RAAS

RAAS US Medical PG Question 1: A 75 year-old gentleman presents to his general practitioner. He is currently being treated for hypertension and is on a multi-drug regimen. His current blood pressure is 180/100. The physician would like to begin treatment with minoxidil or hydralazine. Which of the following side effects is associated with administration of these drugs?

• A. Persistent cough
• B. Cyanosis in extremities
• C. Fetal renal toxicity
• D. Systemic volume loss
• E. Reflex tachycardia (Correct Answer)

RAAS Explanation: ***Reflex tachycardia*** - Both **minoxidil** and **hydralazine** are direct arterial vasodilators, causing a significant drop in **peripheral vascular resistance**. - This vasodilation triggers a **baroreflex response**, leading to an increase in heart rate and **cardiac contractility** to maintain cardiac output, resulting in reflex tachycardia. *Persistent cough* - **Persistent cough** is a common side effect associated with **ACE inhibitors**, such as lisinopril or enalapril, due to the accumulation of **bradykinin**. - This side effect is not typically seen with **minoxidil** or **hydralazine**, which act directly on vascular smooth muscle to cause vasodilation. *Cyanosis in extremities* - **Cyanosis** (bluish discoloration of the skin and mucous membranes) usually indicates **hypoxemia** or poor peripheral perfusion. - While sometimes associated with severe cardiogenic shock or specific drug toxicities like methemoglobinemia (not related to minoxidil or hydralazine), it is not a direct or typical side effect of these vasodilators. *Fetal renal toxicity* - **Fetal renal toxicity**, including **fetal renal dysfunction** and **oligohydramnios**, is a well-known risk associated with **ACE inhibitors** and **ARBs** during pregnancy. - Neither **minoxidil** nor **hydralazine** are primarily linked to this specific fetal adverse effect, though hydralazine can be used in pregnancy for severe hypertension. *Systemic volume loss* - **Systemic volume loss** is usually caused by conditions like **dehydration**, excessive diuresis, or hemorrhage. - While vasodilators can reduce blood pressure, they do not directly cause **systemic volume depletion**; rather, the reflex response to vasodilation can include fluid retention to counteract the blood pressure drop.

RAAS US Medical PG Question 2: A 32-year-old African American man presents to the office for a routine examination. He has no complaints at this time. Records show that his systolic blood pressure was in the 130–138 range and diastolic blood pressure in the 88–95 range despite counseling on lifestyle modification. He admits that he was not compliant with this advice. He takes no medications and works at home as a web designer. He does not drink alcohol but smokes marijuana on a weekly basis. Temperature is 37°C (98.6°F), blood pressure is 138/90 mm Hg, pulse is 76/min, and respirations are 12/min. BMI is 29.8 kg/m2. Physical examination is normal except for truncal obesity, with a waist circumference of 44 inches. Fasting laboratory results are as follows: Blood glucose 117 mg/dL Total cholesterol 210 mg/dL LDL cholesterol 120 mg/dL HDL cholesterol 38 mg/dL Triglycerides 240 mg/dL Which of the following mechanisms contribute to this patient’s condition?

• A. Excessive cortisol secretion and activity
• B. Granulomatous inflammation in medium-sized vessels
• C. LDL receptor gene mutation
• D. Insulin receptor resistance (Correct Answer)
• E. Autoimmune destruction of pancreatic beta cells

RAAS Explanation: ***Insulin receptor resistance*** - The patient exhibits features of **metabolic syndrome**, including **truncal obesity** (BMI 29.8 kg/m², waist circumference 44 inches), **elevated blood pressure** (138/90 mm Hg), **impaired fasting glucose** (117 mg/dL), **high triglycerides** (240 mg/dL), and **low HDL cholesterol** (38 mg/dL). These are all key manifestations of insulin resistance. - **Insulin resistance** is central to metabolic syndrome, leading to compensatory hyperinsulinemia, which contributes to hypertension, dyslipidemia, and impaired glucose tolerance, eventually progressing to type 2 diabetes if pancreatic beta cells fail. *Excessive cortisol secretion and activity* - **Cushing's syndrome**, characterized by excessive cortisol, also causes truncal obesity, hypertension, and hyperglycemia, but typically presents with additional features like **moon facies**, **buffalo hump**, and **skin striae**, which are not mentioned here. - The patient's blood pressure and glucose levels, while elevated, are not severe enough to strongly suggest Cushing's syndrome in the absence of other characteristic signs. *Granulomatous inflammation in medium-sized vessels* - This description is characteristic of various forms of **vasculitis**, such as **Polyarteritis Nodosa** or **Giant Cell Arteritis**. - Vasculitis typically presents with constitutional symptoms, organ ischemia, and specific inflammatory markers, none of which are present in this patient's routine examination. *LDL receptor gene mutation* - An **LDL receptor gene mutation** is associated with **familial hypercholesterolemia**, primarily causing greatly elevated LDL cholesterol levels and premature cardiovascular disease. - While this patient has elevated LDL, his overall lipid profile with high triglycerides and low HDL is more consistent with metabolic syndrome than a primary LDL receptor defect. *Autoimmune destruction of pancreatic beta cells* - This is the underlying mechanism of **type 1 diabetes mellitus**, which usually presents with profound hyperglycemia, polyuria, polydipsia, and weight loss, typically in younger patients. - This patient's mild hyperglycemia and features of metabolic syndrome are more indicative of **insulin resistance (type 2 diabetes)** rather than autoimmune beta-cell destruction.

RAAS US Medical PG Question 3: A 33-year-old woman presents to her primary care physician for a wellness check-up. She states that recently she has been feeling well other than headaches that occur occasionally, which improve with ibuprofen and rest. She has a past medical history of hypertension and headaches and is currently taking hydrochlorothiazide. Her temperature is 99.2°F (37.3°C), blood pressure is 157/108 mmHg, pulse is 90/min, respirations are 14/min, and oxygen saturation is 98% on room air. Physical exam reveals a young woman who appears healthy. A normal S1 and S2 are auscultated on cardiac exam, and her lungs are clear with good air movement bilaterally. From her previous visit, it was determined that she has an elevated aldosterone and low renin level. Laboratory values are ordered as seen below. Serum: Na+: 139 mEq/L Cl-: 100 mEq/L K+: 3.7 mEq/L HCO3-: 29 mEq/L BUN: 20 mg/dL Creatinine: 1.1 mg/dL Which of the following is the most likely diagnosis?

• A. Benign essential hypertension
• B. Pheochromocytoma
• C. Cushing syndrome
• D. Narrowing of the renal arteries
• E. Primary hyperaldosteronism (Correct Answer)

RAAS Explanation: ***Primary hyperaldosteronism*** - The patient presents with **hypertension**, **mild hypokalemia (K+ of 3.7 mEq/L)**, and **metabolic alkalosis (HCO3- of 29 mEq/L)**, which are classic signs of primary hyperaldosteronism. - The elevated aldosterone and low renin levels, as noted from her previous visit, are diagnostic for primary hyperaldosteronism. *Benign essential hypertension* - While essential hypertension is common, the presence of **hypokalemia**, **metabolic alkalosis**, and particularly the **elevated aldosterone with low renin** points away from benign essential hypertension, which typically has normal renin-aldosterone ratios. - This patient's hypertension is likely **secondary** due to a specific endocrine imbalance. *Pheochromocytoma* - This condition presents with **episodic or paroxysmal hypertension**, **tachycardia**, **sweating**, and headaches, often in a more dramatic fashion. - The patient's blood pressure is consistently elevated, and she lacks the typical paroxysmal symptoms and signs of catecholamine excess. *Cushing syndrome* - Cushing syndrome is characterized by **hypertension**, central obesity, moon facies, buffalo hump, and striae, none of which are described. - While it can cause hypertension, it is due to cortisol excess and does not typically present with the specific aldosterone-renin profile seen in this patient. *Narrowing of the renal arteries* - **Renal artery stenosis** causes **renovascular hypertension** and is associated with **elevated renin levels** as the kidney perceives hypoperfusion and activates the renin-angiotensin-aldosterone system. - This patient presents with **low renin levels**, which directly contradicts the pathophysiology of renal artery stenosis.

RAAS US Medical PG Question 4: A 55-year-old woman comes to the physician because of involuntary hand movements that improve with alcohol consumption. Physical examination shows bilateral hand tremors that worsen when the patient is asked to extend her arms out in front of her. The physician prescribes a medication that is associated with an increased risk of bronchospasms. This drug has which of the following immediate effects on the cardiovascular system? Stroke volume | Heart rate | Peripheral vascular resistance

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

RAAS Explanation: ***↓ ↓ ↑*** - This patient likely has **essential tremor**, which is characterized by **bilateral hand tremors** that improve with alcohol and worsen with intention (postural tremor). The prescribed medication is a **beta-blocker** (e.g., propranolol), which is associated with an increased risk of bronchospasms due to blocking **beta-2 receptors** in the airways. - Beta-blockers **decrease heart rate** (negative chronotropic effect) and **stroke volume** (negative inotropic effect) by blocking beta-1 receptors in the heart, reducing cardiac output. - **Peripheral vascular resistance increases** acutely due to: (1) **unopposed alpha-1 adrenergic tone** in blood vessels (loss of beta-2 mediated vasodilation), and (2) baroreceptor-mediated reflex vasoconstriction in response to decreased cardiac output. This helps maintain blood pressure despite reduced cardiac output. *↓ ↓ ↓* - While beta-blockers decrease **heart rate** and **stroke volume**, peripheral vascular resistance does not decrease acutely. A decrease in all three parameters would cause severe hypotension. - The loss of beta-2 receptor-mediated vasodilation and baroreceptor reflexes lead to increased, not decreased, peripheral vascular resistance. *↓ ↑ ↑* - Beta-blockers **decrease heart rate** through beta-1 blockade, not increase it. This is their primary cardiac mechanism of action. - An increase in heart rate would be expected with sympathomimetic drugs or anticholinergics, not beta-blockers. *↑ ↑ ↑* - This combination indicates increased cardiovascular activity, which is the opposite effect of **beta-blockers**. - Beta-blockers reduce heart rate and stroke volume by blocking beta-1 receptors; they do not increase these parameters. - This pattern would suggest sympathetic activation or administration of an adrenergic agonist. *↑ ↑ ↓* - Beta-blockers **decrease** (not increase) both heart rate and stroke volume through beta-1 receptor blockade. - While decreased peripheral vascular resistance occurs with vasodilators, beta-blockers acutely **increase** PVR due to unopposed alpha-adrenergic tone.

RAAS US Medical PG Question 5: A 32-year-old man presents with hypertension that has been difficult to control with medications. His symptoms include fatigue, frequent waking at night for voiding, and pins and needles in the legs. His symptoms started 2 years ago. Family history is positive for hypertension in his mother. His blood pressure is 160/100 mm Hg in the right arm and 165/107 mm Hg in the left arm, pulse is 85/min, and temperature is 36.5°C (97.7°F). Physical examination reveals global hyporeflexia and muscular weakness. Lab studies are shown: Serum sodium 147 mEq/L Serum creatinine 0.7 mg/dL Serum potassium 2.3 mEq/L Serum bicarbonate 34 mEq/L Plasma renin activity low Which of the following is the most likely diagnosis?

• A. Renal artery stenosis
• B. Coarctation of aorta
• C. Cushing syndrome
• D. Primary aldosteronism (Correct Answer)
• E. Essential hypertension

RAAS Explanation: ***Primary aldosteronism*** - The patient presents with **resistant hypertension**, **hypokalemia** (2.3 mEq/L), **metabolic alkalosis** (bicarbonate 34 mEq/L), and **low plasma renin activity**, which are classic features of primary aldosteronism. - Symptoms like **fatigue**, **nocturia**, and **paresthesias** (pins and needles) in the legs are consistent with severe hypokalemia, directly resulting from excessive aldosterone secretion. *Renal artery stenosis* - This condition typically causes **secondary hypertension** with **elevated renin levels** due to decreased renal perfusion, which contradicts the low plasma renin activity seen in this patient. - While it can cause hypokalemia because of increased renin-angiotensin-aldosterone system activation, the **primary driver** in this case, based on low renin, points away from renal artery stenosis. *Coarctation of aorta* - Characterized by **differential blood pressures** between the upper and lower extremities and sometimes between the arms, and a **systolic murmur** that is often present. - It does not typically present with severe **hypokalemia** or metabolic alkalosis or the low plasma renin activity observed in this patient. *Cushing syndrome* - This syndrome is caused by **excessive cortisol** and can lead to hypertension and hypokalemia, but it is also associated with distinct clinical features like **central obesity**, buffalo hump, moon facies, and proximal muscle weakness, which are not described. - While it can cause similar electrolyte imbalances, the lack of classic Cushingoid features makes it less likely, and the specific **low plasma renin** points more strongly to aldosterone excess. *Essential hypertension* - This is a diagnosis of exclusion, typically presenting without a clear secondary cause and with **normal electrolyte levels**. - The presence of severe **hypokalemia**, **metabolic alkalosis**, and **low plasma renin activity** indicates a secondary cause, ruling out essential hypertension.

RAAS US Medical PG Question 6: A newborn female is found to have ambiguous genitalia and hypotension. Laboratory workup reveals hyperkalemia, hyperreninemia, and elevated levels of 17-hydroxyprogesterone in the patient's urine. Which of the following enzymes would you expect to be deficient in this patient?

• A. 11-hydroxylase
• B. 3β-hydroxysteroid dehydrogenase
• C. 11β-hydroxysteroid dehydrogenase
• D. 21-hydroxylase (Correct Answer)
• E. 17-hydroxylase

RAAS Explanation: ***21-hydroxylase*** - **21-hydroxylase deficiency** is the most common cause of **congenital adrenal hyperplasia (CAH)**, leading to a build-up of **17-hydroxyprogesterone** and its metabolites, which are shunted into androgen pathways. - The deficiency in cortisol and aldosterone synthesis results in **hyponatremia**, **hyperkalemia**, and **hypotension** (due to salt-wasting) and **ambiguous genitalia** in females due to excess androgens. *11-hydroxylase* - **11-hydroxylase deficiency** also causes **CAH** and leads to ambiguous genitalia in females, but it is typically associated with **hypertension** due to the accumulation of 11-deoxycorticosterone, a mineralocorticoid, not hypotension. - While 17-hydroxyprogesterone might be elevated, the defining feature of this deficiency is elevated levels of **11-deoxycorticosterone** and **11-deoxycortisol**. *3β-hydroxysteroid dehydrogenase* - **3β-hydroxysteroid dehydrogenase deficiency** leads to impaired synthesis of all adrenal steroids (glucocorticoids, mineralocorticoids, and androgens), resulting in severe **salt-wasting** and **hypotension**. - However, females with this deficiency would typically present with **undervirilized** or normal genitalia, rather than ambiguous genitalia, due to reduced androgen synthesis. *11β-hydroxysteroid dehydrogenase* - **11β-hydroxysteroid dehydrogenase deficiency** is typically associated with **apparent mineralocorticoid excess syndrome**, leading to **hypertension** and **hypokalemia**, not hyperkalemia or ambiguous genitalia. - This enzyme is responsible for converting cortisol to cortisone, preventing cortisol from activating mineralocorticoid receptors. *17-hydroxylase* - **17-hydroxylase deficiency** impairs the synthesis of sex hormones and cortisol, leading to **hypertension** and **hypokalemia** due to increased mineralocorticoid production (e.g., corticosterone, 11-deoxycorticosterone). - Females would typically have **normal female external genitalia** but lack pubertal development, and males would present with **undervirilized external genitalia**.

RAAS US Medical PG Question 7: A 35-year-old African American woman comes to the physician because of intermittent palpitations over the past 2 weeks. During this period she has also had constipation and has felt more tired than usual. She was diagnosed with hypertension 4 weeks ago and treatment with chlorthalidone was begun. Her temperature is 36.5°C (97.7°F), pulse is 75/min, and blood pressure is 158/97 mm Hg. Physical examination shows a soft and nontender abdomen. There is mild weakness of the upper and lower extremities. Deep tendon reflexes are 1+ bilaterally. Laboratory studies show: Hemoglobin 13.5 g/dL Leukocyte count 5,000/mm3 Serum Na+ 146 mEq/L Cl− 100 mEq/L K+ 2.8 mEq/L HCO3− 30 mEq/L Glucose 97 mg/dL Urea nitrogen 10 mg/dL Creatinine 0.8 mg/dL Test of the stool for occult blood is negative. An ECG shows premature atrial complexes. Chlorthalidone is discontinued and oral potassium chloride therapy is begun. One week later, the patient's plasma aldosterone concentration is 26 ng/dL (N=3.6 to 24.0 ng/dL) and plasma renin activity is 0.8 ng/mL/h (N=0.3 to 4.2 ng/mL/h). Which of the following is the most appropriate next step in management?

• A. Perform adrenalectomy
• B. Perform saline infusion test (Correct Answer)
• C. Measure urine pH and anion gap
• D. Perform CT scan of the abdomen
• E. Perform dexamethasone suppression test

RAAS Explanation: ***Perform saline infusion test*** - The patient's **hypokalemia**, **hypertension**, and **high aldosterone-to-renin ratio (ARR)**, even after discontinuing chlorthalidone, are highly suggestive of **primary hyperaldosteronism (Conn's syndrome)**. - A **saline infusion test** is the most appropriate next step to confirm primary hyperaldosteronism by assessing **aldosterone suppressibility**. Failure to suppress aldosterone after saline infusion confirms the diagnosis. *Perform adrenalectomy* - Adrenalectomy is a treatment for aldosterone-producing adenomas, but it is not the next step before confirming the diagnosis and localizing the lesion. - The diagnosis of primary hyperaldosteronism first needs biochemical confirmation, usually with a saline suppression test. *Measure urine pH and anion gap* - Measuring urine pH and anion gap is useful in evaluating acid-base disorders or certain renal tubular conditions, but it is not directly relevant to diagnosing primary hyperaldosteronism. - The primary concern here is the workup of hypertension and hypokalemia with suspected endocrine etiology. *Perform CT scan of the abdomen* - While an abdominal CT scan is used to localize an adrenal adenoma, it should be done after biochemical confirmation of primary hyperaldosteronism. - Imaging should not precede diagnostic confirmation, as incidentalomas are common and may lead to unnecessary procedures. *Perform dexamethasone suppression test* - A dexamethasone suppression test is used to evaluate **Cushing's syndrome** (hypercortisolism), which is characterized by symptoms different from this patient's presentation. - This patient's symptoms of hypokalemia and hypertension point toward mineralocorticoid excess, not glucocorticoid excess.

RAAS US Medical PG Question 8: A 42-year-old man comes to the physician for a health maintenance examination. He has had generalized fatigue and muscle aches since his previous visit 6 months ago. He has hypertension and gastroesophageal reflux disease. Current medications include amlodipine and omeprazole. His temperature is 37.1°C (98.1°F), pulse is 88/min and blood pressure is 156/102 mm Hg. Physical examination shows no abnormalities. Serum studies show: Na+ 143 mEq/L K+ 2.3 mEq/L Cl- 100 mEq/L HCO3- 31 mEq/L Urea nitrogen 14 mg/dL Creatinine 1 mg/dL His blood pressure medication is discontinued. One week later his plasma aldosterone concentration is 35 ng/dL (N=3.6 - 24.0 ng/dL) and plasma renin activity is 0.4 ng/mL/h (N=0.3 to 4.2 ng/mL/h). An oral sodium loading test over 3 days fails to reduce aldosterone. A contrast-enhanced CT scan of the abdomen and pelvis shows a 3-cm, homogenous, right-sided adrenal mass with rapid contrast washout. He is counseled about his treatment options and chooses to pursue surgery. Which of the following is the most appropriate next step in management?

• A. Right adrenalectomy
• B. Fludrocortisone suppression test
• C. Adrenal vein sampling (Correct Answer)
• D. Spironolactone therapy
• E. Bilateral adrenalectomy

RAAS Explanation: ***Adrenal vein sampling*** - This patient presents with **hypokalemia**, **hypertension**, elevated **plasma aldosterone concentration** with suppressed **plasma renin activity**, and unsuppressed aldosterone after a sodium loading test, all highly suggestive of **primary hyperaldosteronism**. - Given the **3-cm adrenal mass** on the right side and the patient's choice for surgery, **adrenal vein sampling (AVS)** is crucial to confirm that the right adrenal gland is the sole source of excess aldosterone production, ensuring that surgery will be curative. *Right adrenalectomy* - Although surgery on the right adrenal gland is the desired outcome, performing a **right adrenalectomy** without prior adrenal vein sampling is premature and potentially harmful. - AVS is essential to differentiate between a unilateral aldosterone-producing adenoma and bilateral adrenal hyperplasia, as the latter would not be cured by unilateral surgery. *Fludrocortisone suppression test* - The **fludrocortisone suppression test** is used to confirm the diagnosis of primary hyperaldosteronism, but the diagnosis in this patient is already strongly supported by the elevated aldosterone-to-renin ratio and lack of suppression with the oral sodium loading test. - This test would not help in localizing the source of aldosterone excess. *Spironolactone therapy* - **Spironolactone** is an **aldosterone antagonist** that can be used to manage primary hyperaldosteronism, especially in cases of bilateral adrenal hyperplasia or if surgery is contraindicated or declined. - However, given the patient's desire for surgery and the presence of a unilateral mass, the goal is curative resection, which requires further localization with AVS. *Bilateral adrenalectomy* - **Bilateral adrenalectomy** is generally reserved for rare cases of bilateral adrenal hyperplasia that are unresponsive to medical therapy or when AVS confirms bilateral disease and surgery is absolutely necessary. - Performing a bilateral adrenalectomy would lead to permanent **adrenal insufficiency**, requiring lifelong corticosteroid replacement, which is a major drawback.

RAAS US Medical PG Question 9: 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

RAAS 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.

RAAS US Medical PG Question 10: Which mechanism primarily regulates sodium reabsorption in the collecting duct?

• A. Glomerulotubular balance
• B. Atrial natriuretic peptide
• C. Antidiuretic hormone
• D. Aldosterone (Correct Answer)

RAAS 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.

RAAS Flashcard 1 of 10

Question: At high concentrations, cortisol can bind to _____ receptors

Answer: mineralocorticoid (aldosterone)

RAAS Flashcard 2 of 10

Question: The renin-angiotensin II-aldosterone system is activated in response to a _____ in mean arterial pressure

Answer: decrease

RAAS Flashcard 3 of 10

Question: The renin-angiotensin II-aldosterone system regulates mean arterial pressure primarily by adjusting blood _____

Answer: volume

RAAS Flashcard 4 of 10

Question: To what receptor does angiotensin II bind?_____

Answer: AT1 receptor

RAAS Flashcard 5 of 10

Question: Secondary hyperaldosteronism is due to activation of _____ system

Answer: renin-angiotensin

RAAS Flashcard 6 of 10

Question: Angiotensin II is a potent vaso-_____

Answer: constrictor

RAAS Flashcard 7 of 10

Question: How do blood sugar levels change in secondary adrenocortical deficiency? _____

Answer: Decreased (hypoglycemia)

Extra Information:   Watch Adrenal Insufficiency [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-endocrine/videos/medical-pathophysiology-endocrine-adrenal-disorders-adrenal-insufficiency?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org/spa/endocrinology/adrenals/acquire?ref=anki 

RAAS Flashcard 8 of 10

Question: How does hyperkalemia influence aldosterone secretion? _____

Answer: Increased aldosterone secretion

Extra Information:  Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/renin-angiotensin-aldosterone-system?index=2] https://onlinemeded.org/spa/nephrology?ref=anki 

RAAS Flashcard 9 of 10

Question: In bone, the long-term effect of PTH is bone _____ via indirect action on _____

Answer: resorption

Extra Information:   Watch Parathyroid Gland Disorders [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-endocrine/videos/medical-pathophysiology-endocrine-thyroid-and-parathyroid-parathyroid-gland-disorders?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/histology/videos/endocrine-system?index=15] https://onlinemeded.org/spa/nephrology/calcium/acquire?ref=anki 

RAAS Flashcard 10 of 10

Question: The zona reticularis secretes _____, such as dehydroepiandrosterone (DHEA) and androstenedione

Answer: androgens

Extra Information:   * "GFR (out to in)" Watch Adrenal Insufficiency [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-endocrine/videos/medical-pathophysiology-endocrine-adrenal-disorders-adrenal-insufficiency?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] Watch Congenital Adrenal Hyperplasia (CAH) [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-endocrine/videos/medical-pathophysiology-endocrine-adrenal-disorders-congenital-adrenal-hyperplasia-cah?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/histology/videos/endocrine-system?index=9] https://onlinemeded.org/spa/endocrinology/adrenals/acquire?ref=anki Atlas: