Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 531: Pheochromocytoma predominantly secretes which hormone?

A. Epinephrine (Correct Answer)
B. Norepinephrine
C. Dopamine
D. DOPA

Explanation: The correct answer is **Epinephrine**. While the normal adrenal medulla secretes approximately 80% epinephrine and 20% norepinephrine, **pheochromocytomas** (tumors arising from chromaffin cells) are unique because they are the only catecholamine-secreting tumors capable of converting norepinephrine to epinephrine [1]. This occurs due to the presence of the enzyme **Phenylethanolamine N-methyltransferase (PNMT)**, which requires high local concentrations of cortisol (from the adjacent adrenal cortex) for induction. Since most pheochromocytomas are intra-adrenal, they have access to this cortisol and thus predominantly secrete epinephrine. **Analysis of Incorrect Options:** * **B. Norepinephrine:** While many extra-adrenal paragangliomas secrete norepinephrine exclusively (as they lack PNMT), the classic adrenal pheochromocytoma predominantly produces epinephrine. However, it is important to note that some tumors may secrete a mixture, but epinephrine remains the hallmark of adrenal origin. * **C. Dopamine:** Secretion of dopamine is rare and usually associated with malignant pheendocrine tumors rather than standard pheochromocytomas. * **D. DOPA:** This is a precursor in the catecholamine synthesis pathway. Elevated DOPA levels are typically markers of poorly differentiated or highly malignant neuroendocrine tumors rather than standard pheochromocytomas. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 10s:** 10% are bilateral, 10% are malignant, 10% are pediatric, and 10% are extra-adrenal (Paragangliomas). * **Diagnosis:** The most sensitive initial screening test is **plasma free metanephrines**; the most specific is **24-hour urinary metanephrines and VMA**. * **Localization:** **MIBG Scan** (I-131 or I-123) is used for localizing extra-adrenal or metastatic tumors [2]. * **Management:** Always start **Alpha-blockers (Phenoxybenzamine)** before Beta-blockers to prevent a hypertensive crisis (unopposed alpha-stimulation).

Question 532: Decreased teeth enamel is seen in all conditions below EXCEPT:

A. Hyperparathyroidism
B. Cushing syndrome
C. Fluorosis (Correct Answer)
D. Osteomalacia

Explanation: The question asks for the condition where decreased enamel (hypoplasia or thinning) is **NOT** seen. **1. Why Fluorosis is the correct answer:** In **Fluorosis**, there is actually an **increase** in the fluoride content of the enamel. While chronic excess fluoride leads to "mottling" (discoloration and pitting), the enamel itself is technically **hyper-mineralized** and more resistant to acid dissolution (caries) compared to normal enamel. Therefore, it is characterized by structural defects and staining rather than a decrease in the quantity of enamel. **2. Analysis of Incorrect Options:** * **Hyperparathyroidism:** Excess Parathyroid Hormone (PTH) leads to increased bone resorption and can interfere with calcium deposition during tooth development, leading to enamel hypoplasia and a characteristic loss of the *lamina dura*. * **Cushing Syndrome:** Chronic hypercortisolism leads to systemic protein catabolism and impaired calcium metabolism. This disrupts the function of ameloblasts (enamel-forming cells), resulting in thinned or decreased enamel. * **Osteomalacia:** This condition (and its pediatric counterpart, Rickets) involves Vitamin D deficiency. Since Vitamin D is essential for calcium and phosphate homeostasis, its deficiency during the formative years leads to significant enamel hypoplasia and delayed tooth eruption. **Clinical Pearls for NEET-PG:** * **Ameloblasts** are highly sensitive to metabolic insults; any condition causing hypocalcemia or malnutrition during tooth development will manifest as enamel hypoplasia. * **Fluorosis High-Yield:** It occurs when fluoride levels in drinking water exceed **1.5 mg/L**. While it causes "mottled enamel," these teeth are paradoxically more resistant to dental caries. * **Radiographic Sign:** Loss of **lamina dura** (the cortical bone lining the tooth socket) is a classic board-exam sign for Hyperparathyroidism.

Question 533: A patient presents with fever and pain in the thyroid gland. Which of the following statements is true?

A. T3 and T4 levels are normal
B. ESR is elevated (Correct Answer)
C. TSH level is normal
D. It is due to Tuberculosis

Explanation: The clinical presentation of **fever and a painful, tender thyroid gland** is the hallmark of **Subacute Granulomatous Thyroiditis** (also known as De Quervain’s Thyroiditis). [1] ### **Explanation of the Correct Answer** * **Option B (ESR is elevated):** This is the most characteristic laboratory finding in De Quervain’s thyroiditis. The condition is an inflammatory response (often post-viral), leading to a significantly high Erythrocyte Sedimentation Rate (ESR), often exceeding 50–100 mm/hr. [1] This "exquisite" tenderness combined with a high ESR is a classic diagnostic clue for NEET-PG. ### **Analysis of Incorrect Options** * **Options A & C (T3, T4, and TSH levels):** In the early (acute) phase of the disease, inflammation causes the destruction of thyroid follicles, leading to the leakage of preformed hormones into the blood. This results in **Hyperthyroidism** (High T3/T4 and Low TSH). [1] Therefore, levels are rarely "normal" during the painful phase. * **Option D (Tuberculosis):** While TB can affect the thyroid, it is extremely rare. De Quervain’s is typically triggered by a **viral infection** (e.g., Coxsackie, Mumps, Adenovirus), not Mycobacterium tuberculosis. ### **High-Yield Clinical Pearls for NEET-PG** 1. **Radioiodine Uptake (RAIU):** Despite high T3/T4 levels, the RAIU is **characteristically low** (near zero) because the inflamed follicular cells cannot trap iodine. [1] 2. **Triphasic Course:** The disease typically follows a sequence: Hyperthyroid phase → Transient Hypothyroid phase → Recovery (Euthyroid). [1] 3. **Histology:** Look for **multinucleated giant cells** and granulomas. 4. **Treatment:** NSAIDs are the first line for pain; Prednisone is used if the pain is severe. [1] Antithyroid drugs (PTU/Methimazole) are **not** indicated as there is no new hormone synthesis. [1]

Question 534: Which is the most common clinical feature of Cushing syndrome?

A. Moon facies
B. Purplish skin striae
C. Hypokalemic alkalosis
D. Weight gain (Correct Answer)

Explanation: Explanation: Weight gain is the most common clinical feature of Cushing syndrome, occurring in approximately 90-95% of patients [1]. It is primarily characterized by centripetal (truncal) obesity, involving the accumulation of adipose tissue in the abdomen, mediastinum, and subcutaneous fat pads (buffalo hump and moon facies). This occurs because chronic hypercortisolism promotes adipogenesis and redistributes fat from the extremities to the trunk. Analysis of Options: * Moon facies (Option A): While a classic and highly frequent sign (appearing in ~75-80% of cases), it is statistically less common than generalized weight gain/truncal obesity. * Purplish skin striae (Option B): These are a highly specific diagnostic clue (especially if >1 cm wide), but they occur in only about 40-50% of patients [1]. They result from cortisol-induced inhibition of fibroblasts and loss of collagen. * Hypokalemic alkalosis (Option C): This is typically seen in Ectopic ACTH syndrome (e.g., Small Cell Lung Cancer) due to the mineralocorticoid effect of massive cortisol excess. it is not a common feature of standard Cushing disease. Clinical Pearls for NEET-PG: * Most Common Feature: Weight gain / Truncal obesity. * Most Specific Feature: Wide (>1 cm) purple striae, proximal muscle weakness, and easy bruisability [1]. * Screening Tests: 24-hour urinary free cortisol (most sensitive), Overnight Dexamethasone Suppression Test (ODST), or Late-night salivary cortisol [2]. * Cushing Disease: Refers specifically to a pituitary adenoma secreting ACTH (the most common cause of endogenous Cushing syndrome) [1].

Question 535: A 23-year-old woman presents with tremor, restlessness, heat intolerance, palpitation, and unexplained weight loss. The thyroid is symmetrically enlarged, the pulse is rapid, the skin is moist and warm, and exophthalmos is apparent. What is the underlying nature of this condition?

A. Autoimmune (Correct Answer)
B. Congenital
C. Infectious
D. Iatrogenic

Explanation: The clinical presentation of tremor, heat intolerance, weight loss, tachycardia, and a symmetrically enlarged thyroid (goiter) indicates **hyperthyroidism** [2]. The presence of **exophthalmos** (thyroid eye disease) is the pathognomonic clinical sign that specifically identifies **Graves' disease** as the underlying cause [1]. 1. **Why Autoimmune is correct:** Graves' disease is an **autoimmune disorder** caused by the production of **Thyroid Stimulating Immunoglobulins (TSI)** [2]. These are Type II hypersensitivity antibodies that bind to and activate the TSH receptors on thyroid follicular cells, leading to autonomous overproduction of thyroid hormones (T3 and T4) and glandular hyperplasia [1]. 2. **Why other options are wrong:** * **Congenital:** While neonatal thyrotoxicosis can occur due to the transplacental passage of maternal antibodies, the primary disease in a 23-year-old is acquired, not a birth defect. * **Infectious:** Subacute thyroiditis (De Quervain's) can follow a viral infection, but it typically presents with a painful, tender thyroid and lacks exophthalmos. * **Iatrogenic:** This refers to hyperthyroidism caused by excessive thyroid hormone replacement (Factitious thyrotoxicosis) [3] or medications like Amiodarone. It would not present with a diffuse goiter or exophthalmos. **NEET-PG High-Yield Pearls:** * **Triad of Graves':** Hyperthyroidism, Diffuse Goiter, and Exophthalmos (Ophthalmopathy) [1]. Dermopathy (Pretibial Myxedema) is also a specific autoimmune feature. * **Diagnosis:** Low TSH, High Free T4, and **diffuse uptake** on Radioactive Iodine Uptake (RAIU) scan. * **Antibody:** TSH-Receptor Antibody (TRAb/TSI) is the most specific marker [1]. * **Histology:** Scalloping of colloid at the margins of follicular cells.

Question 536: A 45-year-old female diabetic patient on insulin is brought to the hospital in an unconscious state. What is the first line of treatment?

A. Intravenous insulin
B. Intravenous infusion of dextrose
C. Intravenous dexamethasone injection
D. Blood glucose test (Correct Answer)

Explanation: In a diabetic patient presenting with unconsciousness (altered sensorium), the primary clinical challenge is differentiating between **Hypoglycemic Coma** and **Diabetic Ketoacidosis (DKA)/Hyperosmolar Hyperglycemic State (HHS)**. ### Why "Blood Glucose Test" is the Correct Answer: The fundamental rule in emergency medicine is: **"Never treat without a diagnosis unless the patient is crashing."** While hypoglycemia is a medical emergency requiring immediate glucose [1], administering insulin to a hypoglycemic patient or concentrated dextrose to a patient with severe DKA can be fatal. A rapid bedside **Capillary Blood Glucose (CBG)** test takes seconds and dictates the entire management algorithm [2]. It is the mandatory first step to confirm the etiology of the coma. ### Why Other Options are Incorrect: * **Intravenous Insulin:** This is the treatment for DKA. If the patient is actually hypoglycemic (a common cause of coma in insulin users), giving insulin will cause irreversible brain damage or death [1]. * **Intravenous Dextrose:** While this is the treatment for hypoglycemia, it should ideally follow a glucose check. In a hospital setting, "blind" dextrose is discouraged if a glucometer is available, as it may worsen cerebral edema in hyperosmolar states. * **Intravenous Dexamethasone:** This is used for cerebral edema or adrenal crisis but has no role in the immediate stabilization of a diabetic coma. ### NEET-PG High-Yield Pearls: 1. **Whipple’s Triad:** Symptoms of hypoglycemia, low plasma glucose, and relief of symptoms after glucose administration. 2. **Neuroglycopenic symptoms** (confusion, coma) usually occur when blood glucose falls below **40–50 mg/dL** [1]. 3. In a **pre-hospital/field setting** where a glucometer is unavailable, the rule is: **"When in doubt, give glucose,"** because hypoglycemia kills faster than hyperglycemia. However, in a **hospital setting**, the "first line" is always the diagnostic test.

Question 537: A patient presents with galactorrhea and visual defects. Which investigation should be performed?

A. Serum prolactin
B. CT scan of the brain
C. MRI (Correct Answer)
D. Angiography

Explanation: **Explanation:** The clinical presentation of **galactorrhea** combined with **visual field defects** (typically bitemporal hemianopia) strongly suggests a **pituitary adenoma** (most likely a Prolactinoma) [1]. Large tumors (macroadenomas >10mm) compress the optic chiasm, leading to visual impairment [1]. 1. **Why MRI is the Correct Answer:** **MRI with gadolinium enhancement** is the gold standard and investigation of choice for visualizing the pituitary gland and the sella turcica [1]. It provides superior soft-tissue resolution compared to CT, allowing for the precise identification of microadenomas (<10mm), macroadenomas, and their relationship to surrounding structures like the optic chiasm and cavernous sinuses [1]. 2. **Why other options are incorrect:** * **Serum Prolactin:** While this is the initial *biochemical* test to confirm hyperprolactinemia, it cannot visualize the anatomical extent of the tumor or the cause of the visual defect [1]. * **CT Scan:** CT is less sensitive than MRI for pituitary lesions and provides poor visualization of the optic chiasm. * **Angiography:** This is an invasive procedure used for vascular pathologies (like aneurysms) and has no role in the routine workup of a suspected pituitary adenoma. **NEET-PG High-Yield Pearls:** * **Investigation of choice for Pituitary lesions:** MRI [1]. * **Most common secretory pituitary tumor:** Prolactinoma. * **Medical Management:** Dopamine agonists (Cabergoline is preferred over Bromocriptine due to better efficacy and fewer side effects) [1]. * **Surgical Indication:** If the patient has visual field defects or is refractory to medical therapy (Transsphenoidal surgery) [1].

Question 538: Which of the following is true regarding galactorrhea?

A. Bilateral
B. Seen in pregnancy and lactation
C. Associated with prolactinomas (Correct Answer)
D. Endocrinopathies

Explanation: **Explanation:** Galactorrhea is defined as the non-puerperal secretion of milk-containing fluid from the breast [1]. It is a clinical sign, not a diagnosis, and is most commonly associated with hyperprolactinemia [1]. **Why Option C is Correct:** Prolactinomas (pituitary adenomas) are the most common cause of pathological hyperprolactinemia [1]. Elevated prolactin levels directly stimulate the mammary glands to produce milk [3]. In women, this typically presents as the triad of **galactorrhea, amenorrhea, and infertility** [2]. **Why the other options are incorrect:** * **Option A (Bilateral):** While galactorrhea is often bilateral and multiductal, this is a **characteristic** of the condition rather than a defining "truth" in the context of etiology [1]. Furthermore, it can occasionally be unilateral, making this a less definitive answer than its association with prolactinomas. * **Option B (Seen in pregnancy and lactation):** This is a distractor. Milk secretion during pregnancy and the postpartum period is considered **physiologic lactation**, not galactorrhea [2]. Galactorrhea, by definition, refers to milk production unrelated to the physiological process of childbearing [2]. * **Option D (Endocrinopathies):** While various endocrinopathies (like hypothyroidism) can cause galactorrhea, this is a broad category [1]. In medical entrance exams, when a specific pathological entity like "Prolactinoma" is provided, it is the preferred, more specific answer. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hypothyroidism Connection:** Primary hypothyroidism can cause galactorrhea because increased **TRH** (Thyrotropin-releasing hormone) acts as a prolactin-releasing factor [1]. 2. **Drug-Induced:** Always rule out dopamine antagonists (e.g., Metoclopramide, Risperidone, Methyldopa) as they inhibit the "prolactin-inhibiting factor" (Dopamine) [1]. 3. **Hook Effect:** In very large macroprolactinomas, extremely high prolactin levels can lead to a false-low lab reading; serial dilutions are required for accurate measurement. 4. **Treatment:** Dopamine agonists like **Cabergoline** (first-line) or Bromocriptine are used to shrink the tumor and normalize prolactin levels [4].

Question 539: A 25-year-old male presents with ophthalmologic signs of thyrotoxicosis. Which of the following is NOT a possible cause?

A. Diffuse thyroid goiter
B. Hashimoto's thyroiditis
C. Riedel's thyroiditis (Correct Answer)
D. Adenomatous goiter

Explanation: The key to solving this question lies in distinguishing between **sympathetic overactivity** (lid lag, lid retraction) and **true infiltrative ophthalmopathy** (proptosis, extraocular muscle palsy) [1]. In the context of thyrotoxicosis, eye signs occur due to either excess thyroid hormones or an underlying autoimmune process. **Why Riedel’s Thyroiditis is the correct answer:** Riedel’s thyroiditis is a rare chronic inflammatory disease characterized by dense **fibrous replacement** of the thyroid parenchyma, often extending to adjacent neck structures. It typically presents as a "stony hard," painless, fixed goiter. Crucially, patients are usually **euthyroid or hypothyroid**, and the condition is not associated with thyrotoxicosis or the autoimmune mechanisms that trigger ophthalmopathy. **Analysis of Incorrect Options:** * **Diffuse Thyroid Goiter (Graves’ Disease):** This is the most common cause of thyrotoxicosis. It features **TSH-receptor antibodies (TRAb)** that cross-react with orbital fibroblasts, leading to true infiltrative ophthalmopathy [1]. * **Hashimoto’s Thyroiditis:** While typically causing hypothyroidism, it can present with a transient hyperthyroid phase (**Hashitoxicosis**). Furthermore, as an autoimmune thyroid disease, it is occasionally associated with Graves'-like ophthalmopathy. * **Adenomatous Goiter:** A toxic multinodular goiter or a toxic adenoma causes excess thyroid hormone production. While these do not cause *infiltrative* disease, the resulting thyrotoxicosis leads to **sympathetic overactivity**, manifesting as lid lag and lid retraction (non-infiltrative signs) [1]. **NEET-PG High-Yield Pearls:** * **Dalrymple Sign:** Palpebral aperture widening (lid retraction) due to sympathetic overactivity of Müller’s muscle. * **Stellwag’s Sign:** Infrequent or incomplete blinking. * **Riedel’s Thyroiditis** is often associated with **IgG4-related systemic diseases** (e.g., retroperitoneal fibrosis, sclerosing cholangitis). * **True Proptosis** is specific to Graves’ Disease and is not seen in other causes of thyrotoxicosis [1].

Question 540: Which of the following is most frequently associated with the typical form of carcinoid syndrome?

A. Foregut carcinoid
B. Midgut carcinoid (Correct Answer)
C. Hindgut carcinoid
D. None of the above

Explanation: **Explanation:** The typical carcinoid syndrome is most frequently associated with **Midgut carcinoids** (originating from the distal duodenum, jejunum, ileum, and ascending colon). **1. Why Midgut Carcinoid is Correct:** Midgut tumors are the most common source of serotonin production. Under normal circumstances, serotonin produced by intestinal tumors is metabolized by the liver into **5-HIAA** via the portal circulation (the "first-pass effect"), preventing systemic symptoms. For carcinoid syndrome to occur, the vasoactive substances (serotonin, bradykinins, prostaglandins) must bypass hepatic metabolism [1]. This typically happens when a midgut carcinoid **metastasizes to the liver**, allowing secretions to enter the systemic circulation directly via the hepatic veins [1]. **2. Why Other Options are Incorrect:** * **Foregut Carcinoids (Bronchus, Stomach, Pancreas):** These are less common causes. Gastric carcinoids often lack the enzyme DOPA decarboxylase, leading to the production of 5-HTP rather than serotonin, resulting in an "atypical" syndrome (characterized by patchy, cherry-red flushing). Bronchial carcinoids can cause syndrome without liver metastasis because they secrete directly into the systemic circulation [1]. * **Hindgut Carcinoids (Descending colon, Rectum):** These tumors are rarely functional. They seldom produce serotonin or other vasoactive peptides and thus almost never present with carcinoid syndrome. **NEET-PG High-Yield Pearls:** * **Classic Triad:** Flushing (most common), Diarrhea, and Right-sided valvular heart disease (Tricuspid Regurgitation/Pulmonary Stenosis). * **Diagnosis:** Best initial screening test is **24-hour urinary 5-HIAA**. * **Localization:** **Octreotide scan** (Somatostatin receptor scintigraphy) is the gold standard for locating the primary tumor. * **Treatment:** **Octreotide** (Somatostatin analog) is used to manage symptoms and prevent a carcinoid crisis during surgery.

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