally intact pupillary light reflexes. The patient is placed in a 30° semi-recumbent position for further examination. What is the most likely finding on the examination of this patient's right ear?

A. Cold water causing ipsilateral saccadic movement.
B. Warm water mimicking the head turning left.
C. Warm water causing contralateral slow tonic deviation. (Correct Answer)
D. Cold water causing contralateral slow tonic deviation.
E. No response to warm water irrigation.

Explanation: ***Warm water causing contralateral slow tonic deviation.*** - The patient has suffered **severe brain injury** with loss of consciousness and absent motor/ocular movements, but **intact pupillary reflexes** indicate the midbrain is functional and suggests an intact brainstem below the level of cortical injury. - **Caloric testing (oculovestibular reflex)** evaluates brainstem function in comatose patients. In a comatose patient with intact brainstem pathways, only the **slow tonic phase** of eye deviation occurs (the fast corrective phase requires an intact cortex). - **Warm water irrigation** in the right ear causes endolymph flow that stimulates the horizontal semicircular canal, mimicking head rotation toward the irrigated side. This triggers the vestibulo-ocular reflex, causing eyes to deviate in the **opposite direction** (contralateral) to maintain gaze stability. - In this comatose patient, **warm water in the right ear** produces **slow tonic deviation to the left** (contralateral), without the fast corrective phase. - Mnemonic: **COWS** - Cold Opposite, Warm Same (refers to fast phase in awake patients); in coma, only slow phase remains, so warm → contralateral deviation. *Cold water causing ipsilateral saccadic movement.* - **Saccadic movements** are rapid, voluntary eye movements that require an intact cortex. In a comatose patient, saccades are absent. - Cold water would cause **ipsilateral tonic deviation** (not saccadic movement) in a comatose patient with intact brainstem. *Warm water mimicking the head turning left.* - This option is ambiguous and doesn't clearly describe the expected eye movement finding. - While warm water does mimic head turning toward the irrigated side, the resulting eye movement is **contralateral deviation**, not simply "mimicking head turning left." *Cold water causing contralateral slow tonic deviation.* - **Cold water irrigation** in the right ear would cause eyes to deviate **ipsilaterally** (toward the right), not contralaterally. - Cold water causes endolymph flow opposite to warm water, resulting in eye deviation toward the irrigated ear in comatose patients. *No response to warm water irrigation.* - **Absent caloric responses** bilaterally indicate severe brainstem damage or brain death. - This patient has **intact pupillary light reflexes**, which demonstrates functional midbrain (cranial nerve III) and suggests preserved brainstem pathways for the vestibulo-ocular reflex. - A complete lack of response would be inconsistent with intact pupillary reflexes.

Question 87: A 38-year-old woman presents to the physician’s clinic with a 6-month history of generalized weakness that usually worsens as the day progresses. She also complains of the drooping of her eyelids and double vision that is worse in the evening. Physical examination reveals bilateral ptosis after a sustained upward gaze and loss of eye convergence which improves upon placing ice packs over the eyes and after the administration of edrophonium. Which of the following is an intrinsic property of the muscle group affected in this patient?

A. A small mass per motor unit
B. High ATPase activity (Correct Answer)
C. High myoglobin content
D. High density of mitochondria
E. Increased amount of ATP generated per molecule of glucose

Explanation: ***High ATPase activity*** - This patient presents with **myasthenia gravis (MG)**, an autoimmune disorder affecting the neuromuscular junction through antibodies against acetylcholine receptors. - **Extraocular muscles** and other muscles affected early in MG contain a high proportion of **fast-twitch (Type II) muscle fibers**, which are characterized by **high ATPase activity**. - **Type II fibers** with high ATPase activity generate rapid, powerful contractions but are **more susceptible to neuromuscular junction dysfunction** due to their higher firing rates and greater dependence on efficient neuromuscular transmission. - This intrinsic property (high ATPase activity) is why these muscles are preferentially affected in myasthenia gravis. *A small mass per motor unit* - While extraocular muscles do have **small motor units** (allowing for precise eye movements), this describes the **innervation pattern** rather than an intrinsic biochemical property of the muscle fibers themselves. - The question specifically asks about an intrinsic property of the muscle group, referring to the metabolic and contractile characteristics of the muscle fibers. *High myoglobin content* - **High myoglobin content** is characteristic of **Type I (slow-twitch) oxidative fibers**, which rely on sustained oxygen delivery for prolonged, fatigue-resistant contractions. - Muscles preferentially affected in MG have a higher proportion of **Type II fibers**, which have lower myoglobin content compared to Type I fibers. *High density of mitochondria* - **High mitochondrial density** is characteristic of **Type I (slow-twitch) oxidative fibers** that depend on aerobic metabolism for sustained energy production. - While extraocular muscles do have oxidative capacity, the **Type II fibers** preferentially affected in MG have relatively lower mitochondrial density compared to Type I fibers and rely more on glycolytic metabolism for rapid energy needs. *Increased amount of ATP generated per molecule of glucose* - **Aerobic respiration** in Type I fibers generates approximately 32 ATP molecules per glucose through oxidative phosphorylation. - **Type II fibers** rely more heavily on **anaerobic glycolysis**, which produces only 2 ATP per glucose molecule, making them less efficient in ATP generation per glucose. - The muscles affected in MG have higher proportions of Type II fibers with lower ATP efficiency per glucose molecule.

Question 88: A 2-month-old girl with a previous diagnosis of DiGeorge syndrome is brought to the emergency department with her parents following a seizure. Her mother states that the baby had been inconsolable all day and refused to feed. She was born at 39 weeks gestation via spontaneous vaginal delivery. She is up to date on all vaccines. Upon arrival to the hospital her heart rate is 120/min, respiratory rate is 40/min, and temperature of 37.0°C (98.6°F). On examination, she is afebrile and somnolent and her fontanelles are open and soft. While attempting to take her blood pressure, the patient’s arm and hand flex sharply and do not relax until the cuff is released. A light tap on the cheek results in an atypical facial muscle twitch. A CMP and CBC are drawn and sent for analysis. Which of the following is the most likely cause?

A. Hypernatremia
B. Hypocalcemia (Correct Answer)
C. Tetanus
D. High fever
E. Meningitis

Explanation: ***Hypocalcemia*** - DiGeorge syndrome is associated with **thymic hypoplasia** and **parathyroid hypoplasia**, leading to **hypocalcemia** due to inadequate parathyroid hormone production. - The symptoms described, including seizures, **Chvostek's sign** (facial muscle twitch with light tap on cheek), and **Trousseau's sign** (carpal spasm with blood pressure cuff inflation), are classic manifestations of **neuromuscular irritability** caused by severe hypocalcemia. *Hypernatremia* - **Hypernatremia** is characterized by excessive sodium levels, typically presenting with symptoms like extreme thirst, lethargy, confusion, or seizures due to **cerebral dehydration**. - It does not cause the specific signs of neuromuscular excitability like Chvostek's or Trousseau's signs seen here. *Tetanus* - **Tetanus** is caused by the bacterium *Clostridium tetani* and manifests with painful muscle spasms, trismus (lockjaw), and opisthotonus, but does not present with Chvostek's or Trousseau's signs. - Furthermore, the child is described as being up to date on all vaccinations, making tetanus unlikely. *High fever* - A **high fever** can cause febrile seizures in young children, but the patient is explicitly stated to be **afebrile** (37.0°C or 98.6°F), ruling out fever as the cause of the seizure. - It also would not explain the other specific signs of neuromuscular irritability. *Meningitis* - **Meningitis** is an inflammation of the meninges, typically presenting with fever, irritability, lethargy, nuchal rigidity, and bulging fontanelles in infants. - The patient is **afebrile** and has **soft, open fontanelles**, and her symptoms are more consistent with metabolic derangements rather than central nervous system infection.

Question 89: A 22-year-old man comes to the physician because of a 2-month history of episodes of shortness of breath, lightheadedness, and palpitations. During the examination, he reports the onset of one such episode. His pulse is 170/min and regular, respirations are 22/min, and blood pressure is 100/65 mm Hg. An ECG shows a regular narrow complex tachycardia; no P waves are visible. A common clinical maneuver to diagnose and/or relieve the patient's symptoms involves stimulation of which of the following nerves?

A. Glossopharyngeal
B. Phrenic
C. Trigeminal
D. Recurrent laryngeal
E. Vagus (Correct Answer)

Explanation: ***Vagus*** - **Vagal maneuvers** (carotid sinus massage, Valsalva maneuver, diving reflex) are the standard clinical approach to terminate **supraventricular tachycardia (SVT)**. - These maneuvers increase **parasympathetic tone** via the **vagus nerve (CN X)** to the **SA and AV nodes**, slowing conduction and heart rate. - Carotid sinus massage stimulates baroreceptors → afferent signals via glossopharyngeal nerve (CN IX) → medullary cardiovascular center → **increased efferent vagal output** to the heart. - The **vagus nerve is the therapeutic effector** that slows the heart and terminates the arrhythmia. *Glossopharyngeal* - The **glossopharyngeal nerve (CN IX)** carries the **afferent (sensory)** signals from carotid sinus baroreceptors to the brainstem. - While technically involved in the reflex arc, the therapeutic effect comes from increased **vagal output**, not glossopharyngeal stimulation. - Clinically, these are called "vagal maneuvers" because the vagus nerve mediates the therapeutic response. *Phrenic* - The **phrenic nerve** (C3-C5) innervates the **diaphragm** and controls breathing. - Not involved in heart rate regulation or termination of SVT. *Trigeminal* - The **trigeminal nerve (CN V)** provides facial sensation and motor innervation to muscles of mastication. - The **diving reflex** (cold water immersion to face) can trigger bradycardia via trigeminal-vagal reflex, but this is not the standard maneuver for SVT. - Carotid sinus massage does not involve the trigeminal nerve. *Recurrent laryngeal* - The **recurrent laryngeal nerve** is a branch of the vagus nerve that innervates **intrinsic laryngeal muscles**. - Controls vocal cord movement, not cardiac function. - Not involved in vagal maneuvers for SVT.

Question 90: Under what physiologic state is the endogenous human analog of nesiritide produced?

A. Increased ventricular stretch (Correct Answer)
B. Increased circulatory volume presenting to the kidneys
C. Increased external stress
D. Increased intracranial pressure
E. Decreased circulatory volume presenting to the kidneys

Explanation: ***Increased ventricular stretch*** - Nesiritide is a recombinant form of **B-type natriuretic peptide (BNP)**, which is endogenously produced by the **ventricular myocardium** in response to increased wall stress or stretch. - This occurs in conditions like **heart failure**, where the ventricles are overfilled and experience elevated pressure. *Increased circulatory volume presenting to the kidneys* - While increased circulatory volume can lead to **atrial natriuretic peptide (ANP)** release from the atria, the primary stimulus for BNP (the analog of nesiritide) production is **ventricular stretch**, not solely renal circulatory volume. - ANP and BNP both contribute to **natriuresis** and vasodilation, but their primary release sites and triggers differ. *Increased external stress* - Increased external stress typically activates the **sympathetic nervous system** and the **hypothalamic-pituitary-adrenal (HPA) axis**, leading to the release of **catecholamines** and **cortisol**. - This response is largely independent of **natriuretic peptide** production. *Increased intracranial pressure* - Increased intracranial pressure can trigger the **Cushing reflex**, characterized by **hypertension**, **bradycardia**, and irregular respiration. - It does not directly stimulate the release of BNP or its analog nesiritide; rather, it represents a response to **cerebral ischemia**. *Decreased circulatory volume presenting to the kidneys* - **Decreased circulatory volume** would activate the **renin-angiotensin-aldosterone system (RAAS)** and **antidiuretic hormone (ADH)**, leading to **fluid retention** and vasoconstriction. - This is opposite to the actions of natriuretic peptides, which promote **diuresis** and vasodilation.

Question 91: A 42-year-old woman presents to her primary care physician with 2 weeks of abdominal pain. She says that the pain is squeezing in character and gets worse after she eats food. The pain is particularly bad after she eats dairy products so she has begun to avoid ice cream and cheese. Furthermore, she has noticed that she has been experiencing episodes of nausea associated with abdominal pain in the last 4 days. Physical exam reveals tenderness to palpation and rebound tenderness in the right upper quadrant of the abdomen. The molecule that is most likely responsible for the increased pain this patient experiences after eating fatty foods is most likely secreted by which of the following cells?

A. G cells
B. Chief cells
C. D cells
D. S cells
E. I cells (Correct Answer)

Explanation: ***I cells*** - The patient's symptoms (worsening pain after fatty meals, particularly dairy; right upper quadrant tenderness; nausea and rebound tenderness) are highly suggestive of **acute cholecystitis**, likely due to **gallstones**. - **Cholecystokinin (CCK)**, secreted by intestinal I cells, is released in response to dietary fats and amino acids, stimulating gallbladder contraction. In the presence of a gallstone obstructing the cystic duct, this contraction causes increased pressure and pain. *G cells* - **G cells** primarily secrete **gastrin** in the stomach, which stimulates gastric acid secretion and mucosal growth. - While gastrin is involved in digestion, it does not directly mediate the pain associated with gallbladder contraction in response to fatty meals. *Chief cells* - **Chief cells** in the stomach secrete **pepsinogen** and gastric lipase, which are involved in protein and fat digestion, respectively. - Their secretions are not directly involved in triggering gallbladder contraction or the associated pain in cholecystitis. *D cells* - **D cells** secrete **somatostatin**, an inhibitory hormone that suppresses the release of many gastrointestinal hormones, including gastrin, secretin, and CCK. - Somatostatin would likely *reduce* gallbladder motility rather than cause the painful contractions seen in this patient. *S cells* - **S cells** in the duodenum secrete **secretin** in response to acidic chyme. Secretin primarily stimulates the pancreas to release bicarbonate and water. - While secretin plays a role in digestion, it does not directly cause gallbladder contraction or the post-fatty meal pain described.

Question 92: Paramedics respond to a call regarding an 18-year-old male with severe sudden-onset heart palpitations. The patient reports symptoms of chest pain, fatigue, and dizziness. Upon examination, his heart rate is 175/min and regular. His blood pressure is 110/75 mm Hg. Gentle massage below the level of the left mandible elicits an immediate improvement in the patient, as his heart rate returns to 70/min. What was the mechanism of action of this maneuver?

A. Decreasing the length of phase 4 of the SA node myocytes
B. Decreasing the firing rate of carotid baroreceptors
C. Increasing the refractory period in ventricular myocytes
D. Increasing sympathetic tone in systemic arteries
E. Slowing conduction in the AV node (Correct Answer)

Explanation: ***Slowing conduction in the AV node*** - The maneuver described, **carotid sinus massage**, stimulates the **baroreceptors** in the carotid artery. This increases **parasympathetic (vagal) tone**. - Increased vagal tone primarily acts on the **AV node** to slow its conduction velocity, thereby terminating reentrant tachycardias that depend on AV nodal conduction, such as AVNRT and AVRT. *Decreasing the length of phase 4 of the SA node myocytes* - **Carotid sinus massage** would actually **increase** the length of phase 4 (spontaneous depolarization) in SA node myocytes, leading to a slower heart rate. - A shorter phase 4 would result in a faster heart rate, which is the opposite of the observed effect. *Decreasing the firing rate of carotid baroreceptors* - The maneuver **stimulates** the carotid baroreceptors, leading to an **increased** firing rate. - A decreased firing rate would normally activate the **sympathetic nervous system**, increasing heart rate, rather than slowing it. *Increasing the refractory period in ventricular myocytes* - While parasympathetic stimulation does affect the heart, its primary action is not to directly increase the **refractory period** in ventricular myocytes. This effect is more directly related to antiarrhythmic drugs. - Carotid massage primarily affects **nodal tissue** (SA and AV nodes) rather than ventricular myocardium directly. *Increasing sympathetic tone in systemic arteries* - Carotid sinus massage **increases parasympathetic tone** and **decreases sympathetic tone**, including that to systemic arteries. - Increased sympathetic tone would lead to **vasoconstriction** and potentially an **increased heart rate**, which is contrary to the therapeutic effect observed.

Question 93: A 72-year-old man comes to the physician for a routine physical examination. He does not take any medications. Physical examination shows no abnormalities. Laboratory studies show a calcium concentration of 8.5 mg/dL, a phosphorus concentration of 3.1 mg/dL, an elevated bone-specific alkaline phosphatase concentration, and a normal urine deoxypyridinoline concentration. Which of the following is the most likely explanation for this patient's laboratory abnormalities?

A. Decreased parathyroid chief cell activity
B. Decreased osteoclast activity
C. Increased chondroblast activity
D. Increased parafollicular C-cell activity
E. Increased osteoblast activity (Correct Answer)

Explanation: ***Increased osteoblast activity*** - An **elevated bone-specific alkaline phosphatase** (BSAP) indicates increased **osteoblast activity**, as BSAP is an enzyme produced by osteoblasts during bone formation. - The combination of **normal calcium, phosphorus**, and **urine deoxypyridinoline** (a marker of bone resorption) suggests a normal overall mineral balance despite increased bone formation, which can be seen in healthy aging or mild stress. *Decreased parathyroid chief cell activity* - **Decreased parathyroid chief cell activity** would lead to **decreased parathyroid hormone (PTH)**. - Low PTH typically causes **low calcium** levels and **high phosphorus** levels, which contradicts the normal calcium and phosphorus seen in this patient. *Decreased osteoclast activity* - **Decreased osteoclast activity** would result in **reduced bone resorption**, leading to **lower urine deoxypyridinoline** levels. - If osteoclast activity were significantly decreased in isolation, it would lead to increased bone density or abnormal bone remodeling that isn't supported by the elevated BSAP as the primary finding. *Increased chondroblast activity* - **Increased chondroblast activity** is primarily associated with **cartilage formation** and would not directly explain an elevated **bone-specific alkaline phosphatase**. - BSAP is a marker of **osteoblastic activity** in bone, not chondroblastic activity in cartilage. *Increased parafollicular C-cell activity* - **Increased parafollicular C-cell activity** would lead to **increased calcitonin** secretion. - Calcitonin’s primary effect is to **lower blood calcium** by inhibiting osteoclasts, which would not typically cause an elevated BSAP.

Question 94: A 45-year-old executive travels frequently around the world. He often has difficulty falling asleep at night when he returns home. You suspect a circadian rhythm disorder is responsible for his pathology. Which of the following regulates the circadian rhythm?

A. Ventromedial area of hypothalamus
B. Suprachiasmatic nucleus of hypothalamus (Correct Answer)
C. Anterior hypothalamus
D. Supraoptic area of hypothalamus
E. Posterior hypothalamus

Explanation: ***Suprachiasmatic nucleus of hypothalamus*** - The **suprachiasmatic nucleus (SCN)** is considered the body's **master circadian clock**, receiving direct input from the retina about light levels. - It plays a crucial role in regulating various bodily functions like sleep-wake cycles and hormone release according to the 24-hour day. *Ventromedial area of hypothalamus* - The **ventromedial nucleus of the hypothalamus** is primarily involved in **satiety** and **feeding behavior**. - Damage to this area can lead to **hyperphagia** and obesity, not circadian rhythm disturbances. *Anterior hypothalamus* - The **anterior hypothalamus** is mainly involved in **thermoregulation**, specifically **heat dissipation**. - It also plays a role in **parasympathetic activities** but is not the primary regulator of circadian rhythms. *Supraoptic area of hypothalamus* - The **supraoptic nucleus** is responsible for producing **vasopressin (ADH)** and **oxytocin**, which are then released by the posterior pituitary. - These hormones are crucial for **water balance** and social bonding, not circadian rhythm regulation. *Posterior hypothalamus* - The **posterior hypothalamus** is responsible for **heat conservation** and sympathetic nervous system activation. - It helps maintain **body temperature** during cold exposure but does not directly control circadian rhythm.

Question 95: A 47-year-old Hispanic man presents with complaints of recent heat intolerance and rapid heart rate. The patient has also experienced recent unintentional weight loss of 15 pounds. Physical exam reveals tachycardia and skin that is warm to the touch. A radioactive iodine uptake scan of the thyroid reveals several focal nodules of increased iodine uptake. Prior to this study, the physician had also ordered a serum analysis that will most likely show which of the following?

A. High TSH and low T4
B. High TSH and normal T4
C. Low TSH and high T4 (Correct Answer)
D. Low TSH and low T4
E. High TSH and high T4

Explanation: ***Low TSH and high T4*** - The patient's symptoms (heat intolerance, rapid heart rate, weight loss, tachycardia, warm skin) are classic for **hyperthyroidism**. - In primary hyperthyroidism, the thyroid gland overproduces **thyroid hormones (T4 and T3)**, which then feedback to inhibit TSH release from the pituitary, leading to **low TSH**. *High TSH and low T4* - This pattern is characteristic of **primary hypothyroidism**, where the thyroid gland is underactive, leading to low T4 and a compensatory high TSH. - The patient's symptoms are inconsistent with hypothyroidism. *High TSH and normal T4* - This could indicate **subclinical hypothyroidism** or a resolving thyroiditis, neither of which aligns with the patient's overt hyperthyroid symptoms. - In subclinical hypothyroidism, there's insufficient T4 to suppress TSH, but T4 levels remain within the normal range. *Low TSH and low T4* - This pattern suggests **central (secondary or tertiary) hypothyroidism**, where the pituitary or hypothalamus is not producing enough TSH, leading to low T4. - The patient's symptoms of hyperthyroidism contradict this diagnosis. *High TSH and high T4* - This uncommon pattern can be seen in cases of **TSH-secreting pituitary adenoma** (secondary hyperthyroidism) or **thyroid hormone resistance**. - However, the focal nodules of increased iodine uptake described in the radioactive iodine uptake scan strongly point to a primary thyroid cause of hyperthyroidism, making this less likely.

Question 96: A 70 year-old man comes to the physician for difficulty swallowing for 6 months. During this time, he has occasionally coughed up undigested food. He did not have weight loss or fever. Four weeks ago, he had an episode of sore throat, that resolved spontaneously. He has smoked one pack of cigarettes daily for 5 years. He has gastroesophageal reflux disease and osteoporosis. Current medications include alendronate and omeprazole. His temperature is 37.0°C (98.6°F), pulse is 84/min, and blood pressure is 130/90 mmHg. On examination, he has foul-smelling breath and a fluctuant mass on the right neck. Which of the following is most likely involved in the pathogenesis of this patient's symptoms?

A. Degeneration of neurons in the esophageal wall
B. Deep neck space infection (Correct Answer)
C. Abnormal esophageal motor function
D. Adverse effect of medication
E. Cellular dysplasia

Explanation: ***Deep neck space infection*** - The patient's presentation with **foul-smelling breath**, difficulty swallowing, a **fluctuant mass on the right neck**, and a recent episode of sore throat are highly suggestive of an evolving deep neck space infection, likely a **peritonsillar abscess** or another neck abscess. - While many symptoms can be explained by a Zenker's diverticulum (undigested food, no weight loss), the **fluctuant neck mass** points more towards an infectious process like a deep neck space infection. *Degeneration of neurons in the esophageal wall* - This typically refers to **achalasia**, characterized by **dysphagia for both solids and liquids**, regurgitation, and sometimes weight loss. - While regurgitation of undigested food can occur, the presence of a **fluctuant neck mass** and foul-smelling breath is not a typical feature of achalasia. *Abnormal esophageal motor function* - This general category includes disorders like **achalasia** and **esophageal spasm**, which can cause dysphagia and regurgitation. - However, the specific finding of a **fluctuant neck mass** is not explained by primary esophageal motility disorders. *Adverse effect of medication* - **Alendronate** can cause **esophagitis** leading to primary dysphagia and pain, but not typically a fluctuant neck mass or regurgitation of undigested food without weight loss. - **Omeprazole** is used to treat GERD and is unlikely to cause these specific symptoms. *Cellular dysplasia* - **Esophageal dysplasia** (often due to **Barrett's esophagus** from GERD) can lead to **esophageal cancer**, which would present with progressive dysphagia, **significant weight loss**, and sometimes pain. - The patient has no weight loss and the fluctuant mass is not typical for primary esophageal malignancy.

Question 97: A 34-year-old woman with a past medical history of obesity and longstanding GERD presents to the emergency room with chest pain. She describes the pain as central with a sensation of something being stuck in her chest, and this is the third episode in the last month. The prior two incidents occurred at the gym while she was drinking a sport drink and resolved after resting for 3-4 minutes. This episode started after she received news that her father had just had a heart attack at age 69 and has lasted for 15 minutes. The patient also notes several months of intermittent difficulty swallowing but denies palpitations, diaphoresis, or shortness of breath. The patient has a family history of scleroderma in her mother. In the emergency room, her temperature is 98.4°F (36.8°C), blood pressure is 143/82 mmHg, pulse is 89/min, and respirations are 16/min. The patient appears mildly uncomfortable but exam is otherwise unremarkable. Which of the following is the most appropriate confirmatory test for this patient’s condition?

A. Troponin I
B. EKG
C. Esophageal manometry (Correct Answer)
D. Barium swallow
E. Endoscopy

Explanation: ***Esophageal manometry*** - This patient presents with **chest pain** and **dysphagia**, worsened by stress (**father's heart attack news**), which are classic symptoms of **esophageal spasm**. - **Esophageal manometry** directly measures the pressure and contractility of the esophageal muscles, making it the most appropriate test to confirm the presence of **esophageal motility disorders** like esophageal spasm. *Troponin I* - While chest pain necessitates cardiac evaluation, this patient's pain has features inconsistent with typical **cardiac ischemia**, such as resolution with rest but also triggered by emotions. - The absence of **diaphoresis** or **shortness of breath** further reduces the likelihood of an acute coronary syndrome, though troponin would still be checked for acute chest pain. *EKG* - An EKG is essential in the initial workup of chest pain to rule out acute cardiac events, but it would not be a **confirmatory test** for an esophageal condition. - The EKG is likely to be normal in esophageal spasm, and while ruling out cardiac ischemia is important, it doesn't diagnose the underlying esophageal issue. *Barium swallow* - A barium swallow is useful for evaluating **structural abnormalities** or **obstructive processes** in the esophagus, such as strictures or masses. - It is less effective for diagnosing **motility disorders** like esophageal spasm, where the issue is functional rather than structural. *Endoscopy* - Endoscopy is primarily used to visualize the esophageal lumen and identify **mucosal abnormalities** like esophagitis, ulcers, or tumors. - While it can rule out some causes of dysphagia and chest pain, it is not the most appropriate test to diagnose **esophageal motility disorders** as it does not assess muscle function directly.

Question 98: A 36-year-old woman comes to the physician because of blurred vision and difficulty keeping her eyes open. She also has occasional difficulty chewing, especially when eating meat or other foods that require prolonged chewing. The symptoms are worse at the end of the day. Physical examination shows bilateral drooping of the eyelids, which becomes more pronounced when she is asked to look upwards for 30 seconds. Which of the following is the most likely cause of this patient's symptoms?

A. Interrupted transmission of T-tubule depolarization
B. Inhibition of calcium release from the sarcoplasmic reticulum
C. Impaired flow of calcium ions between gap junctions
D. Decreased generation of end plate potential (Correct Answer)
E. Sustained blockade of actin myosin-binding sites

Explanation: ***Decreased generation of end plate potential*** - This patient's symptoms of **ptosis**, **diplopia**, and **fatigable chewing difficulties** are highly suggestive of **myasthenia gravis**. - In myasthenia gravis, **autoantibodies block or destroy acetylcholine receptors** at the neuromuscular junction, leading to a reduced response to acetylcholine and thus a **decreased end-plate potential**. *Interrupted transmission of T-tubule depolarization* - This mechanism is characteristic of conditions that affect **muscle excitation-contraction coupling**, such as certain **myopathies** or disorders involving ion channels in muscle fibers. - It does not explain the **fatigability** and specific pattern of muscle weakness seen with acetylcholine receptor dysfunction. *Inhibition of calcium release from the sarcoplasmic reticulum* - This could lead to muscle weakness by preventing contraction, as **calcium release** is essential for initiating muscle contraction. - However, this is typically involved in disorders like **malignant hyperthermia** or certain **store-operated calcium entry (SOCE) channelopathies**, not myasthenia gravis. *Impaired flow of calcium ions between gap junctions* - **Gap junctions** are primarily found in **cardiac and smooth muscle**, facilitating direct electrical communication between cells. - They are **not present at the neuromuscular junction** of skeletal muscles, therefore, impairment here would not explain the patient's symptoms. *Sustained blockade of actin myosin-binding sites* - A sustained blockade of actin-myosin binding would lead to **persistent muscle rigidity** or contracture, preventing relaxation, rather than the presented **fatigable weakness**. - This mechanism is associated with conditions like **rigor mortis** or certain drug toxicities, not myasthenia gravis, which is characterized by impaired muscle activation due to issues at the neuromuscular junction.

Question 99: A team of researchers is investigating different mechanisms of transmitting sensory information in the body. They are particularly interested in the different types of sensory receptors. From a sample of tissue, they isolate a receptor that is encased in deep skin layers and joints. The receptor adapts quickly and they discover its role is to sense vibration and pressure. Which of the following types of nerve fibers is most likely used by this receptor to transmit sensory information?

A. Small, myelinated fibers
B. Small, unmyelinated fibers
C. Large, myelinated fibers (Correct Answer)
D. Large, unmyelinated fibers
E. Medium, myelinated fibers

Explanation: ***Large, myelinated fibers*** - The described receptor, located in deep skin layers and joints, sensing **vibration and pressure** and having **quick adaptation**, is characteristic of a **Pacinian corpuscle**. - **Pacinian corpuscles** and other mechanoreceptors transmitting fine touch, proprioception, and vibratory sensations utilize **large, myelinated (Aβ) nerve fibers** for rapid conduction. *Small, myelinated fibers* - **Small, myelinated fibers (Aδ fibers)** transmit sensations like **fast pain** and **cold temperature**. - These are not associated with the rapid transmission of vibration or pressure from deep mechanoreceptors. *Small, unmyelinated fibers* - **Small, unmyelinated fibers (C fibers)** conduct sensations of **slow, burning pain**, warmth, and itch. - Their slow conduction velocity is not suitable for the quick adaptation and rapid transmission required for vibration and pressure. *Large, unmyelinated fibers* - **Large nerve fibers** are typically **myelinated** in the peripheral nervous system to ensure efficient and fast signal transmission. - **Unmyelinated large fibers** are generally not a recognized category for sensory transmission in the human body; myelination is crucial for speed in large axons. *Medium, myelinated fibers* - While there are various sizes of myelinated fibers, Aβ fibers, which transmit signals from Pacinian corpuscles, are specifically categorized as **large**. - The term "medium" is less precise for describing the most appropriate fiber type for this specific sensory function, which requires the largest and fastest fibers.

Question 100: A 58-year-old man with history of diabetes and hypertension suffers a cardiac arrest at home. The family calls 911, yet no one performs CPR. Five minutes after the arrest, EMS arrives to begin resuscitation. At this point, which region of the CNS is most likely to suffer ischemic damage?

A. Thalamus
B. Hippocampus (Correct Answer)
C. Pons
D. Medulla
E. Spinal cord

Explanation: ***Hippocampus*** - The **hippocampus** (particularly the **CA1 region**) is the **most vulnerable** area of the CNS to global cerebral ischemia and demonstrates the greatest **selective vulnerability** among all brain structures. - After just **5 minutes** of cardiac arrest without perfusion, hippocampal neurons begin to suffer **irreversible ischemic damage** due to their extremely high metabolic demand and dense concentration of **NMDA receptors**, which mediate excitotoxic injury. - This selective vulnerability explains why cardiac arrest survivors often develop **anterograde amnesia** and memory deficits even when other brain functions are preserved. - Other highly vulnerable areas include cerebellar Purkinje cells and cortical layers 3, 5, and 6, but the hippocampus is typically affected **first and most severely**. *Thalamus* - While the **thalamus** can be affected by prolonged global ischemia, it demonstrates **intermediate vulnerability** and is generally less susceptible to early damage compared to the hippocampus. - Thalamic damage typically requires more prolonged ischemia and manifests as sensory or consciousness deficits rather than the profound memory impairment characteristic of hippocampal injury. *Pons* - The **pons** is part of the brainstem and demonstrates **relative resistance** to hypoxic-ischemic injury compared to cortical and hippocampal structures. - Its lower metabolic demand and role in controlling vital functions means it is typically damaged only after more prolonged periods of ischemia (>10 minutes). - Severe pontine damage results in locked-in syndrome or coma, but this is not the primary concern at 5 minutes post-arrest. *Medulla* - The **medulla oblongata** is the most **ischemia-resistant** brain region due to its critical role in maintaining cardiovascular and respiratory reflexes. - Like the pons, it requires prolonged and severe global ischemia before suffering significant damage, typically well beyond the 5-minute timeframe in this scenario. *Spinal cord* - The **spinal cord** has a relatively robust blood supply and is **not typically affected** by global cerebral ischemia from cardiac arrest unless there is specific compromise to spinal arterial circulation. - Spinal cord ischemia is more commonly associated with aortic pathology, hypotension during surgery, or watershed infarction rather than cardiac arrest scenarios.

Question 101: A 4-day-old healthy male infant is born with normal internal and external male reproductive organs. Karyotype analysis reveals a 46XY genotype. Production of what substance by which cell type is responsible for the development of the normal male seminal vesicles, epididymides, ejaculatory ducts, and ductus deferens?

A. Testosterone; Leydig cells (Correct Answer)
B. Testis-determining factor; Sertoli cells
C. Testis-determining factor; Leydig cells
D. Testosterone; Sertoli cells
E. Mullerian inhibitory factor; Sertoli cells

Explanation: ***Testosterone; Leydig cells*** - **Testosterone**, produced by fetal **Leydig cells**, is responsible for stimulating the development and differentiation of the **Wolffian ducts** into the epididymis, vas deferens, seminal vesicles, and ejaculatory ducts. - This process is crucial for the formation of the internal male reproductive organs, as described in the healthy male infant. *Testis-determining factor; Sertoli cells* - **Testis-determining factor (TDF)**, expressed from the SRY gene, initiates the differentiation of the indifferent gonad into a testis but does not directly stimulate Wolffian duct development. - **Sertoli cells** primarily produce anti-Müllerian hormone (AMH), which causes the regression of Müllerian ducts, and also support spermatogenesis later in life. *Testis-determining factor; Leydig cells* - While **Leydig cells** are the correct cell type for producing the necessary hormone, the substance responsible for Wolffian duct differentiation is **testosterone**, not testis-determining factor (TDF). - TDF is involved in gonadal differentiation, not directly in ductal development. *Testosterone; Sertoli cells* - **Testosterone** is the correct hormone for promoting Wolffian duct development, but it is produced by **Leydig cells**, not Sertoli cells. - **Sertoli cells** mainly produce **anti-Müllerian hormone (AMH)** to inhibit female internal reproductive organ development. *Mullerian inhibitory factor; Sertoli cells* - **Müllerian inhibitory factor (MIF)**, also known as **anti-Müllerian hormone (AMH)**, is indeed produced by **Sertoli cells**. - However, MIF causes the **regression of the Müllerian ducts** (structures that would otherwise develop into female internal reproductive organs), rather than stimulating the development of male internal structures.

Question 102: A 39-year-old woman presents to her primary care physician because she has been experiencing intermittent abdominal pain for the last 2 weeks. She says that the pain is squeezing in nature, is located in the right upper quadrant, and is particularly severe after eating a meal. After a diagnosis is made, the patient asks why the pain gets worse after eating. The physician explains that food is detected by the gastrointestinal tract through numerous receptors and that this information is transmitted to other parts of the body to cause compensatory changes. The neurons responsible for transmitting this information are most likely located in a layer of the intestine that has which of the following characteristics?

A. Contracts to generate local movement in mucosa
B. Contains cells that primarily absorb nutrients
C. Connective tissue that envelops the other layers
D. Contracts to generate peristaltic waves (Correct Answer)
E. Contains large blood vessels and large lymphatic vessels

Explanation: ***Contracts to generate peristaltic waves*** - This describes the **muscularis propria** (external muscle layer), which contains the **myenteric plexus (Auerbach's plexus)** between its inner circular and outer longitudinal smooth muscle layers. - The **myenteric plexus is the primary neural network** responsible for detecting food through mechanoreceptors and chemoreceptors, transmitting sensory information, and coordinating both local reflexes and systemic compensatory responses throughout the gastrointestinal tract. - These neurons communicate with the **autonomic nervous system** and coordinate the release of hormones like **cholecystokinin (CCK)** after eating, which causes gallbladder contraction (relevant to this patient's postprandial pain from cholecystitis). - While this layer's most obvious function is generating peristalsis, it contains the most extensive enteric nervous system network for sensory integration and motor coordination. *Contains large blood vessels and large lymphatic vessels* - This describes the **submucosa**, which contains the **submucosal plexus (Meissner's plexus)**. - While the submucosal plexus does contain sensory neurons, it primarily regulates **local functions** such as mucosal secretion, absorption, and blood flow rather than the broader systemic compensatory responses described in the question. - The submucosa's neural network is more limited compared to the myenteric plexus. *Contracts to generate local movement in mucosa* - This describes the **muscularis mucosae**, a thin layer of smooth muscle within the mucosa that causes local folding and movement of the mucosal surface. - This layer lacks significant neural plexuses and is not involved in transmitting sensory information for systemic responses. *Contains cells that primarily absorb nutrients* - This refers to the **mucosa**, specifically the epithelial cells lining the intestinal surface. - While the mucosa contains chemoreceptors and mechanoreceptors, the question asks about the neurons that **transmit** this information, which are located in the deeper neural plexuses (primarily myenteric), not in the absorptive epithelium itself. *Connective tissue that envelops the other layers* - This describes the **serosa** (or adventitia), the outermost protective layer. - The serosa contains minimal neural tissue and is not involved in sensory detection or transmission of gastrointestinal information.

Question 103: A 32-year-old woman patient presents to her family physician with recurrent retrosternal chest pain. She has had similar episodes for the past 7 months along with difficulty swallowing solid as well as liquid food. She recently completed an 8-week course of a proton pump inhibitor, but she is still bothered by the feeling that food gets stuck down her 'food pipe'. Her pain is not related to exertion. She denies any history of acid reflux disease. Her blood pressure is 125/81 mm Hg, respirations are 21/min, pulse is 78/min, and temperature is 36.7°C (98.1°F). She currently does not have pain. A barium swallow X-ray image is normal. Which of the following tests would aid in the diagnosis of this patient's condition?

A. Electrocardiogram
B. Upper GI endoscopy
C. Manometry (Correct Answer)
D. Injection of botulinum toxin
E. Additional therapy with proton pump inhibitors

Explanation: ***Manometry*** - The patient's symptoms of **recurrent retrosternal chest pain** and **dysphagia for both solids and liquids** suggest a **motility disorder** of the esophagus, such as **achalasia** or **diffuse esophageal spasm**. - **Esophageal manometry** directly measures the pressure and coordination of muscle contractions in the esophagus, identifying abnormalities in peristalsis and sphincter relaxation. *Electrocardiogram* - While chest pain can be cardiac in origin, the patient's symptoms are primarily related to **swallowing** and not exertion, making a primary cardiac cause less likely. - An ECG would be unable to diagnose an **esophageal motility disorder**. *Upper GI endoscopy* - An **upper GI endoscopy** is primarily used to visualize the mucosa of the esophagus, stomach, and duodenum to detect structural abnormalities, inflammation, or ulcers. - It would likely be normal in a pure **motility disorder** and would not provide functional information about esophageal contractions. *Injection of botulinum toxin* - **Botulinum toxin injection** is a treatment option for some esophageal motility disorders (e.g., achalasia), but it is not a diagnostic test. - It works by paralyzing muscles, thereby reducing lower esophageal sphincter pressure. *Additional therapy with proton pump inhibitors* - The patient has already completed an 8-week course of a **PPI** without improvement, and she explicitly denies a history of **acid reflux disease**. - This suggests that her symptoms are unlikely to be acid-related, making further PPI therapy ineffective for diagnosis or treatment.

Question 104: A physiologist is studying various mediators that modulate coronary circulation. He is particularly looking at mediators that are activated via the clotting cascade, primarily activated factor XII. He finds that when the clotting cascade starts, it leads to the activation of factor XII, which in turn activates the enzyme kallikrein. This enzyme activates high and low-molecular-weight precursors of certain mediators, which work by contracting the visceral smooth muscle while relaxing the vascular smooth muscle. They are primarily associated with hypersensitivity and can cause an increase in capillary permeability, pain, and mobilize leukocytes. Which of the following is the precursor protein for the mediators the physiologist is studying?

A. L-Arginine
B. Prothrombin
C. Arachidonic acid
D. Kininogen (Correct Answer)
E. Hydroxytryptophan

Explanation: ***Kininogen*** - **Kininogen** is the precursor protein for **kinins**, such as **bradykinin**, which are activated by **kallikrein** following factor XII activation. - Kinins cause **vasodilation**, increase **capillary permeability**, induce **pain**, and contribute to inflammation and smooth muscle contraction. *L-Arginine* - **L-Arginine** is a precursor for **nitric oxide (NO)**, a vasodilator, but it is not directly activated by the clotting cascade or kallikrein. - NO primarily acts on vascular smooth muscle to cause relaxation, but its production pathway differs from the one described. *Prothrombin* - **Prothrombin** is a precursor to **thrombin**, a key enzyme in the coagulation cascade that converts **fibrinogen into fibrin**. - While activated by the clotting cascade, prothrombin's primary role is in clot formation, not in generating mediators with the described effects on vascular smooth muscle, pain, or leukocyte mobilization. *Arachidonic acid* - **Arachidonic acid** is a precursor for **eicosanoids** (prostaglandins, leukotrienes, thromboxanes) which are involved in inflammation and vascular responses. - Its metabolism is by cyclooxygenases and lipoxygenases, not directly by kallikrein or the factor XII pathway described. *Hydroxytryptophan* - **Hydroxytryptophan** is a precursor to **serotonin**, a neurotransmitter and vasoconstrictor. - Serotonin is involved in various physiological processes, but its synthesis and activation pathway are distinct from the kallikrein-kinin system described.

Question 105: A 30-year-old woman comes to the physician because of a 1-month history of intermittent abdominal pain, flatulence, and watery diarrhea. The episodes typically occur 2–3 hours after meals, particularly following ingestion of ice cream, cheese, and pizza. She is administered 50 g of lactose orally. Which of the following changes is most likely to be observed in this patient?

A. Decreased breath hydrogen content
B. Increased stool osmotic gap (Correct Answer)
C. Decreased fecal fat content
D. Increased serum glucose concentration
E. Decreased urinary D-xylose concentration

Explanation: ***Increased stool osmotic gap*** - The patient's symptoms (abdominal pain, flatulence, watery diarrhea after dairy) suggest **lactose intolerance**, a form of **osmotic diarrhea**. - In osmotic diarrhea, unabsorbed solutes in the gut (like lactose) draw water into the lumen, increasing the **osmotic gap** in the stool by reducing the contribution of electrolytes to total osmolality. *Decreased breath hydrogen content* - In **lactose intolerance**, unabsorbed lactose is fermented by colonic bacteria, producing **hydrogen gas**, which is then absorbed and exhaled. - Therefore, one would expect an **increased breath hydrogen content** after lactose ingestion in a patient with lactose intolerance, not a decrease. *Decreased fecal fat content* - **Malabsorption of fat** (steatorrhea) would lead to an **increased fecal fat content**. - Lactose intolerance primarily involves carbohydrate malabsorption, not fat malabsorption, so fecal fat content would likely be normal or unchanged. *Increased serum glucose concentration* - For serum glucose to increase after lactose ingestion, the lactose must be broken down into **glucose and galactose** and then absorbed. - In lactose intolerance, the deficiency of **lactase enzyme** prevents this breakdown, so glucose absorption is impaired and serum glucose would show little to no rise. *Decreased urinary D-xylose concentration* - **D-xylose absorption** tests assess the absorptive function of the small intestine for **monosaccharides**, independent of enzyme hydrolysis. - Lactose intolerance is an enzyme deficiency, not a generalized mucosal absorption defect (like celiac disease), so D-xylose absorption and subsequent urinary excretion would likely be normal.

Question 106: A 29-year-old man is brought to the emergency room 6 hours after the onset of severe epigastric pain and vomiting. His heart rate is 110/min and blood pressure is 98/72 mm Hg. He is diagnosed with acute pancreatitis, and fluid resuscitation with normal saline is initiated. Which of the following is the most likely immediate effect of fluid resuscitation in this patient?

A. Increase in plasma oncotic pressure
B. Increase in glomerular filtration fraction
C. Increase in volume of distribution
D. Increase in cardiac afterload
E. Increase in myocardial oxygen demand (Correct Answer)

Explanation: ***Increase in myocardial oxygen demand*** - Fluid resuscitation in a hypotensive patient with tachycardia increases **cardiac preload** and **stroke volume**, leading to higher cardiac output. - This increased workload on the heart, especially when the patient is already tachycardic, directly translates to an **increased demand for oxygen** by the myocardium. *Increase in plasma oncotic pressure* - Fluid resuscitation with **normal saline** (crystalloid solution) primarily increases intravascular volume but does not significantly increase plasma proteins, which are responsible for oncotic pressure. - In fact, large volumes of crystalloids can sometimes **slightly decrease oncotic pressure** due to hemodilution. *Increase in glomerular filtration fraction* - Fluid resuscitation improves **renal perfusion** and **glomerular filtration rate (GFR)** by restoring blood pressure and intravascular volume. - However, the glomerular filtration fraction, which is the ratio of GFR to renal plasma flow, does not necessarily increase; it might even decrease as renal plasma flow improves. *Increase in volume of distribution* - Volume of distribution refers to the apparent volume into which a drug distributes in the body. Fluid resuscitation **increases the intravascular fluid volume**, which is part of the total body water, but this is a change in actual volume, not a change in a pharmacokinetic parameter for drug distribution. - It would more accurately be described as increasing the **effective circulating volume**, not the **volume of distribution** in a pharmacological sense. *Increase in cardiac afterload* - Cardiac afterload refers to the resistance the heart must overcome to eject blood. While fluid resuscitation increases **intravascular volume**, it primarily affects **preload**. - Although indirectly, by improving cardiac output and maintaining blood pressure, there might be a slight increase in afterload, an **increase in myocardial oxygen demand** is a more direct and immediate consequence of the increased workload.

Question 107: A 55-year-old man comes to the physician because of progressive daytime sleepiness and exertional dyspnea for the past 6 months. Physical examination shows conjunctival pallor and several subcutaneous purple spots on his legs. His hemoglobin concentration is 8.5 g/dL, leukocyte count is 3,000/mm3, and platelet count is 16,000/mm3. Which of the following laboratory values is most likely to be increased in this patient?

A. Reticulocyte count
B. Lactate dehydrogenase concentration
C. Transferrin concentration
D. Erythropoietin concentration (Correct Answer)
E. Haptoglobin concentration

Explanation: ***Erythropoietin concentration*** - The patient presents with severe **anemia (Hb 8.5 g/dL)**, **leukopenia**, and **thrombocytopenia**, indicating **pancytopenia**. This severe decrease in red blood cells will trigger the kidneys to produce more **erythropoietin** in an attempt to stimulate red blood cell production in the bone marrow. - Given the pancytopenia, the underlying pathology is likely bone marrow failure (e.g., aplastic anemia, myelodysplastic syndrome), which would explain why the bone marrow is not responding effectively to increased erythropoietin. *Reticulocyte count* - A low or inappropriately normal reticulocyte count in the presence of severe anemia would suggest **bone marrow suppression** or ineffective erythropoiesis, which is consistent with the pancytopenia observed. - An **increased reticulocyte count** would typically be seen in hemolytic anemia or acute blood loss, where the bone marrow is hyperactive in response to RBC destruction or loss. *Lactate dehydrogenase concentration* - **Elevated LDH** is a marker of **cellular damage** or high cell turnover, commonly seen in hemolytic anemia or certain hematologic malignancies. - While it could be elevated in some conditions causing pancytopenia, it's not the most direct or specific compensatory response to chronic anemia as erythropoietin. *Transferrin concentration* - **Transferrin** levels usually **increase** in **iron deficiency anemia** as the body attempts to maximize iron absorption and transport. - While anemia is present, the broad pancytopenia suggests a bone marrow problem rather than a primary iron deficiency, and increased transferrin isn't a direct compensatory mechanism for severe pancytopenia. *Haptoglobin concentration* - **Haptoglobin levels decrease** in conditions involving **intravascular hemolysis**, as haptoglobin binds to free hemoglobin and is then cleared from circulation. - There is no evidence in the clinical picture to suggest hemolysis as the primary cause of anemia; the pancytopenia points to bone marrow pathology.

Question 108: A 56-year-old woman presents to the emergency department with several episodes in which she felt "dizzy." She has had these symptoms on and off for the past year and can recall no clear exacerbating factor or time of day when her symptoms occur. She has a perpetual sensation of fullness in her ear but otherwise has no symptoms currently. Her temperature is 97.6°F (36.4°C), blood pressure is 122/77 mmHg, pulse is 85/min, respirations are 13/min, and oxygen saturation is 98% on room air. Cardiopulmonary exam is unremarkable. The patient's gait is stable. Which of the following is also likely to be found in this patient?

A. Gradually improving symptoms
B. Conductive hearing loss
C. Positional vertigo
D. Sensorineural hearing loss (Correct Answer)
E. Vertical nystagmus

Explanation: ***Sensorineural hearing loss*** - The sensation of **aural fullness**, recurrent dizzy spells without clear triggers, and the episodic nature of symptoms are classic for **Ménière's disease**. - **Ménière's disease** is characterized by the triad of **vertigo**, **tinnitus**, and **sensorineural hearing loss**, often accompanied by ear fullness. *Gradually improving symptoms* - **Ménière's disease** is a chronic, progressive condition, and symptoms typically **fluctuate** in severity and can worsen over time, rather than gradually improving. - While periods of remission can occur, the underlying pathology does make a steady improvement unlikely without intervention. *Conductive hearing loss* - **Conductive hearing loss** results from problems with sound transmission to the inner ear, such as **earwax** or **ossicular chain dysfunction**. - **Ménière's disease** specifically affects the inner ear (cochlea and vestibular system), leading to **sensorineural hearing loss** due to endolymphatic hydrops. *Positional vertigo* - **Positional vertigo** suggests conditions like **Benign Paroxysmal Positional Vertigo (BPPV)**, where vertigo is triggered by specific head movements due to otolith displacement. - In this patient, the vertigo is described as recurrent and "on and off" without "clear exacerbating factor," which is less consistent with positional vertigo. *Vertical nystagmus* - **Vertical nystagmus** is typically indicative of **central vestibular lesions** or brainstem dysfunction. - The symptoms presented, including aural fullness and episodic dizziness, point towards a **peripheral vestibular disorder** like Ménière's disease, which usually causes horizontal or rotatory nystagmus during acute attacks.

Question 109: A scientist is studying the mechanism by which the gastrointestinal system coordinates the process of food digestion. Specifically, she is interested in how distension of the lower esophagus by a bolus of food changes responses in the downstream segments of the digestive system. She observes that there is a resulting relaxation and opening of the lower esophageal (cardiac) sphincter after the introduction of a food bolus. She also observes a simultaneous relaxation of the orad stomach during this time. Which of the following substances is most likely involved in the process being observed here?

A. Neuropeptide-Y
B. Secretin
C. Ghrelin
D. Vasoactive intestinal polypeptide (Correct Answer)
E. Motilin

Explanation: ***Vasoactive intestinal polypeptide*** - **VIP (Vasoactive intestinal polypeptide)** is a neuropeptide that mediates **relaxation** of the **smooth muscle** in the gastrointestinal tract, including the **lower esophageal sphincter** and the **orad stomach**, facilitating the passage of food. - This relaxation is part of the **receptive relaxation** process, allowing the stomach to accommodate food without a significant increase in intragastric pressure. *Neuropeptide-Y* - **Neuropeptide-Y (NPY)** is primarily involved in stimulating **food intake** and **reducing energy expenditure**, acting as an orexigenic peptide. - It does not directly mediate the relaxation of the **lower esophageal sphincter** or **orad stomach** in response to food bolus distension. *Secretin* - **Secretin** is a hormone released in response to **acid in the duodenum** and primarily stimulates the pancreas to release **bicarbonate-rich fluid**. - Its main role is to neutralize stomach acid, not to mediate sphincter relaxation or stomach accommodation. *Ghrelin* - **Ghrelin** is known as the "**hunger hormone**" and primarily stimulates **appetite** and **growth hormone release**. - It does not play a direct role in the relaxation of the **lower esophageal sphincter** or **orad stomach** during swallowing. *Motilin* - **Motilin** promotes **gastric and intestinal motility** during the **interdigestive phase**, responsible for the migrating motor complex (MMC). - Its actions are generally prokinetic, rather than causing relaxation of the upper GI tract in response to a food bolus.

Question 110: Fertilization begins when sperm binds to the corona radiata of the egg. Once the sperm enters the cytoplasm, a cortical reaction occurs which prevents other sperm from entering the oocyte. The oocyte then undergoes an important reaction. What is the next reaction that is necessary for fertilization to continue?

A. The second meiotic division (Correct Answer)
B. Degeneration of the sperm tail
C. Release of a polar body
D. Formation of the spindle apparatus
E. Acrosome reaction

Explanation: ***The second meiotic division*** - Upon **sperm penetration**, the secondary oocyte completes its **meiosis II**, forming a mature ovum and a second polar body. - This completion of meiosis II is a critical step for the pronuclear fusion and subsequent **zygote formation**. *Degeneration of the sperm tail* - While the sperm tail does degenerate within the ooplasm, it occurs **after** the genetic material has been released and is not the immediate next critical reaction for continued fertilization. - This is a process of degradation and assimilation, not an active cellular reaction of the oocyte vital for fertilization progression. *Release of a polar body* - The first polar body is released **before fertilization** (at the completion of meiosis I), and the second polar body is released **concomitantly with the completion of meiosis II**, which is the required reaction. - Releasing a polar body is a consequence of meiotic division, not an independent reaction that drives fertilization forward. *Formation of the spindle apparatus* - The **spindle apparatus** is formed during both meiotic divisions to separate chromosomes, but its formation itself is not the immediate "next reaction" necessary for fertilization to continue after cortical reaction. - The key event is the progression of meiosis, which the spindle facilitates, not the mere formation of the apparatus. *Acrosome reaction* - The **acrosome reaction** occurs **before** the sperm binds to the zona pellucida and penetrates the oocyte, enabling the release of enzymes to digest the egg's outer layers. - This reaction has already taken place for the sperm to have entered the oocyte and initiated the cortical reaction.

Question 111: An investigator is studying the physiological response during congestive heart failure exacerbations in patients with systolic heart failure. A hormone released by ventricular cardiomyocytes in response to increased wall stress is isolated from a patient's blood sample. The intracellular mechanism by which this hormone acts is most similar to the effect of which of the following substances?

A. Aldosterone
B. Platelet-derived growth factor
C. Nitric oxide (Correct Answer)
D. Angiotensin II
E. Human chorionic gonadotropin

Explanation: ***Nitric oxide*** - The hormone described is likely **Brain Natriuretic Peptide (BNP)**, released from ventricular cardiomyocytes in response to **increased wall stress** during heart failure. BNP acts by increasing intracellular **cGMP** to cause vasodilation and natriuresis. - **Nitric oxide (NO)** also works by stimulating **guanylyl cyclase** to increase intracellular cGMP, leading to smooth muscle relaxation and vasodilation, thus mimicking the intracellular mechanism of BNP. *Aldosterone* - **Aldosterone** is a steroid hormone that acts on intracellular mineralocorticoid receptors, altering gene expression to promote **sodium reabsorption** and potassium excretion. - This mechanism is distinct from the **second messenger system** involving cGMP. *Platelet-derived growth factor* - **Platelet-derived growth factor (PDGF)** binds to cell surface receptor tyrosine kinases, initiating a signaling cascade that primarily involves **phosphorylation** and leads to cell growth and proliferation. - This mechanism is different from the direct activation of **guanylyl cyclase** by BNP. *Angiotensin II* - **Angiotensin II** primarily acts on G protein-coupled receptors (GPCRs), leading to vasoconstriction, aldosterone release, and other effects, often through **IP3/DAG** or **cAMP** pathways. - Its intracellular signaling mechanism is not primarily centered on **cGMP**. *Human chorionic gonadotropin* - **Human chorionic gonadotropin (hCG)** is a glycoprotein hormone that binds to **G protein-coupled receptors (GPCRs)**, primarily stimulating the production of **cAMP** as a second messenger. - While it uses a second messenger system, the specific pathway (cAMP) differs from the **cGMP** pathway activated by BNP.

Question 112: A 42-year-old woman comes to the physician for a routine health maintenance examination. She is doing well. She is 168 cm (5 ft 6 in) tall and weighs 75 kg (165 lb); BMI is 27 kg/m2. Her BMI had previously been stable at 24 kg/m2. The patient states that she has had decreased appetite over the past month. The patient's change in appetite is most likely mediated by which of the following?

A. Increased fatty acid oxidation
B. Potentiation of cholecystokinin
C. Decreased hypothalamic neuropeptide Y (Correct Answer)
D. Increased hepatic somatomedin C secretion
E. Inhibition of proopiomelanocortin neurons

Explanation: ***Decreased hypothalamic neuropeptide Y*** - **Neuropeptide Y (NPY)** is a powerful **orexigenic** (appetite-stimulating) peptide produced by neurons in the arcuate nucleus of the hypothalamus - **Decreased NPY activity** leads to **reduced appetite** and decreased food intake - In this patient, the weight gain (BMI 24→27) likely occurred over a period preceding the past month, resulting in increased adiposity and elevated **leptin levels** - **Leptin** from adipose tissue acts on the hypothalamus to **suppress NPY production**, creating a negative feedback mechanism to prevent further weight gain - This explains the subsequent **decreased appetite over the past month** as an adaptive response to the positive energy balance and increased fat stores - The chronology: weight gain → increased leptin → decreased NPY → decreased appetite *Increased fatty acid oxidation* - While **fatty acid oxidation** increases when energy stores are adequate, it is not a primary signaling mechanism for appetite regulation - Metabolic fuel utilization does not directly mediate appetite changes through established neuroendocrine pathways *Potentiation of cholecystokinin* - **Cholecystokinin (CCK)** is a gut peptide that promotes **post-prandial satiety** in response to nutrients (especially fats and proteins) in the duodenum - CCK acts acutely during and after meals, not as a chronic appetite regulator over weeks to months - The prolonged decrease in appetite described here suggests a **central hypothalamic mechanism** rather than peripheral meal-related satiety signals *Increased hepatic somatomedin C secretion* - **Somatomedin C (IGF-1)** is produced by the liver in response to growth hormone and primarily mediates growth and anabolic effects - IGF-1 has **no established role** as a primary mediator of appetite suppression in clinical physiology - This is not a recognized mechanism for appetite regulation *Inhibition of proopiomelanocortin neurons* - **POMC neurons** in the arcuate nucleus produce **α-melanocyte-stimulating hormone (α-MSH)**, which acts on MC4 receptors to **suppress appetite** (anorexigenic effect) - **Inhibition of POMC neurons** would decrease α-MSH release, leading to **increased appetite**, not decreased - This would cause weight gain, not the appetite suppression seen in this patient - Leptin normally **activates** POMC neurons as part of appetite suppression

Question 113: A 28-year-old patient comes to the physician’s office with complaints of headaches and difficulty seeing out of the corner of her eye. She gave birth to her son 1 year ago. Further visual testing reveals the patient has bitemporal hemianopsia. The patient undergoes brain MRI which shows an anterior pituitary mass, likely adenoma. The patient has her blood tested to see if the adenoma is secreting extra hormone. The patient is found to have a slight excess of a hormone that uptakes a basophilic stain. Which of the following is most likely to be the hormone detected in her blood?

A. Prolactin
B. Growth hormone
C. Thyroid stimulating hormone (Correct Answer)
D. Antidiuretic hormone
E. Oxytocin

Explanation: ***Thyroid stimulating hormone*** - **Thyroid-stimulating hormone (TSH)** is synthesized by **thyrotroph cells** which are basophilic, making it the most likely hormone to stain basophilically in this context. - An excess of TSH from a pituitary adenoma could lead to clinical symptoms of **hyperthyroidism**, although the question states it's only a "slight excess." *Prolactin* - **Prolactin** is secreted by **lactotrophs**, which are acidophilic and would not take up a basophilic stain. - While **prolactinomas** are the most common pituitary adenomas, their cells are not basophilic, and this patient does not exhibit common symptoms of hyperprolactinemia (galactorrhea, amenorrhea). *Growth hormone* - **Growth hormone (GH)** is produced by **somatotrophs**, which are acidophilic and would not take up a basophilic stain. - Excess GH typically causes **acromegaly** in adults, characterized by distinctive physical changes not mentioned in the patient's presentation. *Antidiuretic hormone* - **Antidiuretic hormone (ADH)**, also known as vasopressin, is synthesized in the **hypothalamus** and released from the posterior pituitary, not secreted by basophilic cells of the anterior pituitary. - Overproduction of ADH leads to **SIADH**, characterized by hyponatremia and concentrated urine, none of which are described. *Oxytocin* - **Oxytocin** is also produced in the **hypothalamus** and released from the posterior pituitary, not by basophilic cells in the anterior pituitary. - Its primary functions relate to uterine contractions and milk ejection and are not associated with pituitary adenomas causing bitemporal hemianopsia.

Question 114: A 17-year-old boy is brought to the emergency department after being stabbed with a knife during an altercation. Physical examination shows a 4-cm stab wound on the right lateral border of the T1 spinous process. An MRI of the spinal cord shows damage to the area of the right lateral corticospinal tract at the level of T1. Further evaluation will most likely show which of the following findings?

A. Absence of right-sided motor function below T1 (Correct Answer)
B. Absence of left-sided proprioception below T1
C. Presence of left-sided Babinski sign
D. Absence of left-sided fine touch sensation below T1
E. Absence of right-sided temperature sensation below T1

Explanation: ***Absence of right-sided motor function below T1*** - The **right lateral corticospinal tract** controls **voluntary motor function** on the **ipsilateral side** of the body. - Damage to this tract at T1 would therefore lead to a loss of motor function on the right side below the level of the injury. *Absence of left-sided proprioception below T1* - **Proprioception** is carried by the **dorsal columns**, which ascend **ipsilaterally** before decussating in the brainstem. - Damage to the right lateral corticospinal tract would not affect left-sided proprioception. *Presence of left-sided Babinski sign* - A **Babinski sign** (upgoing plantar reflex) indicates an **upper motor neuron lesion**. - Since the corticospinal tract decussates in the **medulla** (before reaching the spinal cord), a lesion in the **right lateral corticospinal tract at T1** affects motor function on the **right side** of the body. - Therefore, if a Babinski sign were present, it would be on the **right side**, not the left. *Absence of left-sided fine touch sensation below T1* - **Fine touch** sensation is transmitted by the **dorsal columns**, which ascend **ipsilaterally** and decussate in the brainstem. - Damage to the right lateral corticospinal tract would not affect fine touch sensation on the left side. *Absence of right-sided temperature sensation below T1* - **Temperature sensation** is carried by the **spinothalamic tracts**, which decussate at the level of entry into the spinal cord. - Therefore, a lesion of the right lateral corticospinal tract would not affect temperature sensation on the right side; ipsilateral temperature loss would be due to damage to the right spinothalamic tract, which is located more anterolaterally in the spinal cord.

Question 115: A 59-year-old man presents to the emergency department with a sudden-onset sensation that the room is spinning causing him to experience several episodes of nausea and vomiting. Upon arriving, the patient’s symptoms have resolved. He states his symptoms occurred as he was going to bed. He has never experienced this before, but felt extremely dizzy for roughly 3 minutes. He currently feels at his baseline. The patient is otherwise healthy and only has a history of eczema. His temperature is 97.7°F (36.5°C), blood pressure is 134/85 mmHg, pulse is 85/min, respirations are 13/min, and oxygen saturation is 98% on room air. Physical exam is notable for a healthy man with a normal gait. The patient has a physiologic nystagmus and his cranial nerve exam is unremarkable. The patient’s head is turned to the left and he is laid back on the stretcher, which exacerbates severe symptoms with a nystagmus notable. The patient’s symptoms improve after 2 minutes of being in this position. Which of the following is the most likely diagnosis?

A. Benign paroxysmal positional vertigo (Correct Answer)
B. Vertebrobasilar stroke
C. Labyrinthitis
D. Vestibular neuritis
E. Meniere disease

Explanation: ***Benign paroxysmal positional vertigo*** - The sudden onset of **vertigo** that is triggered by specific **head movements** (e.g., lying in bed, Dix-Hallpike maneuver causing severe symptoms with nystagmus, resolving in 2 minutes) is highly characteristic of BPPV. - The **transient nature** of the vertigo (3 minutes), resolution of symptoms, and absence of other neurological deficits further support this diagnosis. *Vertebrobasilar stroke* - A vertebrobasilar stroke would typically present with more persistent and severe neurological symptoms, such as **diplopia**, **dysarthria**, **ataxia**, or significant motor/sensory deficits. - The patient's rapid resolution of symptoms and normal neurological exam upon presentation make a stroke less likely. *Labyrinthitis* - Labyrinthitis is characterized by sudden, severe, and **prolonged vertigo** (days to weeks) often accompanied by **hearing loss** and **tinnitus**, which are not reported in this case. - The transient, position-triggered nature of the patient's symptoms does not fit labyrinthitis. *Vestibular neuritis* - Vestibular neuritis presents with an acute onset of **severe vertigo** that is usually **persistent** for days, associated with **nausea and vomiting**, but **without hearing loss**. - Unlike BPPV, it is not typically triggered by specific head movements and continues for much longer periods. *Meniere disease* - Meniere disease classically involves recurrent episodes of **vertigo**, **tinnitus**, **fluctuating hearing loss**, and aural fullness. - The isolated, transient, and position-triggered vertigo without any mention of hearing changes or tinnitus makes Meniere disease unlikely.

Question 116: A 72-year-old woman is brought to the emergency department for right hip pain 1 hour after she fell while walking around in her house. She has been unable to stand or walk since the fall. She has hypertension and gout. Her sister died of multiple myeloma at the age of 55 years. Current medications include amlodipine and febuxostat. She does not smoke cigarettes. She drinks a glass of wine daily. Her temperature is 37.3°C (99.1°F), pulse is 101/min, and blood pressure is 128/86 mm Hg. Examination shows right groin tenderness. Range of motion of the right hip is limited by pain. The remainder of the examination shows no abnormalities. A complete blood count and serum creatinine concentration are within the reference range. An x-ray of the hip shows a linear fracture of the right femoral neck. She is scheduled for surgery. Which of the following is the most likely underlying cause of this patient's fracture?

A. Defective osteoclast function
B. Impaired bone mineralization
C. Monoclonal antibody production
D. Interrupted vascular supply
E. Reduced osteoblastic activity (Correct Answer)

Explanation: ***Reduced osteoblastic activity*** - In a 72-year-old woman, a **femoral neck fracture** following a fall typically indicates underlying **osteoporosis**, which is characterized by reduced **osteoblastic activity** and overall bone density loss. - As women age, particularly after menopause, **estrogen deficiency** leads to an imbalance in bone remodeling, with bone resorption outpacing bone formation, thus leading to weaker bones. *Defective osteoclast function* - **Defective osteoclast function** is primarily associated with conditions like **osteopetrosis**, where bones become dense and brittle due to impaired bone resorption, making them prone to fracture, which is not consistent with the typical presentation of a hip fracture in an elderly woman. - This condition is rare and usually presents earlier in life, often with symptoms such as **anemia**, **hepatosplenomegaly**, and **cranial nerve compression**. *Impaired bone mineralization* - **Impaired bone mineralization** is characteristic of **osteomalacia** (in adults) or **rickets** (in children), usually due to **vitamin D deficiency** or phosphate imbalances. - While it can lead to bone pain and increased fracture risk, osteoporosis due to aging is a much more common cause of hip fractures in this demographic, and there are no signs of osteomalacia such as **pseudofractures** or specific biochemical abnormalities like **hypophosphatemia** or **elevated alkaline phosphatase** without other causes. *Monoclonal antibody production* - **Monoclonal antibody production** is associated with **multiple myeloma**, a plasma cell malignancy that causes **lytic bone lesions** and diffuse osteopenia. - While the patient's sister died of multiple myeloma, her normal complete blood count and creatinine, and the absence of specific myeloma-related symptoms (e.g., **hypercalcemia**, **renal failure**, **anemia**, or **CRAB criteria**) make this diagnosis less likely for her acute hip fracture. *Interrupted vascular supply* - **Interrupted vascular supply** can lead to **avascular necrosis (AVN)**, which weakens the bone and can cause collapse, eventually leading to a fracture. - However, for an acute traumatic hip fracture, especially in the femoral neck, the primary underlying cause in an elderly person is generally **osteoporosis**, and AVN would typically present with chronic pain and characteristic imaging findings prior to an acute traumatic event.

Question 117: A 16-year-old male comes to his doctor worried that he has not yet gone through puberty. He feels that his genitals are less developed than they should be for his age. On physical exam, you note an absence of facial hair and that his voice has not yet deepened. Your exam confirms that he is Tanner Stage 1. On a thorough review of systems, you learn that the patient has lacked a sense of smell from birth. Which of the following is implicated in the development of this patient's underlying condition?

A. Defect in steroid production
B. Exposure to radiation
C. Chromosomal duplication
D. Failure of normal neuronal migration during development (Correct Answer)
E. Expansile suprasellar tumor

Explanation: ***Failure of normal neuronal migration during development*** - The constellation of **delayed puberty** (Tanner Stage 1, absence of facial hair, lack of voice deepening) and **anosmia** (lack of smell) is characteristic of **Kallmann syndrome**. - Kallmann syndrome is caused by the failure of **GnRH-producing neurons** to migrate from the olfactory placode to the hypothalamus during embryonic development, leading to **hypogonadotropic hypogonadism** and anosmia. *Defect in steroid production* - Defects in steroid production, such as **congenital adrenal hyperplasia** or **gonadal dysgenesis**, would affect hormone levels but would not explain the accompanying **anosmia**. - These conditions typically present with different hormonal profiles and physical exam findings related to sex steroid deficiencies. *Exposure to radiation* - Exposure to radiation can cause damage to various tissues, including the gonads or pituitary gland, potentially leading to **hypogonadism**. - However, radiation exposure does not typically cause **isolated anosmia** in conjunction with hypogonadism, and there is no mention of such exposure in the patient's history. *Chromosomal duplication* - **Chromosomal anomalies**, like some duplications, can be associated with developmental delays and various syndromes. - While some genetic syndromes might include delayed puberty, a chromosomal duplication is not the characteristic underlying mechanism for the specific combination of **hypogonadotropic hypogonadism** and **anosmia** seen in Kallmann syndrome. *Expansile suprasellar tumor* - An **expansile suprasellar tumor**, such as a **craniopharyngioma**, can compress the pituitary stalk or hypothalamus, leading to **hypopituitarism** and delayed puberty. - While it can affect hormonal function, a suprasellar tumor would not typically cause **congenital anosmia** as a primary feature, and neuroimaging would usually reveal the mass.

Question 118: A 21-year-old man presents to the physician with numbness and weakness in both legs for about a day. He also mentions that both thighs ache. His past medical history is not significant except for some diarrhea about 3 weeks ago. On physical examination, his temperature is 37.2ºC (99.0ºF), pulse rate is 108/min and respiratory rate is 14/min. His blood pressure is 122/82 mm Hg and 100/78 mm Hg in supine and upright positions, respectively. His neurologic evaluation reveals the presence of bilateral symmetrical weakness of the lower limbs, the absence of deep tendon reflexes, and negative Babinski sign. His sensorium and higher brain functions are normal. Which of the following options best explains the pathophysiological mechanism underlying the patient’s clinical features?

A. Autoantibody-mediated destruction of Ca2+ channels in the nerve endings at the neuromuscular junction
B. Decreased neuronal excitability (Correct Answer)
C. Genetic overexpression of K+ channels in skeletal muscle
D. Decreased threshold for the generation and propagation of the action potential
E. Toxin-mediated blockade of voltage-gated fast Na+ channels

Explanation: ***Decreased neuronal excitability*** - This patient's presentation with **ascending paralysis**, **areflexia**, and a history of antecedent infection (diarrhea) is highly suggestive of **Guillain-Barré Syndrome (GBS)**. - GBS involves **demyelination** of peripheral nerves, leading to decreased conduction velocity and, consequently, decreased neuronal excitability and signal transmission. *Autoantibody-mediated destruction of Ca2+ channels in the nerve endings at the neuromuscular junction* - This mechanism describes **Lambert-Eaton Myasthenic Syndrome (LEMS)**, which typically presents with proximal muscle weakness that improves with activity and is often associated with small cell lung cancer. - Unlike GBS, LEMS primarily affects the **presynaptic neuromuscular junction**, and the weakness usually *improves* with repetitive stimulation, contrasting with the progressive weakness seen here. *Genetic overexpression of K+ channels in skeletal muscle* - **Overexpression of K+ channels** in skeletal muscle is not a recognized direct cause of acute ascending paralysis or GBS. - This mechanism is more relevant to certain channelopathies causing episodic muscle weakness or paralysis, distinct from the autoimmune demyelination seen in GBS. *Decreased threshold for the generation and propagation of the action potential* - A decreased threshold implies **hyperexcitability** or easier generation of action potentials, which would typically lead to symptoms like muscle spasms, cramps, or even seizures. - This is the opposite of what is observed in GBS, where nerve conduction is impaired, leading to **weakness and numbness**. *Toxin-mediated blockade of voltage-gated fast Na+ channels* - **Toxin-mediated blockade of Na+ channels** can certainly cause paralysis (e.g., tetrodotoxin, saxitoxin) by preventing action potential generation. - However, the clinical context of antecedent diarrhea and ascending paralysis points much more strongly to an autoimmune demyelinating condition like GBS rather than an acute poisoning.

Question 119: In a patient with acute myocardial ischemia, which of the following cardiovascular structures is at greatest risk of damage?

A. Pulmonary valve
B. Cardiac conduction system (Correct Answer)
C. Coronary artery
D. Cardiac septum
E. Temporal artery

Explanation: ***Cardiac conduction system*** - The **cardiac conduction system** is highly dependent on a constant oxygen supply, and its disruption by ischemia can lead to serious **arrhythmias** and **heart blocks**. - Ischemia in critical areas like the **AV node** (supplied by the RCA) or the **bundle branches** can severely impair the heart's electrical activity. *Pulmonary valve* - The **pulmonary valve** is primarily a passive structure and is generally not directly damaged by acute myocardial ischemia. - Its function is more affected by changes in **pulmonary artery pressure** or **ventricular remodeling**, not immediate ischemic injury. *Coronary artery* - While **coronary artery disease (CAD)** is the *cause* of myocardial ischemia, the coronary artery itself is not the structure *damaged* in the sense of functional impairment due to lack of blood flow in acute ischemia. - The damage occurs downstream in the **myocardium** that the artery supplies. *Cardiac septum* - The **cardiac septum** can be damaged by myocardial ischemia, particularly the **interventricular septum**, leading to complications like **septal rupture**. - However, the conduction system is at *greatest* immediate risk of functional damage leading to life-threatening events due to its critical role in rhythm generation. *Temporal artery* - The **temporal artery** is a blood vessel located in the head, entirely separate from the heart. - It is not involved in myocardial ischemia and is not at risk of damage from a cardiac event.

Question 120: A 66-year-old male presents to the emergency room with shortness of breath with exertion and at rest for the past 5 days. His shortness of breath is mostly at night, and he is also concerned about bilateral leg swelling. He is a heart failure patient who is being managed with oral medication and has been compliant with his drugs. Physical examination reveals an elderly man in respiratory distress with abdominal distention and bilateral pitting ankle edema. Respiratory rate is 32/min, SpO2 is 93% in room air, and coarse crepitations are heard on both lung bases. Pulse rate is 73/min and barely palpable. His blood pressure is 79/54 mm Hg. On auscultation, a blowing holosystolic murmur is heard at the apex radiating to the left axilla. An echocardiography shows an ejection fraction of 18%. The physician decides to include an inotropic agent in his current medication. What would likely result from this intervention?

A. A decrease in the interval between the heart sounds S2 and S1
B. A decrease in the systemic vascular resistance
C. A decrease in the left ventricular end-diastolic pressure
D. A decrease in the interval between the heart sounds S1 and S2 (Correct Answer)
E. An increase in the left ventricular end-systolic volume

Explanation: ***A decrease in the interval between the heart sounds S1 and S2*** - The patient has severe **heart failure with reduced ejection fraction** (HFrEF) and likely cardiogenic shock, indicated by **hypotension** and **respiratory distress**. The **holosystolic murmur at the apex radiating to the left axilla** suggests **mitral regurgitation**, exacerbating his condition. - An **inotropic agent** (e.g., dobutamine) increases myocardial contractility, leading to a **more forceful and faster ventricular ejection**. This causes the **aortic valve to close earlier**, effectively **shortening systole** and thus the interval between S1 (mitral valve closure) and S2 (aortic valve closure). *A decrease in the interval between the heart sounds S2 and S1* - The interval between S2 and S1 represents **diastole**. An inotropic agent primarily affects **systolic function**, and while improved cardiac output can influence diastolic filling times, a primary and direct decrease in the S2-S1 interval is not the expected or most significant effect. - In cases of severe heart failure, changes to diastolic timing are complex and secondary to changes in systolic function and filling pressures, but not a direct result of inotropic therapy in this manner. *A decrease in the systemic vascular resistance* - While some inotropic agents like **dobutamine** have **beta-2 agonist activity** that can cause some vasodilation and thus a decrease in SVR, their primary effect is to **increase contractility**. - Other inotropes, like **norepinephrine**, can actually **increase SVR**. The main therapeutic goal here is to improve cardiac output, and a direct and primary decrease in SVR isn't the guaranteed or most significant outcome from the inotropic effect itself. *A decrease in the left ventricular end-diastolic pressure* - An inotropic agent increases cardiac output, which can lead to better systemic perfusion and **reduce venous congestion** over time. However, in the acute setting of severe heart failure with volume overload, **LVEDP** is initially high due to impaired relaxation and increased preload. - While improved contractility might lead to more effective forward flow, it does not directly or immediately decrease LVEDP; rather, this is often achieved through diuretics or vasodilators. In some cases, increased contractility itself can even transiently increase LVEDP if there's significant myocardial stiffness. *An increase in the left ventricular end-systolic volume* - An inotropic agent directly **enhances myocardial contractility**, allowing the left ventricle to **eject more blood** with each beat. - This increased contractility leads to a **more complete emptying of the left ventricle** during systole, resulting in a **decrease** (not an increase) in the **left ventricular end-systolic volume** (LVESV).

Question 121: A 70-year-old woman presents to her primary care physician with sudden episodes of dizziness that resolve in certain positions. On further questioning she describes a false sense of motion with occasional spinning sensation consistent with vertigo. She denies any recent illnesses or hearing loss aside from presbycusis. Her vital signs are normal. During the physical exam the patient reports an episode of vertigo after transitioning from sitting to supine and horizontal nystagmus is concurrently noted. What is the most likely diagnosis?

A. Vestibular migraine
B. Vestibular neuritis
C. Benign Paroxysmal Positional Vertigo (BPPV) (Correct Answer)
D. Meniere's disease
E. Labyrinthitis

Explanation: ***Benign Paroxysmal Positional Vertigo (BPPV)*** - The presentation of sudden **positional vertigo** and **positional nystagmus** (triggered by changing from sitting to supine) in an elderly patient is classic for BPPV. - BPPV is caused by displaced **otoconia** within the semicircular canals, which inappropriately stimulate hair cells with head movements. *Vestibular migraine* - This condition involves recurrent vertigo attacks often associated with **migrainous headaches** or other migraine features (photophobia, phonophobia), which are not described here. - While vertigo can be positional, the lack of headache or migraine history makes BPPV a more likely diagnosis. *Vestibular neuritis* - Typically presents with a **sudden onset of severe vertigo** that is constant and can last for days, often accompanied by **nausea and vomiting**, but without hearing loss. - The vertigo in this case is *episodic* and *positional*, which does not fit the typical pattern of vestibular neuritis. *Meniere's disease* - Characterized by a classic triad of **episodic vertigo, fluctuating sensorineural hearing loss, and tinnitus**, often with aural fullness. - While vertigo attacks can be sudden, the absence of **tinnitus** or *significant* hearing loss (beyond age-related presbycusis) makes Meniere's less likely. *Labyrinthitis* - Involves inflammation of the inner ear, presenting with **sudden, severe vertigo, nausea, and vomiting**, similar to vestibular neuritis, but also includes **unilateral hearing loss**. - The patient specifically denies recent illnesses and significant hearing loss, which rules out labyrinthitis.

Question 122: A 71-year-old man with hypertension comes to the physician for a follow-up examination. Cardiovascular exam shows the point of maximal impulse to be in the mid-axillary line. A transthoracic echocardiogram shows concentric left ventricular hypertrophy with a normal right ventricle. Which of the following is the most likely underlying mechanism of this patient's ventricular hypertrophy?

A. Accumulation of protein fibrils
B. Accumulation of glycogen
C. Infiltration of T lymphocytes
D. Deposition of endomyocardial collagen
E. Accumulation of sarcomeres in parallel (Correct Answer)

Explanation: ***Accumulation of sarcomeres in parallel*** - **Concentric left ventricular hypertrophy** (LVH) is primarily caused by **pressure overload**, such as from **hypertension**. The heart muscle cells respond to this increased afterload by adding new sarcomeres predominantly in parallel, leading to an increase in wall thickness with a relatively preserved chamber size. - This structural adaptation helps the ventricle generate greater force to overcome the elevated systemic vascular resistance. *Accumulation of protein fibrils* - Accumulation of protein fibrils, specifically **amyloid protein**, is characteristic of **cardiac amyloidosis**, which typically causes **restrictive cardiomyopathy**. - While amyloidosis can cause thickening of the ventricular walls, its clinical presentation (e.g., often with proteinuria, peripheral neuropathy) and echocardiographic findings (e.g., granular "sparkling" myocardium) differ from classic concentric LVH due to hypertension. *Accumulation of glycogen* - Excessive accumulation of glycogen within cardiac myocytes is a hallmark of **glycogen storage diseases**, such as **Pompe disease**. - These conditions often lead to hypertrophic cardiomyopathy, but they are genetic disorders usually presenting earlier in life, and hypertension is not the underlying mechanism for the hypertrophy. *Infiltration of T lymphocytes* - Infiltration of T lymphocytes is a characteristic feature of **inflammatory myocarditis**, which can lead to various cardiac dysfunctions including hypertrophy, but the primary mechanism is inflammation and myocyte damage, not a direct response to pressure overload. - The patient's history of **hypertension** and the specific finding of **concentric LVH** strongly point away from an inflammatory cause. *Deposition of endomyocardial collagen* - Deposition of endomyocardial collagen is associated with conditions like **restrictive cardiomyopathy**, where there is excessive fibrosis leading to stiffening of the ventricular walls and impaired diastolic filling. - While hypertension can eventually lead to some degree of fibrosis, the initial and primary mechanism of concentric hypertrophy is the addition of sarcomeres due to increased pressure overload, rather than collagen deposition being the dominant cause of the hypertrophy itself.

Question 123: A 49-year-old woman presents to the office because of tremors for 2 months. She says that her hands have been shaking a lot, especially when she feels stressed. In addition, she has been sweating more than usual and has lost 8 kg (17.6 lb) in the last 2 months. She has a past medical history of vitiligo. Her vital signs are a heart rate of 98/min, a respiratory rate of 14/min, a temperature of 37.6°C (99.7°F), and a blood pressure of 115/75 mm Hg. Physical examination shows a fine, bilateral hand tremor and a diffuse goiter. Which of the following hormonal imbalances is most likely present?

A. Low TSH, high free T4, and high free T3 (Correct Answer)
B. High TSH, high free T4, and high free T3
C. High TSH, normal free T4, and normal free T3
D. Low TSH, normal free T4, and normal free T3
E. High TSH, low free T4, and low free T3

Explanation: ***Low TSH, high free T4, and high free T3*** - The patient's symptoms (tremors, sweating, weight loss, tachycardia, goiter) are classic for **hyperthyroidism**, which is typically characterized by **low TSH** due to negative feedback and **elevated free T4 and T3** levels. - Her history of **vitiligo**, an autoimmune condition, further supports an autoimmune thyroid disorder like **Graves' disease**, a common cause of hyperthyroidism. *High TSH, high free T4, and high free T3* - This pattern would indicate **secondary hyperthyroidism**, caused by a TSH-secreting pituitary adenoma. - While TSH would be high, it is a much rarer cause of hyperthyroidism compared to primary causes. *High TSH, normal free T4, and normal free T3* - This hormonal profile is characteristic of **subclinical hypothyroidism** or a **compensated primary hypothyroidism** early in its course. - The patient's symptoms are inconsistent with hypothyroidism. *Low TSH, normal free T4, and normal free T3* - This suggests **subclinical hyperthyroidism**, where TSH is suppressed but thyroid hormone levels are still within the normal range. - The patient's prominent and severe symptoms (tremors, significant weight loss, goiter) indicate overt hyperthyroidism, not subclinical disease. *High TSH, low free T4, and low free T3* - This is the classic hormonal profile for **primary hypothyroidism**, where the thyroid gland is failing to produce sufficient hormones, leading to elevated TSH. - The patient's symptoms of nervousness, weight loss, and tremors are directly opposite to those seen in hypothyroidism.

Question 124: A previously healthy 57-year-old man comes to the emergency department because of acute retrosternal chest pain that radiates to his back. The pain started suddenly while he was having dinner. A few moments prior to the onset of the pain, he experienced discomfort when trying to eat or drink anything. On the way to the hospital he took a sublingual nitrate tablet that he had at home, which helped relieve the pain. His pulse is 80/min, respirations are 14/min, and blood pressure is 144/88 mm Hg. Examination shows no other abnormalities. An ECG shows a normal sinus rhythm with no ST-segment abnormalities. An esophagogram is done and shows areas of diffuse, uncoordinated spasms in several segments along the length of the esophagus. This patient's condition is most likely to show which of the following findings?

A. Esophageal manometry shows hypertensive contractions
B. Ultrasonography shows a mass at the gastroesophageal junction
C. Esophageal manometry shows simultaneous multi-peak contractions (Correct Answer)
D. Endoscopy shows multiple mucosal erosions
E. Serology shows elevated CK-MB levels

Explanation: ***Esophageal manometry shows simultaneous multi-peak contractions*** - The patient's symptoms of sudden retrosternal chest pain radiating to the back, discomfort with eating and drinking, and pain relief with nitrates suggest an **esophageal spasm**, which is confirmed by the esophagogram showing **diffuse, uncoordinated spasms**. **Simultaneous, multi-peak contractions** are characteristic manometric findings in **diffuse esophageal spasm**. - Relief with **nitrates** is common in esophageal spasms because they relax smooth muscle. *Esophageal manometry shows hypertensive contractions* - **Hypertensive contractions** are characteristic of **nutcracker esophagus** (or hypercontractile esophagus), a condition marked by high-amplitude peristaltic contractions, which are distinct from the uncoordinated spasms seen in this patient. - While both can cause chest pain, the esophagogram showing **diffuse, uncoordinated spasms** points away from nutcracker esophagus. *Ultrasonography shows a mass at the gastroesophageal junction* - A mass at the **gastroesophageal junction** would suggest a **tumor** or other structural lesion, which would typically cause progressive dysphagia and weight loss, not acute, intermittent pain relieved by nitrates. - **Esophageal spasms** are functional disorders of motility, not structural abnormalities detectable by ultrasound at the GE junction. *Endoscopy shows multiple mucosal erosions* - **Mucosal erosions** are indicative of **gastroesophageal reflux disease (GERD)** or esophagitis, which would present with heartburn, regurgitation, and pain primarily related to acid exposure, not the acute, spasm-like pain described. - Endoscopy is usually normal in **diffuse esophageal spasm**. *Serology shows elevated CK-MB levels* - **Elevated CK-MB levels** are a marker for **myocardial infarction (MI)**, which is an important differential for chest pain. However, the normal ECG and relief with nitrates (though nitrates can relieve both cardiac and esophageal pain) coupled with the esophagogram findings definitively rule out MI as the primary diagnosis. - The patient's symptoms are fully explained by the **esophageal findings and history**.

Question 125: An investigator is studying cardiomyocytes in both normal and genetically modified mice. Both groups are observed after aerobic exercise and their heart rates are recorded and compared. After a 10-minute session on a treadmill, the average pulse measured in the normal mice is 680/min, whereas in the genetically modified mice it is only 160/min. Which of the following is most likely to account for the normal mice's ability to achieve higher heart rates during exercise stress?

A. Lower threshold potential for Ca2+ channel opening
B. Greater cardiomyocyte size
C. Lower number of gap junctions
D. Greater ratio of heart to body weight
E. Greater T-tubule density (Correct Answer)

Explanation: ***Greater T-tubule density*** - A **greater T-tubule density** in normal mice's cardiomyocytes enhances **calcium-induced calcium release**, allowing for more efficient and rapid muscle contraction and relaxation cycles, supporting higher heart rates. - T-tubules facilitate the rapid propagation of the **action potential** deep into the myocyte, ensuring synchronized contraction. *Lower threshold potential for Ca2+ channel opening* - A lower threshold potential for Ca2+ channel opening would likely lead to increased contractility at baseline or earlier excitation, but it does not directly explain the ability to sustain a high heart rate during exercise. - This effect might even lead to earlier fatigue or arrhythmias without proper regulation. *Greater cardiomyocyte size* - While larger cardiomyocytes might indicate hypertrophy, it generally implies **slower contraction and relaxation kinetics** due to increased diffusion distances and a larger volume to depolarize. - This would typically lead to a **lower maximum heart rate** rather than a higher one during intense exercise. *Lower number of gap junctions* - A lower number of **gap junctions** would impair the efficient and rapid **electrical coupling** between cardiomyocytes. - This would result in **slower conduction velocity** and a less coordinated, slower heart rate, making higher heart rates more difficult to achieve. *Greater ratio of heart to body weight* - A greater heart-to-body weight ratio could indicate a larger heart, which might be correlated with greater stroke volume, but doesn't specifically explain the cellular mechanism for achieving a **higher heart rate**. - While larger hearts might be more efficient, the question focuses on the cellular ability to beat faster during stress, which relates more to excitation-contraction coupling.

Question 126: A 33-year-old female presents to her primary care physician complaining of heat intolerance and difficulty sleeping over a one month period. She also reports that she has lost 10 pounds despite no changes in her diet or exercise pattern. More recently, she has developed occasional unprovoked chest pain and palpitations. Physical examination reveals a nontender, mildly enlarged thyroid gland. Her patellar reflexes are 3+ bilaterally. Her temperature is 99°F (37.2°C), blood pressure is 135/85 mmHg, pulse is 105/min, and respirations are 18/min. Laboratory analysis is notable for decreased TSH. Which of the following pathophysiologic mechanisms contributed to the cardiovascular symptoms seen in this patient?

A. Increased numbers of α1-adrenergic receptors
B. Increased sensitivity of β1-adrenergic receptors (Correct Answer)
C. Decreased numbers of α2-adrenergic receptors
D. Decreased sensitivity of β2-adrenergic receptors
E. Decreased numbers of α1-adrenergic receptors

Explanation: ***Increased sensitivity of β1-adrenergic receptors*** - Elevated thyroid hormone levels in **hyperthyroidism** increase the expression and sensitivity of **β1-adrenergic receptors** in the heart. - This heightened sensitivity leads to an exaggerated response to **catecholamines**, contributing to symptoms like **tachycardia**, **palpitations**, and **chest pain**. *Increased numbers of α1-adrenergic receptors* - While thyroid hormones can influence adrenergic receptor expression, the primary cardiovascular effects of hyperthyroidism are mediated by **β-adrenergic receptors**, not α1. - An increase in α1-adrenergic receptors would primarily lead to **vasoconstriction**, which is not the predominant cardiovascular pathology in hyperthyroidism where **increased heart rate** and contractility are key. *Decreased numbers of α1-adrenergic receptors* - This would generally lead to **vasodilation** and possibly hypotension, which is contrary to the **palpitations** and **chest pain** seen in the patient's hyperthyroid state. - Hyperthyroidism tends to increase cardiac output and contractility rather than decrease peripheral resistance through reduced α1 receptors. *Decreased numbers of α2-adrenergic receptors* - **Alpha-2 adrenergic receptors** are often involved in **negative feedback** to reduce sympathetic outflow from the central nervous system. - A decrease in these receptors would theoretically increase sympathetic activity, but the direct cardiovascular effects in hyperthyroidism are primarily due to altered **β-adrenergic receptor** function. *Decreased sensitivity of β2-adrenergic receptors* - **Beta-2 adrenergic receptors** are primarily found in smooth muscle (e.g., bronchioles, blood vessels) and mediate **vasodilation and bronchodilation**. - Decreased sensitivity would lead to **vasoconstriction** and **bronchoconstriction**, which are not characteristic cardiovascular or pulmonary findings in hyperthyroidism.

Question 127: Certain glucose transporters that are expressed predominantly on skeletal muscle cells and adipocytes are unique compared to those transporters found on other cell types within the body. Without directly affecting glucose transport in other cell types, which of the following would be most likely to selectively increase glucose uptake in skeletal muscle cells and adipocytes?

A. Increased plasma glucose concentration
B. It is physiologically impossible to selectively increase glucose uptake in specific cells
C. Increased levels of circulating insulin (Correct Answer)
D. Decreased plasma glucose concentration
E. Decreased levels of circulating insulin

Explanation: ***Increased levels of circulating insulin*** - Insulin stimulates the translocation of **GLUT4 transporters** from intracellular vesicles to the cell membrane in **skeletal muscle** and **adipocytes**, thereby increasing glucose uptake. - This mechanism is **selective** because other cell types (e.g., brain, liver) primarily use insulin-independent glucose transporters (e.g., GLUT1, GLUT2, GLUT3) that are constitutively active or respond to different signals. *Increased plasma glucose concentration* - While increased glucose concentration would drive glucose uptake in many cells, it is not **selective** for skeletal muscle and adipocytes since other cells also take up glucose. - Insulin-independent tissues would also increase glucose uptake, making this a non-specific effect. *It is physiologically impossible to selectively increase glucose uptake in specific cells* - This statement is incorrect because the body has mechanisms, such as **insulin-mediated GLUT4 translocation**, that specifically regulate glucose uptake in certain cell types like skeletal muscle and adipocytes. - This regulatory specificity is crucial for maintaining **glucose homeostasis**. *Decreased plasma glucose concentration* - A decrease in plasma glucose would generally **reduce** glucose uptake across all cell types, including skeletal muscle and adipocytes. - It would not selectively increase uptake in any specific cell population. *Decreased levels of circulating insulin* - Decreased insulin levels would lead to **reduced** glucose uptake in insulin-sensitive tissues like skeletal muscle and adipocytes, as GLUT4 transporters would remain sequestered intracellularly. - This would result in higher circulating glucose levels rather than increased uptake.

Question 128: An investigator is studying obesity in mice. Over the course of 2 weeks, mice in the experimental group receive a daily injection with a synthetic analog of an endogenous hormone. Compared to the control group, the hormone-injected mice eat more and gain significantly more weight. Which of the following is the most likely explanation for the observed weight gain in the experimental group?

A. Leptin stimulation of the ventromedial hypothalamus
B. Somatostatin inhibition of the anterior pituitary
C. Cholecystokinin stimulation of the nucleus tractus solitarius
D. Ghrelin stimulation of the lateral hypothalamus (Correct Answer)
E. Glucagon stimulation of hepatocytes

Explanation: ***Ghrelin stimulation of the lateral hypothalamus*** - **Ghrelin** is a hormone that stimulates **hunger** and promotes **weight gain**. Stimulation of the **lateral hypothalamus** specifically leads to increased appetite and food intake. - The experimental mice are exhibiting increased eating and weight gain consistent with the effects of an analogue that mimics or enhances ghrelin's action. *Leptin stimulation of the ventromedial hypothalamus* - **Leptin** is a hormone that suppresses appetite and induces satiety, promoting **weight loss**. - Stimulation of the **ventromedial hypothalamus** also leads to satiety and reduced food intake, which is contrary to the observed weight gain. *Somatostatin inhibition of the anterior pituitary* - **Somatostatin** primarily inhibits the release of various hormones, including **growth hormone** and **thyroid-stimulating hormone**, from the anterior pituitary. - It does not directly regulate appetite or mediate acute changes in food intake and weight in the manner described. *Cholecystokinin stimulation of the nucleus tractus solitarius* - **Cholecystokinin (CCK)** is a gut hormone involved in digestion and induces **satiety** and reduces food intake. - Its action on the **nucleus tractus solitarius** contributes to feelings of fullness, which would lead to decreased eating and weight, not increased. *Glucagon stimulation of hepatocytes* - **Glucagon** primarily functions to raise blood glucose levels by stimulating **glycogenolysis** and **gluconeogenesis** in hepatocytes. - While it plays a role in metabolism, it does not directly drive increased food intake and weight gain as the primary mechanism for the observed effect.

Question 129: A healthy 22-year-old male participates in a research study you are leading to compare the properties of skeletal and cardiac muscle. You conduct a 3-phased experiment with the participant. In the first phase, you get him to lift up a 2.3 kg (5 lb) weight off a table with his left hand. In the second phase, you get him to do 20 burpees, taking his heart rate to 150/min. In the third phase, you electrically stimulate his gastrocnemius with a frequency of 50 Hz. You are interested in the tension and electrical activity of specific muscles as follows: Biceps in phase 1, cardiac muscle in phase 2, and gastrocnemius in phase 3. What would you expect to be happening in the phases and the respective muscles of interest?

A. Increase of tension in experiments 2 and 3, with the same underlying mechanism
B. Increase of tension in all phases (Correct Answer)
C. Recruitment of large motor units followed by small motor units in experiment 1
D. Fused tetanic contraction at the end of all three experiments
E. Recruitment of small motor units at the start of experiments 1 and 2

Explanation: ***Increase of tension in all phases*** - In **phase 1**, lifting a 2.3 kg weight requires the **biceps** to contract, generating sufficient force (**tension**) to overcome gravity. - In **phase 2**, the **cardiac muscle** increases its contractile force (**tension**) to meet the metabolic demands of **exercise**, leading to a heart rate of 150/min. - In **phase 3**, electrical stimulation of the **gastrocnemius** at 50 Hz triggers muscle contraction, leading to an increase in **tension**. *Increase of tension in experiments 2 and 3, with the same underlying mechanism* - While tension increases in phases 2 and 3, the **underlying mechanisms differ**: cardiac muscle tension increases due to increased sympathetic stimulation and preload, while skeletal muscle tension increases due to unfused or fused tetanus from electrical stimulation. - Cardiac muscle contraction is regulated by **calcium-induced calcium release**, while skeletal muscle involves direct coupling of DHP receptor and ryanodine receptor. *Recruitment of large motor units followed by small motor units in experiment 1* - **Motor unit recruitment** follows the **size principle**, meaning smaller, more easily excitable motor units are activated first, followed by larger ones as more force is needed. - Therefore, in phase 1, **small motor units** would be recruited first, not large ones. *Fused tetanic contraction at the end of all three experiments* - **Fused tetanic contraction** occurs in **skeletal muscle** when stimulation frequency is high enough that individual twitches summate completely, leading to sustained contraction. - This phenomenon is **not possible in cardiac muscle** due to its long **refractory period**, which prevents sustained contraction and allows for adequate filling time. *Recruitment of small motor units at the start of experiments 1 and 2* - **Motor unit recruitment** applies to **skeletal muscle** (phase 1) and involves recruiting small motor units first for fine or gentle movements. - **Cardiac muscle** (phase 2) does not have motor units; instead, it relies on the **Frank-Starling mechanism** and hormonal/nervous regulation to adjust its contractile force as a syncytium.

Question 130: An investigator is studying the function of the lateral nucleus of the hypothalamus in an experimental animal. Using a viral vector, the genes encoding chloride-conducting channelrhodopsins are injected into this nucleus. Photostimulation of the channels causes complete inhibition of action potential generation. Persistent photostimulation is most likely to result in which of the following abnormalities in these animals?

A. Hyperthermia
B. Anorexia (Correct Answer)
C. Nocturnal hyperactivity
D. Polydipsia
E. Hypothermia

Explanation: ***Anorexia*** - The **lateral nucleus of the hypothalamus** is primarily associated with **hunger** and **feeding behavior**; its destruction or inhibition leads to aphagia and reduced food intake. - Inhibiting action potential generation in this region would mimic a lesion, preventing the animal from feeling hunger and consequently leading to anorexia. *Hyperthermia* - The **anterior hypothalamus** is more involved in **heat dissipation** (cooling), while the posterior hypothalamus handles heat conservation. - Disrupting the lateral hypothalamus would not directly lead to hyperthermia. *Nocturnal hyperactivity* - The **suprachiasmatic nucleus** and other areas of the hypothalamus regulate circadian rhythms, but the lateral hypothalamus is not primarily associated with activity levels or sleep-wake cycles in this manner. - Activation or inhibition of the lateral hypothalamus typically affects feeding, not general activity levels in a nocturnal pattern. *Polydipsia* - **Thirst regulation** is primarily attributed to the **supraoptic** and **paraventricular nuclei** and the **organum vasculosum of the lamina terminalis (OVLT)**. - The lateral hypothalamus also plays a role in **drinking behavior**, and its inhibition would cause **adipsia** (decreased drinking), not polydipsia (increased drinking). *Hypothermia* - While the hypothalamus regulates body temperature, direct inhibition of the lateral **"hunger center"** would not cause systemic hypothermia. - **Heat conservation** and **production** are more closely linked to the **posterior hypothalamus**.

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