Endocrinology Practice Questions

Q: All are features of Cushing's syndrome except?

Hypotension. **Explanation:** Cushing’s syndrome is characterized by a chronic excess of glucocorticoids (cortisol). The correct answer is **Hypotension**, as cortisol excess typically leads to **Hypertension**. **1. Why Hypotension is the correct answer (The Exception):** Cortisol causes hypertension through several mechanisms: it increases the sensitivity of blood vessels to catecholamines (permissive action), inhibits vasodilators like nitric oxide, and at high levels, exerts a **mineralocorticoid effect** by binding to aldosterone receptors. This leads to sodium and water retention, expanding ECF volume and raising blood pressure. Therefore, hypotension is not a feature of Cushing's syndrome. **2. Analysis of Incorrect Options:** * **Central Obesity (A):** This is the most common clinical feature [1]. Cortisol promotes lipogenesis in the trunk and face while causing lipolysis in the extremities, leading to "buffalo hump," "moon facies," and truncal obesity [1]. * **Diabetes (B):** Cortisol is a counter-regulatory hormone that increases gluconeogenesis in the liver and decreases peripheral glucose uptake (insulin resistance), leading to "Steroid Diabetes." * **Hypokalaemia (D):** At high concentrations (especially in Ectopic ACTH syndrome), cortisol acts on the renal mineralocorticoid receptors, leading to potassium excretion in exchange for sodium reabsorption. **NEET-PG High-Yield Pearls:** * **Screening Test of Choice:** 24-hour urinary free cortisol or Overnight Dexamethasone Suppression Test (ONDST) [2]. * **Gold Standard Test:** Low-dose dexamethasone suppression test (LDDST) [2]. * **Most common cause:** Iatrogenic (exogenous steroids). * **Most common endogenous cause:** Cushing’s Disease (Pituitary adenoma) [1]. * **Clinical Sign:** Purple striae (wider than 1 cm) are highly specific for Cushing’s.

Q: 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?

Klinefelter syndrome. **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].

Q: 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?

Phenoxybenzamine and propranolol. ### **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]

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

Usually intrasellar in location. 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].

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

Decreased sweating. 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].

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

Gastrinoma. 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].

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

Intravenous fluid resuscitation with isotonic saline. **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].

Q: 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?

Oral glucose tolerance test (OGTT). ### 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).

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

Increased carotene. **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 1

All are features of Cushing's syndrome except?

Accepted Answer

Hypotension

Answer

Central obesity

Answer

Diabetes

Answer

Hypokalaemia

Question 2

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?

Accepted Answer

Klinefelter syndrome

Answer

Vanishing testis syndrome

Answer

Noonan syndrome

Answer

Adrenal hyperplasia

Question 3

Primary hyperparathyroidism is suggested by which of the following findings?

Accepted Answer

Increased serum calcium

Answer

Low urinary calcium (<200 mg/day)

Answer

Decreased alkaline phosphatase

Answer

Calcitonin level

Question 4

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?

Accepted Answer

Phenoxybenzamine and propranolol

Answer

Phentolamine and phenoxybenzamine

Answer

Propranolol

Answer

Nitroglycerine

Question 5

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

Accepted Answer

Usually intrasellar in location

Answer

Arise from Rathke's pouch

Answer

Can cause visual disturbances

Answer

Presents with hypopituitarism in adults

Question 6

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

Accepted Answer

Decreased sweating

Answer

Visceromegaly

Answer

Hypertension

Answer

Soft tissue and bone enlargement

Question 7

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

Accepted Answer

Gastrinoma

Answer

Insulinoma

Answer

Lipoma

Answer

Glucagonoma

Question 8

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

Accepted Answer

Intravenous fluid resuscitation with isotonic saline

Answer

Insulin administration

Answer

Administration of sodium bicarbonate

Answer

Potassium repletion

Question 9

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?

Accepted Answer

Oral glucose tolerance test (OGTT)

Answer

Urine glucose estimation hourly for 5 hours

Answer

Repeat Benedict's test

Answer

24-hour urine sugar estimation

Question 10

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

Accepted Answer

Increased carotene

Answer

Increased bilirubin

Answer

Increased cholesterol

Answer

Increased levels of thyroid hormones

Endocrinology — MCQs

Endocrinology — MCQs

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