Endocrinology — MCQs
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All are the features of carcinoid syndrome except?
A 17-year-old male presents with a 3-month history of headache, weight gain, decreased concentration, polyuria, and polydipsia. His headaches are mostly in the morning and involve the frontal region. On examination, he was found to have a bitemporal visual field defect and no facial hair. An MRI scan revealed a suprasellar partially calcified cystic lesion with displacement of the optic chiasm. What is the most likely pathology?
A 36-year-old male presents with recent darkening of his skin, which has a dark, bronze color. Workup reveals signs of diabetes mellitus. His serum iron is 1150 mg/dL, and his transferrin saturation is 98%. A liver biopsy reveals extensive deposits of hemosiderin in hepatocytes and Kupffer cells. What is the most likely mechanism responsible for this constellation of findings?
Which laboratory value is most indicative of central diabetes insipidus?
All of the following will be seen in a patient with hyperthyroidism except?
Which of the following features is NOT typically seen in Cushing's Syndrome?
Which of the following are the extraintestinal manifestations of Sipple syndrome?
Werner syndrome is associated with which of the following endocrine neoplasia syndromes?
A 25-year-old female, several months postpartum and breast-feeding, presents with acute cessation of lactation. She has not menstruated since delivery and reports fatigue and cold intolerance. Laboratory workup reveals deficiency of ACTH and other anterior pituitary hormones. What is the most likely cause of this patient's signs and symptoms?
What is the most common neuropathy in Diabetes Mellitus?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 341: All are the features of carcinoid syndrome except?
- A. Wheezing
- B. Diarrhea
- C. Acute appendicitis (Correct Answer)
- D. Flushing
Explanation: **Explanation:** Carcinoid syndrome occurs when vasoactive substances (primarily **serotonin**, but also histamine, beautykinin, and prostaglandins) enter the systemic circulation. This typically happens with carcinoid tumors of the midgut that have metastasized to the liver, bypassing the "first-pass" metabolism that normally inactivates these substances [1]. **Why "Acute Appendicitis" is the correct answer:** While the **appendix** is the most common site for a carcinoid tumor, the tumor itself is usually an incidental finding during surgery. Carcinoid syndrome is a systemic manifestation of advanced disease (metastasis) [1]. Acute appendicitis is a localized inflammatory process caused by luminal obstruction; it is a potential *presentation* of a tumor, but it is **not a feature** of the systemic "Carcinoid Syndrome" complex [1]. **Analysis of other options:** * **Flushing (Option D):** The most common clinical feature (85%). It is a paroxysmal cyanotic/erythematous redness of the face and neck triggered by alcohol, exercise, or stress. * **Diarrhea (Option B):** Occurs in ~80% of cases due to increased intestinal motility caused by serotonin. It is typically secretory and does not resolve with fasting. * **Wheezing (Option A):** Seen in ~15% of patients. It is caused by serotonin-induced bronchospasm, mimicking asthma. **NEET-PG High-Yield Pearls:** * **Diagnosis:** The best initial screening test is **24-hour urinary 5-HIAA** (a metabolite of serotonin). * **Localization:** **Somatostatin receptor scintigraphy** (OctreoScan) is the imaging of choice. * **Cardiac Involvement:** Right-sided heart failure (Tricuspid regurgitation/Pulmonary stenosis) is common because the lungs contain monoamine oxidase (MAO) which inactivates serotonin before it reaches the left heart. * **Treatment:** **Octreotide** (Somatostatin analog) is used to manage symptoms and prevent a "carcinoid crisis" during surgery.
Question 342: A 17-year-old male presents with a 3-month history of headache, weight gain, decreased concentration, polyuria, and polydipsia. His headaches are mostly in the morning and involve the frontal region. On examination, he was found to have a bitemporal visual field defect and no facial hair. An MRI scan revealed a suprasellar partially calcified cystic lesion with displacement of the optic chiasm. What is the most likely pathology?
- A. Giant aneurysm of the carotid artery
- B. Pituitary macroadenoma
- C. Glioblastoma multiforme
- D. Craniopharyngioma (Correct Answer)
Explanation: **Explanation:** The clinical presentation is classic for a **Craniopharyngioma**, a benign but locally aggressive tumor derived from remnants of **Rathke’s pouch** [1]. **Why Craniopharyngioma is correct:** 1. **Age & Symptoms:** It has a bimodal distribution (5–14 years and >50 years) [1]. In this 17-year-old, the tumor causes mass effect (morning headaches, bitemporal hemianopia due to optic chiasm compression) and endocrine dysfunction (delayed puberty/lack of facial hair due to GH/LH/FSH deficiency). 2. **Diabetes Insipidus (DI):** Polyuria and polydipsia indicate central DI, a hallmark of craniopharyngiomas due to hypothalamic-pituitary axis disruption [1]. 3. **Imaging:** The description of a **suprasellar, cystic, and calcified lesion** is pathognomonic [1]. Calcification is seen in ~90% of pediatric cases. **Why other options are incorrect:** * **Giant aneurysm:** While it can cause mass effect, it would not typically present with a cystic, calcified appearance on MRI or cause DI in a teenager. * **Pituitary macroadenoma:** These are rare in adolescents. While they cause bitemporal hemianopia [2], they are usually solid and **rarely calcified**. * **Glioblastoma multiforme:** This is a high-grade intraparenchymal malignancy, not a suprasellar cystic/calcified lesion, and is rare in this age group. **High-Yield Pearls for NEET-PG:** * **Histology:** Look for "Adamantinomatous" type (machinery oil fluid, wet keratin, stellate reticulum) in children. * **Imaging Triad:** Suprasellar location, Cystic components, and Calcification. * **Most common cause** of hypopituitarism in children. * **Visual field defect:** Bitemporal hemianopia (starts in the **inferior** quadrants because the tumor compresses the chiasm from above).
Question 343: A 36-year-old male presents with recent darkening of his skin, which has a dark, bronze color. Workup reveals signs of diabetes mellitus. His serum iron is 1150 mg/dL, and his transferrin saturation is 98%. A liver biopsy reveals extensive deposits of hemosiderin in hepatocytes and Kupffer cells. What is the most likely mechanism responsible for this constellation of findings?
- A. Defective excretion of copper into the bile
- B. Defective synthesis of a1 antitrypsin
- C. Excessive reabsorption of iron from the small intestines (Correct Answer)
- D. Excessive absorption of galactose from the small intestines
Explanation: The clinical presentation of **bronze skin pigmentation**, **diabetes mellitus** ("bronze diabetes"), and evidence of iron overload (high serum iron, 98% transferrin saturation, and hemosiderin deposits in the liver) is a classic description of **Hereditary Hemochromatosis (HH)** [1, 3]. **1. Why Option C is Correct:** Hereditary Hemochromatosis is most commonly caused by a mutation in the **HFE gene** (C282Y) [2]. This mutation leads to a deficiency in **Hepcidin**, the master regulator of iron homeostasis. Low hepcidin levels result in the upregulation of **ferroportin** on the basolateral membrane of enterocytes, leading to **excessive and uncontrolled reabsorption of dietary iron from the small intestine** [2]. Over decades, this iron accumulates in organs (liver, pancreas, heart, skin), causing oxidative damage and fibrosis [1, 3]. **2. Why the Other Options are Incorrect:** * **Option A:** Defective copper excretion into bile describes **Wilson’s Disease** [3]. While it affects the liver, it presents with Kayser-Fleischer rings and low ceruloplasmin, not iron overload or bronze skin. * **Option B:** Defective synthesis of **α1-antitrypsin** leads to its accumulation in the liver (PAS-positive globules) and emphysema, but does not cause systemic iron overload. * **Option D:** Excessive galactose absorption is associated with **Galactosemia**, a metabolic disorder presenting in infancy with cataracts and jaundice, unrelated to adult-onset bronze diabetes. ### High-Yield Clinical Pearls for NEET-PG: * **Classic Triad:** Cirrhosis, Diabetes Mellitus, and Skin Pigmentation ("Bronze Diabetes") [2]. * **Diagnosis:** Initial screening is **Transferrin Saturation** (>45% is suggestive). Gold standard for diagnosis is **HFE gene analysis** [1, 3]. * **MRI Finding:** Low signal intensity on T2-weighted images (due to paramagnetic effect of iron) [1]. * **Treatment:** The mainstay of treatment is **therapeutic phlebotomy** [1]. * **Complication:** Patients have a significantly increased risk (up to 200-fold) of developing **Hepatocellular Carcinoma (HCC)** [2].
Question 344: Which laboratory value is most indicative of central diabetes insipidus?
- A. Low urinary osmolality and high serum osmolality (Correct Answer)
- B. High urinary osmolality and low serum osmolality
- C. Low urinary osmolality and low serum osmolality
- D. High urinary osmolality and very low serum osmolality
Explanation: Diabetes Insipidus (DI) is characterized by a deficiency of Antidiuretic Hormone (ADH) in Central DI or resistance to its action in Nephrogenic DI [1]. ADH is responsible for water reabsorption in the collecting ducts of the kidney. **1. Why Option A is Correct:** In Central DI, the lack of ADH prevents the kidneys from concentrating urine [1]. This leads to the excretion of large volumes of dilute urine, resulting in **low urinary osmolality** (typically <300 mOsm/kg). As the body loses pure water, the blood becomes concentrated, leading to hypernatremia and **high serum osmolality** (>295 mOsm/kg) [3]. This "dilute urine in the face of concentrated plasma" is the hallmark of DI. **2. Why Incorrect Options are Wrong:** * **Option B:** High urinary and low serum osmolality is characteristic of **SIADH** (Syndrome of Inappropriate ADH), where excess ADH causes water retention and concentrated urine [2]. * **Option C:** Low urinary and low serum osmolality is seen in **Primary Polydipsia** [2]. Here, the patient drinks excessive water, lowering serum osmolality, which physiologically suppresses ADH, leading to dilute urine [3]. * **Option D:** This pattern is not typical for DI; very low serum osmolality would suggest severe water intoxication or SIADH. **Clinical Pearls for NEET-PG:** * **Water Deprivation Test:** The gold standard to differentiate DI from Primary Polydipsia [3]. * **Desmopressin (DDAVP) Challenge:** Used to differentiate Central from Nephrogenic DI. In **Central DI**, urinary osmolality increases by >50%; in **Nephrogenic DI**, there is little to no response (<10%) [3]. * **Imaging:** In Central DI, MRI may show the "loss of the posterior pituitary bright spot." * **Drug of Choice:** Desmopressin is the treatment of choice for Central DI [3].
Question 345: All of the following will be seen in a patient with hyperthyroidism except?
- A. Myxedema
- B. Dalrymple sign
- C. Moist warm hands
- D. Constipation (Correct Answer)
Explanation: In hyperthyroidism, the excess of circulating thyroid hormones ($T_3$ and $T_4$) leads to a hypermetabolic state and increased sympathetic nervous system activity. [1] **Explanation of the Correct Answer:** * **D. Constipation:** This is the correct answer because it is **not** seen in hyperthyroidism. Excess thyroid hormone increases gastrointestinal motility and transit time, typically resulting in **increased frequency of bowel movements** or diarrhea. Constipation is a classic feature of *hypothyroidism*. [2] **Analysis of Incorrect Options:** * **A. Myxedema:** While "Generalized Myxedema" is seen in hypothyroidism, **Pretibial Myxedema** (Graves' dermopathy) is a specific feature of Graves' disease, the most common cause of hyperthyroidism. [3] It occurs due to the deposition of glycosaminoglycans in the dermis. * **B. Dalrymple sign:** This refers to the widening of the palpebral fissures (staring look) due to upper eyelid retraction. It is a classic ocular sign of thyrotoxicosis caused by sympathetic overactivity of the Müller’s muscle. [2] * **C. Moist warm hands:** Hyperthyroidism increases the basal metabolic rate and cutaneous vasodilation to dissipate heat. This results in skin that is characteristically warm, moist (due to diaphoresis), and smooth. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Cardiac:** Sinus tachycardia and Atrial Fibrillation (especially in elderly) are common. [2] * **Neuromuscular:** Fine tremors of outstretched hands and proximal muscle weakness (thyrotoxic myopathy). [1] * **Eye Signs:** Stellwag’s sign (infrequent blinking), Joffroy’s sign (absence of forehead wrinkling on upward gaze), and Von Graefe’s sign (lid lag). [2] * **Apathetic Hyperthyroidism:** Seen in the elderly; presents with depression and lethargy rather than typical hyperactivity.
Question 346: Which of the following features is NOT typically seen in Cushing's Syndrome?
- A. Hypoglycemia (Correct Answer)
- B. Hypertension
- C. Frank psychosis
- D. Hypokalemia
Explanation: Cushing’s Syndrome is characterized by chronic exposure to excess glucocorticoids (cortisol). Cortisol is a "stress hormone" that acts as a potent **insulin antagonist**. **1. Why Hypoglycemia is the Correct Answer:** Glucocorticoids stimulate gluconeogenesis in the liver and decrease peripheral glucose uptake in muscles and adipose tissue. Therefore, excess cortisol leads to **Hyperglycemia** (impaired glucose tolerance or "Steroid Diabetes"), not hypoglycemia. Hypoglycemia is instead a hallmark of Adrenal Insufficiency (Addison’s Disease). **2. Analysis of Incorrect Options:** * **Hypertension (B):** This is a classic feature. Cortisol causes hypertension by increasing peripheral vascular resistance, enhancing sensitivity to catecholamines, and exerting mineralocorticoid effects (sodium and water retention) at high levels. * **Frank Psychosis (C):** Glucocorticoids significantly impact the central nervous system. Neuropsychiatric manifestations range from emotional lability and depression to overt "steroid psychosis" and cognitive deficits. * **Hypokalemia (D):** At high concentrations (especially in Ectopic ACTH syndrome), cortisol overwhelms the 11β-HSD2 enzyme in the kidneys and binds to mineralocorticoid receptors, leading to potassium excretion and metabolic alkalosis. **Clinical Pearls for NEET-PG:** * **Screening Test of Choice:** 24-hour urinary free cortisol or Low-dose Dexamethasone Suppression Test (LDDST) [2]. * **Most Common Cause:** Iatrogenic (exogenous steroids). * **Most Common Endogenous Cause:** Cushing’s Disease (Pituitary adenoma) [1]. * **High-Yield Sign:** Proximal muscle wasting (due to protein catabolism) with centripetal obesity and violaceous striae (>1cm wide) [1].
Question 347: Which of the following are the extraintestinal manifestations of Sipple syndrome?
- A. Cutaneous lichen
- B. Amyloidosis
- C. Hirschsprung disease
- D. All the above (Correct Answer)
Explanation: **Sipple Syndrome**, also known as **Multiple Endocrine Neoplasia Type 2A (MEN 2A)**, is an autosomal dominant disorder caused by a germline mutation in the **RET proto-oncogene**. It is classically characterized by the triad of Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, and Parathyroid Hyperplasia. The correct answer is **"All the above"** because MEN 2A is uniquely associated with several non-endocrine (extraintestinal) manifestations: 1. **Cutaneous Lichen Amyloidosis (Option A & B):** This is a highly specific dermatological marker for MEN 2A. It presents as intensely pruritic, scaly, pigmented papules, typically located in the interscapular region of the back. The "amyloidosis" here refers to localized cutaneous deposits, not systemic amyloidosis. 2. **Hirschsprung Disease (Option C):** There is a known genetic association between RET mutations and Hirschsprung disease (congenital megacolon). Patients with MEN 2A may present with chronic constipation or bowel obstruction due to colonic aganglionosis. **Clinical Pearls for NEET-PG:** * **MEN 2A (Sipple):** MTC (100%), Pheo (50%), Parathyroid (20-30%) + Lichen Amyloidosis + Hirschsprung. * **MEN 2B (Wermer):** MTC, Pheo + **Mucosal Neuromas** (lips/tongue), **Marfanoid habitus**, and Medullated corneal nerve fibers. (Note: MEN 2B does *not* usually feature parathyroid hyperplasia). * **Screening:** The most important initial step in a suspected case is checking for **RET proto-oncogene mutations**. If positive, prophylactic thyroidectomy is often indicated. * **Rule of Thumb:** Always exclude/treat Pheochromocytoma *before* any surgery (including thyroidectomy) to prevent a hypertensive crisis.
Question 348: Werner syndrome is associated with which of the following endocrine neoplasia syndromes?
- A. Multiple Endocrine Neoplasia Type 1 (MEN 1) (Correct Answer)
- B. Multiple Endocrine Neoplasia Type IIA (MEN IIA)
- C. Multiple Endocrine Neoplasia Type IIB (MEN IIB)
- D. Acute Intermittent Porphyria (AIP)
Explanation: **Explanation:** **Werner Syndrome** is the eponymous name for **Multiple Endocrine Neoplasia Type 1 (MEN 1)**. It is an autosomal dominant disorder caused by a mutation in the *MEN1* gene on chromosome 11q13, which encodes the protein **menin**, a tumor suppressor. The syndrome is classically characterized by the **"3 Ps"**: 1. **Parathyroid:** Primary Hyperparathyroidism (most common initial manifestation, >95% of cases). 2. **Pancreas:** Enteropancreatic neuroendocrine tumors (e.g., Gastrinoma/Zollinger-Ellison Syndrome, Insulinoma). 3. **Pituitary:** Anterior pituitary adenomas (most commonly Prolactinomas). **Analysis of Incorrect Options:** * **MEN IIA (Sipple Syndrome):** Characterized by Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, and Parathyroid hyperplasia. It is associated with the *RET* proto-oncogene. * **MEN IIB (Wagenmann-Froboese Syndrome):** Characterized by MTC, Pheochromocytoma, mucosal neuromas, and Marfanoid habitus. It does *not* typically involve the parathyroid glands. * **Acute Intermittent Porphyria (AIP):** A metabolic disorder of heme biosynthesis; it has no association with the MEN syndromes. **High-Yield Clinical Pearls for NEET-PG:** * **Wermer vs. Werner:** Do not confuse **Wermer** Syndrome (MEN 1) with **Werner** Syndrome (Adult Progeria/Premature Aging). * **Screening:** The first biochemical sign of MEN 1 is usually an elevated serum Calcium and PTH. * **Cutaneous Markers:** MEN 1 is also associated with non-endocrine tumors like angiofibromas, collagenomas, and lipomas. * **Most common cause of death** in MEN 1 is now malignant pancreatic neuroendocrine tumors (pNETs).
Question 349: A 25-year-old female, several months postpartum and breast-feeding, presents with acute cessation of lactation. She has not menstruated since delivery and reports fatigue and cold intolerance. Laboratory workup reveals deficiency of ACTH and other anterior pituitary hormones. What is the most likely cause of this patient's signs and symptoms?
- A. Craniopharyngioma
- B. Cushing's disease
- C. Empty sella syndrome
- D. Sheehan's syndrome (Correct Answer)
Explanation: ### Explanation **Correct Option: D. Sheehan’s Syndrome** Sheehan’s syndrome is **postpartum pituitary necrosis** caused by severe hypotension or hemorrhagic shock during or after childbirth. During pregnancy, the pituitary gland undergoes physiological hypertrophy (mainly lactotrophs), increasing its oxygen demand. However, the blood supply (portal venous system) does not increase proportionally, making the gland highly susceptible to ischemia. The clinical presentation in this patient is classic: 1. **Failure to lactate/Acute cessation of lactation:** Due to Prolactin deficiency (usually the earliest sign). 2. **Persistent amenorrhea:** Due to Gonadotropin (FSH/LH) deficiency. 3. **Fatigue and Cold intolerance:** Due to Secondary Hypothyroidism (TSH deficiency). 4. **ACTH deficiency:** Leads to secondary adrenal insufficiency. --- ### Why Other Options are Incorrect: * **A. Craniopharyngioma:** While it can cause hypopituitarism, it is a slow-growing tumor typically presenting with visual field defects (bitemporal hemianopia) and headaches. It is not specifically linked to the postpartum period. * **B. Cushing’s Disease:** This involves an ACTH-secreting pituitary adenoma leading to *excess* cortisol. Symptoms include weight gain, striae, and hypertension, which are opposite to this patient’s hormone deficiencies. * **C. Empty Sella Syndrome:** This is often an incidental radiological finding where the sella turcica is filled with CSF. While it can cause mild endocrine dysfunction, it does not typically present with acute postpartum panhypopituitarism. --- ### High-Yield Clinical Pearls for NEET-PG: * **Earliest sign:** Failure to lactate (Prolactin deficiency). * **Most common initial symptom (long-term):** Failure to resume menses. * **Pathophysiology:** Ischemic necrosis of the **Anterior Pituitary**. The posterior pituitary is usually spared as it receives direct arterial supply. * **Diagnosis:** Growth Hormone (GH) is often the first hormone lost, but Prolactin deficiency is the most clinically apparent early sign. * **Treatment:** Lifelong hormone replacement (Cortisones, Thyroxine, Estrogen/Progesterone). **Always replace glucocorticoids before thyroxine** to avoid precipitating an adrenal crisis.
Question 350: What is the most common neuropathy in Diabetes Mellitus?
- A. Distal symmetric neuropathy (Correct Answer)
- B. Autonomic neuropathy
- C. Mononeuropathy
- D. Amyotrophy
Explanation: **Explanation:** **Distal Symmetric Polyneuropathy (DSPN)** is the most common form of diabetic neuropathy, affecting approximately 50% of all patients with diabetes during their lifetime. It typically presents in a "stocking-and-glove" distribution because the longest nerve fibers are the most vulnerable to metabolic and microvascular injury [1]. The underlying pathophysiology involves chronic hyperglycemia leading to polyol pathway activation, oxidative stress, and advanced glycation end-products (AGEs), which cause progressive axonal degeneration [1]. **Analysis of Incorrect Options:** * **Autonomic Neuropathy:** While common and clinically significant (causing resting tachycardia, gastroparesis, or orthostatic hypotension), it usually occurs alongside or after the development of DSPN [1]. * **Mononeuropathy:** This involves isolated damage to a single nerve (e.g., Cranial Nerve III or Median nerve). While diabetes is a leading cause of mononeuropathies, they are far less frequent than the symmetric variety. * **Amyotrophy (Diabetic Lumbosacral Radiculoplexus Neuropathy):** This is a rare manifestation characterized by severe pain followed by muscle weakness and atrophy, usually in the proximal thigh muscles. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Loss of vibration sense (tested with a 128 Hz tuning fork) and loss of ankle reflex are often the earliest clinical findings [1]. * **Screening:** The **10g Semmes-Weinstein monofilament test** is the gold standard for identifying a "foot at risk" for ulceration [1]. * **Cranial Nerve Involvement:** CN III is the most common cranial nerve affected; it typically presents with **pupillary sparing** (due to the peripheral location of parasympathetic fibers). * **First-line Treatment:** Pregabalin, Duloxetine, or Gabapentin are preferred for symptomatic pain management.
Practice by Chapter
Diabetes Mellitus
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Thyroid Disorders
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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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