Endocrinology — MCQs

A 62-year-old Type 2 diabetic patient presents with complaints of malaise, myalgias, respiratory distress, and increased somnolence. Laboratory examination reveals an anion gap of 26mmol/L, HCO3- of 17 mmol/L, and an arterial blood pH of 7.27. Suspecting lactic acidosis, which of the following medications is the patient most likely receiving?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 161: Which of the following is true about hypercalcemia?

A. Treatment of the primary cause (Correct Answer)
B. Malignancy does not produce hypercalcemia
C. Intravenous fluids with furosemide are given
D. Amidarone is not effective

Explanation: Hypercalcemia is a common clinical scenario in internal medicine, most frequently caused by **Primary Hyperparathyroidism (PHPT)** in the outpatient setting and **Malignancy** in hospitalized patients [1]. **1. Why Option A is Correct:** The definitive management of hypercalcemia always focuses on **treating the underlying cause**. For instance, if the cause is PHPT, surgical parathyroidectomy is the cure [1]. If it is due to sarcoidosis, steroids are used. While acute stabilization is necessary for severe cases, the hypercalcemia will recur unless the primary pathology is addressed. **2. Analysis of Incorrect Options:** * **Option B:** This is incorrect. Malignancy is the **second most common cause** of hypercalcemia. It occurs via three mechanisms: secretion of PTHrP (Squamous cell CA), local osteolytic bone destruction (Breast CA, Multiple Myeloma), or 1,25-dihydroxyvitamin D production (Lymphomas) [1]. * **Option C:** While IV fluids (Normal Saline) are the first-line treatment to restore volume, the routine use of **Furosemide is no longer recommended** unless the patient is in fluid overload (heart failure/renal failure). It can worsen dehydration and electrolyte imbalances if used prematurely. * **Option D:** This is a distractor. **Amiodarone** is associated with thyroid dysfunction (hypo/hyperthyroidism) but is not a standard treatment modality for hypercalcemia. **Clinical Pearls for NEET-PG:** * **First-line treatment:** Aggressive hydration with 0.9% Normal Saline [1]. * **Drug of choice for Malignancy-associated hypercalcemia:** Intravenous Bisphosphonates (e.g., Zoledronic acid) [1]. * **ECG finding:** Shortened QT interval (mnemonic: "Short cow" - Short QT in Hypercalcemia). * **Milk-Alkali Syndrome:** Characterized by the triad of hypercalcemia, metabolic alkalosis, and renal insufficiency [1].

Question 162: Congenital adrenal hyperplasia due to 11 beta hydroxylase deficiency presents with all the following except?

A. Metabolic acidosis (Correct Answer)
B. Hypokalemia
C. Hypernatremia
D. Hypertension

Explanation: In **11β-hydroxylase deficiency**, the final step of cortisol synthesis is blocked. This leads to an accumulation of precursor steroids, specifically **11-deoxycorticosterone (DOC)** and **11-deoxycortisol**. [1] **1. Why Metabolic Acidosis is the Correct Answer:** 11-deoxycorticosterone (DOC) is a potent **mineralocorticoid**. Excess DOC acts on the renal collecting ducts similarly to aldosterone, causing sodium retention and the excretion of potassium and hydrogen ions ($H^+$). The loss of $H^+$ ions leads to **Metabolic Alkalosis**, not acidosis. Therefore, metabolic acidosis is the "except" in this clinical presentation. **2. Why the other options are incorrect:** * **Hypertension (D) and Hypernatremia (C):** The mineralocorticoid effect of excess DOC causes significant water and sodium retention, leading to volume expansion and hypertension. This distinguishes 11β-hydroxylase deficiency from 21-hydroxylase deficiency (where salt-wasting and hypotension occur). [1] * **Hypokalemia (B):** Increased mineralocorticoid activity promotes potassium secretion into the urine, resulting in low serum potassium levels. **Clinical Pearls for NEET-PG:** * **The "Rule of 1s":** If the enzyme deficiency starts with **1** (11β-hydroxylase or 17α-hydroxylase), it causes **Hypertension** (due to mineralocorticoid excess). * **Virilization:** Since the block is below the androgen pathway, excess substrate is shunted toward androgens. This causes **ambiguous genitalia** in females and **precocious puberty** in males. [1] * **Differential:** 11β-hydroxylase deficiency presents with hypertension + virilization, whereas 17α-hydroxylase deficiency presents with hypertension + sexual infantilism (no androgens).

Question 163: Which type of thyroid carcinoma is associated with Multiple Endocrine Neoplasia (MEN) syndromes?

A. Follicular Carcinoma
B. Papillary Carcinoma
C. Medullary Carcinoma (Correct Answer)
D. Thyroid Lymphoma

Explanation: Explanation: **Medullary Thyroid Carcinoma (MTC)** is the correct answer because it originates from the **parafollicular C-cells**, which are neuroendocrine cells derived from the neural crest. These cells secrete calcitonin. Approximately 25% of MTC cases are hereditary and occur as part of **Multiple Endocrine Neoplasia (MEN) type 2A and 2B** syndromes, caused by germline mutations in the **RET proto-oncogene**. **Analysis of Incorrect Options:** * **A. Follicular Carcinoma:** This is a well-differentiated thyroid cancer derived from follicular cells. It typically spreads hematogenously (to bone/lungs) and is associated with iodine deficiency and RAS mutations, not MEN syndromes. * **B. Papillary Carcinoma:** The most common thyroid malignancy. It is associated with radiation exposure and BRAF mutations. While it is the most common thyroid cancer overall, it is not a component of MEN syndromes. * **D. Thyroid Lymphoma:** Usually a B-cell (MALT) lymphoma, it typically arises in the background of chronic autoimmune inflammation, such as **Hashimoto’s Thyroiditis**. **High-Yield NEET-PG Pearls:** * **MEN 2A:** MTC + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN 2B:** MTC + Pheochromocytoma + Mucosal Neuromas/Marfanoid habitus. * **Tumor Marker:** Calcitonin is used for diagnosis and monitoring recurrence. CEA is also often elevated. * **Amyloid Stroma:** Histologically, MTC is characterized by nests of cells in a prominent **amyloid stroma** (stained by Congo Red). * **Prophylaxis:** In families with known RET mutations, prophylactic thyroidectomy is often performed in early childhood.

Question 164: True about rickets?

A. Decreased alkaline phosphatase
B. Hyperphosphatemia
C. Hypophosphatemia (Correct Answer)
D. Hypophosphaturia

Explanation: Rickets is a disorder of defective mineralization of the osteoid matrix in growing bone, most commonly due to Vitamin D deficiency [1]. **Why Hypophosphatemia is Correct:** In Vitamin D deficiency, there is decreased intestinal absorption of Calcium ($Ca^{2+}$). This leads to **Secondary Hyperparathyroidism** (elevated PTH). PTH acts on the kidneys to increase calcium reabsorption but simultaneously **decreases phosphate reabsorption** in the proximal convoluted tubule (phosphaturia). This renal wasting of phosphate leads to **Hypophosphatemia**, which is a hallmark of rickets and a primary driver of impaired bone mineralization [1]. **Analysis of Incorrect Options:** * **A. Decreased alkaline phosphatase:** Incorrect. Serum Alkaline Phosphatase (ALP) is **elevated** in rickets due to increased osteoblastic activity attempting to compensate for the poor mineralization [1]. * **B. Hyperphosphatemia:** Incorrect. As explained, PTH-mediated renal excretion causes low, not high, serum phosphate levels [1]. * **D. Hypophosphaturia:** Incorrect. There is actually **Hyperphosphaturia** (increased phosphate in urine) because PTH inhibits the Na-Pi cotransporters in the renal tubules. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Craniotabes (softening of skull bones) [1]. * **Radiological Signs:** Cupping, fraying, and splaying of the metaphysis (best seen at the wrist or knee). * **Biochemical Profile:** Low/Normal Calcium, Low Phosphate, **High ALP (most sensitive marker)**, and High PTH [1]. * **Rachitic Rosary:** Palpable enlargement of the costochondral junctions [1]. * **Harrison’s Sulcus:** A horizontal groove along the lower border of the thorax corresponding to the insertion of the diaphragm.

Question 165: Which of the following tests is best for diagnosing carcinoid tumor?

A. 24-hour urinary 5-hydroxyindoleacetic acid (HIAA) (Correct Answer)
B. 24-hour urinary catecholamines
C. 24-hour urinary vanillylmandelic acid (VMA)
D. 24-hour urinary metanephrine levels

Explanation: ### Explanation **Correct Option: A. 24-hour urinary 5-hydroxyindoleacetic acid (5-HIAA)** **Medical Concept:** Carcinoid tumors are neuroendocrine tumors that frequently secrete excessive amounts of **serotonin (5-hydroxytryptamine)**. Serotonin is metabolized by the enzyme monoamine oxidase (MAO) and aldehyde dehydrogenase into **5-hydroxyindoleacetic acid (5-HIAA)**, which is then excreted in the urine. Measuring 5-HIAA in a 24-hour urine collection is the gold-standard biochemical screening test for diagnosing carcinoid syndrome. It has high specificity (approx. 90%) for the condition. **Analysis of Incorrect Options:** * **B, C, and D (Catecholamines, VMA, and Metanephrines):** These are metabolites of epinephrine and norepinephrine. They are used in the diagnostic workup of **Pheochromocytoma** and **Neuroblastoma**, not carcinoid tumors. Metanephrines (Option D) are currently considered the most sensitive screening test for Pheochromocytoma. **NEET-PG High-Yield Pearls:** * **Dietary Interference:** Patients must avoid serotonin-rich foods (bananas, walnuts, pineapples, avocados, tomatoes) for 24–48 hours before the 5-HIAA test to prevent false-positive results. * **Localization:** Once biochemically confirmed, the most sensitive imaging for localization is **Somatostatin Receptor Scintigraphy (OctreoScan)** or **68Ga-DOTATATE PET/CT** [1]. * **Clinical Triad:** Carcinoid syndrome (usually occurring with liver metastasis) presents with **flushing, diarrhea, and right-sided valvular heart disease** (tricuspid regurgitation/pulmonary stenosis) [1]. * **Chromogranin A:** This is a non-specific but useful serum marker for monitoring tumor burden and recurrence in neuroendocrine tumors [2].

Question 166: Which of the following statements regarding DeQuervain thyroiditis is true?

A. Low ESR
B. Infectious disorder
C. Increased radio-iodine uptake
D. Self-limiting condition (Correct Answer)

Explanation: **De Quervain Thyroiditis (Subacute Granulomatous Thyroiditis)** **Explanation of the Correct Answer:** De Quervain thyroiditis is a **self-limiting** inflammatory condition of the thyroid gland. It typically follows a predictable triphasic clinical course: an initial **thyrotoxic phase** (due to the release of preformed hormones from damaged follicles), followed by a transient **hypothyroid phase**, and finally **euthyroid recovery** within 2–6 months [1]. Treatment is primarily supportive, focusing on pain relief with NSAIDs or corticosteroids [1]. **Analysis of Incorrect Options:** * **A. Low ESR:** Incorrect. A **markedly elevated ESR** (often >50–100 mm/hr) and high C-reactive protein (CRP) are hallmark laboratory findings [1]. A "normal ESR" virtually excludes this diagnosis. * **B. Infectious disorder:** Incorrect. While it often follows a viral upper respiratory tract infection (e.g., Coxsackie, Mumps, Adenovirus), it is considered a **post-viral inflammatory** or immune-mediated response, not a direct infection of the gland itself. * **C. Increased radio-iodine uptake:** Incorrect. During the thyrotoxic phase, follicular destruction prevents the gland from trapping iodine [2]. Therefore, the **Radioactive Iodine Uptake (RAIU) is characteristically low/depressed** (<5%), which helps distinguish it from Graves' disease (where RAIU is high) [1]. **Clinical Pearls for NEET-PG:** * **Most Common Cause:** It is the most common cause of a **painful/tender thyroid gland**. * **Pathology:** Characterized by **multinucleated giant cells** and granulomatous inflammation on biopsy. * **HLA Association:** Strongly associated with **HLA-B35**. * **Key Diagnostic Clue:** A patient presenting with jaw/ear pain, fever, and a tender goiter following a "flu-like" illness.

Question 167: Which of the following is a surgical cause of hypercalcemia?

A. Hyperparathyroidism (Correct Answer)
B. Multiple Endocrine Neoplasia (MEN)
C. Hyperthyroidism
D. Pheochromocytoma

Explanation: **Explanation:** **Correct Answer: A. Hyperparathyroidism** Hyperparathyroidism (specifically Primary Hyperparathyroidism) is the most common cause of hypercalcemia in the outpatient setting. It is considered a **surgical cause** because the definitive treatment for symptomatic or meeting-criteria patients is a **parathyroidectomy** (removal of the overactive parathyroid gland/adenoma) [1]. The underlying mechanism involves the autonomous secretion of Parathyroid Hormone (PTH), which increases bone resorption, renal calcium reabsorption, and intestinal calcium absorption via Vitamin D activation [2]. **Analysis of Incorrect Options:** * **B. Multiple Endocrine Neoplasia (MEN):** While MEN syndromes (Type 1 and 2A) *feature* hyperparathyroidism, MEN itself is a genetic syndrome/predisposition rather than a single surgical cause [1]. Hyperparathyroidism is the manifestation within the syndrome that leads to hypercalcemia. * **C. Hyperthyroidism:** This is a medical cause of hypercalcemia [1]. Increased thyroid hormone levels lead to increased bone turnover, but the primary management is medical (antithyroid drugs) rather than surgical. * **D. Pheochromocytoma:** While associated with MEN 2 syndromes, pheochromocytoma itself causes hypertension via catecholamine excess, not hypercalcemia [1]. It only co-exists with hypercalcemia if hyperparathyroidism is also present (MEN 2A). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Hypercalcemia:** "Stones (renal), Bones (aches), Groans (abdominal pain/constipation), and Psychic Moans (depression/confusion)." * **Primary Hyperparathyroidism:** Most common cause is a **single solitary adenoma** (85%) [1]. * **Lab Findings:** High Serum Calcium, **Low Serum Phosphate**, and inappropriately High/Normal PTH [3]. * **ECG Finding:** Shortened QT interval is a classic sign of hypercalcemia.

Question 168: A young female presents with a history of abdominal pain, headache, nausea, and vomiting, along with sudden loss of movement of the right upper limb. What is the most likely diagnosis?

A. Conversion disorder
B. Migraine
C. Right lower limb paralysis
D. Acute intermittent porphyria (Correct Answer)

Explanation: **Explanation:** The clinical presentation of abdominal pain, neuropsychiatric symptoms (headache, nausea, vomiting), and motor weakness (monoparesis/paralysis) in a young female is a classic triad for **Acute Intermittent Porphyria (AIP)** [1]. **1. Why Acute Intermittent Porphyria is correct:** AIP is an autosomal dominant metabolic disorder caused by a deficiency of the enzyme **Porphobilinogen (PBG) deaminase** [2]. It typically presents in young females (often triggered by drugs, fasting, or hormonal changes) [1]. The "classic triad" includes: * **Abdominal Pain:** Severe, poorly localized, and out of proportion to physical findings (neurogenic pain) [1]. * **Autonomic Instability:** Nausea, vomiting, tachycardia, and hypertension [1]. * **Neurological Involvement:** Peripheral neuropathy (often motor), which can manifest as sudden limb weakness or paralysis, and CNS symptoms like headaches or seizures [1]. **2. Why other options are incorrect:** * **Conversion Disorder:** While it can present with sudden motor loss, it is a diagnosis of exclusion and does not typically account for severe systemic symptoms like acute abdominal pain and vomiting. * **Migraine:** While migraines cause headaches and nausea, they do not typically cause acute abdominal pain or focal limb paralysis (except in rare hemiplegic migraines, which wouldn't explain the abdominal crisis). * **Right lower limb paralysis:** This is a clinical sign, not a diagnosis. Furthermore, the question specifies right *upper* limb involvement. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Elevated urinary **PBG (Porphobilinogen)** and ALA levels during an attack. * **Urine Finding:** Urine may turn **"port-wine" red** upon standing (exposure to light). * **Management:** Intravenous **Hemin** (first-line) and high-dose **Glucose** (inhibits ALA synthase). * **Avoid:** Barbiturates and Sulfonamides, as they induce the cytochrome P450 system and precipitate attacks [1].

Question 169: What is the commonest cause of Cushing syndrome?

A. Adrenal adenoma
B. Adrenal carcinoma
C. Adrenal atrophy
D. Adrenal hyperplasia (Correct Answer)

Explanation: **Explanation:** The question asks for the commonest cause of **Cushing Syndrome** (the clinical state of hypercortisolism). **Why Adrenal Hyperplasia is correct:** Cushing syndrome is broadly classified into ACTH-dependent and ACTH-independent causes [1]. The most common cause overall is **Exogenous (Iatrogenic) steroid use** [1]. However, among endogenous causes, **Cushing Disease** (an ACTH-secreting pituitary adenoma) accounts for approximately 70% of cases. In Cushing Disease, the excess ACTH chronically stimulates both adrenal glands, leading to **bilateral adrenal hyperplasia**. Therefore, pathologically, adrenal hyperplasia is the most frequent finding in endogenous Cushing syndrome. **Analysis of Incorrect Options:** * **A & B (Adrenal Adenoma/Carcinoma):** These are ACTH-independent causes [1]. While they result in hypercortisolism, they are less common than pituitary-driven disease. Adrenal adenomas account for ~10-15% of cases, and carcinomas are rare (<5%). * **C (Adrenal Atrophy):** This occurs in the contralateral gland when a unilateral functional adrenal tumor is present, or bilaterally due to prolonged exogenous steroid use (due to negative feedback suppression of ACTH). It is a consequence, not a cause, of the syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause overall:** Iatrogenic (Exogenous steroids). * **Most common endogenous cause:** Cushing Disease (Pituitary Adenoma). * **Ectopic ACTH secretion:** Most commonly associated with Small Cell Carcinoma of the Lung; presents with rapid onset and severe hypokalemia [1]. * **Screening tests:** 24-hour urinary free cortisol, Low-dose dexamethasone suppression test (LDDST), or Late-night salivary cortisol [2]. * **Gold standard for source localization:** Inferior Petrosal Sinus Sampling (IPSS).

Question 170: A 62-year-old Type 2 diabetic patient presents with complaints of malaise, myalgias, respiratory distress, and increased somnolence. Laboratory examination reveals an anion gap of 26mmol/L, HCO3- of 17 mmol/L, and an arterial blood pH of 7.27. Suspecting lactic acidosis, which of the following medications is the patient most likely receiving?

A. Glucagon
B. Glyburide
C. Metformin (Correct Answer)
D. Miglitol

Explanation: **Explanation:** The patient presents with **Metformin-Associated Lactic Acidosis (MALA)**, characterized by a high anion gap metabolic acidosis (HAGMA), low pH, and non-specific symptoms like malaise and respiratory distress (Kussmaul breathing) [2]. **1. Why Metformin is correct:** Metformin, a biguanide, inhibits mitochondrial glycerophosphate dehydrogenase and the mitochondrial respiratory chain complex I. This leads to a shift toward anaerobic metabolism, increasing the conversion of pyruvate to **lactate** [2]. While rare, MALA typically occurs in patients with predisposing factors such as renal impairment, hepatic failure, or severe sepsis, where lactate clearance is reduced [2]. The laboratory findings (pH 7.27, HCO3- 17, and Anion Gap 26) are classic for this condition [1]. **2. Why other options are incorrect:** * **Glyburide:** A second-generation sulfonylurea. Its primary side effect is **hypoglycemia** and weight gain; it does not cause lactic acidosis. * **Miglitol:** An alpha-glucosidase inhibitor that acts locally in the GI tract to delay carbohydrate absorption. Its side effects are primarily gastrointestinal (flatulence, diarrhea). * **Glucagon:** A hormone used to treat severe hypoglycemia. It promotes glycogenolysis and gluconeogenesis, which would typically oppose the metabolic state of lactic acidosis. **Clinical Pearls for NEET-PG:** * **MALA Risk Factor:** The most significant risk factor for MALA is **renal insufficiency**. Metformin is generally contraindicated if the eGFR is <30 mL/min/1.73m². * **Management:** The treatment of choice for severe MALA with renal failure is **Hemodialysis**, which removes both metformin and lactate. * **Contrast Media:** Metformin should be withheld for 48 hours after procedures involving IV iodinated contrast to prevent acute kidney injury-induced MALA.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

Pituitary Disorders

Practice Questions

Calcium and Bone Metabolism

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Reproductive Endocrinology

Practice Questions

Lipid Disorders

Practice Questions

Endocrine Hypertension

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Neuroendocrine Tumors

Practice Questions

Endocrine Emergencies

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