Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 491: A 35-year-old female patient with a history of amenorrhea and galactorrhea presents with elevated prolactin levels on blood examination. What is the most likely finding on a CT scan of the head?

A. Pituitary adenoma (Correct Answer)
B. Craniopharyngioma
C. Sheehan's syndrome
D. Pinealoma

Explanation: The clinical triad of **amenorrhea, galactorrhea, and hyperprolactinemia** in a young female is the classic presentation of a **Prolactinoma**, which is a functional **Pituitary Adenoma** [1]. Prolactinomas are the most common type of secretory pituitary tumor [1]. Elevated prolactin inhibits the pulsatile release of GnRH, leading to decreased LH/FSH, which results in secondary amenorrhea and infertility. **Analysis of Options:** * **A. Pituitary Adenoma (Correct):** Specifically, a lactotroph adenoma. It directly secretes prolactin. On imaging (MRI is preferred, but CT shows sellar enlargement/mass), this is the most common cause of pathological hyperprolactinemia [1]. * **B. Craniopharyngioma:** These are suprasellar tumors derived from Rathke’s pouch. While they can cause "stalk effect" (compression of the pituitary stalk leading to mild prolactin elevation) [1], they typically present with visual field defects (bitemporal hemianopia) and calcifications on CT, rather than primary galactorrhea. * **C. Sheehan’s Syndrome:** This is postpartum pituitary necrosis. It typically presents with a **failure to lactate** (due to prolactin deficiency) and loss of other anterior pituitary hormones, rather than hyperprolactinemia. * **D. Pinealoma:** These tumors are located in the pineal gland (posterior to the midbrain). They typically present with Parinaud syndrome (upward gaze palsy) and precocious puberty, not isolated galactorrhea. **High-Yield Clinical Pearls for NEET-PG:** * **Drug-induced hyperprolactinemia:** Always rule out dopamine antagonists (e.g., Metoclopramide, Risperidone) before diagnosing an adenoma [1]. * **Hook Effect:** In extremely high prolactin levels, lab assays may show falsely low levels; serial dilution is required. * **Treatment:** First-line treatment for prolactinomas is medical (Dopamine agonists like **Cabergoline** or Bromocriptine) [1], NOT surgery [3]. * **Imaging:** MRI Brain with gadolinium (Sella protocol) is the gold standard, though CT can detect macroadenomas [2].

Question 492: Which of the following statements is true about SIADH?

A. Hypovolemic Hyponatremia
B. Euvolemic Hyponatremia (Correct Answer)
C. Hypervolemic Hyponatremia
D. Hypervolemic Hypernatremia

Explanation: **Explanation:** **SIADH (Syndrome of Inappropriate Antidiuretic Hormone)** is characterized by the excessive release of ADH from the posterior pituitary or ectopic sources, regardless of serum osmolality. **Why Euvolemic Hyponatremia is Correct:** In SIADH, excess ADH leads to increased water reabsorption in the renal collecting ducts [1]. This causes **dilutional hyponatremia**. While there is an initial increase in total body water, the body compensates through **pressure natriuresis** (atrial natriuretic peptide release and inhibition of the RAAS system). This results in the excretion of sodium and water in the urine, bringing the clinical volume status back to near-normal. Therefore, patients appear **clinically euvolemic** (no edema, no jugular venous distension) [2]. **Why Other Options are Incorrect:** * **Hypovolemic Hyponatremia (A):** Seen in conditions with fluid loss, such as vomiting, diarrhea, or diuretic use [2]. In SIADH, the patient is not volume-depleted. * **Hypervolemic Hyponatremia (C):** Characterized by "dilutional" states with clinical edema, such as Congestive Heart Failure, Cirrhosis, or Nephrotic Syndrome [2]. * **Hypervolemic Hypernatremia (D):** Usually results from the administration of hypertonic saline or mineralocorticoid excess (e.g., Conn’s Syndrome). **NEET-PG High-Yield Pearls:** 1. **Diagnostic Criteria:** Low serum osmolality (<275 mOsm/kg), inappropriately high urine osmolality (>100 mOsm/kg), and high urine sodium (>40 mEq/L). 2. **Common Causes:** Small cell carcinoma of the lung (ectopic ADH), CNS disorders (stroke, trauma), and drugs (SSRIs, Carbamazepine, Cyclophosphamide). 3. **Management:** Fluid restriction is the first-line treatment. For severe/symptomatic cases, use hypertonic saline (3%) and V2-receptor antagonists (**Vaptans**) [3]. 4. **Caution:** Rapid correction of hyponatremia can lead to **Osmotic Demyelination Syndrome** (Central Pontine Myelinolysis). Keep correction <8–10 mmol/L in 24 hours.

Question 493: What is the intravenous fluid of choice in the management of diabetic ketoacidosis?

A. Normal saline (Correct Answer)
B. Colloids
C. 5% dextrose
D. Dextran-70

Explanation: **Explanation:** The primary goal in the initial management of Diabetic Ketoacidosis (DKA) is the restoration of circulatory volume and correction of profound dehydration caused by osmotic diuresis. **Why Normal Saline (0.9% NaCl) is the Correct Choice:** Normal saline is an **isotonic crystalloid** and remains the fluid of choice for initial resuscitation. It effectively expands the extracellular fluid (ECF) volume, improves renal perfusion (which helps clear ketones and glucose), and stabilizes blood pressure. In DKA, there is a significant deficit of both water and sodium; 0.9% NaCl provides a rapid way to replenish these without causing a sudden drop in serum osmolality. **Analysis of Incorrect Options:** * **Colloids (B) and Dextran-70 (D):** These are large-molecule fluids used primarily for rapid intravascular volume expansion in hemorrhagic shock. They are not indicated in DKA as they do not address the total body water deficit and are more expensive with no proven benefit over crystalloids in this setting. * **5% Dextrose (C):** Giving dextrose initially would worsen hyperglycemia and osmotic diuresis. However, it is **added** to the regimen (usually as 5% Dextrose in 0.45% saline) only once the blood glucose falls below **200–250 mg/dL** to prevent hypoglycemia and allow continued insulin infusion to close the anion gap. **High-Yield Clinical Pearls for NEET-PG:** * **Initial Rate:** Typically 1 liter of 0.9% NaCl is given in the first hour. * **Switching Fluids:** If the corrected serum sodium is high or normal, the fluid is often switched to **0.45% (half-normal) saline** after the first hour. * **Potassium Rule:** Never start insulin if K+ is **<3.3 mEq/L**; always replenish potassium early as insulin causes an intracellular shift of K+. * **Resolution Criteria:** DKA is considered resolved when the pH >7.3, bicarbonate ≥18 mEq/L, and the anion gap is closed.

Question 494: Myopathy is seen in all except?

A. X-linked hypophosphatemic rickets (Correct Answer)
B. Oncogenic osteomalacia
C. Nutritional osteomalacia
D. Cushing syndrome

Explanation: The presence of myopathy in metabolic bone diseases is primarily linked to **Vitamin D deficiency** and **hypophosphatemia**. However, the underlying pathophysiology determines whether muscle weakness occurs. [1] **1. Why Option A is the Correct Answer:** In **X-linked hypophosphatemic (XLH) rickets**, the primary defect is a mutation in the *PHEX* gene leading to elevated levels of **FGF-23**. While FGF-23 causes profound renal phosphate wasting and low 1,25(OH)₂D levels, **myopathy is characteristically absent**. This is a classic "except" in medical exams because, despite severe hypophosphatemia and rickets/osteomalacia, these patients maintain normal muscle strength. **2. Analysis of Incorrect Options:** * **Oncogenic Osteomalacia (B):** Like XLH, this is mediated by FGF-23 (secreted by mesenchymal tumors). However, unlike the congenital form, patients with acquired oncogenic osteomalacia frequently present with **severe proximal muscle weakness** and bone pain. * **Nutritional Osteomalacia (C):** Vitamin D is essential for calcium handling in muscle cells. Deficiency leads to secondary hyperparathyroidism and hypophosphatemia, resulting in **proximal myopathy** (waddling gait) [1]. * **Cushing Syndrome (D):** Excess glucocorticoids cause **steroid myopathy** via protein catabolism and type II muscle fiber atrophy. This is a hallmark clinical feature of the disease. **High-Yield Clinical Pearls for NEET-PG:** * **Proximal Myopathy** is a feature of both Hyperthyroidism and Hypothyroidism, but "pseudohypertrophy" (Hoffman’s syndrome) is specific to Hypothyroidism. * **Hypophosphatemia** causes myopathy because ATP (Adenosine Triphosphate) cannot be adequately synthesized, leading to muscle cell dysfunction. * **Rule of Thumb:** If a patient has rickets/osteomalacia *with* muscle weakness, think Nutritional or Vitamin D-dependent; if *without* weakness, think XLH.

Question 495: Which of the following findings are seen in Hyperparathyroidism?

A. Osteitis fibrosa cystica
B. Osteoporosis
C. Dissecting osteitis
D. All the above (Correct Answer)

Explanation: **Explanation:** Primary Hyperparathyroidism (PHPT) is characterized by the overproduction of Parathyroid Hormone (PTH), which leads to increased bone resorption by stimulating osteoclast activity [1]. This process results in a spectrum of skeletal manifestations. * **Osteitis Fibrosa Cystica (Option A):** This is the classic, advanced skeletal manifestation of PHPT. Chronic PTH excess leads to the replacement of bone marrow with fibrous tissue and the formation of cystic lesions (Brown tumors). * **Osteoporosis (Option B):** PTH has a catabolic effect on cortical bone [1]. In modern clinical practice, asymptomatic PHPT often presents as generalized bone loss or decreased bone mineral density (BMD), particularly at the distal radius (cortical bone), mimicking or exacerbating osteoporosis [3]. * **Dissecting Osteitis (Option C):** This is the pathognomonic histological feature of hyperparathyroidism. Osteoclasts tunnel into the center of bony trabeculae, creating a "railroad track" appearance. This "dissecting" nature of bone resorption distinguishes it from other metabolic bone diseases. **Conclusion:** Since all three findings are characteristic pathological or radiological features of hyperparathyroidism, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** "Stones (Renal), Bones (Aches/Fractures), Abdominal Groans (Peptic ulcers/Pancreatitis), and Psychic Moans (Depression)." [2] * **Radiology:** Look for **subperiosteal bone resorption**, most specifically on the radial aspect of the middle phalanges of the 2nd and 3rd fingers. * **Skull finding:** "Salt and pepper" appearance (mottled lucencies). * **Biochemical profile:** High Calcium, Low Phosphate, High PTH, and High Alkaline Phosphatase (if bone involvement is significant) [2].

Question 496: Which of the following is NOT considered an exclusive or strongly associated infection in diabetes mellitus?

A. Mucormycosis
B. Atypical mycobacterial infection
C. Emphysematous appendicitis
D. Hansen's disease (Correct Answer)

Explanation: ### **Explanation** In the context of Diabetes Mellitus (DM), certain infections occur with significantly higher frequency or severity due to hyperglycemia, impaired neutrophil function (chemotaxis and phagocytosis), and microvascular complications. **Why Hansen’s Disease is the Correct Answer:** **Hansen’s Disease (Leprosy)** is caused by *Mycobacterium leprae*. While diabetic patients may develop secondary infections in neuropathic ulcers (similar to leprosy), there is **no established epidemiological or pathophysiological link** suggesting that DM increases the susceptibility to or the incidence of leprosy itself. It is not considered an "opportunistic" or "exclusive" infection of the diabetic state. **Analysis of Incorrect Options:** * **Mucormycosis (Rhinocerebral):** This is a classic "exclusive" association. Rhizopus species thrive in acidic, glucose-rich environments. Diabetic Ketoacidosis (DKA) provides the ideal milieu for these fungi to invade blood vessels, leading to tissue necrosis. * **Atypical Mycobacterial Infections:** Patients with DM have impaired cell-mediated immunity, making them more susceptible to non-tuberculous mycobacteria (NTM) like *M. avium complex* and *M. kansasii*. * **Emphysematous Appendicitis:** DM is a major risk factor for

Question 497: A 63-year-old man recently treated for renal tuberculosis presents with weight loss, diarrhea, hypoglycemia, hypotension, and is noted to have hyperpigmented buccal mucosa, palmar and hand creases. Which investigation is most suitable for this clinical presentation?

A. Serum iron and ferritin
B. Serum copper and ceruloplasmin
C. Plasma ACTH and cortisol (Correct Answer)
D. Gene XPERT and Intravenous pyelography

Explanation: **Explanation:** The clinical presentation of weight loss, diarrhea, hypoglycemia, and hypotension, combined with characteristic **hyperpigmentation** (buccal mucosa and palmar creases), is a classic description of **Primary Adrenal Insufficiency (Addison’s Disease)** [1]. In this patient, the history of **renal tuberculosis** is a critical clue, as TB remains a leading cause of adrenal destruction (Adrenal TB) [2]. 1. **Why Option C is correct:** The diagnosis of adrenal insufficiency is confirmed by demonstrating low cortisol levels. High **Plasma ACTH** levels (due to loss of negative feedback) confirm the site of pathology is the adrenal gland (Primary) rather than the pituitary (Secondary) [1]. Hyperpigmentation occurs because ACTH and Melanocyte-Stimulating Hormone (MSH) share a common precursor, Pro-opiomelanocortin (POMC). 2. **Why other options are incorrect:** * **Option A:** Iron studies are for Hemochromatosis. While it causes skin bronzing, it typically presents with diabetes ("bronze diabetes") and cirrhosis, not hypotension or hypoglycemia. * **Option B:** Copper studies are for Wilson’s disease, which presents with liver failure and neuropsychiatric symptoms, not adrenal crisis. * **Option D:** While GeneXpert is used to diagnose active TB, it does not assess organ function. IVP is an outdated imaging modality for renal anatomy and is not used to diagnose endocrine failure. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause worldwide:** Autoimmune adrenalitis. * **Most common cause in India:** Tuberculosis [2]. * **Electrolyte Triad:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis. * **Gold Standard Test:** ACTH Stimulation Test (Cosyntropin test) [1]. * **Imaging:** In TB, CT may show enlarged, calcified adrenal glands [1].

Question 498: Conn's syndrome is associated with all of the following, except:

A. Hypertension
B. Muscle weakness
C. Hypokalemia
D. Edema (Correct Answer)

Explanation: Explanation: Conn’s Syndrome (Primary Hyperaldosteronism) is characterized by the autonomous overproduction of aldosterone, usually due to an adrenal adenoma [2]. Why Edema is the Correct Answer (The "Aldosterone Escape" Phenomenon): Despite significant sodium and water retention caused by excess aldosterone, patients with Conn’s syndrome **do not** typically present with clinical edema [1]. This is due to the **"Aldosterone Escape"** mechanism: the initial volume expansion triggers the release of Atrial Natriuretic Peptide (ANP) and increases the glomerular filtration rate (GFR), leading to pressure natriuresis [1]. This compensates for the sodium retention, preventing fluid overload and edema. Analysis of Incorrect Options: * **A. Hypertension:** Aldosterone increases sodium reabsorption in the distal tubules, leading to volume expansion and high blood pressure. It is a classic cause of secondary hypertension [3]. * **B. Muscle Weakness:** This is a clinical manifestation of severe hypokalemia [4]. Low potassium levels interfere with muscle cell membrane potential, leading to fatigue or even paralysis. * **C. Hypokalemia:** Aldosterone promotes potassium excretion in exchange for sodium at the cortical collecting duct [4]. This results in low serum potassium, often accompanied by metabolic alkalosis (plasma HCO₃⁻ elevation [3]). NEET-PG High-Yield Pearls: 1. **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A ratio **>20-30** is highly suggestive. 2. **Confirmatory Test:** Saline infusion test (failure to suppress aldosterone) or Oral Salt Loading test. 3. **Triad:** Hypertension + Hypokalemia + Metabolic Alkalosis [3]. 4. **Treatment:** Surgical excision for adenoma (Conn's); Spironolactone (Aldosterone antagonist) for bilateral adrenal hyperplasia.

Question 499: Hepatomegaly is a feature of all of the following, except:

A. Von Girke's Disease
B. Hurler's Disease
C. Niemann Pick Disease
D. Hepatic porphyrias (Correct Answer)

Explanation: The correct answer is **Hepatic porphyrias**. In medical diagnostics, hepatomegaly typically results from the accumulation of substances (glycogen, lipids, or glycosaminoglycans) within hepatocytes or Kupffer cells. **Hepatic porphyrias** (such as Acute Intermittent Porphyria) are enzymatic defects in the heme biosynthesis pathway [1]. While the liver is the primary site of the metabolic error, these conditions manifest with systemic symptoms like abdominal pain, neuropsychiatric issues, and photosensitivity. Crucially, they **do not cause hepatomegaly** because there is no significant storage or structural infiltration within the liver parenchyma. Analysis of Incorrect Options: **Von Gierke’s Disease (GSD Type I):** A glycogen storage disorder caused by Glucose-6-Phosphatase deficiency. It leads to massive accumulation of glycogen in the liver, resulting in prominent **hepatomegaly**, renomegaly, and hypoglycemia. **Hurler’s Disease (MPS I):** A lysosomal storage disorder where alpha-L-iduronidase deficiency leads to the buildup of dermatan and heparan sulfate. This causes multi-organ infiltration, including significant **hepatosplenomegaly**. **Niemann-Pick Disease:** A lipid storage disorder (Sphingomyelinase deficiency) characterized by the accumulation of sphingomyelin in the reticuloendothelial system, leading to marked **hepatosplenomegaly** and "foam cells" on biopsy. Clinical Pearls for NEET-PG: **Porphyria Cutanea Tarda (PCT):** The most common porphyria; it is the only hepatic porphyria that may show mild liver damage/cirrhosis, but classic "Hepatic Porphyrias" (AIP) are defined by metabolic crises, not organomegaly [1]. **Gaucher’s Disease:** The most common lysosomal storage disorder; it presents with massive splenomegaly (more than hepatomegaly). **Zellweger Syndrome:** A peroxisomal disorder that also presents with hepatomegaly and impaired liver function.

Question 500: All the following statements regarding postpartum thyroiditis are true, EXCEPT:

A. Hyperthyroidism may be present in the first 3 months after delivery.
B. Hypothyroidism may be present a few months after delivery.
C. Thyroid function may be normal after 1 year.
D. The risk of recurrence in subsequent pregnancy is < 10%. (Correct Answer)

Explanation: **Explanation:** Postpartum Thyroiditis (PPT) is an autoimmune destructive thyroiditis occurring within one year of delivery in women without a prior history of thyroid disease. It is essentially a variant of Hashimoto’s thyroiditis, triggered by the rebound of the immune system following the immunosuppression of pregnancy. **Why Option D is the correct answer (False statement):** The risk of recurrence in subsequent pregnancies is significantly high, estimated at **approximately 70%**. Therefore, the statement that the risk is < 10% is incorrect [1]. Patients with a history of PPT should be closely monitored in future pregnancies. **Analysis of other options:** * **Option A:** PPT typically follows a triphasic course. The **thyrotoxic phase** occurs first (usually 1–4 months postpartum) due to the release of preformed hormones from damaged follicles [1]. * **Option B:** The **hypothyroid phase** typically follows the thyrotoxic phase, occurring 4–8 months after delivery. Some patients may present with only hypothyroidism without a preceding toxic phase [1]. * **Option C:** In the majority of cases (**~80%**), thyroid function returns to **euthyroid status** within one year. However, these women have an increased risk of developing permanent hypothyroidism later in life [1]. **NEET-PG High-Yield Pearls:** * **Antibody Association:** Strongly associated with **Anti-TPO (Thyroid Peroxidase)** antibodies. * **Radioiodine Uptake (RAIU):** During the thyrotoxic phase, RAIU is **low/absent** (distinguishes it from Graves' disease) [1]. * **Treatment:** The thyrotoxic phase is usually mild and treated with **Beta-blockers** (Propranolol) if symptomatic; Antithyroid drugs (PTU/Methimazole) are **not** indicated as there is no excess synthesis [1]. * **Risk Factor:** Type 1 Diabetes Mellitus increases the risk of PPT three-fold.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

Pituitary Disorders

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Calcium and Bone Metabolism

Practice Questions

Reproductive Endocrinology

Practice Questions

Lipid Disorders

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Endocrine Hypertension

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

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Neuroendocrine Tumors

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Endocrine Emergencies

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