Angiotensinogen to angiotensin I conversion US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Angiotensinogen to angiotensin I conversion. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Angiotensinogen to angiotensin I conversion US Medical PG Question 1: A new drug has been shown to block epithelial sodium channels in the cortical collecting duct. Which of the following is most likely to be decreased upon drug administration?
- A. Urea reabsorption in the collecting tubules
- B. Hydrogen ion secretion in the collecting tubules
- C. Potassium secretion in the collecting tubules (Correct Answer)
- D. Sodium secretion in the collecting tubules
- E. Sodium chloride reabsorption in the distal tubule
Angiotensinogen to angiotensin I conversion Explanation: ***Potassium secretion in the collecting tubules***
- Blocking **epithelial sodium channels (ENaC)** in the cortical collecting duct reduces sodium reabsorption, which in turn diminishes the electrochemical gradient driving **potassium secretion** into the lumen.
- This is because sodium reabsorption creates a more negative luminal charge, attracting potassium ions to move from the cell into the tubule.
- This is the mechanism of **potassium-sparing diuretics** like amiloride and triamterene.
*Urea reabsorption in the collecting tubules*
- Urea **reabsorption** primarily occurs in the **medullary collecting duct** via urea transporters (UT-A1, UT-A3) and is influenced by the inner medullary osmolarity and ADH.
- Blocking ENaC would primarily affect sodium flux and potassium secretion, with minimal direct impact on urea reabsorption in the collecting duct.
*Hydrogen ion secretion in the collecting tubules*
- **Hydrogen ion (H+) secretion** occurs in the collecting tubules via intercalated cells (α-intercalated cells), which is important for acid-base balance.
- While blocking ENaC can indirectly reduce H+ secretion (by decreasing the lumen-negative potential), the primary and most significant effect is on **potassium secretion**, making this a less likely answer.
*Sodium secretion in the collecting tubules*
- The primary function of ENaC is to **reabsorb sodium** from the tubular lumen back into the blood, not to secrete it.
- Sodium is not normally secreted in the collecting tubules; blocking ENaC would decrease sodium **reabsorption**, not affect sodium secretion.
*Sodium chloride reabsorption in the distal tubule*
- **Sodium chloride reabsorption** in the distal convoluted tubule is mainly mediated by the **thiazide-sensitive Na-Cl co-transporter (NCC)**.
- ENaC are predominantly located in the cortical collecting duct (downstream from the DCT), so blocking them would not directly impact NaCl reabsorption in the distal tubule.
Angiotensinogen to angiotensin I conversion US Medical PG Question 2: Which hormone's secretion is primarily stimulated by increased plasma osmolality?
- A. EPO
- B. PTH
- C. ADH (Correct Answer)
- D. Aldosterone
- E. ANP
Angiotensinogen to angiotensin I conversion Explanation: ***ADH***
- **Antidiuretic hormone (ADH)**, also known as vasopressin, is primarily released in response to an increase in **plasma osmolality**.
- Its main function is to promote water reabsorption in the kidneys, thereby decreasing osmolality and concentrating urine.
*EPO*
- **Erythropoietin (EPO)** is a hormone primarily produced by the kidneys in response to **hypoxia** (low oxygen levels), not increased plasma osmolality.
- It stimulates the production of **red blood cells** in the bone marrow.
*PTH*
- **Parathyroid hormone (PTH)** regulates **calcium** and phosphate levels in the blood, primarily stimulated by low plasma calcium concentrations.
- It does not directly respond to changes in plasma osmolality.
*Aldosterone*
- **Aldosterone** is a mineralocorticoid hormone involved in regulating **blood pressure** and electrolyte balance, particularly sodium and potassium.
- Its secretion is primarily stimulated by the **renin-angiotensin-aldosterone system** in response to low blood volume or pressure, and high potassium levels, not plasma osmolality.
Angiotensinogen to angiotensin I conversion US Medical PG Question 3: A 29-year-old patient presents to her primary care physician with persistent amenorrhea and inability to breastfeed over the last 5 months. She says that she has also been very tired since her baby was born and this fatigue was accompanied by an inability to deal with cold weather despite having no problem with cold prior to becoming pregnant. She has gained an additional 5 pounds since delivery. Review of her hospital records reveals that she had a vaginal delivery that was complicated by severe hemorrhage and episodes of hypotension. Which of the following hormone levels is most likely to be normal in this patient?
- A. Thyroid hormone
- B. Cortisol
- C. Aldosterone (Correct Answer)
- D. Follicle-stimulating hormone (FSH)
- E. Prolactin
Angiotensinogen to angiotensin I conversion Explanation: **Aldosterone**
- **Aldosterone** is primarily regulated by the **renin-angiotensin-aldosterone system** (RAAS) and is produced by the adrenal cortex, which is not directly affected by pituitary ischemia in Sheehan's syndrome.
- The symptoms described (amenorrhea, inability to breastfeed, fatigue, cold intolerance, weight gain) are classic for **Sheehan's syndrome**, which involves panhypopituitarism due to **ischemic necrosis of the pituitary gland** following severe postpartum hemorrhage. However, aldosterone production generally remains intact.
*Thyroid hormone*
- The pituitary gland produces **thyroid-stimulating hormone (TSH)**, which is essential for thyroid hormone production. Sheehan's syndrome leads to TSH deficiency, resulting in **secondary hypothyroidism** (low thyroid hormone).
- The patient's symptoms of fatigue, cold intolerance, and weight gain are consistent with hypothyroidism.
*Cortisol*
- The pituitary gland produces **adrenocorticotropic hormone (ACTH)**, which stimulates cortisol production from the adrenal cortex. Sheehan's syndrome causes ACTH deficiency, leading to **secondary adrenal insufficiency** (low cortisol).
- Fatigue is a common symptom of cortisol deficiency.
*Follicle-stimulating hormone (FSH)*
- **FSH** is produced by the pituitary gland and is crucial for ovarian function, including follicular development and estrogen production.
- Deficiency of FSH (and LH) due to Sheehan's syndrome results in **secondary amenorrhea** and an inability to ovulate.
*Prolactin*
- **Prolactin** is produced by the pituitary gland and is necessary for lactation.
- In Sheehan's syndrome, prolactin deficiency directly leads to the **inability to breastfeed**.
Angiotensinogen to angiotensin I conversion US Medical PG Question 4: A researcher is studying receptors that respond to epinephrine in the body and discovers a particular subset that is expressed in presynaptic adrenergic nerve terminals. She discovers that upon activation, these receptors will lead to decreased sympathetic nervous system activity. She then studies the intracellular second messenger changes that occur when this receptor is activated. She records these changes and begins searching for analogous receptor pathways. Which of the following receptors would cause the most similar set of intracellular second messenger changes?
- A. Muscarinic cholinoreceptors in the gastrointestinal tract
- B. Growth hormone receptors in the musculoskeletal system
- C. Vasopressin receptors in the kidney
- D. Dopamine receptors in the brain (Correct Answer)
- E. Aldosterone receptors in the kidney
Angiotensinogen to angiotensin I conversion Explanation: ***Dopamine receptors in the brain***
- The described presynaptic receptors for epinephrine that decrease sympathetic activity are **alpha-2 adrenergic receptors**, which are **G inhibitory protein (Gi)-coupled receptors**.
- Gi-coupled receptors **inhibit adenylyl cyclase**, leading to a **decrease in intracellular cAMP**, a signaling pathway shared by **D2 dopamine receptors**.
*Muscarinic cholinoreceptors in the gastrointestinal tract*
- Most muscarinic receptors (M1 and M3) in the GI tract are **Gq-coupled**, leading to an **increase in phospholipase C (PLC) activity**, ultimately increasing intracellular **IP3 and DAG** and promoting smooth muscle contraction.
- This mechanism is distinct from the **Gi-mediated inhibition of cAMP** described for the presynaptic adrenergic receptor.
*Growth hormone receptors in the musculoskeletal system*
- Growth hormone receptors are **tyrosine kinase-associated receptors** (specifically, they are linked to **JAK/STAT pathways**), not G protein-coupled receptors.
- Their intracellular signaling involves **protein phosphorylation cascades**, which are fundamentally different from second messenger changes involving cAMP.
*Vasopressin receptors in the kidney*
- Vasopressin (ADH) acts on **V2 receptors** in the kidney, which are **G stimulatory protein (Gs)-coupled receptors**.
- Activation of V2 receptors leads to an **increase in adenylyl cyclase activity** and thus an **increase in intracellular cAMP**, the opposite effect of the described Gi-coupled receptor.
*Aldosterone receptors in the kidney*
- Aldosterone receptors are **intracellular steroid hormone receptors** that directly bind to DNA and regulate gene transcription.
- They do not engage in rapid intracellular second messenger changes like G protein-coupled receptors, but rather alter **protein synthesis** over hours to days.
Angiotensinogen to angiotensin I conversion US Medical PG Question 5: A 33-year-old male presents to his primary care physician with complaints of headaches and muscle weakness. His physical exam is entirely within normal limits except for a blood pressure of 150/95. Subsequent routine blood lab work showed a sodium level of 146 and potassium level of 3.0. What is the best pharmacological therapy for this patient?
- A. Fludrocortisone
- B. Spironolactone (Correct Answer)
- C. Lisinopril
- D. Hydrochlorothiazide
- E. Propranolol
Angiotensinogen to angiotensin I conversion Explanation: ***Spironolactone***
- This patient's symptoms (hypertension, **hypokalemia**, and **hypernatremia**) are classic for **primary hyperaldosteronism**. **Spironolactone** is an **aldosterone antagonist** that blocks the effects of aldosterone, effectively treating both the hypertension and electrolyte abnormalities.
- Aldosterone antagonists directly target the underlying pathology by countering the excessive mineralocorticoid activity, making it the most appropriate pharmacological therapy for primary hyperaldosteronism.
*Fludrocortisone*
- **Fludrocortisone** is a **mineralocorticoid** used to *replace* aldosterone in conditions like Addison's disease where aldosterone production is deficient.
- Administering fludrocortisone in a patient with excessive aldosterone (primary hyperaldosteronism) would worsen their condition by exacerbating hypertension, hypokalemia, and hypernatremia.
*Lisinopril*
- **Lisinopril** is an **ACE inhibitor** that works by blocking the conversion of angiotensin I to angiotensin II, leading to vasodilation and decreased aldosterone secretion.
- While ACE inhibitors can lower blood pressure, they are not the primary treatment for **primary hyperaldosteronism** because the condition involves autonomous aldosterone production **independent of the renin-angiotensin-aldosterone system (RAAS)**.
*Hydrochlorothiazide*
- **Hydrochlorothiazide** is a **thiazide diuretic** that works by increasing the excretion of sodium and water, thereby lowering blood pressure.
- However, thiazide diuretics also increase potassium excretion, which would further worsen the patient's existing **hypokalemia**, making it an inappropriate choice.
*Propranolol*
- **Propranolol** is a **non-selective beta-blocker** that lowers blood pressure by reducing heart rate and cardiac output.
- While useful for hypertension, beta-blockers do not address the underlying electrolyte disturbances characteristic of **primary hyperaldosteronism** and are not a first-line treatment for this specific condition.
Angiotensinogen to angiotensin I conversion US Medical PG Question 6: Which mechanism primarily regulates sodium reabsorption in the collecting duct?
- A. Glomerulotubular balance
- B. Atrial natriuretic peptide
- C. Antidiuretic hormone
- D. Aldosterone (Correct Answer)
Angiotensinogen to angiotensin I conversion Explanation: ***Aldosterone***
- **Aldosterone** is the primary hormone that stimulates **sodium reabsorption** and **potassium secretion** in the principal cells of the collecting duct.
- It acts by increasing the synthesis and activity of **ENaC channels** on the apical membrane and **Na+/K+-ATPase pumps** on the basolateral membrane.
*Glomerulotubular balance*
- **Glomerulotubular balance** refers to the mechanism by which the **proximal tubule** reabsorbs a constant fraction of the filtered load, regardless of changes in glomerular filtration rate (GFR).
- This mechanism maintains a relatively constant delivery of fluid and solutes to downstream segments but does not primarily regulate sodium in the collecting duct.
*Atrial natriuretic peptide*
- **Atrial natriuretic peptide (ANP)** primarily **inhibits sodium reabsorption** in the collecting duct, leading to **natriuresis** and **diuresis**, which is the opposite of sodium reabsorption.
- ANP is released in response to atrial stretch, indicating increased blood volume.
*Antidiuretic hormone*
- **Antidiuretic hormone (ADH)** primarily regulates **water reabsorption** in the collecting duct by increasing the insertion of **aquaporin-2 channels** into the apical membrane, making the collecting duct permeable to water.
- While ADH can indirectly affect sodium concentration by influencing water movement, it does not directly regulate sodium transport to the same extent as aldosterone.
Angiotensinogen to angiotensin I conversion US Medical PG Question 7: 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
Angiotensinogen to angiotensin I conversion 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.
Angiotensinogen to angiotensin I conversion US Medical PG Question 8: A 52-year-old man is brought to the emergency department by ambulance after a motor vehicle accident. He was an unrestrained passenger who was ejected from the vehicle. On presentation, he is found to be actively bleeding from numerous wounds. His blood pressure is 76/42 mmHg and pulse is 152/min. Attempts at resuscitation fail, and he dies 25 minutes later. Autopsy shows blood in the peritoneal cavity, and histology of the kidney reveals swelling of the proximal convoluted tubule epithelial cells. Which of the following is most likely the mechanism underlying the renal cell findings?
- A. Decreased activity of caspase 7
- B. Increased activity of caspase 9
- C. Increased function of the Na+/K+-ATPase
- D. Increased activity of caspase 8
- E. Decreased function of the Na+/K+-ATPase (Correct Answer)
Angiotensinogen to angiotensin I conversion Explanation: ***Decreased function of the Na+/K+-ATPase***
- The patient experienced **hypovolemic shock** due to severe blood loss, leading to a significant drop in blood pressure and organ perfusion. This results in **ischemia** of the renal cells.
- **Ischemic injury** impairs ATP production, which is essential for the function of the **Na+/K+-ATPase pump**. Failure of this pump leads to intracellular accumulation of sodium and water, causing **cellular swelling**, particularly noticeable in the proximal convoluted tubules.
*Decreased activity of caspase 7*
- **Caspases**, including caspase 7, are involved in **apoptosis** (programmed cell death), which involves cell shrinkage and fragmentation, not the swelling observed here.
- Decreased caspase activity would generally *reduce* apoptosis, which is not the primary mechanism of acute cell injury in shock.
*Increased activity of caspase 9*
- Increased activity of **caspase 9** is indicative of the **intrinsic apoptotic pathway**, typically initiated by mitochondrial damage.
- While prolonged ischemia can eventually lead to apoptotic changes, the acute finding of **cellular swelling** points more directly to immediate membrane pump dysfunction due to ATP depletion.
*Increased function of the Na+/K+-ATPase*
- **Increased function** of the Na+/K+-ATPase would actively pump sodium out of the cell and potassium in, *preventing* intracellular swelling.
- This option contradicts the observed finding of proximal convoluted tubule epithelial cell swelling, which is characteristic of acute cellular injury due to pump failure.
*Increased activity of caspase 8*
- **Caspase 8** is a key initiator caspase in the **extrinsic apoptotic pathway**, often triggered by death receptor signaling.
- Similar to caspase 9, increased caspase 8 activity would lead to apoptosis, characterized by cell shrinkage, not the **cellular swelling** seen in acute ischemic injury.
Angiotensinogen to angiotensin I conversion US Medical PG Question 9: A 63-year-old man comes to the physician because of fatigue and muscle cramps for 6 weeks. He also noticed several episodes of tingling around the mouth and in the fingers and toes. He has osteoarthritis of his knees and hypertension. Current medications include ibuprofen and ramipril. He has smoked one pack of cigarettes daily for 35 years. Tapping over the facial nerve area in front of the ear elicits twitching of the facial muscles on the same side of the face. His serum alkaline phosphatase activity is 66 U/L. An ECG shows sinus rhythm with a prolonged QT interval. Which of the following is the most likely underlying cause of this patient's symptoms?
- A. Medication side effect
- B. Ectopic hormone production
- C. Vitamin D deficiency
- D. Destruction of parathyroid glands (Correct Answer)
- E. Albright hereditary osteodystrophy
Angiotensinogen to angiotensin I conversion Explanation: ***Destruction of parathyroid glands***
- The patient presents with **fatigue**, **muscle cramps**, and **paresthesias** (tingling around the mouth, fingers, and toes), which are classic symptoms of **hypocalcemia**.
- The positive **Chvostek's sign** (tapping over the facial nerve leading to facial muscle twitching) further confirms hypocalcemia, and a **prolonged QT interval** on ECG is also a known manifestation of low calcium levels. Destruction of the parathyroid glands (e.g., due to surgery, autoimmune disease, or radiation) leads to primary hypoparathyroidism and subsequent hypocalcemia.
*Medication side effect*
- While some medications can affect calcium levels, neither **ibuprofen** nor **ramipril** are typically associated with profound hypocalcemia leading to such prominent symptoms.
- The constellation of symptoms and signs (Chvostek's sign, prolonged QT) strongly points to an underlying calcium metabolism disorder, not a common drug side effect.
*Ectopic hormone production*
- **Ectopic hormone production** (e.g., PTHrP from tumors) usually causes **hypercalcemia**, not hypocalcemia, by mimicking parathyroid hormone action.
- Tumors that could lead to hypocalcemia are rare and usually involve extensive osteoblastic metastases consuming calcium, which is not suggested by the patient's presentation.
*Vitamin D deficiency*
- **Vitamin D deficiency** primarily causes osteomalacia in adults and rickets in children and can lead to **secondary hyperparathyroidism** as the body tries to compensate for low calcium.
- While severe vitamin D deficiency can cause some hypocalcemia symptoms, it doesn't typically present with the acute, symptomatic hypocalcemia signs like Chvostek's sign and prolonged QT interval in this direct manner without other signs of bone disease.
*Albright hereditary osteodystrophy*
- **Albright hereditary osteodystrophy** is a genetic disorder causing **pseudohypoparathyroidism**, where the body is resistant to PTH, leading to hypocalcemia.
- This condition is often associated with characteristic physical features such as **short stature**, **brachydactyly**, and **obesity**, which are not mentioned in this patient.
Angiotensinogen to angiotensin I conversion US Medical PG Question 10: A 23-year-old woman presents to a medical clinic for a follow-up visit. She initially came with complaints of recurrent headaches and darkening of her knuckles and skin creases, which first began 6 months ago after she underwent bilateral adrenalectomy. Today, she says that she frequently bumps into people and objects while walking. Which of the following mechanisms most likely account for this patient’s symptoms?
- A. Feedback inhibition by an exogenous source
- B. Hormonal receptor downregulation
- C. Dissemination of tumor to distant sites
- D. Ectopic secretion of a trophic hormone
- E. Loss of a regulatory process (Correct Answer)
Angiotensinogen to angiotensin I conversion Explanation: ***Loss of a regulatory process***
- This patient likely has **Nelson's syndrome**, which develops after bilateral adrenalectomy for **Cushing's disease**. The removal of adrenal glands eliminates the **negative feedback** normally exerted by cortisol on the pituitary gland.
- This leads to unchecked growth of a pre-existing corticotroph adenoma, causing excessive **ACTH** secretion. The high ACTH levels result in **hyperpigmentation** (darkening knuckles and skin creases) due to its melanocyte-stimulating properties, and the growing tumor can cause **visual field defects** (bumping into objects) due to compression of the optic chiasm.
*Feedback inhibition by an exogenous source*
- This mechanism involves the suppression of endogenous hormone production by an external agent, such as corticosteroid medication.
- In this case, the patient's symptoms are due to a lack of feedback, not an excess.
*Hormonal receptor downregulation*
- This process involves a decrease in the number or sensitivity of receptors in response to prolonged high hormone levels, making the cells less responsive.
- While relevant in some endocrine disorders, it does not explain the pituitary tumor growth or the specific constellation of symptoms seen here.
*Dissemination of tumor to distant sites*
- This option refers to metastasis, where a cancer spreads from its primary location to other parts of the body.
- Although the pituitary adenoma grows, Nelson's syndrome is primarily characterized by local tumor expansion and hormonal effects, not distant metastasis.
*Ectopic secretion of a trophic hormone*
- Ectopic secretion refers to the production of hormones by tissues that do not normally produce them, often associated with paraneoplastic syndromes.
- In this scenario, the ACTH is secreted by an adenoma within the pituitary gland, which is its normal site of production, albeit in an unregulated and excessive manner.
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