Endocrinology — MCQs

A 25-year-old man presents with a confused state, intense headache, profuse sweating, and eye rolling. His wife reports similar past events that resolved spontaneously. He smokes 20 packs of cigarettes per year and drinks 2-3 beers on weekends. On examination, he is confused, obeys simple commands, has intact deep tendon reflexes, and vital signs show BP 210/108 mm Hg and pulse 124/min. Laboratory results are: Na+ 142 meq/L, K+ 3.8 meq/L, BUN 30 mg/dL, S creatinine 1.0 mg/dL, and Blood sugar 110 mg/dL. What medication should be started preoperatively given the patient's condition?

Q484Medium

All of the following statements regarding Craniopharyngiomas are true, except:

Q485Easy

In Acromegaly, which of the following is NOT typically seen?

Q486Easy

What is the most common association in Multiple Endocrine Neoplasia type 1 (MEN I)?

Q487Medium

What is the most important initial step in the management of diabetic ketoacidosis?

Q488Medium

A 42-year-old male has a strongly positive Benedict's test, random blood sugar is > 163 mg%, and fasting blood sugar is > 200 mg%. What is the next line of investigation?

Q489Medium

Yellowing of the skin occurs in hypothyroidism because of which of the following?

Q490Medium

Which of the following is true about Cushing's syndrome?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 481: A 23-year-old tall male presents with complaints of absent pubic hair, axillary hair, infantile genitalia, high LH, FSH levels, and XXY karyotype. What is the most probable diagnosis?

A. Vanishing testis syndrome
B. Noonan syndrome
C. Adrenal hyperplasia
D. Klinefelter syndrome (Correct Answer)

Explanation: **Explanation:** The clinical presentation of a tall male with signs of hypogonadism (absent secondary sexual hair, infantile genitalia) and hypergonadotropic hypogonadism (elevated LH and FSH) is classic for **Klinefelter Syndrome (47, XXY)**. **1. Why Klinefelter Syndrome is correct:** Klinefelter syndrome is the most common cause of primary hypogonadism in males [1]. The presence of an extra X chromosome leads to **dysgenesis of seminiferous tubules** (causing low inhibin and high FSH) and **damage to Leydig cells** (causing low testosterone and high LH) [2]. The lack of testosterone results in "eunuchoid" body habitus (tall stature due to delayed epiphyseal closure) and failure of secondary sexual characteristic development [1]. **2. Why other options are incorrect:** * **Vanishing Testis Syndrome (Congenital Anorchia):** While this presents with high LH/FSH and infantile genitalia, the karyotype is a normal **46, XY**, and patients are typically not tall. * **Noonan Syndrome:** Often called "Male Turner Syndrome," it presents with short stature, webbed neck, and pulmonary stenosis [3]. The karyotype is usually **46, XY**. * **Adrenal Hyperplasia (CAH):** In males, this typically causes precocious (early) puberty and virilization, not infantile genitalia or delayed puberty. **High-Yield Clinical Pearls for NEET-PG:** * **Karyotype:** Most common is 47, XXY (due to meiotic non-disjunction). * **Testicular Findings:** Characteristically **small, firm testes** (due to hyalinization and fibrosis) [1]. * **Biochemical Profile:** ↓ Testosterone, ↑ LH, ↑ FSH, ↑ Estradiol (leading to gynecomastia) [1]. * **Increased Risks:** Breast cancer (20x higher than normal males), extragonadal germ cell tumors, and autoimmune diseases (like SLE) [3]. * **Intellectual Disability:** Usually mild; IQ may be slightly lower than siblings but often within the normal range [1].

Question 482: Primary hyperparathyroidism is suggested by which of the following findings?

A. Increased serum calcium (Correct Answer)
B. Low urinary calcium (<200 mg/day)
C. Decreased alkaline phosphatase
D. Calcitonin level

Explanation: **Explanation:** **Primary Hyperparathyroidism (PHPT)** is most commonly caused by a solitary parathyroid adenoma (85%). The fundamental pathology is the autonomous overproduction of Parathyroid Hormone (PTH), which acts on the bones and kidneys to elevate serum calcium levels [1]. **Why Option A is Correct:** The hallmark of PHPT is **hypercalcemia** (increased serum calcium) [4]. PTH increases calcium levels through three mechanisms: 1. Stimulating osteoclastic bone resorption [1]. 2. Increasing renal distal tubular calcium reabsorption [1]. 3. Stimulating the synthesis of 1,25-dihydroxyvitamin D in the kidneys, which enhances intestinal calcium absorption [1]. **Why the Other Options are Incorrect:** * **Option B:** In PHPT, urinary calcium is typically **high or normal** (Hypercalciuria) [3]. While PTH increases renal reabsorption, the filtered load of calcium (due to high serum levels) overwhelms the kidneys, leading to net excretion. *Low urinary calcium (<100 mg/day)* is characteristic of Familial Hypocalciuric Hypercalcemia (FHH), a key differential [2]. * **Option C:** Alkaline phosphatase (ALP) is often **elevated** (not decreased) in PHPT, especially when there is significant bone involvement (Osteitis Fibrosa Cystica), reflecting increased osteoblastic activity following bone resorption. * **Option D:** Calcitonin is a marker for Medullary Thyroid Carcinoma (MTC). While MTC is associated with MEN 2A/2B [2], calcitonin itself is not a diagnostic finding for hyperparathyroidism. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Hypercalcemia, elevated PTH, and low/normal serum phosphate [4]. * **Radiological Sign:** Subperiosteal bone resorption, most classically seen on the radial aspect of the middle phalanges. * **Brown Tumors:** These are non-neoplastic cystic lesions of the bone caused by rapid osteoclast activity in PHPT. * **Most common presentation:** Today, most patients are asymptomatic and detected via routine biochemical screening showing isolated hypercalcemia [4].

Question 483: A 25-year-old man presents with a confused state, intense headache, profuse sweating, and eye rolling. His wife reports similar past events that resolved spontaneously. He smokes 20 packs of cigarettes per year and drinks 2-3 beers on weekends. On examination, he is confused, obeys simple commands, has intact deep tendon reflexes, and vital signs show BP 210/108 mm Hg and pulse 124/min. Laboratory results are: Na+ 142 meq/L, K+ 3.8 meq/L, BUN 30 mg/dL, S creatinine 1.0 mg/dL, and Blood sugar 110 mg/dL. What medication should be started preoperatively given the patient's condition?

A. Phentolamine and phenoxybenzamine
B. Propranolol
C. Nitroglycerine
D. Phenoxybenzamine and propranolol (Correct Answer)

Explanation: ### **Explanation** The clinical presentation—episodic headache, profuse sweating, palpitations (tachycardia), and severe hypertension (210/108 mmHg)—is the classic triad of **Pheochromocytoma**. The "eye rolling" and confusion represent hypertensive encephalopathy or transient neurological symptoms during a paroxysm. **1. Why Option D is Correct:** The cornerstone of preoperative management for pheochromocytoma is **combined alpha and beta-adrenergic blockade** [1]. * **Phenoxybenzamine** (an irreversible, non-selective alpha-blocker) is started first to control hypertension and expand the contracted intravascular volume [1]. * **Propranolol** (a beta-blocker) is added only **after** adequate alpha-blockade is achieved to manage tachycardia or arrhythmias. **2. Why Other Options are Incorrect:** * **Option A:** Phentolamine is a short-acting alpha-blocker used for hypertensive crises, but it is not the standard long-term preoperative oral regimen. Using two alpha-blockers together is redundant. * **Option B:** Giving a beta-blocker alone is **contraindicated**. Blocking vasodilatory beta-2 receptors while alpha-1 receptors are unopposed leads to "unopposed alpha stimulation," causing a catastrophic rise in blood pressure. [1] * **Option C:** Nitroglycerine is a vasodilator used in acute hypertensive emergencies but does not address the underlying catecholamine excess required for surgical stabilization. **3. Clinical Pearls for NEET-PG:** * **Rule of 10s:** 10% bilateral, 10% malignant, 10% extra-adrenal (Paraganglioma), 10% pediatric, 10% familial. * **Sequence Matters:** Always **Alpha before Beta** (usually 7–14 days before surgery) [1]. * **Diagnosis:** Best initial screening test is **Plasma free metanephrines**; most specific is **24-hour urinary catecholamines/metanephrines**. * **Associated Syndromes:** MEN 2A, MEN 2B, von Hippel-Lindau (VHL), and Neurofibromatosis type 1 (NF1). [1]

Question 484: All of the following statements regarding Craniopharyngiomas are true, except:

A. Arise from Rathke's pouch
B. Can cause visual disturbances
C. Presents with hypopituitarism in adults
D. Usually intrasellar in location (Correct Answer)

Explanation: Craniopharyngiomas are benign but locally aggressive tumors that account for about 3-5% of all intracranial tumors. **1. Why Option D is the Correct Answer (The False Statement):** Craniopharyngiomas are **primarily suprasellar** in location (about 75-90% of cases). While they can have an intrasellar component, a purely intrasellar craniopharyngioma is rare. They typically arise along the pituitary stalk and expand into the suprasellar cistern, often compressing the optic chiasm and hypothalamus [1]. **2. Analysis of Other Options:** * **Option A (True):** These tumors are derived from the remnants of **Rathke’s pouch** (ectodermal origin), which is the same embryological precursor as the anterior pituitary gland [1]. * **Option B (True):** Due to their suprasellar location, they frequently compress the **optic chiasm**, leading to visual field defects, most classically **bitemporal hemianopia** [1]. * **Option C (True):** In adults, the gradual expansion of the tumor compresses the normal pituitary gland or stalk, leading to **hypopituitarism** (growth hormone deficiency is most common, followed by gonadotropin deficiency). **Clinical Pearls for NEET-PG:** * **Bimodal Age Distribution:** Peaks at 5–14 years and 50–75 years [1]. * **Imaging Triad:** Suprasellar mass showing **calcification** (very common in children), **cystic components** (filled with "machinery oil" fluid), and **solid enhancement** [1]. * **Histology:** Two types—**Adamantinomatous** (common in children, shows "wet keratin" and calcification) and **Papillary** (common in adults, lacks calcification). * **Clinical Presentation:** Often presents with the triad of headaches, visual disturbances, and endocrine dysfunction (including Diabetes Insipidus) [1].

Question 485: In Acromegaly, which of the following is NOT typically seen?

A. Visceromegaly
B. Decreased sweating (Correct Answer)
C. Hypertension
D. Soft tissue and bone enlargement

Explanation: In Acromegaly, the clinical presentation is driven by the chronic hypersecretion of **Growth Hormone (GH)** and its mediator, **IGF-1**, leading to widespread anabolic effects [1]. ### **Why "Decreased Sweating" is the Correct Answer** In Acromegaly, patients actually experience **increased sweating (hyperhidrosis)** and oily skin (seborrhea). This occurs because GH causes hypertrophy of the sweat (eccrine) and sebaceous glands. Hyperhidrosis is a sensitive clinical marker of disease activity; its resolution often indicates successful treatment. ### **Explanation of Incorrect Options** * **Visceromegaly (A):** GH/IGF-1 stimulate the growth of internal organs [3]. Common findings include cardiomegaly, hepatomegaly, splenomegaly, and thyroid enlargement [3]. * **Hypertension (C):** Approximately 30–50% of acromegalic patients have hypertension. It is caused by increased plasma volume (due to renal sodium retention) and increased peripheral vascular resistance. * **Soft tissue and bone enlargement (D):** This is the hallmark of the disease [3]. It manifests as increased glove/shoe size, "spade-like" hands, frontal bossing, and macroglossia [3]. ### **NEET-PG High-Yield Clinical Pearls** * **Screening Test:** Serum **IGF-1** levels (more stable than GH, which is pulsatile) [1]. * **Confirmatory Test:** **Oral Glucose Tolerance Test (OGTT)**; failure to suppress GH to <1 ng/mL after 75g glucose load is diagnostic [2]. * **Most Common Cause:** Somatotroph adenoma of the anterior pituitary [2]. * **Metabolic Associations:** Impaired glucose tolerance or Diabetes Mellitus (GH is a counter-regulatory hormone that causes insulin resistance). * **Mortality:** Most commonly due to **Cardiovascular disease** (congestive heart failure/arrhythmias). There is also an increased risk of **Colonic polyps/Carcinoma** [2].

Question 486: What is the most common association in Multiple Endocrine Neoplasia type 1 (MEN I)?

A. Gastrinoma (Correct Answer)
B. Insulinoma
C. Lipoma
D. Glucagonoma

Explanation: Multiple Endocrine Neoplasia type 1 (MEN 1), also known as **Wermer’s Syndrome**, is an autosomal dominant disorder caused by a mutation in the *MEN1* gene (encoding the protein Menin) [1]. It is classically characterized by the "3 Ps": **P**arathyroid (95%), **P**ancreatic Islet Cells (40-70%), and **P**ituitary (30-40%) [1]. **Why Gastrinoma is correct:** Among the pancreatic neuroendocrine tumors (NETs) associated with MEN 1, **Gastrinoma** is the most common functional tumor (occurring in ~40% of patients). It often leads to Zollinger-Ellison Syndrome, characterized by refractory peptic ulcers. While Parathyroid hyperplasia is the most common overall manifestation of MEN 1, among the options provided (which focus on pancreatic/associated tumors), Gastrinoma is the most frequent. **Analysis of Incorrect Options:** * **B. Insulinoma:** This is the second most common functional pancreatic NET in MEN 1, but it occurs less frequently than Gastrinoma (approx. 10-30%). * **C. Lipoma:** While cutaneous manifestations like lipomas, angiofibromas, and collagenomas are common in MEN 1, they are non-endocrine associations and occur less frequently or are less clinically diagnostic than Gastrinomas in the context of the syndrome's classic triad. * **D. Glucagonoma:** These are rare functional pancreatic tumors in MEN 1, occurring in less than 3% of cases. **NEET-PG High-Yield Pearls:** * **Most common initial presentation:** Hyperparathyroidism (Hypercalcemia). * **Most common Pituitary tumor:** Prolactinoma. * **Most common cause of death:** Malignant pancreatic NETs or Thymic carcinoids. * **Screening:** Genetic testing for *MEN1* gene mutations is the gold standard for family members [2].

Question 487: What is the most important initial step in the management of diabetic ketoacidosis?

A. Insulin administration
B. Intravenous fluid resuscitation with isotonic saline (Correct Answer)
C. Administration of sodium bicarbonate
D. Potassium repletion

Explanation: **Explanation:** The management of Diabetic Ketoacidosis (DKA) follows a prioritized sequence, where **Intravenous (IV) fluid resuscitation with isotonic saline (0.9% NaCl)** is the most critical initial step [1]. Patients with DKA typically have a massive fluid deficit (averaging 6–9 liters) due to osmotic diuresis [1]. Immediate hydration restores intravascular volume, improves renal perfusion (allowing for glucose excretion), and reduces the concentration of counter-regulatory hormones, which helps lower blood glucose levels even before insulin is started [2]. **Why other options are incorrect:** * **Insulin administration:** While essential to stop ketogenesis, insulin should only be started *after* fluid resuscitation has commenced and potassium levels are confirmed to be >3.3 mEq/L [2]. Starting insulin too early can cause an intracellular shift of water and potassium, potentially leading to vascular collapse or fatal arrhythmias [3]. * **Potassium repletion:** Although DKA involves a total body potassium deficit, repletion is secondary to ensuring adequate urine output via fluid resuscitation [3]. * **Sodium bicarbonate:** This is rarely indicated and only considered in extreme acidosis (pH < 6.9), as it can worsen intracellular acidosis and cause a rebound shift in the oxyhemoglobin dissociation curve. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of 10":** Initial fluid bolus is typically 10-20 mL/kg in the first hour. * **Potassium Check:** Always check serum K+ before starting insulin [2]. If K+ < 3.3 mEq/L, hold insulin and replace potassium first. * **Switching Fluids:** Change from 0.9% NS to 5% Dextrose (D5) once blood glucose reaches ~200–250 mg/dL to prevent hypoglycemia while continuing the insulin infusion to clear ketones [2]. * **Resolution Marker:** DKA is considered resolved based on the **anion gap** and pH, not just the normalization of blood glucose [2].

Question 488: A 42-year-old male has a strongly positive Benedict's test, random blood sugar is > 163 mg%, and fasting blood sugar is > 200 mg%. What is the next line of investigation?

A. Urine glucose estimation hourly for 5 hours
B. Oral glucose tolerance test (OGTT) (Correct Answer)
C. Repeat Benedict's test
D. 24-hour urine sugar estimation

Explanation: ### Explanation **1. Why the Correct Answer (B) is Right:** The patient presents with symptoms and biochemical findings suggestive of Diabetes Mellitus (DM). However, the values provided are borderline or inconsistent with standard diagnostic criteria (e.g., a Fasting Blood Sugar (FBS) of >200 mg/dL is diagnostic, but a Random Blood Sugar (RBS) of >163 mg/dL is not). According to the **WHO and ADA guidelines**, when blood glucose levels are equivocal or do not clearly meet the diagnostic threshold for DM (FBS ≥126 mg/dL or RBS/2-hour post-load ≥200 mg/dL), the **Oral Glucose Tolerance Test (OGTT)** is the gold standard for confirmation [1]. It assesses the body's ability to handle a standardized glucose load (75g) and helps differentiate between Impaired Glucose Tolerance (IGT) and overt Diabetes Mellitus. **2. Why the Other Options are Incorrect:** * **A & D (Urine Glucose Estimation):** Benedict’s test and urine sugar levels are poor diagnostic tools for DM. The **renal threshold for glucose** is approximately 180 mg/dL; glucose only appears in urine once this is exceeded. Furthermore, urine testing cannot distinguish between DM and renal glycosuria. * **C (Repeat Benedict’s Test):** Benedict’s test is a non-specific semi-quantitative test for reducing sugars. Repeating it adds no diagnostic value to the management of hyperglycemia. **3. Clinical Pearls for NEET-PG:** * **Diagnostic Criteria for DM:** * FBS ≥ 126 mg/dL [1] * 2-hour OGTT (75g) ≥ 200 mg/dL * HbA1c ≥ 6.5% * Random Plasma Glucose ≥ 200 mg/dL (with classic symptoms of hyperglycemia). * **Benedict’s Test:** It detects reducing sugars (Glucose, Fructose, Lactose, Maltose, Galactose). It is **negative** for Sucrose (non-reducing). * **Renal Glycosuria:** Presence of glucose in urine despite normal blood glucose levels (seen in pregnancy or Fanconi syndrome).

Question 489: Yellowing of the skin occurs in hypothyroidism because of which of the following?

A. Increased bilirubin
B. Increased cholesterol
C. Increased carotene (Correct Answer)
D. Increased levels of thyroid hormones

Explanation: **Explanation:** In hypothyroidism, the yellowing of the skin is primarily due to **Hypercarotenemia**. Thyroid hormones are essential for the hepatic conversion of dietary beta-carotene into Vitamin A (Retinol) [1]. In a hypothyroid state, this enzymatic conversion is impaired, leading to an accumulation of carotene in the serum and its subsequent deposition in the stratum corneum of the skin. **Analysis of Options:** * **A. Increased bilirubin:** While jaundice (hyperbilirubinemia) causes yellowing, it typically involves the **sclera** (icterus). In hypothyroidism, the yellowing spares the sclera, distinguishing it from liver disease. * **B. Increased cholesterol:** Hypothyroidism does cause hypercholesterolemia (due to decreased LDL receptor expression [2]), but cholesterol itself does not impart a yellow pigment to the skin. * **C. Increased carotene (Correct):** The lack of thyroxine prevents the breakdown of carotene, leading to "Carotenemic xanthoderma." * **D. Increased levels of thyroid hormones:** This describes hyperthyroidism, which is associated with warm, moist, and often flushed skin, not yellowing. **High-Yield Clinical Pearls for NEET-PG:** * **Scleral Sparing:** Carotenemia (hypothyroidism) causes yellowing of the palms and soles but **never** the sclera. Jaundice **always** involves the sclera. * **Vitamin A Connection:** Hypothyroidism can lead to functional Vitamin A deficiency despite high carotene levels because the conversion process is blocked [1]. * **Skin Texture:** The skin in hypothyroidism is classically described as **"Cold, Dry, and Coarse"** with non-pitting edema (Myxedema) due to the accumulation of glycosaminoglycans (hyaluronic acid) in the dermis.

Question 490: Which of the following is true about Cushing's syndrome?

A. Red striae are present
B. Increased adrenalin secretion
C. Proximal muscle weakness is present (Correct Answer)
D. Edema is present

Explanation: **Explanation:** **Proximal muscle weakness (Option C)** is a hallmark clinical feature of Cushing’s syndrome, occurring in approximately 60–80% of patients. It is caused by the **catabolic effect of excess cortisol** on skeletal muscle, leading to the breakdown of muscle proteins (proteolysis) and subsequent atrophy of Type II fast-twitch muscle fibers [3]. This typically manifests as difficulty climbing stairs or rising from a seated position. **Analysis of Incorrect Options:** * **Option A:** While striae are characteristic, they are classically **purple/violaceous** and wide (>1 cm), not simply red. This color is due to the thinning of the dermis, making the underlying vascular subcutaneous tissue visible [3]. * **Option B:** Cushing’s syndrome involves the overproduction of **cortisol** (from the adrenal cortex), not adrenalin (from the adrenal medulla) [2]. * **Option C:** While cortisol has some mineralocorticoid activity that can cause fluid retention, **overt edema** is not a primary diagnostic feature of Cushing's unless there is severe ectopic ACTH production or co-existing heart/renal failure. **NEET-PG High-Yield Pearls:** * **Most common cause:** Overall, the most common cause is **exogenous steroid use**. The most common endogenous cause is **Cushing’s Disease** (ACTH-secreting pituitary adenoma) [2]. * **Screening Tests:** 24-hour urinary free cortisol, Low-dose dexamethasone suppression test (LDDST), or Late-night salivary cortisol [1], [4]. * **Hypokalemic Metabolic Alkalosis:** Often seen in ectopic ACTH syndrome (e.g., Small Cell Lung Cancer) due to massive cortisol levels saturating the 11β-HSD2 enzyme, leading to mineralocorticoid excess.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

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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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