Endocrinology — MCQs

A 35-year-old female presents with complaints of fatigue, weakness, decreased appetite, weight loss, and severe light-headedness upon standing. Physical examination reveals oral mucosal pigmentation, proximal muscle weakness of the lower extremities, and hyperpigmentation of the palmar creases, knuckles, and knees. What is the most likely diagnosis?

Q405Easy

What is the most common cause of Addison's disease?

Q406Medium

A 15-year-old girl presents with complaints of puffy eyes, swelling in the neck, weight gain, and fatigue. Investigations reveal the presence of thyroid peroxidase antibodies and elevated TSH levels. What is the most likely diagnosis?

Q407Easy

Brown pigmentation is seen in which disease?

Q408Easy

Tetany may be present in all the following conditions except?

Q409Medium

A patient presents with headache and flushing, and has a family history of medullary thyroid carcinoma. What investigation is most appropriate for this patient?

Q410Easy

Medical adrenalectomy is seen with:

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 401: A 30-year-old female presents with increased thirst and polyuria. Her random plasma glucose is 230 mg/dL. Which of the following tests differentiates type 1 diabetes mellitus from type 2 diabetes mellitus?

A. Anti-GAD-65 antibody (Correct Answer)
B. Peroxisome proliferator-activated receptor gamma-2 polymorphism testing
C. Plasma insulin level
D. Testing for human leukocyte antigen (HLA) DR3

Explanation: The clinical presentation of polyuria, polydipsia, and a random plasma glucose of 230 mg/dL confirms a diagnosis of Diabetes Mellitus [1]. To differentiate between Type 1 (T1DM) and Type 2 (T2DM), we must identify the underlying pathophysiology: autoimmune destruction of beta cells versus insulin resistance [1]. **Why Anti-GAD-65 is correct:** **Glutamic Acid Decarboxylase (GAD-65) antibodies** are the most sensitive and persistent markers for autoimmune T1DM. They are present in approximately 70-80% of newly diagnosed T1DM patients. Their presence confirms an autoimmune etiology, helping distinguish T1DM (or LADA) from T2DM, where these antibodies are absent. **Analysis of Incorrect Options:** * **B. PPAR-gamma-2 polymorphism:** While associated with T2DM risk and insulin sensitivity, this is a research tool and has no clinical utility in differentiating diabetes types. * **C. Plasma insulin level:** Insulin and C-peptide levels can be low in long-standing T2DM (due to beta-cell exhaustion) or "falsely" normal in early T1DM (the "honeymoon phase"). Thus, they are less reliable than antibody testing for definitive classification. * **D. HLA DR3:** While HLA-DR3 and DR4 are strongly associated with a genetic predisposition to T1DM [1], they are also present in a significant portion of the general healthy population [1]. Therefore, HLA typing lacks the specificity required for diagnosis. **NEET-PG High-Yield Pearls:** * **Most common antibody in T1DM:** Anti-GAD-65 (also the most persistent). * **Earliest antibody to appear:** Anti-IAA (Insulin Autoantibodies), especially in children. * **Zinc Transporter 8 (ZnT8):** A newer, highly specific marker for T1DM. * **C-peptide:** Used to assess endogenous insulin production; it is low/absent in T1DM and initially high/normal in T2DM.

Question 402: Hypokalemia may be a feature of all the following diseases, except?

A. Addison's disease (Correct Answer)
B. Cushing's syndrome
C. Bartter syndrome
D. Gitelman syndrome

Explanation: **Explanation:** The core concept behind this question is the role of **Aldosterone** and **Cortisol** in renal potassium handling [1]. **1. Why Addison’s Disease is the Correct Answer:** Addison’s disease (Primary Adrenocortical Insufficiency) is characterized by the destruction of the adrenal cortex, leading to a deficiency of both cortisol and **aldosterone** [2]. Aldosterone normally acts on the distal convoluted tubule and collecting duct to reabsorb sodium and **excrete potassium/hydrogen ions** [1]. In its absence, potassium is retained in the blood, leading to **Hyperkalemia**, not hypokalemia. This is often accompanied by hyponatremia and metabolic acidosis. **2. Why the other options are incorrect:** * **Cushing’s Syndrome:** High levels of cortisol exert a "mineralocorticoid effect" when the enzyme 11β-HSD2 is overwhelmed. This leads to excessive sodium reabsorption and increased potassium excretion, resulting in **hypokalemia** [3]. * **Bartter Syndrome:** A genetic defect in the thick ascending limb of the Loop of Henle (mimicking Loop diuretics). It causes salt wasting, activation of the RAAS pathway, and subsequent **hypokalemia** and metabolic alkalosis. * **Gitelman Syndrome:** A genetic defect in the distal convoluted tubule (mimicking Thiazide diuretics). It presents with **hypokalemia**, metabolic alkalosis, and characteristically low urinary calcium (hypocalciuria). **Clinical Pearls for NEET-PG:** * **Conn’s Syndrome:** Primary hyperaldosteronism is a classic cause of resistant hypertension with hypokalemia [3]. * **Liddle’s Syndrome:** "Pseudo-hyperaldosteronism" (gain of function of ENaC channels) presents with hypertension and hypokalemia but **low** aldosterone levels. * **Addisonian Crisis:** Always look for the triad of Hypotension, Hyponatremia, and Hyperkalemia in clinical vignettes.

Question 403: Which of the following is NOT found in Maturity Onset Diabetes of the Young (MODY)?

A. Family history positive
B. Young onset
C. Insulin receptor resistance
D. Glucokinase deficiency (Correct Answer)

Explanation: **Explanation:** Maturity-Onset Diabetes of the Young (MODY) is a group of monogenic disorders characterized by **primary defects in beta-cell function**, leading to impaired insulin secretion [1]. It is not a disorder of insulin resistance. **Why Option D is the "Correct" Answer (Contextual Note):** There appears to be a technical error in the question's framing. **Glucokinase deficiency (MODY 2)** is actually one of the most common causes of MODY. However, in the context of standard medical examinations, if this question is presented as "Which is NOT found," and the key points to "Glucokinase deficiency," it may be a distractor or a miskeyed question. **Pathophysiologically, the correct answer should be Option C (Insulin receptor resistance)**, as MODY is defined by insulin *deficiency* due to genetic mutations, not resistance. Insulin resistance is the hallmark of Type 2 Diabetes Mellitus, not MODY. [1] **Analysis of Options:** * **A. Family History Positive:** MODY follows an **Autosomal Dominant** inheritance pattern [1]. A strong three-generation family history is a diagnostic hallmark. * **B. Young Onset:** By definition, MODY presents in young individuals, typically **before the age of 25**. * **C. Insulin receptor resistance:** This is **NOT** a feature of MODY. Patients are usually non-obese and have high insulin sensitivity; the problem lies in the "sensing" of glucose or the secretion of insulin. * **D. Glucokinase deficiency:** This is the cause of **MODY 2**, characterized by a stable, mild fasting hyperglycemia. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Type:** MODY 3 (HNF-1 alpha mutation). * **Most Common in Pregnancy:** MODY 2 (Glucokinase mutation). * **Clinical Clue:** A young, non-obese patient with a strong family history of diabetes who is **C-peptide positive** (unlike Type 1) and **antibody negative**. * **Treatment:** MODY 3 is exquisitely sensitive to low-dose **Sulfonylureas**.

Question 404: A 35-year-old female presents with complaints of fatigue, weakness, decreased appetite, weight loss, and severe light-headedness upon standing. Physical examination reveals oral mucosal pigmentation, proximal muscle weakness of the lower extremities, and hyperpigmentation of the palmar creases, knuckles, and knees. What is the most likely diagnosis?

A. Adrenal insufficiency (Correct Answer)
B. Depression
C. Anorexia with surreptitious diuretic use
D. Hypothyroidism

Explanation: The clinical presentation described is a classic case of **Primary Adrenal Insufficiency (Addison’s Disease)** [1]. The hallmark of this condition is the deficiency of cortisol and aldosterone due to adrenal cortex destruction [1]. 1. **Why Adrenal Insufficiency is correct:** * **Hyperpigmentation:** This is the most specific sign of *primary* adrenal insufficiency. Low cortisol levels trigger a compensatory increase in ACTH (Adrenocorticotropic hormone). ACTH is derived from POMC (Pro-opiomelanocortin), which also produces MSH (Melanocyte-stimulating hormone), leading to hyperpigmentation in sun-exposed areas, pressure points (knuckles, knees), and mucosal surfaces [2]. * **Postural Hypotension:** Aldosterone deficiency leads to sodium wasting and volume depletion, causing severe light-headedness upon standing [1]. * **Systemic Symptoms:** Fatigue, weight loss, and muscle weakness are common due to glucocorticoid deficiency [2]. 2. **Why other options are incorrect:** * **Depression:** While it causes fatigue and weight loss, it does not explain hyperpigmentation or postural hypotension. * **Anorexia with diuretic use:** May cause weight loss and hypotension, but would not cause mucosal or palmar crease hyperpigmentation. * **Hypothyroidism:** Presents with fatigue and weight gain (not loss), and typically features dry skin or myxedema rather than hyperpigmentation. **NEET-PG High-Yield Pearls:** * **Most common cause:** Autoimmune adrenalitis (developed countries); Tuberculosis (developing countries like India) [2]. * **Electrolyte Triad:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis. * **Diagnosis:** Best initial test is the **ACTH Stimulation Test** (Cosyntropin test) [2]. * **Treatment:** Glucocorticoid (Hydrocortisone) and Mineralocorticoid (Fludrocortisone) replacement [2]. Stress doses are required during illness or surgery.

Question 405: What is the most common cause of Addison's disease?

A. Autoimmune adrenalitis (Correct Answer)
B. Meningococcal septicemia
C. Malignancy
D. Tuberculosis

Explanation: **Explanation:** **Addison’s Disease (Primary Adrenal Insufficiency)** occurs when the adrenal cortex is destroyed, leading to a deficiency of glucocorticoids, mineralocorticoids, and adrenal androgens. 1. **Why Autoimmune Adrenalitis is Correct:** In developed countries and globally as a whole, **autoimmune adrenalitis** is the most common cause (responsible for ~80% of cases) [1]. It involves the production of antibodies against the enzyme **21-hydroxylase**, leading to lymphocytic infiltration and atrophy of the adrenal cortex. It can occur in isolation or as part of Autoimmune Polyglandular Syndromes (APS I and II) [1]. 2. **Why the Other Options are Incorrect:** * **Tuberculosis (D):** Historically, TB was the leading cause. While it remains a significant cause in developing nations (like India), it has been overtaken by autoimmune etiology globally. In TB, the adrenals are often enlarged and calcified [1] (unlike the atrophy seen in autoimmune cases). * **Meningococcal Septicemia (B):** This causes **Waterhouse-Friderichsen Syndrome**, characterized by acute adrenal insufficiency due to massive bilateral adrenal hemorrhage. It is an *acute* crisis rather than the chronic presentation of Addison’s. * **Malignancy (C):** Metastatic spread (commonly from lung or breast cancer) can cause adrenal insufficiency, but it is a relatively rare cause compared to autoimmune destruction [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Hyperpigmentation:** A hallmark of primary adrenal insufficiency (due to increased ACTH/POMC levels), seen in skin creases, buccal mucosa, and scars. * **Biochemical Profile:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis [1]. * **Diagnosis:** The screening test of choice is the **ACTH Stimulation Test (Cosyntropin test)** [1]. A subnormal cortisol response confirms the diagnosis. * **Treatment:** Lifelong replacement of glucocorticoids (Hydrocortisone) and mineralocorticoids (Fludrocortisone) [1].

Question 406: A 15-year-old girl presents with complaints of puffy eyes, swelling in the neck, weight gain, and fatigue. Investigations reveal the presence of thyroid peroxidase antibodies and elevated TSH levels. What is the most likely diagnosis?

A. Hashimoto thyroiditis (Correct Answer)
B. Graves' disease
C. Iodine deficiency
D. Congenital hypothyroidism

Explanation: **Explanation:** The clinical presentation of puffy eyes (periorbital edema), neck swelling (goiter), weight gain, and fatigue in a young girl is classic for **hypothyroidism**. The presence of **Thyroid Peroxidase (TPO) antibodies** and **elevated TSH** confirms an autoimmune etiology, specifically **Hashimoto thyroiditis**. **Why Hashimoto thyroiditis is correct:** Hashimoto thyroiditis is the most common cause of hypothyroidism in iodine-sufficient regions. It is characterized by autoimmune-mediated destruction of the thyroid gland. The hallmark laboratory findings include elevated TSH, low T4, and high titers of anti-TPO and anti-thyroglobulin antibodies. Histologically, it shows diffuse lymphocytic infiltration with germinal centers and **Hürthle cells** (Askanazy cells). **Why other options are incorrect:** * **Graves' disease:** Typically presents with hyperthyroidism (weight loss, tachycardia, tremors). While it involves antibodies (TSH-receptor antibodies), the TSH would be suppressed, not elevated. Management of Graves' ophthalmopathy may involve selenium or glucocorticoids for inflammatory episodes. * **Iodine deficiency:** While it causes goiter and hypothyroidism, it would not typically present with positive TPO antibodies. * **Congenital hypothyroidism:** This presents in infancy (cretinism) with features like prolonged jaundice, macroglossia, and umbilical hernia, rather than an adolescent presentation. **High-Yield NEET-PG Pearls:** * **Most common cause of goitrous hypothyroidism:** Hashimoto thyroiditis. * **Associated HLA:** HLA-DR3 and HLA-DR5. * **Increased Risk:** Patients with Hashimoto’s have an increased risk of **B-cell Non-Hodgkin Lymphoma** of the thyroid. * **Initial Phase:** Some patients may experience a transient hyperthyroid phase known as **"Hashitoxicosis"** due to the release of preformed hormones during gland destruction.

Question 407: Brown pigmentation is seen in which disease?

A. Addison's disease (Correct Answer)
B. Hyperthyroidism
C. Nephritis
D. All of the above

Explanation: **Explanation:** **1. Why Addison’s Disease is Correct:** In primary adrenal insufficiency (Addison’s disease), the adrenal cortex fails to produce cortisol [1]. This lack of negative feedback leads to a compensatory increase in **Adrenocorticotropic Hormone (ACTH)** secretion by the anterior pituitary [2]. ACTH is derived from a precursor molecule called **Pro-opiomelanocortin (POMC)**. When POMC is cleaved to produce ACTH, it also produces **Melanocyte-Stimulating Hormone (MSH)**. High levels of ACTH and MSH stimulate melanocytes in the skin, leading to characteristic **hyperpigmentation** (brownish/bronze discoloration) [2]. This is most prominent in skin creases, pressure points (elbows, knees), oral mucosa, and recent scars. **2. Why the other options are incorrect:** * **Hyperthyroidism:** While skin changes occur (warm, moist, velvety skin), generalized brown pigmentation is not a hallmark. In Graves' disease, one might see pretibial myxedema, but not systemic hyperpigmentation. * **Nephritis:** Chronic Kidney Disease (CKD) can cause a sallow, yellowish-brown tint due to the accumulation of urochromes, but "brown pigmentation" specifically linked to the ACTH mechanism is unique to Addison’s. **3. Clinical Pearls for NEET-PG:** * **Primary vs. Secondary:** Hyperpigmentation occurs **only** in primary adrenal insufficiency. In secondary adrenal insufficiency (pituitary failure), ACTH levels are low, so the skin remains pale [3]. * **The "Tan" that doesn't fade:** Suspect Addison's in a patient with unexplained hypotension, hyponatremia, hyperkalemia, and a "tan" in non-exposed areas (like palmar creases). * **Nelson’s Syndrome:** Rapidly progressive hyperpigmentation following bilateral adrenalectomy due to an enlarging ACTH-secreting pituitary adenoma.

Question 408: Tetany may be present in all the following conditions except?

A. Acute pancreatitis
B. Hysterical hyperventilation
C. Hyperkalemia (Correct Answer)
D. Hypomagnesemia

Explanation: Tetany is a state of increased neuromuscular excitability characterized by carpopedal spasms, paresthesia, and laryngospasm. It is primarily caused by a decrease in the threshold for nerve depolarization. **Why Hyperkalemia is the Correct Answer:** Hyperkalemia (Option C) actually **decreases** neuromuscular excitability by causing persistent depolarization of the cell membrane, which eventually leads to a state of inactivation of sodium channels (refractoriness) [1]. This typically results in muscle weakness or paralysis, not tetany. In contrast, **Hypokalemia** can occasionally be associated with tetany, particularly when it coexists with metabolic alkalosis. **Analysis of Incorrect Options:** * **Acute Pancreatitis (Option A):** This condition often leads to **hypocalcemia** due to the saponification of calcium in necrotic fat (calcium soaps) [2]. Low ionized calcium levels reduce the threshold for action potentials, leading to tetany. * **Hysterical Hyperventilation (Option B):** Hyperventilation causes respiratory alkalosis. The increase in blood pH promotes the binding of ionized calcium to albumin, leading to **decreased ionized calcium** levels (despite normal total calcium), which triggers tetany [2]. * **Hypomagnesemia (Option D):** Magnesium is a cofactor for PTH secretion and action. Severe magnesium deficiency leads to secondary hypocalcemia and can also directly increase neuromuscular excitability, both of which cause tetany [2]. **NEET-PG High-Yield Pearls:** * **Trousseau’s Sign:** Induction of carpal spasm by inflating a BP cuff above systolic pressure for 3 minutes (more sensitive than Chvostek). * **Chvostek’s Sign:** Tapping the facial nerve leads to twitching of facial muscles. * **The "Ionized" Rule:** Tetany is always a function of **ionized calcium** levels, not total calcium [2]. * **Metabolic Alkalosis:** Always consider tetany in alkalotic states due to increased calcium-albumin binding [2].

Question 409: A patient presents with headache and flushing, and has a family history of medullary thyroid carcinoma. What investigation is most appropriate for this patient?

A. Chest X-ray
B. Measurement of 5-hydroxyindoleacetic acid (5-HIAA)
C. Fractionated plasma metanephrines (Correct Answer)
D. Intravenous pyelography

Explanation: ### Explanation **Clinical Reasoning:** The patient presents with symptoms of **episodic flushing and headache** alongside a significant family history of **Medullary Thyroid Carcinoma (MTC)**. This clinical constellation strongly suggests **Multiple Endocrine Neoplasia type 2 (MEN 2A or 2B)**. MTC is a hallmark of MEN 2, and these patients have a high risk of developing **Pheochromocytoma** [1]. The symptoms of headache and flushing (paroxysms) are classic indicators of catecholamine excess. Therefore, the priority is to screen for pheochromocytoma before any other intervention. **Why Option C is Correct:** Measurement of **fractionated plasma metanephrines** (or 24-hour urinary metanephrines) is the initial screening test of choice for pheochromocytoma due to its high sensitivity [1]. In the context of MEN 2, ruling out pheochromocytoma is a critical first step because performing surgery on an undiagnosed pheochromocytoma can trigger a fatal hypertensive crisis. **Why Other Options are Incorrect:** * **Option A (Chest X-ray):** This is a non-specific investigation and does not help in diagnosing neuroendocrine tumors of the adrenal or thyroid. * **Option B (5-HIAA):** This is the metabolite of serotonin used to diagnose **Carcinoid Syndrome**. While carcinoid causes flushing [2], it is not associated with MTC or MEN 2 syndromes. * **Option D (Intravenous pyelography):** This is an outdated imaging modality for the renal collecting system and has no role in the modern workup of endocrine hypertension or MEN syndromes. **NEET-PG High-Yield Pearls:** * **MEN 2A (Sipple Syndrome):** MTC + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN 2B:** MTC + Pheochromocytoma + Mucosal Neuromas/Marfanoid habitus. * **Rule of 10s for Pheochromocytoma:** 10% bilateral, 10% malignant, 10% extra-adrenal, 10% familial [1]. * **Gold Standard Rule:** Always screen for and treat Pheochromocytoma *before* MTC surgery in MEN 2 patients to prevent intraoperative hypertensive crisis.

Question 410: Medical adrenalectomy is seen with:

A. Vincristine
B. Vinblastine
C. Mitotane (Correct Answer)
D. Methotrexate

Explanation: **Explanation:** **Correct Answer: C. Mitotane** **Medical Adrenalectomy** refers to the pharmacological destruction or functional suppression of the adrenal cortex, mimicking a surgical removal. **Mitotane** is the drug of choice for this process. It is a derivative of the insecticide DDT and acts as a **cytotoxic antineoplastic agent** specifically targeting the adrenal cortex. It works via two primary mechanisms: 1. **Direct Adrenolytic Action:** It causes mitochondrial damage and necrosis of the cells in the *zona fasciculata* and *zona reticularis*, leading to atrophy of the gland. 2. **Biochemical Inhibition:** It inhibits enzymes involved in steroidogenesis (such as 11-beta-hydroxylase) and alters the peripheral metabolism of steroids. It is primarily used in the treatment of **inoperable Adrenocortical Carcinoma** and occasionally in refractory Cushing’s Syndrome. **Why other options are incorrect:** * **Vincristine & Vinblastine (Options A & B):** These are Vinca alkaloids that inhibit microtubule formation (M-phase specific). Their primary toxicities are neurological (Vincristine) and bone marrow suppression (Vinblastine), with no specific destructive effect on the adrenal glands. * **Methotrexate (Option D):** An antimetabolite that inhibits dihydrofolate reductase (DHFR). It is used for malignancies, ectopic pregnancy, and autoimmune conditions (RA/Psoriasis), but does not cause adrenal necrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Other drugs causing "Medical Adrenalectomy" (Functional):** Ketoconazole, Metyrapone, and Aminoglutethimide (these inhibit steroid synthesis rather than destroying the tissue). * **Mitotane Side Effect:** It is highly lipophilic and can cause significant GI distress and neurological symptoms (ataxia, lethargy). * **Nelson’s Syndrome:** Be aware that rapid reduction of cortisol (via surgery or drugs) can lead to an ACTH-secreting pituitary adenoma and hyperpigmentation.

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

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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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