Endocrinology — MCQs
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A 35-year-old man develops symptoms of hyperthyroidism with tachycardia and heat intolerance over a one-month period. Thyroid biopsy demonstrates a heavy mononuclear cell infiltrate with multinucleated giant cells, follicular disruption, and loss of colloid. About one month later, the patient develops symptoms of hypothyroidism. To which of the following is this patient's condition thought to be most closely related?
Which of the following is NOT a characteristic of inappropriate ADH secretion?
Phaeochromocytoma arises from which of the following structures?
What is the most common cause of spontaneous hypoglycemia in a non-diabetic individual?
Which of the following is NOT a manifestation of carcinoid syndrome?
Which of the following is true about the therapy of obesity?
Non-pitting edema is seen in which of the following conditions?
A 29-year-old male on oral hypoglycemic drugs has never had ketonuria. His BMI is 20.5. His grandfather had diabetes, and his father, who was his grandfather's only son, also had the disease. Which type of diabetes mellitus is this person most likely to have?
Which of the following signs is characteristic of Graves' disease?
A 58-year-old man is referred for evaluation of a 2-cm adrenal mass discovered incidentally on a CT scan performed for abdominal pain. The patient has no history of malignancy and denies erectile dysfunction. Physical examination reveals a blood pressure of 122/78 mmHg with no gynecomastia or evidence of Cushing syndrome. His serum potassium is normal. What is the next step in determining whether this patient's adrenal mass should be resected?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 791: A 35-year-old man develops symptoms of hyperthyroidism with tachycardia and heat intolerance over a one-month period. Thyroid biopsy demonstrates a heavy mononuclear cell infiltrate with multinucleated giant cells, follicular disruption, and loss of colloid. About one month later, the patient develops symptoms of hypothyroidism. To which of the following is this patient's condition thought to be most closely related?
- A. Blocking TSH receptor autoantibodies
- B. Carcinoma
- C. Lymphoma
- D. Viral infection (Correct Answer)
Explanation: The patient’s presentation—acute onset of hyperthyroidism followed by hypothyroidism, coupled with a biopsy showing **multinucleated giant cells** and a mononuclear infiltrate—is classic for **Subacute Granulomatous Thyroiditis (De Quervain’s Thyroiditis).** ### 1. Why Viral Infection is Correct Subacute thyroiditis is a self-limiting inflammatory condition typically preceded by an **upper respiratory tract infection**. It is thought to be triggered by a **viral infection** (e.g., Coxsackievirus, Mumps, Adenovirus) or a post-viral inflammatory response in genetically susceptible individuals (HLA-B35). * **Pathophysiology:** Viral-induced inflammation causes follicular destruction, leading to a "leak" of preformed thyroid hormones (initial hyperthyroid phase). As stores are depleted and follicles are damaged, a transient hypothyroid phase follows before eventual recovery [1]. * **Histology:** The hallmark is a granulomatous inflammation featuring **multinucleated giant cells** surrounding fragments of colloid. ### 2. Why Other Options are Incorrect * **A. Blocking TSH receptor autoantibodies:** These are characteristic of **Atrophic Thyroiditis** or a subset of Graves' disease. They cause hypothyroidism without an initial hyperthyroid phase or giant cell histology [2]. * **B. Carcinoma:** While some cancers (like Anaplastic) can be painful, they do not typically present with a classic triphasic thyroid function (hyper-to-hypo) or granulomatous histology. * **C. Lymphoma:** Thyroid lymphoma usually presents as a rapidly enlarging goiter, often in the setting of pre-existing Hashimoto’s thyroiditis. Histology shows malignant lymphoid cells, not giant cells. ### 3. High-Yield Clinical Pearls for NEET-PG * **Clinical Hallmark:** The most common cause of a **painful/tender thyroid gland**. * **Lab Findings:** Elevated ESR and CRP; **Low radioactive iodine uptake (RAIU)** during the hyperthyroid phase (due to follicular damage) [1]. * **Treatment:** NSAIDs for mild cases; Steroids for severe pain. It is usually self-limiting [1]. * **Differential:** Do not confuse with *Subacute Lymphocytic (Painless) Thyroiditis*, which lacks the pain and the giant cell histology.
Question 792: Which of the following is NOT a characteristic of inappropriate ADH secretion?
- A. Hypo-osmolar urine (Correct Answer)
- B. Water intoxication
- C. Expanded fluid volume
- D. Hypomagnesemia
Explanation: **Explanation:** The hallmark of **Syndrome of Inappropriate Antidiuretic Hormone (SIADH)** is the excessive release of ADH despite low plasma osmolality. ADH acts on the V2 receptors in the renal collecting ducts, causing water reabsorption [1], [3]. **1. Why "Hypo-osmolar urine" is the correct answer:** In SIADH, the kidneys reabsorb excessive amounts of water, leading to concentrated urine. Therefore, the urine is **hyper-osmolar** (typically >100 mOsm/kg, and often greater than the plasma osmolality). **Hypo-osmolar urine** is characteristic of Diabetes Insipidus, not SIADH. **2. Analysis of incorrect options:** * **Water intoxication:** The continuous water reabsorption leads to dilutional hyponatremia, essentially a state of "water intoxication" where the body has too much water relative to sodium. * **Expanded fluid volume:** SIADH causes mild ECF volume expansion. However, it is clinically **euvolemic** [2] because the body compensates via pressure natriuresis (excreting sodium and water) to prevent overt edema or hypertension. * **Hypomagnesemia:** Chronic SIADH is frequently associated with secondary electrolyte disturbances, including hypomagnesemia and hypokalemia, due to increased urinary excretion of these ions alongside the natriuresis. **NEET-PG High-Yield Pearls:** * **Diagnosis:** Look for the triad of Hyponatremia + Low Plasma Osmolality (<275 mOsm/kg) + High Urine Osmolality (>100 mOsm/kg) in a clinically euvolemic patient [2]. * **Urine Sodium:** Typically high (>40 mEq/L) due to the body's attempt to shed volume. * **Treatment:** Fluid restriction is the first-line treatment. For severe cases, use hypertonic saline (3%) but avoid rapid correction to prevent **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis).** * **Drug of choice (Vaptans):** Tolvaptan (oral) or Conivaptan (IV) are vasopressin receptor antagonists used in refractory cases.
Question 793: Phaeochromocytoma arises from which of the following structures?
- A. Adrenal gland (Correct Answer)
- B. Mediastinum
- C. Chest wall
- D. Neck
Explanation: **Explanation:** **Phaeochromocytoma** is a catecholamine-secreting tumor that arises from the **chromaffin cells** of the adrenal medulla. These cells are derived from the neural crest and are responsible for synthesizing and secreting epinephrine and norepinephrine. * **Why Option A is correct:** Approximately **85-90%** of these tumors arise from the **adrenal gland**. The adrenal medulla is the primary site for chromaffin tissue in adults, making it the most common location for phaeochromocytoma. * **Why Options B, C, and D are incorrect:** While catecholamine-secreting tumors can occur outside the adrenal gland (in the mediastinum, neck, or abdomen), these are technically termed **Paragangliomas** (extra-adrenal phaeochromocytomas). While they share similar clinical features, the term "Phaeochromocytoma" specifically refers to the adrenal tumor in standard nomenclature. The chest wall is not a typical site for chromaffin tissue. **High-Yield Clinical Pearls for NEET-PG:** 1. **The Rule of 10s:** 10% are bilateral, 10% are malignant, 10% are extra-adrenal (paragangliomas), and 10% occur in children. 2. **Clinical Triad:** Episodic headache, sweating (diaphoresis), and tachycardia/palpitations, usually accompanied by hypertension. 3. **Diagnosis:** The best initial screening test is **24-hour urinary fractionated metanephrines** or plasma free metanephrines. 4. **Genetic Associations:** Often associated with **MEN 2A and 2B**, von Hippel-Lindau (VHL) syndrome, and Neurofibromatosis type 1 (NF1). 5. **Management:** Always start **Alpha-blockade** (e.g., Phenoxybenzamine) *before* Beta-blockade to prevent a hypertensive crisis caused by unopposed alpha-receptor stimulation.
Question 794: What is the most common cause of spontaneous hypoglycemia in a non-diabetic individual?
- A. Insulin
- B. Oral hypoglycemic agents
- C. Von Gierke's disease
- D. Alcohol consumption (Correct Answer)
Explanation: The most common cause of spontaneous hypoglycemia in a non-diabetic individual is **alcohol consumption** [3]. **Mechanism of Alcohol-Induced Hypoglycemia:** Alcohol metabolism by the enzyme *alcohol dehydrogenase* increases the **NADH/NAD+ ratio** in the liver. High levels of NADH inhibit gluconeogenesis by diverting key substrates (pyruvate to lactate and oxaloacetate to malate). In individuals with depleted glycogen stores (e.g., due to fasting or malnutrition), the body becomes entirely dependent on gluconeogenesis to maintain blood glucose. When this pathway is blocked by alcohol [3], profound hypoglycemia occurs. **Analysis of Incorrect Options:** * **A & B (Insulin and Oral Hypoglycemic Agents):** While these are the most common causes of hypoglycemia in **diabetic** patients (iatrogenic), they are considered "factitious" or accidental rather than "spontaneous" [1] in non-diabetics. * **C (Von Gierke’s Disease):** This is a Type I Glycogen Storage Disease (Glucose-6-Phosphatase deficiency). While it causes severe fasting hypoglycemia, it is a rare genetic disorder typically diagnosed in infancy, not the most common cause in the general population. **NEET-PG High-Yield Pearls:** * **Whipple’s Triad:** Essential for diagnosing true hypoglycemia: (1) Symptoms of hypoglycemia, (2) Low plasma glucose level, and (3) Relief of symptoms when glucose is raised. [2] * **Fasting vs. Postprandial:** Alcohol causes *fasting* hypoglycemia. In contrast, Insulinoma (a rare neuroendocrine tumor) also causes fasting hypoglycemia but is characterized by high insulin and C-peptide levels [2]. * **Key Lab Finding:** In alcohol-induced hypoglycemia, look for an elevated **Lactate:Pyruvate ratio** due to the high NADH state.
Question 795: Which of the following is NOT a manifestation of carcinoid syndrome?
- A. Retroperitoneal fibrosis
- B. Peyronie's disease of the penis
- C. Occlusion of the mesenteric arteries
- D. Steatorrhea (Correct Answer)
Explanation: Explanation: Carcinoid syndrome results from the systemic release of vasoactive substances (primarily **serotonin**, histamine, and bradykinin) by neuroendocrine tumors, typically after they have metastasized to the liver [1]. **Why Steatorrhea is the Correct Answer:** Steatorrhea is **not** a direct manifestation of the syndrome itself. In fact, the diarrhea in carcinoid syndrome is **secretory** in nature (due to increased intestinal motility and fluid secretion caused by serotonin). However, steatorrhea can occur as a **side effect of treatment** with Somatostatin analogs (like Octreotide), which inhibit pancreatic enzyme secretion. It is not a primary clinical feature of the disease process. **Analysis of Other Options:** * **Retroperitoneal Fibrosis & Peyronie’s Disease:** High levels of serotonin stimulate fibroblast proliferation. This leads to **fibrotic complications**, including right-sided endocardial fibrosis, retroperitoneal fibrosis, and Peyronie’s disease (fibrosis of the corpus cavernosum). * **Occlusion of Mesenteric Arteries:** The intense local fibrotic reaction (desmoplastic reaction) in the mesentery can lead to kinking of the bowel and vascular compromise, potentially causing mesenteric ischemia or occlusion. **NEET-PG High-Yield Pearls:** * **Classic Triad:** Flushing (most common), Secretory Diarrhea, and Right-sided heart failure (Tricuspid regurgitation/Pulmonary stenosis) [1]. * **Diagnosis:** Best initial screening test is **24-hour urinary 5-HIAA** (metabolite of serotonin). * **Localization:** Somatostatin receptor scintigraphy (OctreoScan) or 68Ga-DOTATATE PET/CT. * **Pellagra Connection:** Serotonin is synthesized from Tryptophan. Excessive production can deplete Tryptophan stores, leading to **Niacin (Vitamin B3) deficiency** and Pellagra (Dermatitis, Dementia, Diarrhea).
Question 796: Which of the following is true about the therapy of obesity?
- A. Bariatric surgery is indicated for BMI > 30 kg/m2.
- B. Adjuvant pharmacotherapy is indicated for BMI > 30 kg/m2. (Correct Answer)
- C. Lifestyle modification is not required.
- D. Reducing appetite by centrally active drugs is not an option.
Explanation: The management of obesity follows a stepwise approach based on Body Mass Index (BMI) and associated comorbidities [1]. **Explanation of the Correct Option:** **Option B** is correct because pharmacological therapy is indicated as an adjunct to lifestyle modification in individuals with a **BMI ≥ 30 kg/m²**, or a **BMI ≥ 27 kg/m²** when there are obesity-related comorbidities (e.g., hypertension, type 2 diabetes, dyslipidemia). Common FDA-approved drugs include Orlistat (lipase inhibitor), Liraglutide (GLP-1 agonist), and Phentermine-Topiramate. **Why the other options are incorrect:** * **Option A:** Bariatric surgery is typically reserved for severe obesity. The standard indications are a **BMI ≥ 40 kg/m²** or a **BMI ≥ 35 kg/m²** with significant comorbidities [2]. (Note: Asian-specific guidelines often lower these thresholds to >37.5 and >32.5 respectively [1], but BMI >30 is still too low for primary surgical indication). * **Option C:** Lifestyle modification (dietary restriction, physical activity, and behavior therapy) is the **cornerstone** of all obesity management and must be continued even if drugs or surgery are initiated. A reasonable goal for most patients is to lose 5–10% of body weight [1]. * **Option D:** Centrally active drugs are a mainstay of treatment. Drugs like **Lorcaserin** (Serotonin agonist) and **Phentermine** act on the hypothalamus to suppress appetite and increase satiety [3]. **High-Yield Clinical Pearls for NEET-PG:** * **First-line treatment:** Lifestyle modification (aim for 5–10% weight loss over 6 months) [1]. * **Orlistat:** Only weight loss drug that acts peripherally (inhibits gastric and pancreatic lipases); side effects include steatorrhea [2]. * **Liraglutide/Semaglutide:** GLP-1 analogues that are highly effective for both weight loss and glycemic control. * **Most effective treatment:** Bariatric surgery (Roux-en-Y Gastric Bypass is the gold standard) provides the most significant and sustained weight loss [2].
Question 797: Non-pitting edema is seen in which of the following conditions?
- A. Congestive cardiac failure
- B. Myxedema (Correct Answer)
- C. Liver failure
- D. Renal failure
Explanation: **Explanation:** **Correct Answer: B. Myxedema** The hallmark of hypothyroidism (specifically severe cases or "myxedema") is **non-pitting edema**. This occurs due to the excessive deposition of **glycosaminoglycans** (primarily hyaluronic acid and chondroitin sulfate) in the dermis. These molecules are osmotic and trap water, but because they are bound in a mucopolysaccharide matrix, the fluid cannot be displaced by manual pressure, resulting in a firm, non-pitting surface [1]. This is most commonly seen in the pretibial area and periorbital tissues. **Incorrect Options:** * **A, C, and D (CCF, Liver Failure, Renal Failure):** These conditions cause **pitting edema**. The underlying mechanism is a disturbance in Starling forces—either an increase in capillary hydrostatic pressure (Heart Failure) or a decrease in plasma oncotic pressure due to hypoalbuminemia (Liver Cirrhosis and Nephrotic Syndrome). In these cases, the edema consists of free-moving interstitial fluid that is easily displaced upon pressure, leaving a "pit." **NEET-PG High-Yield Pearls:** * **Pretibial Myxedema:** Despite the name, this is actually a feature of **Graves' disease** (Hyperthyroidism), caused by thyroid-stimulating antibodies reacting with TSH receptors on fibroblasts [1]. It is also non-pitting. * **Lymphedema:** Another classic cause of non-pitting edema (e.g., in Filariasis or post-mastectomy) due to impaired lymphatic drainage and subsequent fibrosis. * **Stem Clue:** If a question mentions "puffy face," "macroglossia," and "non-pitting edema," always think of **Hypothyroidism**.
Question 798: A 29-year-old male on oral hypoglycemic drugs has never had ketonuria. His BMI is 20.5. His grandfather had diabetes, and his father, who was his grandfather's only son, also had the disease. Which type of diabetes mellitus is this person most likely to have?
- A. Pancreatic diabetes
- B. Maturity-onset diabetes of the young (MODY) (Correct Answer)
- C. Type I diabetes mellitus
- D. Type II diabetes mellitus
Explanation: ### Explanation The clinical presentation strongly suggests **Maturity-Onset Diabetes of the Young (MODY)**, a group of monogenic disorders characterized by non-insulin-dependent diabetes occurring at a young age [1]. **1. Why MODY is the correct answer:** * **Autosomal Dominant Inheritance:** The question describes a clear vertical transmission across three generations (Grandfather → Father → Son). This "three-generation rule" is a hallmark of MODY, which is caused by single gene defects with autosomal dominant inheritance [1]. * **Age and Phenotype:** The patient is young (29 years old) and lean (BMI 20.5). Unlike Type 2 DM, MODY typically occurs in non-obese individuals under the age of 25–30 [1]. * **Absence of Ketosis:** The lack of ketonuria indicates significant residual beta-cell function, which distinguishes it from Type 1 DM [1]. **2. Why the other options are incorrect:** * **Type I DM:** Usually presents with an absolute insulin deficiency, leading to ketonuria/ketoacidosis [2]. It does not follow a strong autosomal dominant inheritance pattern [2]. * **Type II DM:** While it has a genetic component, it is typically associated with insulin resistance, obesity (high BMI), and older age of onset [3]. * **Pancreatic Diabetes:** This refers to secondary diabetes due to chronic pancreatitis or cystic fibrosis [2]. There is no history of abdominal pain, steatorrhea, or pancreatic insult provided. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most Common Type:** MODY 3 (HNF-1α mutation) is the most common subtype globally. * **MODY 2 (Glucokinase mutation):** Characterized by mild, stable fasting hyperglycemia that often doesn't require treatment. * **Treatment:** Patients with MODY 1 and 3 are exquisitely sensitive to **Sulfonylureas**, which is often the first-line treatment instead of insulin. * **Key Differentiator:** MODY is **C-peptide positive** (unlike T1DM) and **Antibody negative** (GAD/ICA).
Question 799: Which of the following signs is characteristic of Graves' disease?
- A. Chemosis
- B. Kocher sign (Correct Answer)
- C. Von Graefe sign
- D. Stellwag sign
Explanation: The correct answer is **Kocher sign**. While all the options listed are ocular signs associated with hyperthyroidism, the question asks for a sign specifically characteristic of **Graves' disease** (Graves' ophthalmopathy), rather than just general thyrotoxicosis. 1. **Kocher Sign:** This refers to an appearance of a "frightened expression" or a fixed stare on upward gaze. It is caused by increased sympathetic activity and, more importantly, the inflammatory involvement of the levator palpebrae superioris muscle. In the context of NEET-PG, it is frequently associated with the infiltrative ophthalmopathy unique to Graves' disease. 2. **Why the others are incorrect:** * **Von Graefe sign:** This is "lid lag" (the upper eyelid fails to follow the globe smoothly on downward gaze). While common in Graves', it is a non-specific sign of thyrotoxicosis caused by sympathetic overactivity of the Müller’s muscle. * **Stellwag sign:** This refers to infrequent or incomplete blinking. Like lid lag, it is a general sign of sympathetic overstimulation seen in any form of hyperthyroidism. * **Chemosis:** This is edema of the conjunctiva. While it occurs in severe Graves' ophthalmopathy due to venous congestion, it is a clinical finding rather than a named "eponymous sign" like Kocher’s. **High-Yield Clinical Pearls for NEET-PG:** * **Dalrymple Sign:** Widening of the palpebral fissures (staring look) at rest [1]. * **Joffroy Sign:** Absence of forehead wrinkling on upward gaze. * **Mobius Sign:** Inability to maintain convergence of the eyes. * **Pathogenesis:** Graves' ophthalmopathy is caused by TSH-receptor antibodies (TRAb) reacting with receptors on orbital fibroblasts, leading to GAG accumulation and muscle edema [1, 2]. Smoking is the most significant modifiable risk factor for progression.
Question 800: A 58-year-old man is referred for evaluation of a 2-cm adrenal mass discovered incidentally on a CT scan performed for abdominal pain. The patient has no history of malignancy and denies erectile dysfunction. Physical examination reveals a blood pressure of 122/78 mmHg with no gynecomastia or evidence of Cushing syndrome. His serum potassium is normal. What is the next step in determining whether this patient's adrenal mass should be resected?
- A. Plasma aldosterone/renin ratio
- B. Estradiol level
- C. Plasma metanephrines and dexamethasone-suppressed cortisol level (Correct Answer)
- D. Testosterone level
Explanation: The patient presents with an **Adrenal Incidentaloma**, defined as an adrenal mass ≥1 cm discovered on imaging performed for reasons other than suspected adrenal disease. The management goal is twofold: determining if the mass is **malignant** and if it is **hormonally active**. **Why Option C is correct:** All patients with an adrenal incidentaloma, regardless of symptoms or blood pressure, must undergo a biochemical workup to rule out hyperfunctioning tumors. 1. **Pheochromocytoma:** Ruled out using **plasma free metanephrines** (or 24-hour urinary metanephrines). This is vital because an undiagnosed pheochromocytoma can lead to a fatal hypertensive crisis during surgery or biopsy [1]. 2. **Subclinical Cushing Syndrome:** Ruled out using a **1-mg overnight dexamethasone suppression test (DST)**. This is the most sensitive screening tool for autonomous cortisol secretion in asymptomatic patients [3]. **Why other options are incorrect:** * **Option A:** Plasma aldosterone/renin ratio is only indicated if the patient is **hypertensive or hypokalemic** (screening for Primary Aldosteronism) [2]. This patient is normotensive with normal potassium. * **Options B & D:** Sex hormone testing (Estradiol/Testosterone) is only indicated if there are clinical signs of virilization or feminization (e.g., gynecomastia, hirsutism). This patient has no such findings. **High-Yield Clinical Pearls for NEET-PG:** * **Size Cut-off:** Masses **>4 cm** have a higher risk of malignancy and are generally recommended for resection even if non-functional [1]. * **Biopsy Rule:** Never perform a Fine Needle Aspiration (FNA) of an adrenal mass until **Pheochromocytoma is biochemically ruled out**, as it can precipitate a catecholamine storm [1]. * **Imaging Characteristics:** A "washout" of >60% on delayed contrast CT and an attenuation value of **<10 Hounsfield Units (HU)** suggest a benign lipid-rich adenoma [1].
Practice by Chapter
Diabetes Mellitus
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Thyroid Disorders
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Adrenal Gland Disorders
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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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