Non-classical RAAS components US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Non-classical RAAS components. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Non-classical RAAS components US Medical PG Question 1: An investigator is studying patients with acute decompensated congestive heart failure. He takes measurements of a hormone released from atrial myocytes, as well as serial measurements of left atrial and left ventricular pressures. The investigator observes a positive correlation between left atrial pressures and the serum level of this hormone. Which of the following is most likely the mechanism of action of this hormone?
- A. Increases potassium excretion at the collecting ducts
- B. Constricts afferent renal arteriole
- C. Decreases sodium reabsorption at the collecting tubules (Correct Answer)
- D. Decreases reabsorption of bicarbonate in the proximal convoluted tubules
- E. Increases free water reabsorption from the distal tubules
Non-classical RAAS components Explanation: ***Decreases sodium reabsorption at the collecting tubules***
- The hormone described, exhibiting a positive correlation with left atrial pressure and released from atrial myocytes, is **Atrial Natriuretic Peptide (ANP)**.
- ANP promotes **natriuresis** (sodium excretion) and **diuresis** by directly inhibiting sodium reabsorption in the collecting tubules, thereby reducing blood volume and cardiac preload.
*Increases potassium excretion at the collecting ducts*
- While ANP does promote fluid and electrolyte excretion, its primary effect is on sodium and water, not a direct increase in **potassium excretion**. **Aldosterone**, not ANP, primarily increases potassium secretion in the collecting ducts.
- This option describes a mechanism more consistent with **mineralocorticoid activity**, which is counteracted by ANP.
*Constricts afferent renal arteriole*
- ANP generally causes **vasodilation** of the afferent arteriole and constriction of the efferent arteriole, increasing glomerular filtration rate (GFR).
- **Angiotensin II** is a primary constrictor of the afferent and efferent renal arterioles, which is the opposite effect of ANP.
*Decreases reabsorption of bicarbonate in the proximal convoluted tubules*
- This mechanism is primarily involved in **acid-base balance** and is influenced by factors like parathyroid hormone or respiratory/metabolic acidosis/alkalosis.
- ANP's main action is on **sodium and water balance**, not directly on bicarbonate reabsorption.
*Increases free water reabsorption from the distal tubules*
- **Vasopressin (Antidiuretic Hormone, ADH)** is responsible for increasing free water reabsorption in the distal tubules and collecting ducts.
- ANP's action is to *increase* water excretion, working in opposition to ADH to reduce circulating fluid volume.
Non-classical RAAS components US Medical PG Question 2: A group of investigators is studying a drug to treat refractory angina pectoris. This drug works by selectively inhibiting the late influx of sodium ions into cardiac myocytes. At high doses, the drug also partially inhibits the degradation of fatty acids. Which of the following is the most likely effect of this drug?
- A. Increased prolactin release
- B. Decreased uric acid excretion
- C. Decreased serum pH
- D. Increased oxygen efficiency (Correct Answer)
- E. Decreased insulin release
Non-classical RAAS components Explanation: ***Increased oxygen efficiency***
- Inhibiting the **late sodium current** reduces intracellular calcium overload, preventing diastolic dysfunction and improving myocardial relaxation.
- Partial inhibition of **fatty acid degradation** shifts myocardial metabolism towards glucose utilization, which is more oxygen-efficient.
*Increased prolactin release*
- This drug does not act on **dopamine receptors**, which are typically involved in regulating prolactin release.
- **Ranolazine**, the drug described, has no known effect on the endocrine system, specifically prolactin.
*Decreased uric acid excretion*
- **Uric acid excretion** is primarily affected by renal handling, often influenced by diuretics or drugs that compete for renal transporters, which is not a mechanism of this drug.
- This drug does not interfere with the **organic anion transporters (OATs)** responsible for uric acid secretion.
*Decreased serum pH*
- Changes in **serum pH** are usually associated with severe metabolic or respiratory disturbances, which are not direct effects of a drug targeting cardiac ion channels and metabolism.
- The drug's mechanism of action does not directly produce **acidic byproducts** or inhibit acid-base regulatory systems.
*Decreased insulin release*
- Insulin release is primarily stimulated by **glucose** and modulated by various endocrine pathways, none of which are directly targeted by a drug that inhibits cardiac sodium channels and fatty acid oxidation.
- There is no evidence that this class of drugs affects **pancreatic beta-cell function**.
Non-classical RAAS components US Medical PG Question 3: A 47-year-old man presents as a new patient at an outpatient clinic. He has never seen a physician before, but was motivated by his 40-year-old brother's recent heart attack and seeks to optimize his health. In particular, he read that uncontrolled atherosclerosis can lead to a heart attack. Which molecule is downregulated in response to the advent of atherosclerosis?
- A. Tumor necrosis factor
- B. Serotonin
- C. Nitric oxide (Correct Answer)
- D. Interleukin 1
- E. Thromboxane A2
Non-classical RAAS components Explanation: ***Nitric oxide***
- **Nitric oxide (NO)** is a potent **vasodilator** and **anti-inflammatory** molecule produced by endothelial cells. In atherosclerosis, endothelial dysfunction leads to reduced NO bioavailability.
- Decreased NO production contributes to vasoconstriction, increased platelet aggregation, and enhanced smooth muscle cell proliferation, all of which promote **atherosclerotic plaque formation** and progression.
*Tumor necrosis factor*
- **Tumor necrosis factor-alpha (TNF-α)** is a **pro-inflammatory cytokine** that plays a significant role in the pathogenesis of atherosclerosis.
- It is **upregulated** in response to atherosclerotic plaque formation, contributing to endothelial activation, leukocyte recruitment, and smooth muscle cell proliferation.
*Serotonin*
- **Serotonin (5-hydroxytryptamine)** is primarily known for its role as a neurotransmitter but also acts as a **vasoconstrictor** and promotes platelet aggregation.
- While it can be released from activated platelets in the context of vascular injury, it is not consistently **downregulated** in atherosclerosis; rather, its effects can contribute to disease progression.
*Interleukin 1*
- **Interleukin-1 (IL-1)**, particularly IL-1β, is a major **pro-inflammatory cytokine** critically involved in the immune response in atherosclerosis.
- It is **upregulated** in atherosclerotic plaques, contributing to systemic inflammation, endothelial dysfunction, and vascular smooth muscle cell activation.
*Thromboxane A2*
- **Thromboxane A2 (TXA2)** is a potent **vasoconstrictor** and **platelet aggregator** produced by activated platelets.
- Its levels are **increased** in atherosclerosis, contributing to hypercoagulability and increased risk of thrombotic events like myocardial infarction.
Non-classical RAAS components US Medical PG Question 4: Activation of the renin-angiotensin-aldosterone system yields a significant physiological effect on renal blood flow and filtration. Which of the following is most likely to occur in response to increased levels of Angiotensin-II?
- A. Decreased renal plasma flow, decreased filtration fraction
- B. Decreased renal plasma flow, increased glomerular capillary oncotic pressure
- C. Increased renal plasma flow, decreased filtration fraction
- D. Increased renal plasma flow, increased filtration fraction
- E. Decreased renal plasma flow, increased filtration fraction (Correct Answer)
Non-classical RAAS components Explanation: ***Decreased renal plasma flow, increased filtration fraction***
- **Angiotensin II** causes **efferent arteriolar constriction**, which reduces blood flow leaving the glomerulus, thereby **decreasing renal plasma flow**.
- This efferent constriction also increases **glomerular hydrostatic pressure** and reduces plasma flow distal to the glomerulus, leading to a **higher filtration fraction** (GFR/RPF).
*Decreased renal plasma flow, decreased filtration fraction*
- While **renal plasma flow decreases**, a **decreased filtration fraction** would imply that either GFR decreases disproportionately more than RPF or GFR does not increase despite the RPF reduction, which is not the typical response to **angiotensin II** due to its predominant effect on the **efferent arteriole**.
*Decreased renal plasma flow, increased glomerular capillary oncotic pressure*
- **Increased glomerular capillary oncotic pressure** is a consequence of increased filtration fraction, as more fluid is filtered out, leaving behind a more concentrated plasma. This option includes a correct element (decreased RPF) but pairs it with a less direct and defining outcome of acute Angiotensin II action as the primary physiological effect.
*Increased renal plasma flow, decreased filtration fraction*
- **Angiotensin II** causes **vasoconstriction**, predominantly of the efferent arteriole, which by definition would **decrease renal plasma flow**, not increase it.
- A **decreased filtration fraction** would be inconsistent with efferent arteriolar constriction which typically raises GFR relative to RPF.
*Increased renal plasma flow, increased filtration fraction*
- **Angiotensin II** causes **vasoconstriction**, leading to a **decrease in renal plasma flow**, not an increase.
- While **filtration fraction is increased**, the initial premise of increased renal plasma flow is incorrect.
Non-classical RAAS components US Medical PG Question 5: A 71-year-old man presents to his cardiologist with a 1-month history of increasing shortness of breath. He says that he is finding it very difficult to walk up the flight of stairs to his bedroom and he is no longer able to sleep flat on his bed because he wakes up choking for breath. His past medical history is significant for a myocardial infarction 3 years ago. On physical exam, he is found to have diffuse, moist crackles bilaterally on pulmonary auscultation and pitting edema in his lower extremities. Serum tests reveal an increased abundance of a product produced by cardiac myocytes. Which of the following most likely describes the function of this product?
- A. Increases water reabsorption in the kidney
- B. Stimulates parasympathetic nerves
- C. Increases conversion of angiotensin
- D. Inhibits release of renin (Correct Answer)
- E. Binds to intracellular receptors in the collecting duct
Non-classical RAAS components Explanation: ***Inhibits release of renin***
- The patient's symptoms (shortness of breath, orthopnea, crackles, edema) and history of MI are consistent with **heart failure**, leading to increased natriuretic peptide production from cardiac myocytes due to ventricular stretch.
- **Brain Natriuretic Peptide (BNP)**, released in heart failure, counteracts fluid retention by inhibiting renin release, thereby reducing aldosterone and angiotensin II, and promoting diuresis and natriuresis.
*Increases water reabsorption in the kidney*
- This is the primary function of **Antidiuretic Hormone (ADH)**, which acts on the collecting ducts to increase water reabsorption.
- Natriuretic peptides, in contrast, promote water excretion rather than retention.
*Stimulates parasympathetic nerves*
- The **parasympathetic nervous system** primarily slows heart rate and promotes digestion through the vagus nerve.
- Natriuretic peptides primarily exert their effects on the cardiovascular and renal systems to regulate blood volume and pressure, not through direct nervous system stimulation.
*Increases conversion of angiotensin*
- The conversion of angiotensin I to **angiotensin II** is mediated by **angiotensin-converting enzyme (ACE)**, primarily in the lungs.
- The product described (natriuretic peptide) works to *inhibit* the renin-angiotensin-aldosterone system (RAAS), thus indirectly reducing angiotensin II levels.
*Binds to intracellular receptors in the collecting duct*
- Hormones that bind to **intracellular receptors** are typically steroid hormones (e.g., aldosterone, cortisol) that regulate gene expression.
- Natriuretic peptides bind to **cell-surface receptors** (guanylyl cyclase receptors) on target cells, activating second messenger systems like cGMP.
Non-classical RAAS components US Medical PG Question 6: A physician is choosing whether to prescribe losartan or lisinopril to treat hypertension in a 56-year-old male. Relative to losartan, one would expect treatment with lisinopril to produce which of the following changes in the circulating levels of these peptides?
- A. Aldosterone increase; bradykinin decrease
- B. Angiotensin II increase; bradykinin decrease
- C. Renin decrease; angiotensin I increase
- D. Bradykinin increase; angiotensin II decrease (Correct Answer)
- E. Renin decrease; angiotensin II increase
Non-classical RAAS components Explanation: ***Bradykinin increase; angiotensin II decrease***
- **Lisinopril** is an **ACE inhibitor**, which directly blocks the conversion of **angiotensin I** to **angiotensin II**, leading to a decrease in circulating **angiotensin II** levels.
- ACE is also responsible for the breakdown of **bradykinin**, so inhibiting ACE with lisinopril will lead to an **increase in bradykinin** levels, contributing to vasodilation but also the characteristic cough.
*Aldosterone increase; bradykinin decrease*
- **Lisinopril** (an ACE inhibitor) decreases **angiotensin II**, which in turn leads to a **decrease in aldosterone** synthesis and release, not an increase.
- **Bradykinin** levels would increase due to ACE inhibition, as ACE is involved in its degradation.
*Angiotensin II increase; bradykinin decrease*
- **Lisinopril** directly inhibits the enzyme responsible for producing **angiotensin II**, thus leading to its **decrease**, not an increase.
- **Bradykinin** levels would increase because its degradation pathway (via ACE) is blocked, not decrease.
*Renin decrease; angiotensin I increase*
- **Lisinopril** reduces the negative feedback on **renin** release, leading to an **increase in renin** levels, not a decrease.
- While ACE is inhibited by lisinopril, this leads to an accumulation of its substrate, **angiotensin I**, resulting in an increase of angiotensin I.
*Renin decrease; angiotensin II increase*
- As an ACE inhibitor, lisinopril would lead to an **increase in renin** due to reduced negative feedback from angiotensin II, not a decrease.
- **Angiotensin II** levels would **decrease** because its production from angiotensin I is directly inhibited by lisinopril.
Non-classical RAAS components US Medical PG Question 7: Which mechanism primarily regulates sodium reabsorption in the collecting duct?
- A. Glomerulotubular balance
- B. Atrial natriuretic peptide
- C. Antidiuretic hormone
- D. Aldosterone (Correct Answer)
Non-classical RAAS components 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.
Non-classical RAAS components US Medical PG Question 8: 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
Non-classical RAAS components 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.
Non-classical RAAS components 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
Non-classical RAAS components 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.
Non-classical RAAS components 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)
Non-classical RAAS components 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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