Endocrinology — MCQs

A 30-year-old woman complains of headache, visual disturbances, deepening of the voice, and generalized weakness. She has amenorrhea for the past year and states that she recently required a larger shoe size. Laboratory studies show impaired glucose tolerance. What procedure would be most useful for establishing your diagnosis?

Q518Easy

All of the following are associated with gigantism / acromegaly, except?

Q519Easy

Which of the following is true about secondary hyperparathyroidism?

Q520Easy

Alkaline phosphatase levels are decreased in which of the following conditions?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 511: Which of the following statements about extra-adrenal pheochromocytomas is FALSE?

A. They constitute 50% of all pheochromocytomas. (Correct Answer)
B. They may occur in the urinary bladder.
C. They may occur in the thorax.
D. They can involve the carotid body.

Explanation: **Explanation:** The correct answer is **A**. This statement is false because extra-adrenal pheochromocytomas (often referred to as **paragangliomas**) constitute only about **10–15%** of all pheochromocytomas in adults. The classic "Rule of 10s" for pheochromocytoma states that 10% are extra-adrenal, 10% are bilateral, 10% are malignant, and 10% occur in children (though modern genetics suggests these percentages are higher in hereditary cases). **Analysis of Options:** * **Option B (Urinary Bladder):** This is a classic site for extra-adrenal paragangliomas. A high-yield clinical sign is **micturition-induced syncope** or paroxysmal hypertension triggered by voiding, due to the release of catecholamines from the bladder wall tumor. * **Option C (Thorax):** Paragangliomas can occur in the posterior mediastinum, arising from the para-aortic sympathetic chain. * **Option D (Carotid Body):** The carotid body is a common site for head and neck paragangliomas. Unlike sympathetic paragangliomas, these are usually parasympathetic and often non-secretory (do not produce catecholamines). **High-Yield NEET-PG Pearls:** * **Most common site:** The most common extra-adrenal site is the **Organ of Zuckerkandl** (located near the origin of the inferior mesenteric artery). * **Malignancy:** Extra-adrenal tumors have a **higher risk of malignancy** (up to 20-40%) compared to adrenal pheochromocytomas (10%). * **Genetics:** Extra-adrenal tumors are frequently associated with **SDHB mutations**. * **Diagnosis:** Initial screening is via plasma or urinary **metanephrines**. Localization is done via CT/MRI, followed by functional imaging like **123I-MIBG** or **68Ga-DOTATATE PET/CT** [1].

Question 512: What is the primary indication for ACE inhibitor use in patients with diabetes mellitus?

A. Diabetic nephropathy
B. Nephropathy unrelated to diabetes
C. Both diabetic nephropathy and nephropathy unrelated to diabetes (Correct Answer)
D. None of the above

Explanation: **Explanation:** The primary indication for ACE inhibitors (ACEIs) in patients with diabetes mellitus is their **renoprotective effect**, which extends beyond simple blood pressure control. **1. Why Option C is correct:** ACE inhibitors (and ARBs) are the standard of care for reducing the progression of chronic kidney disease (CKD) [1]. * **In Diabetic Nephropathy:** They reduce intraglomerular pressure by causing vasodilation of the **efferent arteriole**. This reduces hyperfiltration and decreases albuminuria, slowing the progression to End-Stage Renal Disease (ESRD) [1], [2]. * **In Non-Diabetic Nephropathy:** The same hemodynamic mechanism applies. ACEIs reduce proteinuria and provide significant cardiovascular protection, making them the first-line antihypertensive for any patient with proteinuric CKD, regardless of the underlying cause [1]. **2. Why other options are incorrect:** * **Option A & B:** While ACEIs are indeed used for diabetic nephropathy (A) and non-diabetic renal disease (B), selecting only one would be incomplete. Clinical guidelines (KDIGO and ADA) recommend ACEIs for any patient with albuminuria (>30mg/g) to prevent renal decline, making Option C the most comprehensive choice [1], [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Selective dilation of the **efferent arteriole** (decreases GFR slightly but protects the basement membrane) [1]. * **Monitoring:** Always monitor Serum Potassium and Creatinine within 1–2 weeks of starting therapy. A rise in creatinine up to **30%** is acceptable [1]. * **Contraindications:** Bilateral renal artery stenosis, pregnancy (teratogenic), and history of angioedema. * **Combination Therapy:** Never combine ACEIs and ARBs; it increases the risk of hyperkalemia and acute kidney injury without added benefit.

Question 513: Hirsutism is caused by all of the following, EXCEPT:

A. Cushing's syndrome
B. Hyperthyroidism (Correct Answer)
C. Hyperprolactinemia
D. Acromegaly

Explanation: Hirsutism is defined as the presence of terminal hair in females in a male-pattern distribution, primarily driven by an excess of androgens or increased sensitivity of hair follicles to androgens. **Why Hyperthyroidism is the Correct Answer:** Hyperthyroidism is **not** a cause of hirsutism. In fact, thyrotoxicosis is typically associated with **thinning of hair or alopecia** (diffuse hair loss) [1]. While thyroid hormones influence the hair cycle, they do not stimulate the conversion of vellus hair to terminal hair in androgen-sensitive areas. **Analysis of Incorrect Options:** * **Cushing’s Syndrome:** Excess cortisol production is often accompanied by increased adrenal androgens (especially in ACTH-dependent causes), leading to hirsutism, acne, and menstrual irregularities. * **Hyperprolactinemia:** Elevated prolactin levels can stimulate the adrenal cortex (specifically the zona fasciculata and reticularis) to produce excess Dehydroepiandrosterone sulfate (DHEAS), which leads to androgenic effects like hirsutism. * **Acromegaly:** Excess Growth Hormone (GH) and IGF-1 stimulate hair follicle growth directly and can also lead to insulin resistance, which decreases Sex Hormone Binding Globulin (SHBG), thereby increasing free testosterone levels. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of hirsutism:** Polycystic Ovary Syndrome (PCOS) [2]. * **Ferriman-Gallwey Score:** Used to clinically quantify hirsutism (Score ≥8 is significant). * **Drug-induced Hirsutism/Hypertrichosis:** Common culprits include Minoxidil, Cyclosporine, Phenytoin, and Anabolic steroids. * **Rapid onset hirsutism + Virilization:** Always suspect an androgen-secreting tumor (Adrenal or Ovarian).

Question 514: Obesity is seen in all of the following conditions EXCEPT?

A. Cushing syndrome
B. Pickwickian syndrome
C. Prader Willi syndrome
D. Sipple syndrome (Correct Answer)

Explanation: **Explanation:** The correct answer is **Sipple syndrome (Option D)**. **1. Why Sipple Syndrome is the Correct Answer:** Sipple syndrome, also known as **Multiple Endocrine Neoplasia type 2A (MEN 2A)**, is an autosomal dominant disorder characterized by the triad of **Medullary Thyroid Carcinoma (MTC)**, **Pheochromocytoma**, and **Parathyroid Hyperplasia**. Unlike the other options, Sipple syndrome is not associated with obesity. In fact, patients with pheochromocytoma often experience **weight loss** due to a hypermetabolic state induced by chronic catecholamine excess. **2. Analysis of Incorrect Options:** * **Cushing Syndrome:** Characterized by hypercortisolism, leading to **centripetal (trunkal) obesity**, "buffalo hump," and "moon facies" due to redistribution of adipose tissue. * **Pickwickian Syndrome (Obesity Hypoventilation Syndrome):** Defined by the triad of obesity (BMI >30 kg/m²), daytime hypoventilation, and sleep-disordered breathing. Here, obesity is a core diagnostic criterion. * **Prader-Willi Syndrome:** A genetic disorder (deletion on chromosome 15q11-q13) characterized by hyperphagia (excessive appetite) leading to **early-onset morbid obesity**, short stature, and hypogonadism [1]. **3. Clinical Pearls for NEET-PG:** * **MEN 2A (Sipple):** MTC (100%), Pheochromocytoma (50%), Parathyroid Hyperplasia (20%). Associated with *RET* proto-oncogene mutations. * **MEN 2B (Wermer-like):** MTC, Pheochromocytoma, Mucosal neuromas, and Marfanoid habitus (not obesity). * **High-yield Obesity Syndromes:** Prader-Willi, Laurence-Moon-Biedl (Bardet-Biedl), Alstrom syndrome, and Frohlich syndrome (Adiposogenital dystrophy) [1].

Question 515: A combination of gynaecomastia, decreased serum testosterone and LH in a male patient is seen in:

A. Testicular failure
B. Sertoli cell tumor (Correct Answer)
C. Gonadotrophins
D. Androgen resistance state

Explanation: The clinical triad of **gynaecomastia, decreased testosterone, and decreased LH** indicates a state of secondary hypogonadism driven by estrogen excess. **Why Sertoli Cell Tumor is correct:** Sertoli cell tumors are rare sex cord-stromal tumors of the testis. These tumors often overexpress the enzyme **aromatase**, which converts androgens into **estrogens** (estradiol) [1]. 1. **Gynaecomastia:** High estrogen levels directly stimulate breast tissue [2]. 2. **Decreased LH:** Elevated estrogen exerts powerful **negative feedback** on the hypothalamus and anterior pituitary, suppressing the secretion of GnRH and LH [1]. 3. **Decreased Testosterone:** Low LH levels result in a lack of stimulation to the Leydig cells, leading to reduced endogenous testosterone production [1]. **Analysis of Incorrect Options:** * **Testicular Failure (Primary Hypogonadism):** Characterized by low testosterone but **elevated LH/FSH** (hypergonadotropic hypogonadism) due to the loss of negative feedback [1]. * **Gonadotrophins (Exogenous administration):** Administration of hCG (which mimics LH) would typically **increase** testosterone levels, not decrease them. * **Androgen Resistance State (e.g., AIS):** Caused by defective androgen receptors. This leads to **elevated LH** and **elevated testosterone** because the pituitary is "blind" to the feedback of circulating androgens. **High-Yield Clinical Pearls for NEET-PG:** * **Leydig Cell Tumors** are the most common sex cord-stromal tumors and can also cause gynaecomastia via similar mechanisms (increased aromatization). * **Feedback Loop:** Always check LH levels to differentiate between primary (High LH) and secondary (Low LH) hypogonadism [1]. * **Estrogen/Androgen Ratio:** Gynaecomastia is fundamentally caused by an increase in the ratio of free estrogen to effective androgens [2].

Question 516: Pseudo-Cushing syndrome is seen in which of the following conditions?

A. Chronic alcoholism (Correct Answer)
B. Incidentaloma
C. Adrenal carcinoma
D. Nelson syndrome

Explanation: **Explanation:** **Pseudo-Cushing syndrome** refers to a clinical state where patients exhibit the physical features (cushingoid habitus) and biochemical evidence (elevated cortisol) of Cushing syndrome, but the underlying cause is not a primary pathology of the Hypothalamic-Pituitary-Adrenal (HPA) axis [1]. 1. **Why Chronic Alcoholism is correct:** Chronic alcoholism is a classic cause of Pseudo-Cushing. Alcohol stimulates the HPA axis, leading to increased CRH secretion and subsequent hypercortisolemia. Additionally, impaired liver function in alcoholics reduces the clearance of cortisol. Other common causes include **major depression** and **morbid obesity**. 2. **Why the other options are incorrect:** * **Incidentaloma:** This refers to an asymptomatic adrenal mass found accidentally on imaging. While some may be secretory (Subclinical Cushing), they represent true adrenal pathology, not "pseudo" states. * **Adrenal Carcinoma:** This is a cause of **ACTH-independent Cushing syndrome** [2]. It involves autonomous, malignant production of cortisol [3]. * **Nelson Syndrome:** This occurs after bilateral adrenalectomy for Cushing disease. The loss of cortisol feedback leads to an aggressive ACTH-secreting pituitary adenoma, causing hyperpigmentation, not Pseudo-Cushing. **High-Yield Clinical Pearls for NEET-PG:** * **Distinguishing Test:** The **Dexamethasone-CRH test** or the **Insulin Tolerance Test (ITT)** can help differentiate true Cushing from Pseudo-Cushing [1]. Patients with Pseudo-Cushing will show a normal GH and ACTH response to insulin-induced hypoglycemia, whereas those with true Cushing will not. * **Reversibility:** The biochemical abnormalities in Pseudo-Cushing typically resolve after 1–4 weeks of alcohol abstinence or treatment of the underlying depression.

Question 517: A 30-year-old woman complains of headache, visual disturbances, deepening of the voice, and generalized weakness. She has amenorrhea for the past year and states that she recently required a larger shoe size. Laboratory studies show impaired glucose tolerance. What procedure would be most useful for establishing your diagnosis?

A. Complete blood count with differential count
B. CT scan of the abdomen
C. MRI of the sella turcica (Correct Answer)
D. Test for serum 21-hydroxylase

Explanation: ### Explanation **Diagnosis: Acromegaly (Growth Hormone-secreting Pituitary Adenoma)** The patient presents with classic features of **Acromegaly**: enlargement of acral parts (increased shoe size), deepening of the voice (due to laryngeal hypertrophy), and metabolic complications like impaired glucose tolerance (GH is a counter-regulatory hormone). The headache and visual disturbances (likely bitemporal hemianopia) suggest a **pituitary macroadenoma** causing mass effect on the optic chiasm and surrounding structures [1]. Amenorrhea occurs due to either co-secretion of prolactin [2] or compression of the pituitary stalk. **Why MRI of the sella turcica is the correct answer:** Once a biochemical diagnosis is suspected (via elevated IGF-1 levels), **MRI of the sella turcica** is the gold standard imaging modality to visualize the pituitary adenoma, assess its size (micro vs. macro), and determine its relationship with the optic chiasm and cavernous sinuses [1]. **Why the other options are incorrect:** * **A. CBC with differential:** This is a non-specific test for infection or anemia and has no diagnostic value for endocrine tumors. * **B. CT scan of the abdomen:** While used to look for ectopic GHRH-secreting tumors (rare), it is not the primary investigation for a patient with classic pituitary mass symptoms. * **D. Test for serum 21-hydroxylase:** This is used to diagnose Congenital Adrenal Hyperplasia (CAH), which presents with virilization but not acral enlargement or pituitary mass symptoms. --- ### High-Yield Clinical Pearls for NEET-PG * **Best Initial Screening Test:** Serum **IGF-1** levels (stable throughout the day) [2]. * **Gold Standard Confirmatory Test:** **Oral Glucose Tolerance Test (OGTT)** with GH measurement. Failure to suppress GH < 1 ng/mL after 75g glucose is diagnostic [2]. * **Most Common Cause of Death:** Cardiovascular disease (specifically dilated cardiomyopathy). * **Associated Conditions:** Carpal tunnel syndrome, sleep apnea, and increased risk of **Colonic Polyps/Carcinoma** (requires screening colonoscopy) [2]. * **Treatment of Choice:** Transsphenoidal surgery (TSS) [2]. Medical management includes Somatostatin analogues (Octreotide) or GH receptor antagonists (Pegvisomant).

Question 518: All of the following are associated with gigantism / acromegaly, except?

A. Mental Retardation (Correct Answer)
B. Hyperhydrosis
C. Visceromegaly
D. Impaired Glucose Tolerance

Explanation: **Explanation:** Acromegaly (in adults) and Gigantism (in children) result from the excessive secretion of **Growth Hormone (GH)**, usually due to a pituitary adenoma [1]. **Why Mental Retardation is the Correct Answer:** Growth hormone excess does **not** cause cognitive impairment or mental retardation. In fact, patients with acromegaly typically have normal intelligence. Mental retardation is more commonly associated with endocrine deficiencies during development, such as **Congenital Hypothyroidism (Cretinism)**, rather than hormone excess. **Analysis of Incorrect Options:** * **Hyperhidrosis (B):** This is one of the most common early clinical signs. GH excess causes hypertrophy of sweat and sebaceous glands, leading to oily skin and excessive sweating. * **Visceromegaly (C):** GH stimulates the growth of internal organs via IGF-1 [1]. This leads to enlargement of the heart (cardiomegaly), liver (hepatomegaly), spleen (splenomegaly), and kidneys [4]. * **Impaired Glucose Tolerance (D):** GH is a "diabetogenic" hormone [3]. It antagonizes the action of insulin and increases hepatic glucose production [3]. Approximately 25-50% of patients develop impaired glucose tolerance or overt Diabetes Mellitus [2]. **NEET-PG High-Yield Pearls:** * **Screening Test:** Serum IGF-1 levels (more stable than pulsatile GH) [2]. * **Confirmatory Test:** Oral Glucose Tolerance Test (OGTT) – failure to suppress GH below 1 ng/mL [2]. * **Most Common Cause of Death:** Cardiovascular disease (specifically dilated cardiomyopathy). * **Classic Sign:** "Spade-like hands" and increased hat/shoe size. * **Drug of Choice:** Transsphenoidal surgery (first-line); Somatostatin analogues (Octreotide) for medical management [2].

Question 519: Which of the following is true about secondary hyperparathyroidism?

A. Commonly occurs in chronic renal failure
B. Related to hyperphosphatemia
C. Patients are generally hypocalcemic
D. All of the above (Correct Answer)

Explanation: **Explanation:** Secondary hyperparathyroidism (sHPT) is a compensatory state where the parathyroid glands overproduce parathyroid hormone (PTH) in response to chronic hypocalcemia. **1. Why Option D is correct (Underlying Medical Concept):** In the context of **Chronic Kidney Disease (CKD)**, which is the most common cause (Option A), the pathophysiology involves a triad of factors: * **Hyperphosphatemia (Option B):** Failing kidneys cannot excrete phosphate. Elevated serum phosphate directly stimulates PTH secretion and binds ionized calcium. * **Vitamin D Deficiency:** Kidneys lose the ability to convert 25-hydroxyvitamin D into its active form, 1,25-dihydroxyvitamin D (Calcitriol). This reduces intestinal calcium absorption [1]. * **Hypocalcemia (Option C):** The combination of phosphate binding and low calcitriol leads to low serum calcium [1]. The parathyroid glands sense this low calcium and high phosphate, leading to **hyperplasia** and increased PTH secretion to normalize calcium levels by mobilizing it from the bones. **2. Analysis of Options:** * **Option A:** CKD is the classic trigger; as GFR declines, sHPT becomes almost universal [1]. * **Option B:** High phosphate is a primary driver of PTH release and a hallmark of renal-induced sHPT [1]. * **Option C:** Unlike primary hyperparathyroidism (where calcium is high), secondary HPT is a response to **low/low-normal calcium** [1]. **Clinical Pearls for NEET-PG:** * **Tertiary Hyperparathyroidism:** Occurs when long-standing sHPT leads to autonomous PTH secretion, resulting in **hypercalcemia** (often seen post-renal transplant). * **Radiology:** Look for "Rugger-jersey spine" and subperiosteal resorption of phalanges (Osteitis Fibrosa Cystica). * **Treatment:** Phosphate binders (Sevelamer), Vitamin D analogues (Calcitriol), and Calcimimetics (Cinacalcet).

Question 520: Alkaline phosphatase levels are decreased in which of the following conditions?

A. Hypophosphatasia (Correct Answer)
B. Primary biliary cirrhosis
C. Hyperphosphatemia
D. Hepatitis A

Explanation: Alkaline phosphatase (ALP) is an enzyme primarily found in the liver, bones, kidneys, and placenta. While elevated ALP is a common clinical finding, **decreased** ALP levels are rare and highly specific for certain conditions. **1. Why Hypophosphatasia is Correct:** Hypophosphatasia is a rare genetic metabolic disorder caused by a loss-of-function mutation in the **ALPL gene**, which encodes the **tissue-nonspecific alkaline phosphatase (TNSALP)** enzyme. This deficiency leads to the accumulation of substrates like inorganic pyrophosphate, which inhibits bone mineralization. Clinically, it manifests as rickets in children or osteomalacia in adults, characterized by low serum ALP levels [1]. **2. Why the Other Options are Incorrect:** * **Primary Biliary Cirrhosis (PBC):** This is a cholestatic liver disease. ALP is a marker of cholestasis; therefore, levels are significantly **elevated** due to increased synthesis and release from the bile duct epithelium. * **Hyperphosphatemia:** High serum phosphate levels do not directly cause low ALP. In fact, in conditions like chronic kidney disease (CKD) where hyperphosphatemia occurs, ALP is often **elevated** (Secondary Hyperparathyroidism). * **Hepatitis A:** Acute viral hepatitis causes hepatocellular injury, leading to an **increase** in ALP (though the rise in transaminases like ALT/AST is usually more prominent). **3. NEET-PG High-Yield Pearls:** * **Causes of Low ALP (Mnemonic: "MAPLE"):** **M**agnesium deficiency, **A**pastic anemia/Achondroplasia, **P**ernicious anemia (Vitamin B12 deficiency), **L**ow Zinc, **E**xcess Vitamin D intake/Hypothyroidism. * **Hypophosphatasia** is the most classic cause of low ALP tested in exams. * **Wilson’s Disease:** In cases of fulminant hepatic failure due to Wilson’s disease, a characteristic finding is a very low ALP to Bilirubin ratio.

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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