Endocrinology — MCQs
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An 18-year-old girl presents with weakness. She reports high stress levels due to academic demands, with most of her time dedicated to studying, dieting, and exercising. Physical examination reveals a height of 5'8", a weight of 85 lbs, and she appears unwell. Her blood pressure is 85/70 mm Hg, heart rate is 50/min, and there is prominent muscle wasting. What is this patient most likely at risk for?
Which of the following is not involved in Multiple Endocrine Neoplasia type 2 (MEN II) syndrome?
Which of the following conditions can lead to increased T4 levels?
Which of the following is an anti-androgenic drug?
Which of the following findings is FALSE regarding primary adrenal hyperplasia?
A 56-year-old man is diagnosed with the metabolic syndrome, which consists of hypertension, insulin resistance, dyslipidemia, and abdominal obesity. He has no prior history of cardiac or vascular disease and is otherwise well. His fasting T-chol is 270 mg/dL, HDL 50 mg/dL, LDL 150 mg/dL, and triglycerides 150 mg/dL. His Framingham risk calculation approximates a 10-year risk for cardiac events of 10%-20%. For the above patient with dyslipidemia, select the most appropriate treatment.
Which of the following is a feature of primary hyperaldosteronism?
Which of the following is NOT true of Verner Morrison syndrome (WDHA syndrome)?
A 30-year-old patient presents with intermittent, severe headaches accompanied by perspiration, palpitations, and pallor. Blood pressure on initial examination was within normal limits, but when the patient came in later with a headache, it was 180/135 mm Hg. Urinary vanillylmandelic acid (VMA) levels were elevated. Roughly, what percentage of the tumors causing this pattern is malignant?
Decreased activity of type I 5'-monodeiodinase could lead to which of the following physiological effects?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 721: An 18-year-old girl presents with weakness. She reports high stress levels due to academic demands, with most of her time dedicated to studying, dieting, and exercising. Physical examination reveals a height of 5'8", a weight of 85 lbs, and she appears unwell. Her blood pressure is 85/70 mm Hg, heart rate is 50/min, and there is prominent muscle wasting. What is this patient most likely at risk for?
- A. Renal failure
- B. Ventricular tachyarrhythmias (Correct Answer)
- C. Diabetes Mellitus
- D. Hyperthermia
Explanation: ### Explanation This clinical presentation is classic for **Anorexia Nervosa (AN)**. The patient exhibits a low BMI (approx. 12.9 kg/m²), bradycardia, hypotension, and a preoccupation with dieting/exercise despite being severely underweight [2]. **1. Why Ventricular Tachyarrhythmias is Correct:** The most common cause of death in patients with severe Anorexia Nervosa is **cardiac complications**. Chronic starvation leads to the depletion of cardiac muscle mass (myocardial atrophy), resulting in a **prolonged QTc interval** [2]. This electrical instability, often exacerbated by electrolyte imbalances (like hypokalemia or hypomagnesemia from purging or malnutrition), predisposes the patient to life-threatening **ventricular tachyarrhythmias**, such as Torsades de Pointes, and sudden cardiac death. **2. Why the Other Options are Incorrect:** * **Renal Failure:** While dehydration can cause pre-renal azotemia, acute renal failure is a less common cause of immediate mortality compared to cardiac arrest in AN. * **Diabetes Mellitus:** Anorexia is associated with **hypoglycemia** due to depleted glycogen stores and lack of precursors for gluconeogenesis [3], not hyperglycemia or diabetes. * **Hyperthermia:** Patients with AN typically suffer from **hypothermia** due to the loss of insulating adipose tissue and a lowered basal metabolic rate [1], which is a compensatory mechanism for starvation. **Clinical Pearls for NEET-PG:** * **Refeeding Syndrome:** The most dangerous complication during treatment. It is characterized by **Hypophosphatemia**, which can lead to heart failure and seizures. * **Hormonal Profile in AN:** Low GnRH, low LH/FSH (Hypogonadotropic hypogonadism), and normal to high Cortisol. * **Physical Sign:** Look for **Lanugo hair** (fine, downy hair) and **Russell’s sign** (calluses on knuckles from self-induced vomiting).
Question 722: Which of the following is not involved in Multiple Endocrine Neoplasia type 2 (MEN II) syndrome?
- A. Pituitary tumor (Correct Answer)
- B. Medullary carcinoma of the thyroid
- C. Pheochromocytoma
- D. Parathyroid adenoma
Explanation: Multiple Endocrine Neoplasia (MEN) syndromes are autosomal dominant disorders characterized by tumors involving two or more endocrine glands [1]. To answer this question correctly, one must distinguish between the components of MEN 1 and MEN 2. **Why Pituitary Tumor is the correct answer:** Pituitary tumors (most commonly prolactinomas) are a hallmark of **MEN 1 (Wermer’s Syndrome)**, often remembered by the "3 Ps": **P**ituitary, **P**arathyroid, and **P**ancreas. They are **not** a component of MEN 2. **Analysis of incorrect options (Components of MEN 2):** * **Medullary Carcinoma of Thyroid (MTC):** This is the most consistent feature of MEN 2 (occurring in nearly 100% of cases). It arises from parafollicular C-cells. * **Pheochromocytoma:** Found in approximately 50% of patients with MEN 2A and 2B. They are frequently bilateral and occur in the adrenal medulla. * **Parathyroid Adenoma/Hyperplasia:** This is seen in **MEN 2A** (Sipple Syndrome) but is notably absent in MEN 2B. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Mutation:** MEN 1 is caused by a mutation in the *MEN1* gene (Menin protein), while MEN 2 (both 2A and 2B) is caused by a gain-of-function mutation in the **RET proto-oncogene**. * **MEN 2B vs. 2A:** MEN 2B is characterized by MTC and Pheochromocytoma (like 2A) but includes **Mucosal neuromas** and a **Marfanoid habitus** instead of parathyroid involvement. * **Screening:** In patients with a known *RET* mutation, prophylactic thyroidectomy is often indicated due to the high virulence of MTC.
Question 723: Which of the following conditions can lead to increased T4 levels?
- A. Hyperparathyroidism
- B. X-linked TBG deficiency (Correct Answer)
- C. Familial dysalbuminemic hyperthyroxinemia
- D. Low T3 syndrome
Explanation: The concentration of total T4 in the blood is dependent on two factors: the amount of hormone produced by the thyroid gland and the concentration of thyroid-binding proteins (primarily **Thyroid-Binding Globulin or TBG**) [1]. **Why Option B is Correct:** In **X-linked TBG deficiency**, there is a genetic decrease in the levels of TBG. Since >99% of T4 is protein-bound, a decrease in binding proteins leads to a **decrease in Total T4** levels [1]. However, the free T4 (fT4) and TSH levels remain normal, and the patient remains euthyroid [1]. *(Note: The question asks which condition leads to increased T4; however, based on standard medical physiology, TBG deficiency leads to **decreased** total T4. If the provided key marks B as correct, it likely refers to a scenario where the
Question 724: Which of the following is an anti-androgenic drug?
- A. Bicalutamide (Correct Answer)
- B. Oxymetholone
- C. Raloxifene
- D. Stanozolol
Explanation: ### Explanation **Correct Option: A. Bicalutamide** Bicalutamide is a potent, non-steroidal **androgen receptor antagonist** [1]. It works by competitively inhibiting the binding of dihydrotestosterone (DHT) and testosterone to their receptors [1]. In clinical practice, it is primarily used in the management of metastatic prostate cancer, often combined with GnRH analogues to prevent the "testosterone flare" phenomenon. **Analysis of Incorrect Options:** * **B. Oxymetholone:** This is a synthetic **androgen/anabolic steroid** [2]. Instead of blocking androgens, it mimics them. It is clinically used to treat certain types of anemia (by stimulating erythropoietin) and muscle-wasting conditions [2]. * **C. Raloxifene:** This is a **Selective Estrogen Receptor Modulator (SERM)**. It acts as an estrogen agonist in the bone (preventing osteoporosis) and an antagonist in the breast and uterus. It has no direct activity on androgen receptors. * **D. Stanozolol:** Similar to oxymetholone, this is an **anabolic steroid** (derived from DHT) [2]. It is often discussed in the context of performance-enhancing drug abuse and the treatment of hereditary angioedema. **NEET-PG High-Yield Pearls:** * **Classification of Anti-androgens:** 1. **Receptor Antagonists:** Flutamide, Bicalutamide (longer half-life, less hepatotoxic), Enzalutamide, and Spironolactone [1]. 2. **5-alpha Reductase Inhibitors:** Finasteride, Dutasteride (used in BPH and male pattern baldness). 3. **Synthesis Inhibitors:** Ketoconazole, Abiraterone. * **Clinical Note:** Bicalutamide is preferred over Flutamide due to its once-daily dosing and significantly lower risk of hepatotoxicity [1]. * **Side Effects:** Common side effects of anti-androgens include gynecomastia, hot flashes, and decreased libido.
Question 725: Which of the following findings is FALSE regarding primary adrenal hyperplasia?
- A. Hyponatremia (Correct Answer)
- B. Hypernatremia
- C. Water retention
- D. Hypokalemia
Explanation: Primary adrenal hyperplasia (a form of **Primary Hyperaldosteronism** or Conn’s syndrome) is characterized by the autonomous overproduction of aldosterone from the adrenal cortex. To answer this question, one must understand the physiological actions of aldosterone on the distal convoluted tubule and collecting ducts of the kidney. **Why Hyponatremia is FALSE (The Correct Answer):** Aldosterone acts on the principal cells to increase the reabsorption of sodium ($Na^+$) and the secretion of potassium ($K^+$) and hydrogen ions ($H^+$) [2]. Consequently, primary hyperaldosteronism leads to **hypernatremia** (or high-normal sodium levels), not hyponatremia [3]. Therefore, Option A is the false statement. **Analysis of Other Options:** * **B. Hypernatremia:** This is a classic finding due to excessive sodium retention mediated by the ENaC channels [2]. * **C. Water Retention:** Sodium reabsorption creates an osmotic gradient that pulls water into the intravascular compartment. This leads to ECF volume expansion and hypertension [1]. (Note: Clinically, edema is usually absent due to the "Aldosterone Escape" phenomenon) [1]. * **D. Hypokalemia:** Excessive aldosterone causes profound renal potassium wasting, which is a hallmark of the disease, often presenting as muscle weakness or cardiac arrhythmias [2]. **NEET-PG High-Yield Pearls:** 1. **Aldosterone Escape:** Despite water retention, patients with primary hyperaldosteronism do not typically have edema because increased stretch in the atria releases **ANP (Atrial Natriuretic Peptide)**, which promotes secondary natriuresis [1]. 2. **Metabolic Profile:** Look for the triad of **Hypertension, Hypokalemia, and Metabolic Alkalosis** [3]. 3. **Screening:** The best initial test is the **Aldosterone-to-Renin Ratio (ARR)**. In primary disease, Aldosterone is high, and Renin is suppressed. 4. **Spironolactone:** This is the medical treatment of choice as it acts as a direct aldosterone antagonist.
Question 726: A 56-year-old man is diagnosed with the metabolic syndrome, which consists of hypertension, insulin resistance, dyslipidemia, and abdominal obesity. He has no prior history of cardiac or vascular disease and is otherwise well. His fasting T-chol is 270 mg/dL, HDL 50 mg/dL, LDL 150 mg/dL, and triglycerides 150 mg/dL. His Framingham risk calculation approximates a 10-year risk for cardiac events of 10%-20%. For the above patient with dyslipidemia, select the most appropriate treatment.
- A. Fibric acid derivatives (clofibrate, gemfibrozil)
- B. Nicotinic acid
- C. Bile acid-binding resins (cholestyramine, colestipol)
- D. Hepatic hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (lovastatin, simvastatin, pravastatin) (Correct Answer)
Explanation: ### Explanation The patient presents with **Metabolic Syndrome** and a moderate-to-high cardiovascular risk profile (10-year Framingham risk of 10-20%). In such patients, the primary goal of lipid management is the reduction of **LDL cholesterol** to prevent atherosclerotic cardiovascular disease (ASCVD). **1. Why Option D is Correct:** **HMG-CoA reductase inhibitors (Statins)** are the first-line therapy for dyslipidemia in patients with elevated LDL and significant cardiovascular risk [1, 3]. They work by inhibiting the rate-limiting enzyme in hepatic cholesterol synthesis, leading to an up-regulation of LDL receptors and increased clearance of LDL from the blood [2]. Statins are the only class of lipid-lowering drugs proven to consistently reduce mortality and major cardiovascular events in both primary and secondary prevention [1]. **2. Why Other Options are Incorrect:** * **A. Fibric acid derivatives:** These are primarily used to lower **Triglycerides** (by activating PPAR-alpha) [3]. Since this patient’s triglycerides are normal (150 mg/dL), fibrates are not the initial drug of choice. * **B. Nicotinic acid (Niacin):** While it increases HDL and lowers LDL/triglycerides, it is poorly tolerated due to side effects (flushing, hyperglycemia, hyperuricemia) and has not shown incremental benefit in reducing CV outcomes when added to statins [3]. * **C. Bile acid-binding resins:** These are less potent than statins at lowering LDL and can actually **increase triglyceride levels**. They are generally reserved as second-line or adjunct therapy [3]. **Clinical Pearls for NEET-PG:** * **Metabolic Syndrome Criteria (ATP III):** Requires 3 of 5: Abdominal obesity, TG ≥150 mg/dL, HDL <40 (men)/<50 (women), BP ≥130/85 mmHg, Fasting Glucose ≥100 mg/dL. * **Statin Side Effects:** Myopathy (check CK if symptomatic) and hepatotoxicity (check LFTs before starting) [1]. * **High-Yield Fact:** Statins are most effective when taken at night (except Rosuvastatin/Atorvastatin) because cholesterol synthesis peaks during sleep.
Question 727: Which of the following is a feature of primary hyperaldosteronism?
- A. Pedal edema
- B. Polyuria
- C. Hyperkalemia
- D. Hypertension (Correct Answer)
Explanation: **Primary Hyperaldosteronism (Conn’s Syndrome)** is characterized by the autonomous overproduction of aldosterone from the adrenal cortex, leading to increased sodium reabsorption and potassium excretion [1]. ### **Explanation of the Correct Answer** **D. Hypertension:** This is the hallmark of the condition. Excess aldosterone acts on the mineralocorticoid receptors in the distal convoluted tubule and collecting ducts, increasing the activity of ENaC channels [2]. This leads to **sodium and water retention**, expanding the extracellular fluid volume and increasing peripheral vascular resistance, resulting in secondary hypertension. ### **Explanation of Incorrect Options** * **A. Pedal Edema:** Despite sodium and water retention, clinically significant edema is typically **absent** due to the **"Aldosterone Escape" phenomenon** [1]. Increased atrial natriuretic peptide (ANP) levels and pressure natriuresis lead to the excretion of excess sodium, preventing overt volume overload. * **B. Polyuria:** While chronic hypokalemia can cause nephrogenic diabetes insipidus leading to polyuria, it is a secondary complication rather than a primary diagnostic feature. Hypertension is the more consistent and defining clinical finding. * **C. Hyperkalemia:** This is incorrect because aldosterone promotes **potassium secretion** into the urine [2]. Therefore, **hypokalemia** (not hyperkalemia) is the classic biochemical finding [1], often associated with metabolic alkalosis. ### **NEET-PG High-Yield Pearls** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A **PAC:PRA ratio > 20-30** is highly suggestive. * **Confirmatory Test:** Oral or Intravenous Saline Suppression Test (failure to suppress aldosterone levels). * **Most Common Cause:** Adrenal Adenoma (Conn’s Syndrome), followed by Bilateral Adrenal Hyperplasia. * **Triad:** Hypertension, Hypokalemia, and Metabolic Alkalosis [1].
Question 728: Which of the following is NOT true of Verner Morrison syndrome (WDHA syndrome)?
- A. It is associated with Vipoma.
- B. It presents with secretory diarrhea.
- C. It can be associated with ganglioneuroblastoma.
- D. It is associated with hyperkalemia. (Correct Answer)
Explanation: Verner-Morrison Syndrome, also known as WDHA syndrome (Watery Diarrhea, Hypokalemia, and Achlorhydria), is caused by a VIPoma—a rare neuroendocrine tumor that secretes excessive Vasoactive Intestinal Peptide (VIP) [1]. ### Explanation of the Correct Option **D. It is associated with hyperkalemia (Incorrect Statement):** This is the correct answer because VIPoma actually causes profound hypokalemia (low potassium), not hyperkalemia. VIP stimulates the massive secretion of fluids and electrolytes (including potassium and bicarbonate) into the intestinal lumen, leading to significant fecal potassium loss. ### Explanation of Incorrect Options * **A. Associated with VIPoma:** This is true. The syndrome is primarily caused by a non-beta islet cell tumor of the pancreas that secretes VIP [1]. * **B. Presents with secretory diarrhea:** This is true. The diarrhea is "tea-colored," voluminous (>3L/day), and persists even during fasting (a hallmark of secretory diarrhea). * **C. Associated with ganglioneuroblastoma:** This is true. While 90% of VIPomas are pancreatic in adults, in children, the syndrome is often associated with neurogenic tumors like ganglioneuroblastomas or ganglioneuromas. ### High-Yield Clinical Pearls for NEET-PG * **Achlorhydria/Hypochlorhydria:** VIP inhibits gastric acid secretion, leading to low stomach acid. * **Metabolic Acidosis:** Due to the loss of bicarbonate in the stool (though some cases may show alkalosis). * **Hypercalcemia and Hyperglycemia:** These are frequently associated metabolic findings in VIPoma patients. * **Diagnosis:** Elevated fasting plasma VIP levels (>200 pg/mL). * **Management:** Initial stabilization involves aggressive fluid/electrolyte replacement and **Octreotide** (somatostatin analog) to inhibit VIP release. Surgical resection is the definitive treatment. * **MEN-1 Association:** Approximately 5% of VIPomas are associated with Multiple Endocrine Neoplasia Type 1.
Question 729: A 30-year-old patient presents with intermittent, severe headaches accompanied by perspiration, palpitations, and pallor. Blood pressure on initial examination was within normal limits, but when the patient came in later with a headache, it was 180/135 mm Hg. Urinary vanillylmandelic acid (VMA) levels were elevated. Roughly, what percentage of the tumors causing this pattern is malignant?
- A. 1%
- B. 10% (Correct Answer)
- C. 50%
- D. 90%
Explanation: ### Explanation The clinical presentation of paroxysmal hypertension, headache, perspiration, and palpitations (the classic triad) strongly suggests **Pheochromocytoma**, a catecholamine-secreting tumor of the adrenal medulla. The diagnosis is further supported by elevated urinary vanillylmandelic acid (VMA) levels. **Why 10% is Correct:** Pheochromocytoma is famously known as the **"10% Tumor"** because it historically follows a specific rule of percentages. According to this rule, approximately **10% of pheochromocytomas are malignant**. Malignancy is defined not by histology, but by the presence of chromaffin tissue in non-chromaffin sites (e.g., bones, liver, or lymph nodes). **Analysis of Incorrect Options:** * **A (1%):** This is too low. While some rare endocrine syndromes have lower malignancy rates, 10% is the established figure for pheochromocytoma. * **C (50%):** This is incorrect for adrenal pheochromocytoma. However, it is worth noting that the risk of malignancy is significantly higher (up to 35-40%) in extra-adrenal paragangliomas. * **D (90%):** This is incorrect; the vast majority (90%) of these tumors are benign. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of 10" for Pheochromocytoma:** * 10% are Malignant. * 10% are Bilateral (more common in familial cases like MEN 2A/2B). * 10% are Extra-adrenal (Paragangliomas; most common site is the **Organ of Zuckerkandl**). * 10% occur in Children. * 10% are Familial (though modern genetics suggests this may be as high as 30-40%). * **Diagnosis:** The most sensitive screening test is **plasma free metanephrines**. * **Management:** Always start **Alpha-blockade (Phenoxybenzamine)** before Beta-blockade to prevent a hypertensive crisis caused by unopposed alpha-receptor stimulation.
Question 730: Decreased activity of type I 5'-monodeiodinase could lead to which of the following physiological effects?
- A. Increased plasma triiodothyronine (T3)
- B. Increased plasma reverse T3 (Correct Answer)
- C. Decreased plasma thyroxine T4
- D. Increased TSH
Explanation: The thyroid gland primarily secretes **Thyroxine (T4)**, which is a pro-hormone. To become biologically active, T4 must be converted into **Triiodothyronine (T3)**. This process is mediated by **deiodinase enzymes**: 1. **Type I and Type II 5'-deiodinase:** These remove iodine from the *outer* ring of T4 to produce active **T3**. 2. **Type III deiodinase:** This removes iodine from the *inner* ring of T4 to produce inactive **reverse T3 (rT3)**. **Why Option B is Correct:** Type I 5'-monodeiodinase is responsible for the peripheral conversion of T4 to T3 and also for the **clearance (degradation) of rT3**. When the activity of this enzyme decreases, two things happen: less T4 is converted to T3, and less rT3 is broken down. This leads to a characteristic rise in plasma **reverse T3** levels. **Analysis of Incorrect Options:** * **Option A:** T3 levels would **decrease**, not increase, because the conversion from T4 is impaired [1]. * **Option C:** T4 levels usually remain **normal or slightly elevated** because its peripheral utilization/conversion is blocked. * **Option D:** TSH typically remains **normal** in these scenarios (like Euthyroid Sick Syndrome) because Type II deiodinase in the pituitary remains active, maintaining local T3 levels and feedback inhibition [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Euthyroid Sick Syndrome:** Characterized by low T3, high rT3, and normal TSH. It is the most common clinical scenario involving decreased Type I deiodinase activity (seen in starvation, trauma, or severe illness). * **Drugs inhibiting Type I deiodinase:** Propylthiouracil (PTU), Propranolol, Glucocorticoids, and Amiodarone. * **Selenium:** This trace element is a crucial cofactor for deiodinase enzymes (selenoproteins). Deficiency can impair T4 to T3 conversion.
Practice by Chapter
Diabetes Mellitus
Practice Questions
Thyroid Disorders
Practice Questions
Adrenal Gland Disorders
Practice Questions
Pituitary Disorders
Practice Questions
Calcium and Bone Metabolism
Practice Questions
Reproductive Endocrinology
Practice Questions
Lipid Disorders
Practice Questions
Endocrine Hypertension
Practice Questions
Multiple Endocrine Neoplasia
Practice Questions
Obesity and Metabolic Syndrome
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Neuroendocrine Tumors
Practice Questions
Endocrine Emergencies
Practice Questions
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