Endocrinology — MCQs
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An overweight 48-year-old male presents with complaints of increased thirst and frequent urination. Laboratory examination reveals a blood glucose level of 180 mg/dL. The patient's past medical history is unremarkable, except for an anaphylactic reaction that occurred one year ago when he was given trimethoprim-sulfamethoxazole for a sinus infection. Based on this information, which of the following agents should be prescribed?
When the patient is asked to look upwards with the head fixed, there is an absence of wrinkling on the forehead. This clinical finding is known as:
Which of the following is NOT typically seen in myxedema coma?
A 60-year-old male presented with skin hyperpigmentation, central obesity, violet striae, and proximal myopathy. His blood pressure is 160/90 mmHg. Lab studies show hypokalemic metabolic alkalosis. Which of the following statements is true regarding this condition?
What is the treatment of Diabetes Insipidus?
In diabetes mellitus, which of the following complications are NOT found?
Chvostek sign is seen in:
Which of the following is not a feature of Sipple syndrome?
Vitamin D resistant rickets occurs due to all EXCEPT:
A smoker presented with altered sensorium. His blood osmolality was found to be 240 mOsm/kg, urine osmolality 340 mOsm/kg, and serum Na+ is 122 mEq/L. What is the most likely diagnosis?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 831: An overweight 48-year-old male presents with complaints of increased thirst and frequent urination. Laboratory examination reveals a blood glucose level of 180 mg/dL. The patient's past medical history is unremarkable, except for an anaphylactic reaction that occurred one year ago when he was given trimethoprim-sulfamethoxazole for a sinus infection. Based on this information, which of the following agents should be prescribed?
- A. Chlorpropamide
- B. Glipizide
- C. Glucagon
- D. Metformin (Correct Answer)
Explanation: The patient presents with classic symptoms of Type 2 Diabetes Mellitus (polyuria, polydipsia) and a blood glucose level of 180 mg/dL. According to current clinical guidelines, **Metformin** is the first-line pharmacological therapy for Type 2 Diabetes, especially in overweight patients, due to its efficacy, weight-neutrality (or modest weight loss), and low risk of hypoglycemia [1]. **Why the other options are incorrect:** * **Chlorpropamide & Glipizide (Options A & B):** These are **Sulfonylureas**. The patient has a documented history of an **anaphylactic reaction to trimethoprim-sulfamethoxazole**. Sulfonylureas contain a sulfonamide moiety; while cross-reactivity between antibiotic sulfonamides and non-antibiotic sulfonamides is debated, it is generally contraindicated or used with extreme caution in patients with a history of severe (anaphylactic) sulfa allergies. Furthermore, Metformin remains the preferred initial agent over sulfonylureas [1]. * **Glucagon (Option C):** Glucagon is used to treat severe hypoglycemia. Prescribing it to a patient with hyperglycemia (180 mg/dL) would worsen their clinical state. **NEET-PG High-Yield Pearls:** * **Mechanism of Action (Metformin):** Primarily inhibits hepatic gluconeogenesis by activating AMP-activated protein kinase (AMPK) [1]. * **Side Effects:** Most common are GI upset (diarrhea, nausea) [1]. The most serious, though rare, is **Lactic Acidosis**. * **Contraindications:** Metformin should be avoided in patients with significant renal impairment (eGFR <30 mL/min/1.73m²) due to the risk of lactic acidosis. * **Sulfa Allergy Cross-reactivity:** Always be cautious with Sulfonylureas, Carbonic anhydrase inhibitors (Acetazolamide), and Loop diuretics (Furosemide) in patients with severe sulfa allergies.
Question 832: When the patient is asked to look upwards with the head fixed, there is an absence of wrinkling on the forehead. This clinical finding is known as:
- A. Joffroy's sign (Correct Answer)
- B. Von Graefe's sign
- C. Moebius sign
- D. Dalrymple's sign
Explanation: The clinical finding described is **Joffroy’s sign**, a characteristic ocular manifestation of **Graves' ophthalmopathy** (Thyroid Eye Disease). **1. Why Joffroy’s Sign is Correct:** In patients with hyperthyroidism, there is often a combination of sympathetic overactivity and infiltrative changes in the extraocular muscles [1]. Joffroy’s sign refers to the **absence of forehead wrinkling** when the patient attempts to look upward with the head fixed. This occurs because the patient relies on the superior rectus muscle rather than the frontalis muscle, or due to the inherent muscle weakness/rigidity associated with thyrotoxicosis. **2. Analysis of Incorrect Options:** * **Von Graefe’s sign:** This refers to **lid lag**. When the patient is asked to look slowly downward, the upper eyelid lags behind the movement of the globe, exposing the white sclera above the cornea. * **Moebius sign:** This is the **inability to maintain convergence** of the eyes when looking at a near object, resulting from weakness of the medial rectus muscles. * **Dalrymple’s sign:** This is the **widening of the palpebral fissures** (staring look) caused by the retraction of the upper eyelids in the primary position of gaze. **3. High-Yield Clinical Pearls for NEET-PG:** * **Stellwag’s sign:** Infrequent or incomplete blinking. * **Enroth’s sign:** Edema of the eyelids. * **Pathophysiology:** These signs are primarily due to overactivity of the **Müller’s muscle** (sympathetic stimulation) and autoimmune-mediated inflammation of orbital tissues [2]. * **Diagnosis:** While these signs suggest thyrotoxicosis, the most specific sign for Graves' disease (vs. other causes of hyperthyroidism) is **Exophthalmos** (proptosis) [1].
Question 833: Which of the following is NOT typically seen in myxedema coma?
- A. Hypothermia
- B. Tachycardia (Correct Answer)
- C. Hypotension
- D. Hyponatremia
Explanation: **Explanation:** Myxedema coma is a life-threatening complication of severe, untreated hypothyroidism. It is characterized by a global slowing of metabolic processes. **1. Why Tachycardia is the correct answer:** In severe hypothyroidism, there is a marked decrease in metabolic rate and sympathetic activity. This leads to **bradycardia** (slow heart rate), not tachycardia [1]. The heart muscle also suffers from decreased contractility and reduced stroke volume. Therefore, tachycardia is inconsistent with the clinical presentation of myxedema coma. **2. Why the other options are wrong:** * **Hypothermia (A):** This is a hallmark feature. Due to the lack of thyroid hormone, thermogenesis is impaired. Patients often present with temperatures below 35°C (95°F). * **Hypotension (C):** Reduced cardiac output and decreased vascular tone lead to low blood pressure. This can progress to shock if not treated promptly. * **Hyponatremia (D):** This is frequently seen due to an increase in Antidiuretic Hormone (ADH) secretion (SIADH-like picture) and reduced free water clearance by the kidneys. **Clinical Pearls for NEET-PG:** * **Precipitating Factors:** Sepsis, cold exposure, myocardial infarction, or sedative use. * **Classic Triad:** Altered mental status (coma/lethargy), hypothermia, and a precipitating event. * **Treatment:** Immediate IV Levothyroxine (T4) and/or Liothyronine (T3). **Crucial:** Always administer **IV Hydrocortisone** before thyroid hormone replacement to avoid precipitating an adrenal crisis (as the patient may have concomitant adrenal insufficiency). * **Lab findings:** High TSH, low Free T4, and often hypoglycemia.
Question 834: A 60-year-old male presented with skin hyperpigmentation, central obesity, violet striae, and proximal myopathy. His blood pressure is 160/90 mmHg. Lab studies show hypokalemic metabolic alkalosis. Which of the following statements is true regarding this condition?
- A. Basal ACTH level is likely to be low.
- B. Circulating corticotropin-releasing hormone is likely to be elevated.
- C. Pituitary magnetic resonance imaging (MRI) will visualize all ACTH-secreting tumors.
- D. Serum potassium level <3.3 mmol/L is suggestive of ectopic ACTH production. (Correct Answer)
Explanation: ### Explanation The patient presents with classic features of **Cushing’s Syndrome** (central obesity, striae, proximal myopathy, hypertension) [3]. However, the presence of **hypokalemic metabolic alkalosis** is a critical diagnostic clue. **1. Why Option D is Correct:** In most cases of pituitary-origin Cushing’s disease, mineralocorticoid effects are mild. However, in **Ectopic ACTH Syndrome** (often due to Small Cell Lung Cancer or Bronchial Carcinoid), ACTH levels are extremely high. This leads to massive cortisol production that overwhelms the **11β-HSD2 enzyme** in the kidney. Excess cortisol then binds to mineralocorticoid receptors, causing severe potassium depletion. A serum potassium **<3.3 mmol/L** is found in ~70% of ectopic cases but only <10% of pituitary cases, making it a strong marker for ectopic production. **2. Why the Other Options are Incorrect:** * **Option A:** In both Cushing’s disease (pituitary) and ectopic ACTH syndrome, the **basal ACTH level is high** (ACTH-dependent) [2]. A low ACTH would suggest an adrenal tumor [2]. * **Option B:** Circulating CRH is usually **low** due to negative feedback from high cortisol, except in the extremely rare case of an ectopic CRH-secreting tumor. * **Option C:** Pituitary MRI has limited sensitivity; approximately **30–50% of ACTH-secreting microadenomas** are too small to be detected on standard MRI. **Clinical Pearls for NEET-PG:** * **Screening Test:** 24-hour urinary free cortisol or Low-Dose Dexamethasone Suppression Test (LDDST) [1]. * **Differentiation:** High-Dose Dexamethasone Suppression Test (HDDST) and CRH stimulation test typically show suppression/response in **Cushing’s Disease** but *not* in ectopic ACTH syndrome. * **Gold Standard:** Inferior Petrosal Sinus Sampling (IPSS) is the most reliable way to differentiate pituitary from ectopic sources.
Question 835: What is the treatment of Diabetes Insipidus?
- A. Antidiuretic Hormone (ADH) (Correct Answer)
- B. Thiazide diuretics
- C. Loop diuretics
- D. Insulin
Explanation: Diabetes Insipidus (DI) is characterized by the inability to concentrate urine due to either a deficiency of **Antidiuretic Hormone (ADH/Vasopressin)** from the posterior pituitary (Central DI) or resistance to its action in the kidneys (Nephrogenic DI) [3]. **Why Option A is Correct:** The primary treatment for Central DI is hormone replacement. **Desmopressin (dDAVP)**, a synthetic analogue of ADH, is the drug of choice [1]. It acts on V2 receptors in the renal collecting ducts to increase water reabsorption, thereby reducing polyuria and correcting hypernatremia [3]. **Why Other Options are Incorrect:** * **B. Thiazide Diuretics:** While used in *Nephrogenic* DI to create a mild hypovolemia-induced increase in proximal sodium/water reabsorption, they are not the primary physiological replacement for the underlying hormone deficiency. * **C. Loop Diuretics:** These (e.g., Furosemide) inhibit water reabsorption in the Thick Ascending Limb and would worsen the polyuria and dehydration seen in DI. * **D. Insulin:** This is the treatment for Diabetes Mellitus (hyperglycemia), which is pathophysiologically unrelated to Diabetes Insipidus [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Water Deprivation Test:** The gold standard for diagnosis [1]. If urine osmolality increases >50% after exogenous ADH administration, it confirms **Central DI**. If there is little to no response, it is **Nephrogenic DI**. * **Drug-Induced Nephrogenic DI:** Most commonly caused by **Lithium**. * **Treatment of Nephrogenic DI:** Amiloride (especially for Lithium-induced cases), Thiazides, and NSAIDs (which inhibit prostaglandins that antagonize ADH).
Question 836: In diabetes mellitus, which of the following complications are NOT found?
- A. Encephalopathy, retinopathy, and diabetes
- B. Myelopathy, retinopathy, and diabetes
- C. Encephalopathy, myelopathy, and myopathy (Correct Answer)
- D. Encephalopathy and myelopathy
Explanation: Diabetes Mellitus (DM) primarily affects the nervous system through **peripheral neuropathy** (sensory, motor, and autonomic) [1] and the vascular system through microvascular (retinopathy, nephropathy) [3] and macrovascular (stroke, MI) complications. **Why Option C is Correct:** The central nervous system (CNS) and skeletal muscles are relatively spared from direct diabetic damage compared to the peripheral nerves. * **Encephalopathy:** While acute metabolic crises (DKA, HHS) or hypoglycemia cause altered sensorium, chronic "diabetic encephalopathy" is not a recognized classical complication of DM. * **Myelopathy:** Spinal cord involvement (myelopathy) is not a feature of diabetes. * **Myopathy:** Diabetes affects nerves (neuropathy), not the primary muscle fibers (myopathy). Although "Diabetic Amyotrophy" exists, it is actually a proximal neuropathy (radiculoplexus neuropathy) rather than a primary myopathy. **Analysis of Incorrect Options:** * **Options A & B:** These are incorrect because they include **Retinopathy**, which is a hallmark microvascular complication of DM caused by chronic hyperglycemia leading to retinal ischemia and neovascularization [3]. * **Option D:** While it correctly identifies encephalopathy and myelopathy as non-complications, it is less comprehensive than Option C, which includes myopathy. **High-Yield NEET-PG Pearls:** * **Most common neuropathy:** Distal Symmetrical Polyneuropathy (DSPN) – "Glove and Stocking" distribution [1]. * **Diabetic Amyotrophy:** Presents as severe pain followed by weakness and atrophy of proximal thigh muscles (L2-L4 distribution). * **Mononeuropathy:** The **3rd Cranial Nerve** (Oculomotor) is most commonly affected; characteristically, **pupillary reflex is spared** (due to the peripheral location of parasympathetic fibers). * **Autonomic Neuropathy:** Look for resting tachycardia, orthostatic hypotension, gastroparesis, and gustatory sweating [2].
Question 837: Chvostek sign is seen in:
- A. Hypercalcemia
- B. Hypothyroidism (Correct Answer)
- C. Insulinoma
- D. Diabetes mellitus
Explanation: **Explanation:** The **Chvostek sign** is a clinical indicator of hyperexcitability of the facial nerve, typically associated with **hypocalcemia**. In the context of this question, **Hypothyroidism** is the correct answer because it is frequently associated with **Hypoparathyroidism** (either due to autoimmune destruction or as a post-surgical complication of thyroidectomy). A deficiency in Parathyroid Hormone (PTH) leads to low serum calcium levels, which decreases the threshold for nerve depolarization [1]. * **Mechanism:** Tapping the facial nerve at the angle of the jaw (anterior to the tragus) causes ipsilateral twitching of the facial muscles (nose or lips). **Analysis of Options:** * **Hypothyroidism (Correct):** Often co-exists with hypocalcemia via associated hypoparathyroidism or as part of polyglandular autoimmune syndromes. * **Hypercalcemia (Incorrect):** High calcium levels actually stabilize neuronal membranes, leading to decreased excitability and diminished reflexes. * **Insulinoma & Diabetes Mellitus (Incorrect):** These are disorders of glucose metabolism and do not typically affect serum ionized calcium levels or neuromuscular irritability. **NEET-PG High-Yield Pearls:** 1. **Trousseau Sign:** Carpopedal spasm induced by inflating a BP cuff above systolic pressure for 3 minutes. It is **more sensitive and specific** than Chvostek sign for latent tetany. 2. **Other causes of Chvostek Sign:** Hypomagnesemia, metabolic alkalosis (which decreases ionized calcium), and hyperventilation. 3. **False Positives:** Approximately 10% of healthy individuals with normal calcium levels may exhibit a positive Chvostek sign. 4. **ECG in Hypocalcemia:** Look for **prolonged QT interval**, a classic exam favorite [1].
Question 838: Which of the following is not a feature of Sipple syndrome?
- A. Pheochromocytoma
- B. Medullary carcinoma thyroid
- C. Hyperthyroidism (Correct Answer)
- D. Hyperparathyroidism
Explanation: **Explanation:** Sipple Syndrome, also known as **Multiple Endocrine Neoplasia Type 2A (MEN 2A)**, is an autosomal dominant disorder caused by a germline mutation in the **RET proto-oncogene** [1]. It is characterized by a specific triad of endocrine tumors. **Why Hyperthyroidism is the Correct Answer:** Hyperthyroidism is **not** a component of MEN 2A [2]. While patients with Sipple syndrome develop thyroid pathology, it is specifically **Medullary Thyroid Carcinoma (MTC)**, which arises from the parafollicular C-cells (secreting calcitonin) rather than the follicular cells. Therefore, it does not typically result in a hypermetabolic thyrotoxic state. **Analysis of Incorrect Options:** * **Medullary Carcinoma Thyroid (MTC):** This is the most common feature (seen in >90% of cases) and is often the first manifestation. It is usually bilateral and multicentric. * **Pheochromocytoma:** Occurs in approximately 50% of patients [2]. It is frequently bilateral and usually develops after the thyroid pathology. * **Hyperparathyroidism:** Seen in about 10–20% of patients, typically due to parathyroid hyperplasia rather than a single adenoma [3]. **High-Yield Clinical Pearls for NEET-PG:** * **MEN 2A (Sipple Syndrome):** MTC + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN 2B (Wermer-Morrison):** MTC + Pheochromocytoma + Mucosal Neuromas + Marfanoid Habitus (Note: No Parathyroid involvement). * **Screening:** All first-degree relatives of a patient with MTC should be screened for the **RET mutation** [3]. * **Prophylactic Thyroidectomy:** Recommended in children carrying the RET mutation to prevent the inevitable development of MTC [3].
Question 839: Vitamin D resistant rickets occurs due to all EXCEPT:
- A. Alpha-1-hydroxylase deficiency (Correct Answer)
- B. Renal tubular acidosis
- C. Fanconi syndrome
- D. Drugs
Explanation: **Explanation:** The term **Vitamin D Resistant Rickets (VDRR)** refers to conditions where rickets occurs despite normal or high intake of Vitamin D, typically due to defects in phosphate metabolism or end-organ resistance [1]. **Why Option A is the Correct Answer:** **Alpha-1-hydroxylase deficiency** is the underlying cause of **Vitamin D Dependent Rickets (VDDR) Type 1**, not Vitamin D *Resistant* Rickets. In this condition, the body cannot convert 25(OH)D into its active form, 1,25(OH)₂D. It is classified as "dependent" because it can be successfully treated with physiological doses of active Vitamin D (Calcitriol). **Analysis of Incorrect Options:** * **Renal Tubular Acidosis (RTA):** Distal (Type 1) and Proximal (Type 2) RTA cause chronic metabolic acidosis, which leads to hypercalciuria and phosphate wasting. This results in rickets that does not respond to standard Vitamin D therapy, classifying it as a "resistant" form. * **Fanconi Syndrome:** This is a generalized dysfunction of the proximal tubule leading to phosphaturia. The resulting hypophosphatemia causes rickets that is resistant to Vitamin D alone and requires phosphate supplementation. * **Drugs:** Long-term use of certain drugs, most notably **Anticonvulsants** (like Phenytoin or Phenobarbital), induces hepatic cytochrome P450 enzymes. This accelerates the catabolism of Vitamin D into inactive metabolites, leading to a resistant state. **High-Yield Clinical Pearls for NEET-PG:** * **X-linked Hypophosphatemic Rickets:** The most common cause of Vitamin D Resistant Rickets (due to PHEX gene mutation and increased FGF-23) [1]. * **VDDR Type 2:** Caused by a mutation in the **Vitamin D Receptor (VDR)**; often presents with **alopecia**. * **Biochemical Hallmark of VDRR:** Low serum phosphate with normal serum calcium and normal/high 1,25(OH)₂D (except in FGF-23 mediated types).
Question 840: A smoker presented with altered sensorium. His blood osmolality was found to be 240 mOsm/kg, urine osmolality 340 mOsm/kg, and serum Na+ is 122 mEq/L. What is the most likely diagnosis?
- A. Diabetes insipidus
- B. Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) (Correct Answer)
- C. Renal tubular acidosis
- D. Cerebellar degeneration
Explanation: ### Explanation The clinical presentation and laboratory findings are classic for **Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH)**. **Why SIADH is the correct diagnosis:** The patient presents with the hallmark triad of SIADH: 1. **Hypotonic Hyponatremia:** Serum Na+ is 122 mEq/L (Normal: 135–145) and serum osmolality is 240 mOsm/kg (Normal: 275–295) [2]. 2. **Inappropriately Concentrated Urine:** Urine osmolality (340 mOsm/kg) is greater than serum osmolality (>100 mOsm/kg), indicating that ADH is acting despite low plasma tonicity [2]. 3. **Clinical Context:** The patient is a smoker, which strongly suggests an underlying **Small Cell Carcinoma of the Lung**, a well-known paraneoplastic cause of ectopic ADH production [1]. The altered sensorium is a direct neurological consequence of severe hyponatremia. **Why the other options are incorrect:** * **Diabetes Insipidus (DI):** This is the functional opposite of SIADH. It presents with hypernatremia and dilute urine (low urine osmolality) due to a lack of ADH or its effect. * **Renal Tubular Acidosis (RTA):** RTA typically presents with normal anion gap metabolic acidosis and electrolyte imbalances like hypokalemia, not isolated hypotonic hyponatremia. * **Cerebellar Degeneration:** While this can be a paraneoplastic syndrome associated with lung cancer, it presents with ataxia and dysarthria, not the biochemical profile of hyponatremia and low serum osmolality [1]. **NEET-PG High-Yield Pearls:** * **Euvolemic Hyponatremia:** SIADH is the most common cause of euvolemic hyponatremia [2]. * **Diagnostic Criteria:** Must exclude renal, adrenal (Addison's), and thyroid (hypothyroidism) dysfunction. * **Management:** Fluid restriction is the first-line treatment [2]. For symptomatic/severe cases, use hypertonic (3%) saline. * **Caution:** Rapid correction of hyponatremia can lead to **Osmotic Demyelination Syndrome** (Central Pontine Myelinolysis) [2]. Rule of thumb: Do not exceed 8–10 mEq/L in 24 hours [2].
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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