Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1121: A 22-year-old woman presents with recent onset of hirsutism and voice changes. What is the most appropriate initial investigation?

A. Urine 17-ketosteroids
B. Blood FSH and LH levels
C. Blood testosterone levels (Correct Answer)
D. Blood thyroxine and TSH levels

Explanation: **Explanation:** The clinical presentation of **rapid-onset hirsutism** accompanied by **virilization** (voice changes/deepening) in a young woman is highly suggestive of an androgen-secreting tumor (ovarian or adrenal). In such cases, the initial step is to document biochemical hyperandrogenism. **1. Why Blood Testosterone is correct:** Serum **Total Testosterone** is the most appropriate initial screening test to assess the severity of androgen excess [1]. Very high levels (>200 ng/dL) are strongly indicative of an androgen-secreting neoplasm [1]. While DHEAS is also measured to rule out adrenal sources, testosterone remains the primary marker for overall androgen status in the initial workup of virilization. **2. Why other options are incorrect:** * **Urine 17-ketosteroids:** This is an obsolete test. It measures metabolites of weak adrenal androgens but is non-specific and has been replaced by more accurate serum assays like DHEAS and Testosterone. * **Blood FSH and LH levels:** These are useful in diagnosing PCOS (where the LH:FSH ratio may be elevated) or primary ovarian failure [1], but they do not help in the direct evaluation of virilizing symptoms. * **Blood Thyroxine and TSH:** While thyroid dysfunction can cause menstrual irregularities, it does not cause virilization or significant hirsutism. **Clinical Pearls for NEET-PG:** * **Rapid progression + Virilization** (clitoromegaly, deepening of voice, male-pattern baldness) = Suspect **Tumor**. * **Gradual onset + Menstrual irregularity** = Suspect **PCOS**. * If Testosterone is >200 ng/dL, perform a Pelvic USG/CT to look for an **Ovarian tumor** (e.g., Sertoli-Leydig cell tumor) [1]. * If DHEAS is >700 µg/dL, perform an Abdominal CT to look for an **Adrenal tumor** [1].

Question 1122: All are true about primary aldosteronism except:

A. It is one of the most common causes of secondary hypertension.
B. Hyperkalemia. (Correct Answer)
C. Sodium retention.
D. Ratio of plasma aldosterone to plasma renin activity (PA/PRA) is a useful screening test.

Explanation: **Explanation:** **Primary Aldosteronism (Conn’s Syndrome)** is characterized by the autonomous overproduction of aldosterone from the adrenal cortex, independent of the renin-angiotensin system. **Why "Hyperkalemia" is the correct (false) statement:** Aldosterone acts on the principal cells of the renal collecting ducts to reabsorb sodium and **excrete potassium and hydrogen ions** [1]. Consequently, the hallmark of primary aldosteronism is **Hypokalemia**, not hyperkalemia [3]. It is important to note that many patients may actually be normokalemic, but they never present with hyperkalemia unless there is concurrent renal failure. **Analysis of other options:** * **Option A:** Primary aldosteronism is indeed the **most common cause of secondary hypertension**, accounting for approximately 5–10% of all hypertensive patients. * **Option C:** Aldosterone causes **sodium retention** by upregulating ENaC channels. While this leads to volume expansion and hypertension, clinical edema is rarely seen due to the "Aldosterone Escape" phenomenon (atrial natriuretic peptide-mediated diuresis) [2]. * **Option D:** The **ARR (Aldosterone-to-Renin Ratio)** is the gold-standard screening test. In primary disease, aldosterone is high while renin is suppressed (due to feedback inhibition), leading to a high ratio (typically >20-30). **NEET-PG High-Yield Pearls:** * **Most common cause:** Adrenal Adenoma (Conn’s Syndrome) > Bilateral Adrenal Hyperplasia. * **Acid-Base Status:** Metabolic alkalosis (due to H+ excretion) [3]. * **Confirmatory Test:** Saline infusion test (failure to suppress aldosterone) or Oral salt loading. * **Treatment:** Spironolactone/Eplerenone (Medical) or Unilateral Adrenalectomy (Surgical).

Question 1123: A 15-year-old girl has been losing weight and exercising vigorously. She feels overweight and wants to lose more weight. On examination, she is thin with muscle wasting. Which of the following physical signs is also suggestive of the diagnosis?

A. Salivary gland enlargement (Correct Answer)
B. Coarse body hair
C. Diarrhea
D. Tachycardia

Explanation: **Explanation:** The clinical presentation of a 15-year-old girl with weight loss, vigorous exercise, and a distorted body image (feeling overweight despite being thin) is highly suggestive of **Anorexia Nervosa**. [1] **Why Salivary Gland Enlargement is Correct:** In patients with eating disorders, particularly those who engage in self-induced vomiting (purging subtype), **bilateral painless enlargement of the parotid glands (Sialadenosis)** is a classic physical sign. This occurs due to hypertrophy of the acinar cells, likely triggered by repeated stimulation of the autonomic nervous system during vomiting or nutritional deficiencies. **Analysis of Incorrect Options:** * **B. Coarse body hair:** Patients with anorexia nervosa typically develop **Lanugo hair**—fine, downy, soft hair on the back and arms—as a physiological response to conserve body heat in the absence of insulating fat. Coarse hair is more characteristic of hypothyroidism or PCOS. * **C. Diarrhea:** Anorexia is associated with slowed gastrointestinal motility and decreased intake, leading to **constipation**, not diarrhea. [2] * **D. Tachycardia:** Malnutrition and starvation lead to a hypometabolic state and increased vagal tone, resulting in **bradycardia** and hypotension. [2] Tachycardia would be an unusual finding unless the patient is severely dehydrated or in heart failure. **NEET-PG High-Yield Pearls:** * **Russell’s Sign:** Calluses or scars on the knuckles from self-induced vomiting. * **Electrolyte Abnormalities:** Hypokalemic hypochloremic metabolic alkalosis (due to vomiting). * **Endocrine Profile:** Low FSH, LH, and Estrogen (leading to amenorrhea); "Sick Euthyroid" syndrome (low T3); and elevated Cortisol levels. * **Most common cause of death:** Cardiac arrhythmias (due to electrolyte imbalance) or suicide.

Question 1124: Which of the following is NOT a component of Werner's syndrome?

A. Pituitary
B. Adrenal (Correct Answer)
C. Parathyroid
D. Pancreas

Explanation: Werner’s syndrome, also known as **Multiple Endocrine Neoplasia Type 1 (MEN1)**, 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, **P**ancreas, and **P**ituitary. * **Why Adrenal is the correct answer:** While adrenal cortical lesions (like adenomas or hyperplasia) can occasionally occur in MEN1 patients, they are **not** considered a primary or defining component of the syndrome. In the context of MEN syndromes, the **Adrenal Medulla** (Pheochromocytoma) is a hallmark of **MEN 2A and 2B**, not MEN 1. * **Why other options are incorrect:** * **Parathyroid (Option C):** This is the most common feature (95% of cases). It typically presents as multiglandular hyperplasia leading to primary hyperparathyroidism. * **Pancreas (Option D):** Enteropancreatic neuroendocrine tumors (NETs) occur in about 40-70% of patients. Gastrinomas (leading to Zollinger-Ellison Syndrome) and Insulinomas are the most frequent. * **Pituitary (Option A):** Anterior pituitary adenomas occur in about 30-40% of cases, with Prolactinomas being the most common subtype. **High-Yield Clinical Pearls for NEET-PG:** 1. **Inheritance:** Autosomal Dominant; Gene located on **Chromosome 11q13**. 2. **Most common initial presentation:** Hypercalcemia due to Hyperparathyroidism. 3. **MEN 2A (Sipple Syndrome):** Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, Parathyroid hyperplasia. 4. **MEN 2B (Williams-Pollock Syndrome):** MTC, Pheochromocytoma, Mucosal neuromas, and Marfanoid habitus. 5. **Memory Aid:** Remember the "3 Ps" for MEN 1 and "MPH" (Medullary, Pheo, Hyperparathyroid) for MEN 2A.

Question 1125: All are TRUE about the management of Humoral hypercalcemia of malignancy (HHM), EXCEPT:

A. Oral phosphorus initially
B. Saline rehydration is used
C. Bisphosphonates are very effective
D. Steroids are not useful (Correct Answer)

Explanation: Humoral Hypercalcemia of Malignancy (HHM) is primarily mediated by the secretion of **Parathyroid Hormone-related Protein (PTHrP)** from solid tumors (e.g., squamous cell carcinoma of the lung, renal cell carcinoma) [2]. PTHrP stimulates osteoclastic bone resorption and renal calcium reabsorption. **Why Option D is the Correct Answer (The "Except"):** Steroids (Glucocorticoids) are generally **not useful** in HHM because PTHrP-mediated hypercalcemia does not involve increased Vitamin D production. However, steroids are highly effective in hypercalcemia caused by **lymphomas, sarcoidosis, or Vitamin D toxicity**, where they inhibit the 1-alpha-hydroxylase enzyme. In the context of HHM, saying they are "not useful" is a clinical fact, making it the correct "Except" choice. **Analysis of Other Options:** * **Option A (Oral Phosphorus):** While not first-line for severe cases, oral phosphorus can be used initially in mild hypercalcemia to inhibit bone resorption and promote calcium deposition in bone, provided renal function is adequate. * **Option B (Saline Rehydration):** This is the **initial step** in management. Isotonic saline (0.9% NaCl) restores extracellular fluid volume and promotes urinary calcium excretion (calciuresis). * **Option C (Bisphosphonates):** IV Bisphosphonates (e.g., **Zoledronic acid**, Pamidronate) are the **most effective** long-term treatment for HHM as they potentally inhibit osteoclast activity [1]. **High-Yield NEET-PG Pearls:** * **Most common cause of HHM:** PTHrP secretion (80% of cases). * **Drug of choice for acute management:** Aggressive IV Saline rehydration. * **Most potent Bisphosphonate:** Zoledronic acid. * **Calcitonin:** Used for rapid, short-term reduction of calcium (works within hours) but develops tachyphylaxis (stops working) after 48 hours. * **Denosumab:** A monoclonal antibody against RANKL used in bisphosphonate-refractory hypercalcemia.

Question 1126: All of the following are true about Hashimoto thyroiditis EXCEPT:

A. Myoclonus
B. Seizures
C. Steroid responsive encephalopathy
D. EEG is normal (Correct Answer)

Explanation: This question refers to **Hashimoto’s Encephalopathy (HE)**, also known as **Steroid-Responsive Encephalopathy associated with Autoimmune Thyroiditis (SREAT)**. This is a rare neuroendocrine syndrome characterized by high titers of anti-thyroid antibodies (Anti-TPO or Anti-Tg) and neuropsychiatric symptoms, occurring independently of the patient's actual thyroid functional status (patients can be euthyroid). **Why Option D is the correct answer:** In Hashimoto’s Encephalopathy, the **EEG is characteristically abnormal** in approximately 90-95% of cases. The most common finding is non-specific **generalized slowing** (delta or theta waves), though periodic sharp wave complexes or triphasic waves may also be seen. Therefore, the statement that the EEG is normal is false. **Analysis of incorrect options:** * **A & B (Myoclonus and Seizures):** These are classic clinical manifestations of HE. Patients often present with a "stroke-like" relapsing-remitting course or a diffuse progressive course involving tremors, myoclonus, and generalized tonic-clonic seizures. * **C (Steroid responsive):** This is the hallmark of the condition. Most patients show dramatic clinical improvement within 24–72 hours of starting high-dose intravenous corticosteroids (e.g., Methylprednisolone). **NEET-PG High-Yield Pearls:** * **Antibody Marker:** Anti-TPO (Thyroid Peroxidase) antibodies are almost always elevated. * **Thyroid Status:** Most patients are clinically euthyroid or only mildly hypothyroid at presentation. * **CSF Findings:** Often shows elevated protein levels with normal cell counts (albuminocytologic dissociation). * **Imaging:** Brain MRI is frequently normal or shows non-specific white matter changes, making EEG a more sensitive (though non-specific) diagnostic tool.

Question 1127: Metyrapone inhibits which of the following enzymes?

A. 11-β-hydroxylase (Correct Answer)
B. 21-β-hydroxylase
C. Both
D. None

Explanation: **Explanation:** **1. Mechanism of Action (Why A is correct):** Metyrapone is a potent inhibitor of the enzyme **11-β-hydroxylase** (*CYP11B1*). This enzyme is responsible for the final step of cortisol synthesis: converting 11-deoxycortisol into cortisol [1]. By blocking this enzyme, metyrapone causes a decrease in plasma cortisol levels. This reduction triggers a compensatory increase in ACTH secretion (via the negative feedback loop), which in turn leads to an accumulation of the precursor **11-deoxycortisol**. **2. Analysis of Incorrect Options:** * **Option B (21-β-hydroxylase):** This enzyme converts Progesterone to 11-deoxycorticosterone (DOC) [3]. Deficiency of this enzyme is the most common cause of Congenital Adrenal Hyperplasia (CAH), but it is not the target of Metyrapone [3]. * **Option C & D:** Since Metyrapone is highly selective for 11-β-hydroxylase, these options are incorrect. **3. Clinical Pearls for NEET-PG:** * **Metyrapone Stimulation Test:** Used to assess the integrity of the Hypothalamic-Pituitary-Adrenal (HPA) axis [2]. In a normal response, blocking cortisol should lead to a rise in ACTH and 11-deoxycortisol. A failure of 11-deoxycortisol to rise suggests pituitary or hypothalamic insufficiency. * **Therapeutic Use:** It is used for the medical management of **Cushing’s Syndrome** (especially when surgery is contraindicated) to control hypercortisolism. * **Side Effects:** Because it blocks the final step of cortisol but not the androgen pathway, it can cause **hirsutism** (due to androgen excess) and **hypertension** (due to the mineralocorticoid effects of accumulated 11-deoxycortisol). * **Pregnancy:** Metyrapone is the drug of choice for treating Cushing’s syndrome in pregnancy.

Question 1128: Lab investigations of a patient show low T4 and elevated TSH. Which of the following is the most likely diagnosis?

A. Graves' disease
B. Hashimoto's disease (Correct Answer)
C. Pituitary failure
D. Hypothalamic failure

Explanation: ### Explanation **Core Concept: Primary Hypothyroidism** The laboratory profile of **low T4 (thyroxine)** and **elevated TSH (Thyroid Stimulating Hormone)** is the hallmark of **Primary Hypothyroidism** [1]. In this condition, the thyroid gland itself is failing to produce hormones. Due to the loss of negative feedback on the pituitary gland, TSH secretion increases significantly to compensate [1]. **Why Hashimoto’s Disease is Correct:** Hashimoto’s thyroiditis is the most common cause of primary hypothyroidism in iodine-sufficient regions [1]. It is an autoimmune destruction of the thyroid gland. Because the pathology resides in the gland, T4 is low and TSH is high. **Analysis of Incorrect Options:** * **Graves’ Disease:** This is a cause of *hyperthyroidism*. It presents with **high T4** and **suppressed (low) TSH** due to thyroid-stimulating antibodies [1]. * **Pituitary Failure (Secondary Hypothyroidism):** If the pituitary fails, it cannot produce TSH. Therefore, the labs would show **low T4** and **low or inappropriately normal TSH** [1]. * **Hypothalamic Failure (Tertiary Hypothyroidism):** Similar to pituitary failure, a lack of TRH leads to **low T4** and **low TSH** [1]. **NEET-PG High-Yield Pearls:** * **Most sensitive initial test** for thyroid function: **Serum TSH**. * **Subclinical Hypothyroidism:** Elevated TSH with **normal** Free T4 levels [1]. * **Antibody Marker:** Anti-TPO (Thyroid Peroxidase) antibodies are positive in >90% of Hashimoto’s cases. * **Histology Hint:** Look for **Hurthle cells** (Askanazy cells) and lymphocytic infiltration with germinal centers on biopsy.

Question 1129: A patient has a pituitary tumor, specifically a prolactinoma, that encircles the carotid artery. What is the best line of management?

A. Observation
B. Transsphenoidal surgical resection (Correct Answer)
C. Radiotherapy
D. Medical management with dopamine agonists

Explanation: ### Explanation The management of prolactinomas typically follows a specific hierarchy based on tumor size, symptoms, and anatomical involvement. [1] **Why Transsphenoidal Surgical Resection (B) is Correct:** While medical management is the first-line treatment for most prolactinomas, **encirclement or invasion of the internal carotid artery (ICA)** represents a complex anatomical challenge. In cases where a tumor is aggressive, causes significant mass effect, or shows signs of potential neurovascular compromise that may not respond rapidly enough to medication, surgical intervention is indicated. For NEET-PG purposes, if a pituitary tumor is causing structural complications or is refractory to medical therapy, **Transsphenoidal Surgery (TSS)** is the definitive management to decompress the area. [1] **Why the other options are incorrect:** * **A. Observation:** Prolactinomas are active tumors. Observation is inappropriate when there is evidence of vascular encirclement or mass effect. * **C. Radiotherapy:** This is generally reserved as a third-line treatment for persistent or recurrent tumors after both medical and surgical interventions have failed. [1] * **D. Medical management with dopamine agonists:** While Cabergoline/Bromocriptine is the standard first-line for *most* prolactinomas (even macroprolactinomas), surgery is prioritized when there is a specific surgical indication like CSF rhinorrhea, visual field defects worsening under treatment, or specific anatomical invasion requiring urgent decompression. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Cabergoline is the preferred dopamine agonist due to higher efficacy and fewer side effects compared to Bromocriptine. [1] * **Surgery Indications:** Surgery is indicated if the patient is intolerant to dopamine agonists, the tumor is resistant, or there is a sudden complication like **Pituitary Apoplexy**. * **Anatomy:** The most common cranial nerve involved in lateral extension (into the cavernous sinus) is the **Abducens nerve (CN VI)**. * **Hook Effect:** In extremely high prolactin levels, a lab artifact may show falsely low levels; serial dilution is required for diagnosis.

Question 1130: Increased serum calcium is seen in all of the following except?

A. Myxedema
B. Sarcoidosis
C. Familial hypocalciuric hypercalcemia
D. Primary hyperparathyroidism (Correct Answer)

Explanation: **Explanation:** The question asks for the condition where increased serum calcium is **NOT** seen. However, there appears to be a discrepancy in the provided key: **Primary Hyperparathyroidism** is a classic cause of hypercalcemia. In the context of NEET-PG, **Myxedema (Hypothyroidism)** is the correct answer for "except," as it is typically associated with normal calcium levels or, rarely, a decrease in bone turnover. **1. Why Myxedema (Option A) is the correct "Except":** In Myxedema (severe hypothyroidism), there is a generalized slowing of metabolic processes. Thyroid hormones normally stimulate bone resorption; thus, in hypothyroidism, bone turnover is decreased. This does not lead to hypercalcemia. In contrast, **Thyrotoxicosis** (hyperthyroidism) is a known cause of increased serum calcium due to increased osteoclastic activity. **2. Analysis of Incorrect Options (Causes of Hypercalcemia):** * **Primary Hyperparathyroidism (Option D):** The most common cause of hypercalcemia in outpatient settings. It is characterized by autonomous secretion of PTH, leading to increased bone resorption, renal calcium reabsorption, and intestinal absorption. * **Sarcoidosis (Option B):** A granulomatous disease where macrophages in the granulomas express 1-alpha-hydroxylase. This converts Vitamin D to its active form (1,25-dihydroxyvitamin D), leading to increased intestinal calcium absorption and hypercalcemia. * **Familial Hypocalciuric Hypercalcemia (FHH) (Option C):** An autosomal dominant condition caused by a mutation in the Calcium-Sensing Receptor (CaSR). It results in a higher "set-point" for calcium, leading to mild hypercalcemia with inappropriately low urinary calcium excretion. **Clinical Pearls for NEET-PG:** * **Mnemonic for Hypercalcemia:** "Stones, Bones, Abdominal Groans, and Psychic Overtones." * **FHH vs. Primary Hyperparathyroidism:** Use the **Urinary Calcium/Creatinine Clearance Ratio**. A ratio <0.01 suggests FHH, while >0.02 suggests Primary Hyperparathyroidism. * **Most common cause of hypercalcemia in hospitalized patients:** Malignancy (often via PTHrP).

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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