Endocrinology — MCQs
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Nephrocalcinosis is associated with all of the following, except?
A 40-year-old male presented with a 2-month history of watery diarrhea and periodic abdominal pain. Examination revealed a warm face, facial engorgement with blood, itching, sweating, and a diastolic murmur in the left 4th intercostal space, parasternal, which increased with inspiration. Lab findings showed increased 5-HIAA secretion in urine. Colonoscopy was performed, and a biopsy of a mass stained positive for chromogranin. With which of the following syndromes may the above condition be associated?
A 54-year-old obese man diagnosed with NIDDM one year ago is on glipizide and metformin. He also takes propranolol and nifedipine for hypertension, and recently started naproxen for severe osteoarthritis. His current BP is 154/92. His BUN is 29 mg/dL and creatinine is 1.8 mg/dL, both of which were normal one year prior. Which medication is most likely responsible for the increase in BUN and creatinine?
What is the investigation of choice for diagnosing primary hypothyroidism?
Primary hypothyroidism is seen in all EXCEPT?
Which of the following is NOT a feature of hypothyroidism?
In which of the following conditions would the patient most likely be normotensive?
A young woman presents with secondary amenorrhea and galactorrhea. MRI shows a pituitary tumor of less than 10 mm diameter. What is the recommended treatment?
A 49-year-old female presents with a non-healing ulcer on the right medial malleolus. On examination, there is symmetrical loss of sensation in both extremities. She also complains of recurrent vaginal discharge and irregular menstrual cycles. She reports experiencing hot flashes. What is the most likely pathological finding to be seen in her peripheral nerves?
Which of the following medications should not be given to a diabetic patient?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 881: Nephrocalcinosis is associated with all of the following, except?
- A. Hypoparathyroidism (Correct Answer)
- B. Multiple myeloma
- C. Milk-alkali syndrome
- D. Hyperparathyroidism
Explanation: **Explanation:** Nephrocalcinosis refers to the deposition of calcium salts (calcium phosphate or calcium oxalate) within the renal parenchyma. It is primarily driven by states of **hypercalcemia** and **hypercalciuria**. **1. Why Hypoparathyroidism is the correct answer:** In **Hypoparathyroidism**, there is a deficiency of Parathyroid Hormone (PTH). This leads to **hypocalcemia** and decreased urinary calcium excretion (initially) [1]. Since nephrocalcinosis requires an excess of calcium to precipitate in the renal tissue, a low-calcium state like hypoparathyroidism does not cause it. *Note:* While treatment of hypoparathyroidism with Vitamin D and Calcium can *induce* hypercalciuria and subsequent nephrocalcinosis [2], the disease state itself is not an associative cause. **2. Analysis of Incorrect Options:** * **Hyperparathyroidism (Option D):** This is the most common cause of nephrocalcinosis. Elevated PTH increases bone resorption and intestinal calcium absorption, leading to hypercalcemia and hypercalciuria [1], [3]. * **Multiple Myeloma (Option B):** Malignant plasma cells produce osteoclast-activating factors, leading to extensive bone destruction and significant hypercalcemia, which promotes renal calcium deposition [1]. * **Milk-Alkali Syndrome (Option C):** Characterized by the triad of hypercalcemia, metabolic alkalosis, and renal insufficiency due to excessive ingestion of calcium and absorbable antacids [1]. The resulting hypercalcemia leads to nephrocalcinosis. **Clinical Pearls for NEET-PG:** * **Distinction:** Nephrocalcinosis (parenchymal deposition) is different from Nephrolithiasis (stones in the pelvicalyceal system), though they often coexist [3]. * **Medullary Nephrocalcinosis:** The most common form (95%). Key causes include Distal Renal Tubular Acidosis (Type 1 RTA), Medullary Sponge Kidney, and Hyperparathyroidism [3]. * **Cortical Nephrocalcinosis:** Rare; typically follows severe renal insult like Acute Tubular Necrosis (ATN), cortical necrosis, or Alport syndrome.
Question 882: A 40-year-old male presented with a 2-month history of watery diarrhea and periodic abdominal pain. Examination revealed a warm face, facial engorgement with blood, itching, sweating, and a diastolic murmur in the left 4th intercostal space, parasternal, which increased with inspiration. Lab findings showed increased 5-HIAA secretion in urine. Colonoscopy was performed, and a biopsy of a mass stained positive for chromogranin. With which of the following syndromes may the above condition be associated?
- A. Sipple syndrome
- B. Wermer syndrome (Correct Answer)
- C. Neurofibromatosis
- D. Tuberous sclerosis
Explanation: ### Explanation **1. Analysis of the Correct Answer (Wermer Syndrome)** The clinical presentation describes **Carcinoid Syndrome**, characterized by the triad of watery diarrhea, cutaneous flushing (facial engorgement/warmth), and right-sided valvular heart disease [1]. The diastolic murmur in the left 4th intercostal space that increases with inspiration indicates **Tricuspid Stenosis** (right-sided murmurs increase with inspiration—Carman’s sign). Elevated urinary **5-HIAA** (a metabolite of serotonin) and **Chromogranin A** positivity are diagnostic markers for neuroendocrine tumors (NETs). **Wermer Syndrome (MEN 1)** is characterized by the "3 Ps": * **P**arathyroid hyperplasia (most common) * **P**ancreatic islet cell tumors (e.g., Gastrinoma, Insulinoma) * **P**ituitary adenomas * *Crucially*, MEN 1 is also associated with **Carcinoid tumors** (bronchial, thymic, or gastric/GI), which can lead to the symptoms described. **2. Why Other Options are Incorrect** * **Sipple Syndrome (MEN 2A):** Characterized by Medullary Thyroid Carcinoma, Pheochromocytoma, and Parathyroid hyperplasia. It is not typically associated with GI carcinoid tumors. * **Neurofibromatosis (NF1):** While associated with some neuroendocrine tumors like Pheochromocytoma or Somatostatinoma (duodenal), it is not the primary syndrome associated with the classic MEN-related carcinoid presentation. * **Tuberous Sclerosis:** A neurocutaneous syndrome (Ash-leaf spots, Shagreen patches, Angiomyolipomas) not linked to serotonin-secreting carcinoid tumors. **3. Clinical Pearls for NEET-PG** * **Carcinoid Heart Disease:** Typically affects the **right side** (Tricuspid/Pulmonary valves) because the lungs contain monoamine oxidase (MAO) which degrades serotonin before it reaches the left heart [1]. Left-sided involvement suggests a bronchial carcinoid or a right-to-left shunt. * **Diagnosis:** Best initial test is 24-hour urinary 5-HIAA. Most sensitive imaging is **Octreoscan** (Somatostatin receptor scintigraphy). * **Treatment:** **Octreotide** (Somatostatin analog) is used to manage symptoms before surgery.
Question 883: A 54-year-old obese man diagnosed with NIDDM one year ago is on glipizide and metformin. He also takes propranolol and nifedipine for hypertension, and recently started naproxen for severe osteoarthritis. His current BP is 154/92. His BUN is 29 mg/dL and creatinine is 1.8 mg/dL, both of which were normal one year prior. Which medication is most likely responsible for the increase in BUN and creatinine?
- A. Glipizide
- B. Metformin
- C. Naproxen (Correct Answer)
- D. Nifedipine
Explanation: ### Explanation The correct answer is **Naproxen**. #### 1. Why Naproxen is the Correct Answer Naproxen is a Non-Steroidal Anti-Inflammatory Drug (NSAID) [1]. NSAIDs inhibit the enzyme cyclooxygenase (COX), leading to decreased synthesis of **prostaglandins** (specifically PGE2 and PGI2). In the kidneys, prostaglandins are essential for maintaining renal blood flow by causing **vasodilation of the afferent arteriole** [1]. In patients with underlying risk factors (diabetes, hypertension, or older age), the inhibition of these vasodilatory prostaglandins leads to afferent arteriolar vasoconstriction. This reduces the glomerular filtration rate (GFR), resulting in **Prerenal Azotemia**, characterized by an increase in Blood Urea Nitrogen (BUN) and Creatinine. #### 2. Why the Other Options are Incorrect * **Glipizide (Sulfonylurea):** Primarily causes hypoglycemia and weight gain; it does not have direct nephrotoxic effects. * **Metformin (Biguanide):** While metformin must be dose-adjusted or discontinued in renal failure to prevent **lactic acidosis**, it does not *cause* the rise in creatinine itself. * **Nifedipine (Calcium Channel Blocker):** CCBs are generally neutral or protective regarding renal hemodynamics and do not cause acute elevations in BUN/Creatinine. #### 3. NEET-PG High-Yield Pearls * **Triple Whammy:** Be cautious of the "Triple Whammy" effect on the kidney: **NSAIDs** (constrict afferent arteriole) + **ACE inhibitors/ARBs** (dilate efferent arteriole) + **Diuretics** (reduce plasma volume). This combination significantly increases the risk of Acute Kidney Injury (AKI). * **Analgesic Nephropathy:** Chronic use of NSAIDs can lead to **Chronic Interstitial Nephritis** and **Renal Papillary Necrosis** [1]. * **Metformin Guideline:** In NEET-PG, remember that Metformin is contraindicated if the eGFR is <30 mL/min/1.73m² due to the risk of lactic acidosis.
Question 884: What is the investigation of choice for diagnosing primary hypothyroidism?
- A. Decreased free T3
- B. Decreased free T4
- C. Elevated TSH (Correct Answer)
- D. Anti-TPO antibodies
Explanation: Explanation: In **Primary Hypothyroidism**, the pathology lies within the thyroid gland itself, leading to reduced production of thyroid hormones [4]. Due to the intact negative feedback loop, the anterior pituitary responds to low circulating T4 levels by increasing the secretion of **Thyroid Stimulating Hormone (TSH)** [1]. **1. Why Elevated TSH is the Correct Answer:** TSH is the most sensitive and specific screening test for primary hypothyroidism [2]. Because of the logarithmic relationship between TSH and free T4, even a minor decrease in T4 results in a significant, disproportionate rise in TSH. Therefore, an elevated TSH is the first biochemical marker to change, often rising even when T4 levels are still within the normal range (Subclinical Hypothyroidism) [2]. **2. Why the other options are incorrect:** * **Decreased free T3:** T3 is not a sensitive indicator of hypothyroidism and should not be requested [2]. The body compensates by increasing the peripheral conversion of T4 to T3; thus, T3 levels often remain normal even in significant disease. * **Decreased free T4:** While low fT4 confirms overt hypothyroidism, it is not the "investigation of choice" because it may remain normal in early or subclinical stages [2]. * **Anti-TPO antibodies:** These are used to determine the *etiology* (e.g., Hashimoto’s Thyroiditis) [3] rather than to diagnose the functional state of hypothyroidism itself. **Clinical Pearls for NEET-PG:** * **Best Screening Test:** Serum TSH. * **Best Monitoring Parameter:** Serum TSH (checked 6–8 weeks after starting Levothyroxine) [3]. * **Secondary (Central) Hypothyroidism:** TSH will be low or inappropriately normal, and fT4 will be low [2]. In this specific case, TSH is *not* a reliable diagnostic tool. * **Subclinical Hypothyroidism:** Elevated TSH with a normal free T4 [2].
Question 885: Primary hypothyroidism is seen in all EXCEPT?
- A. Iodine deficiency
- B. Iodine excess
- C. Lithium
- D. Bexarotene (Correct Answer)
Explanation: **Explanation:** The key to this question lies in distinguishing between **Primary** and **Central (Secondary/Tertiary)** hypothyroidism [1]. **Correct Answer: D. Bexarotene** Bexarotene is a selective Retinoid X Receptor (RXR) agonist used in the treatment of cutaneous T-cell lymphoma. It causes **Central Hypothyroidism** by suppressing the thyrotropin ̢-subunit gene expression, leading to a profound suppression of TSH secretion. Unlike primary hypothyroidism, patients on Bexarotene will show low T4 levels with a low or inappropriately normal TSH [1]. **Why the other options are incorrect (Causes of Primary Hypothyroidism):** * **A. Iodine Deficiency:** The most common cause of primary hypothyroidism worldwide. Lack of iodine prevents the synthesis of T3 and T4, leading to a compensatory rise in TSH. * **B. Iodine Excess:** High doses of iodine can inhibit the organification of iodine and the synthesis of thyroid hormones, a phenomenon known as the **Wolff-Chaikoff effect**. While usually transient, it can lead to permanent primary hypothyroidism in patients with underlying thyroid disease. * **C. Lithium:** Lithium inhibits the release of thyroid hormones from the thyroid gland. It is a well-known pharmacological cause of primary hypothyroidism and goiter. **High-Yield Clinical Pearls for NEET-PG:** * **Wolff-Chaikoff Effect:** Autoregulation where excess iodine inhibits thyroid hormone synthesis. * **Jod-Basedow Phenomenon:** Iodine-induced hyperthyroidism (opposite of Wolff-Chaikoff). * **Amiodarone:** A high-yield drug that can cause both hypothyroidism (via Wolff-Chaikoff) and hyperthyroidism (Type 1 and Type 2) [2]. * **TSH Levels:** In Primary Hypothyroidism, TSH is **elevated**. In Central Hypothyroidism (e.g., Bexarotene, Pituitary adenoma), TSH is **low or normal** [1].
Question 886: Which of the following is NOT a feature of hypothyroidism?
- A. Obesity
- B. Hypertension
- C. High TSH levels
- D. Increased risk of infections (Correct Answer)
Explanation: Hypothyroidism is characterized by a generalized slowing of metabolic processes. The correct answer is **Option D (Increased risk of infections)** because, unlike Diabetes Mellitus or Cushing’s syndrome, hypothyroidism is not typically associated with impaired immunity or a significantly increased risk of infections. **Why the other options are features of Hypothyroidism:** * **Obesity (Option A):** A decrease in the Basal Metabolic Rate (BMR) leads to weight gain [2]. This is primarily due to fluid retention (accumulation of glycosaminoglycans) and decreased thermogenesis, rather than just fat accumulation. * **Hypertension (Option B):** While hyperthyroidism causes systolic hypertension, hypothyroidism often causes **diastolic hypertension**. This occurs due to increased systemic vascular resistance and arterial stiffness. * **High TSH levels (Option C):** In primary hypothyroidism (the most common form), the loss of negative feedback from low T4/T3 levels leads the pituitary to secrete compensatory high levels of TSH [3]. **Clinical Pearls for NEET-PG:** * **Wolff-Chaikoff Effect:** Hypothyroidism induced by excessive iodine ingestion (e.g., amiodarone). * **Myxedema Coma:** The most severe form of hypothyroidism, presenting with hypothermia, bradycardia, and altered sensorium. * **Dyslipidemia:** Hypothyroidism is a common secondary cause of hypercholesterolemia (due to decreased LDL receptor expression [1]). * **Anemia:** Most commonly normocytic normochromic, but can be macrocystic (if associated with Pernicious Anemia in Schmidt’s Syndrome).
Question 887: In which of the following conditions would the patient most likely be normotensive?
- A. Primary hyperparathyroidism
- B. Hypothyroidism
- C. Cushing syndrome
- D. Bartter syndrome (Correct Answer)
Explanation: **Explanation:** The correct answer is **Bartter syndrome**. This condition is a rare autosomal recessive renal tubular disorder characterized by defective salt reabsorption in the thick ascending limb of the loop of Henle. This leads to salt wasting, which triggers the Renin-Angiotensin-Aldosterone System (RAAS). While aldosterone levels are high (secondary hyperaldosteronism), the patient remains **normotensive or hypotensive** because the primary defect is volume depletion due to salt loss. **Analysis of Options:** * **Primary Hyperparathyroidism:** Approximately 20–40% of these patients have hypertension [1]. The mechanism is multifactorial, involving hypercalcemia-induced increase in peripheral vascular resistance and potential renal impairment. * **Hypothyroidism:** Often associated with **diastolic hypertension**. This occurs due to increased peripheral vascular resistance and low-turnover states despite a decrease in cardiac output. * **Cushing Syndrome:** Hypertension is present in over 80% of cases. It is caused by increased mineralocorticoid activity of cortisol, enhanced sensitivity to catecholamines, and activation of the RAAS. **High-Yield Clinical Pearls for NEET-PG:** * **Bartter vs. Gitelman:** Bartter syndrome presents early in life with polyuria and growth retardation (mimics Loop diuretics). Gitelman syndrome presents later with prominent hypomagnesemia and hypocalciuria (mimics Thiazides). * **Key Triad of Bartter:** Hypokalemia, Metabolic Alkalosis, and **Normotension** (despite high renin/aldosterone). * **Differential Diagnosis:** If a patient has hypokalemia, metabolic alkalosis, and **hypertension**, think of Conn’s syndrome (Primary Hyperaldosteronism) or Liddle syndrome.
Question 888: A young woman presents with secondary amenorrhea and galactorrhea. MRI shows a pituitary tumor of less than 10 mm diameter. What is the recommended treatment?
- A. Hormonal therapy for withdrawal bleeding
- B. Radiotherapy
- C. Chemotherapy
- D. Bromocriptine (Correct Answer)
Explanation: **Explanation:** The clinical presentation of secondary amenorrhea and galactorrhea in a young woman, combined with an MRI showing a pituitary tumor <10 mm (Microadenoma), is classic for a **Prolactinoma**. [1] **1. Why Bromocriptine is Correct:** Prolactinomas are unique among pituitary tumors because **medical management is the first-line treatment**, regardless of size. [1] Dopamine agonists like **Bromocriptine** or Cabergoline act on D2 receptors in the pituitary to inhibit prolactin secretion and shrink the tumor mass. [1] They effectively restore menses, stop galactorrhea, and achieve tumor shrinkage in over 80% of patients. **2. Why Incorrect Options are Wrong:** * **Hormonal therapy (Option A):** While OCPs can induce withdrawal bleeding, they do not address the underlying hyperprolactinemia or the pituitary tumor. In fact, estrogen can theoretically stimulate lactotroph hyperplasia. * **Radiotherapy (Option B):** This is reserved for refractory cases or aggressive macroadenomas that fail both medical and surgical therapy due to long-term risks like hypopituitarism. * **Chemotherapy (Option C):** Cytotoxic chemotherapy is not used for benign pituitary adenomas. Temozolomide is only considered for rare, malignant pituitary carcinomas. **3. NEET-PG High-Yield Pearls:** * **Drug of Choice:** While Bromocriptine is the traditional answer, **Cabergoline** is now preferred in clinical practice due to higher efficacy and better tolerability (longer half-life). * **Micro vs. Macro:** Microadenomas are <10 mm; Macroadenomas are ≥10 mm. [1] * **Surgery (Transsphenoidal):** Indicated only if the patient is intolerant to dopamine agonists or if the tumor is resistant to medical therapy. * **Hook Effect:** In very large macroadenomas, extremely high prolactin levels can cause a false low reading in lab assays; serial dilution is required for diagnosis.
Question 889: A 49-year-old female presents with a non-healing ulcer on the right medial malleolus. On examination, there is symmetrical loss of sensation in both extremities. She also complains of recurrent vaginal discharge and irregular menstrual cycles. She reports experiencing hot flashes. What is the most likely pathological finding to be seen in her peripheral nerves?
- A. Axonal neuropathy (Correct Answer)
- B. Acute inflammation
- C. Wallerian degeneration
- D. Lymphocytic infiltration in the endoneurium
Explanation: **Explanation:** The clinical presentation describes a 49-year-old female with classic signs of **Diabetes Mellitus (DM)**. The non-healing ulcer and symmetrical sensory loss indicate **Diabetic Peripheral Neuropathy (DPN)**, while recurrent vaginal discharge (likely Candidiasis) is a common opportunistic infection in hyperglycemic states. Her hot flashes and irregular cycles suggest she is perimenopausal, a period where metabolic syndrome and DM often manifest. **Why Axonal Neuropathy is Correct:** In Diabetes Mellitus, the primary pathological process in peripheral nerves is **distal symmetric axonal degeneration**. Chronic hyperglycemia leads to the accumulation of advanced glycation end-products (AGEs) and increased oxidative stress, causing microvascular damage (vasa nervorum ischemia) and direct metabolic injury to the axons. This results in a "dying-back" phenomenon where the longest axons are affected first (stocking-and-glove distribution). **Why Other Options are Incorrect:** * **Acute inflammation:** This is characteristic of vasculitic neuropathies or certain infections, not the chronic metabolic damage seen in DM. * **Wallerian degeneration:** This refers to the process where a nerve fiber degenerates distal to a site of **acute transection** or focal crush injury. While it involves axonal loss, it is not the primary mechanism of chronic diabetic neuropathy. * **Lymphocytic infiltration:** This is the hallmark of **Guillain-Barré Syndrome (GBS)** or Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP), which are autoimmune and demyelinating in nature. **Clinical Pearls for NEET-PG:** * **Most common type of Diabetic Neuropathy:** Distal Symmetrical Polyneuropathy (Sensory > Motor). * **Earliest sign:** Loss of vibratory sense (tested with a 128 Hz tuning fork) and loss of ankle jerk. * **Pathological hallmark:** Axonal degeneration and "onion bulb" formations (due to repetitive demyelination/remyelination in some cases), but **axonal loss** is the predominant feature. * **Microscopy:** Thickening of the basement membrane of endoneurial capillaries.
Question 890: Which of the following medications should not be given to a diabetic patient?
- A. Propranolol (Correct Answer)
- B. Theophylline
- C. Digoxin
- D. Glyburide
Explanation: **Explanation:** The correct answer is **Propranolol**. **Why Propranolol is contraindicated:** Propranolol is a non-selective beta-blocker that poses two significant risks to diabetic patients: 1. **Masking Hypoglycemia:** The most critical danger is that it masks the sympathetic "warning signs" of hypoglycemia, such as tachycardia, palpitations, and tremors. A patient may slip into a severe hypoglycemic coma without realizing their blood sugar has dropped. (Note: Sweating is mediated by cholinergic receptors and is usually not masked). 2. **Inhibition of Glycogenolysis:** Beta-2 receptors mediate the breakdown of glycogen into glucose in the liver. By blocking these receptors, Propranolol impairs the body's compensatory mechanism to raise blood glucose levels during a hypoglycemic episode, leading to prolonged and more severe hypoglycemia. **Analysis of Incorrect Options:** * **Theophylline:** A methylxanthine used in asthma/COPD. While it can cause mild hyperglycemia in toxicity, it is not contraindicated in diabetes. * **Digoxin:** A cardiac glycoside used in heart failure and atrial fibrillation. It has no significant effect on glucose metabolism. * **Glyburide:** This is a second-generation Sulfonylurea. It is a standard treatment for Type 2 Diabetes (though used less frequently now due to the risk of hypoglycemia). **NEET-PG High-Yield Pearls:** * If a beta-blocker must be used in a diabetic patient (e.g., post-MI), **Cardioselective (Beta-1) blockers** like Metoprolol or Atenolol are preferred, as they have less effect on glucose metabolism. * **Sweating** is the only sympathetic symptom of hypoglycemia not masked by beta-blockers. * Other drugs causing hyperglycemia: Thiazides, Corticosteroids, and Atypical Antipsychotics (e.g., Olanzapine).
Practice by Chapter
Diabetes Mellitus
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Thyroid Disorders
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Adrenal Gland Disorders
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Pituitary Disorders
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Calcium and Bone Metabolism
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Reproductive Endocrinology
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Lipid Disorders
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Endocrine Hypertension
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Multiple Endocrine Neoplasia
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Obesity and Metabolic Syndrome
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Neuroendocrine Tumors
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Endocrine Emergencies
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