Endocrinology Practice Questions

Q: Which of the following is a symptom of hypothyroidism?

Hair loss. **Explanation:** Hypothyroidism is a clinical syndrome resulting from a deficiency of thyroid hormones (T3 and T4), leading to a generalized slowing of metabolic processes [1]. **Why Hair Loss is Correct:** Thyroid hormones are essential for the initiation of the anagen (growth) phase of the hair cycle. In hypothyroidism, hair follicles enter the telogen (resting) phase prematurely, leading to diffuse **alopecia** and thinning of the hair. A classic high-yield sign is **Madarosis**—the loss of the outer one-third of the eyebrows. Additionally, decreased sebum production makes the hair dry, brittle, and coarse. **Analysis of Incorrect Options:** * **A. Hyperactivity:** Hypothyroidism causes psychomotor retardation, lethargy, and "myxedema madness" (slowing of mental processes), whereas hyperactivity is a hallmark of hyperthyroidism. * **B. Palpitation:** This is a symptom of increased sympathetic activity and tachycardia seen in hyperthyroidism [2]. Hypothyroidism typically presents with **bradycardia** and decreased cardiac output. * **C. Diarrhoea:** Hypothyroidism leads to decreased gastrointestinal motility, resulting in **constipation**. Frequent bowel movements or diarrhea are characteristic of hyperthyroidism. **NEET-PG High-Yield Pearls:** * **Most common cause:** Hashimoto’s Thyroiditis (autoimmune) in iodine-sufficient areas. * **Key metabolic feature:** Weight gain despite poor appetite and **cold intolerance**. * **Neuromuscular sign:** Delayed relaxation of deep tendon reflexes (Woltman sign) [1]. * **Dermatological feature:** Non-pitting edema (Myxedema) due to glycosaminoglycan deposition in the dermis.

Q: A 53-year-old woman with a past medical history of chronic kidney disease due to diabetic nephropathy is noted to have hyperphosphatemia and hypocalcemia on routine electrolyte measurement. The disturbance is likely a result of metabolic bone disease seen in patients with chronic kidney disease. Which of the following findings is most likely associated with this electrolyte disturbance?

Neuromuscular irritability. The patient presents with **hypocalcemia** and **hyperphosphatemia** secondary to Chronic Kidney Disease (CKD), a condition known as **CKD-Mineral and Bone Disorder (CKD-MBD)**. In CKD, the kidneys fail to excrete phosphate and cannot adequately convert 25-hydroxyvitamin D into its active form, 1,25-dihydroxyvitamin D (calcitriol) [3], [4]. This leads to decreased intestinal calcium absorption and reciprocal hypocalcemia. **1. Why Neuromuscular Irritability is Correct:** Low extracellular calcium levels decrease the threshold for depolarization of excitable membranes. This increases the permeability of neuronal membranes to sodium ions, leading to spontaneous action potentials. Clinically, this manifests as **neuromuscular irritability**, which includes: * **Paresthesias** (perioral and fingertips) [1]. * **Tetany** (involuntary muscle contractions). * **Chvostek sign** (facial twitching on tapping the facial nerve). * **Trousseau sign** (carpopedal spasm induced by BP cuff inflation). **2. Why the other options are incorrect:** * **Lethargy and Anorexia:** These are classic symptoms of **hypercalcemia**, not hypocalcemia [2]. Hypercalcemia "moans" include CNS depression and GI upset. * **Tachyarrhythmias:** Hypocalcemia typically causes **QT interval prolongation**, which can lead to Torsades de Pointes (a form of ventricular tachycardia), but it is more classically associated with bradycardia or heart block rather than simple tachyarrhythmias. **High-Yield Clinical Pearls for NEET-PG:** * **CKD-MBD Triad:** Hyperphosphatemia, Hypocalcemia, and Secondary Hyperparathyroidism [3]. * **ECG in Hypocalcemia:** Prolonged QT interval (specifically the ST segment). * **Phosphate Binders:** Used in CKD to manage hyperphosphatemia (e.g., Sevelamer, Calcium acetate). * **Hungry Bone Syndrome:** Severe hypocalcemia seen post-parathyroidectomy in patients with long-standing hyperparathyroidism.

Q: What is the treatment for neurogenic diabetes insipidus?

Desmopressin. **Explanation:** **Neurogenic (Central) Diabetes Insipidus (DI)** is characterized by a deficiency in the synthesis or release of Antidiuretic Hormone (ADH) from the posterior pituitary [1]. This leads to the inability to concentrate urine, resulting in polyuria and polydipsia. **Why Desmopressin is the Correct Answer:** **Desmopressin (dDAVP)** is a synthetic analogue of vasopressin and is the **drug of choice** for Central DI [1]. It is highly selective for **V2 receptors** located in the renal collecting ducts, which mediate the antidiuretic effect [2]. Unlike natural vasopressin, it has minimal activity at V1 receptors (vasoconstrictor receptors), meaning it does not cause significant hypertension or cramping [2]. It also has a longer half-life, allowing for twice-daily dosing via nasal spray, oral, or parenteral routes. **Analysis of Incorrect Options:** * **Vasopressin (A):** While it works, it is non-selective (stimulates both V1 and V2) and has a very short half-life (minutes), making it impractical for long-term maintenance compared to Desmopressin. * **Terlipressin (C):** This is a prodrug of lysine vasopressin with high affinity for **V1 receptors** [2]. It is primarily used in the management of esophageal variceal bleeding and Hepatorenal Syndrome, not DI. * **Amiodarone (D):** This is a Class III antiarrhythmic drug. It is not used to treat DI; in fact, it is more commonly associated with thyroid dysfunction. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** The **Water Deprivation Test** is used to diagnose DI [1]. In Central DI, the administration of exogenous Desmopressin will result in a significant increase in urine osmolality (>50%), whereas Nephrogenic DI shows little to no response. * **Nephrogenic DI Treatment:** The drug of choice is **Thiazide diuretics** (paradoxical effect) or Amiloride (especially if lithium-induced). * **Pregnancy:** Desmopressin is safe to use for DI during pregnancy.

Q: All of the following are features of pheochromocytoma except?

Wheezing. **Explanation:** Pheochromocytoma is a catecholamine-secreting tumor arising from the chromaffin cells of the adrenal medulla. The clinical presentation is primarily driven by the excessive release of epinephrine and norepinephrine. **Why Wheezing is the Correct Answer:** Wheezing is not a feature of pheochromocytoma. In fact, catecholamines (especially epinephrine) act on **$\beta_2$-adrenergic receptors** in the bronchioles to cause **bronchodilation**. Therefore, pheochromocytoma would physiologically oppose wheezing rather than cause it. Wheezing is more characteristic of **Carcinoid Syndrome**, which is a common differential diagnosis. **Analysis of Incorrect Options:** * **Hypertensive Paroxysm:** This is the hallmark of the disease. Sudden bursts of catecholamines cause severe vasoconstriction ($\alpha_1$ effect), leading to episodic, life-threatening hypertension. * **Headache:** This is the most common symptom during a paroxysm (seen in >90% of symptomatic patients) due to the sudden increase in cerebral blood pressure. * **Orthostatic Hypotension:** Though counterintuitive, this is a classic feature. It occurs due to **decreased intravascular volume** (chronic vasoconstriction leads to pressure natriuresis) and impaired autonomic reflexes. **High-Yield Clinical Pearls for NEET-PG:** * **The Rule of 10s:** 10% bilateral, 10% malignant, 10% pediatric, 10% extra-adrenal (Paragangliomas), and 10% familial. * **The Classic Triad:** Episodic headache, sweating (diaphoresis), and tachycardia. * **Diagnosis:** Best initial screening test is **24-hour urinary fractionated metanephrines** or plasma free metanephrines. * **Management:** Always give **$\alpha$-blockers first** (e.g., Phenoxybenzamine) before $\beta$-blockers to avoid an unopposed $\alpha$-mediated hypertensive crisis.

Q: Hypogonadotropic hypogonadism with diabetes mellitus is seen in which of the following conditions?

Prader-Willi Syndrome. **Explanation:** **Prader-Willi Syndrome (PWS)** is the correct answer because it is a complex multisystem genetic disorder (deletion of the paternal copy of chromosome 15q11-q13) characterized by hypothalamic dysfunction [1]. This dysfunction leads to **Hypogonadotropic Hypogonadism** (due to GnRH deficiency) and **Hyperphagia**, which results in morbid obesity [1]. The severe obesity and associated insulin resistance frequently lead to the development of **Type 2 Diabetes Mellitus** in these patients. **Analysis of Incorrect Options:** * **Kallman Syndrome:** Characterized by hypogonadotropic hypogonadism and anosmia due to failure of GnRH neuron migration. While it causes infertility, it is not classically associated with obesity or diabetes mellitus. * **Hypothalamic Hamartoma:** These are benign tumors typically presenting with **Precocious Puberty** (due to ectopic GnRH secretion) and gelastic seizures, rather than hypogonadism. * **Granulomatous Hypophysitis:** An inflammatory condition of the pituitary (often associated with Sarcoidosis or TB). While it can cause panhypopituitarism (including hypogonadism), it does not have a primary association with diabetes mellitus; in fact, pituitary failure often *increases* insulin sensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **PWS Triad:** Hypotonia (infancy), Hyperphagia/Obesity (childhood), and Hypogonadism. * **Genetics:** Paternal deletion of 15q11-q13 or Maternal Uniparental Disomy (UPD). * **Hand/Foot findings:** Small hands and feet (acromicria) are characteristic. * **Contrast:** **Angelman Syndrome** involves the same locus but results from *maternal* deletion ("Happy Puppet" syndrome).

Q: MEN 1 syndrome is associated with all EXCEPT:

Medullary carcinoma of the thyroid. **Explanation:** Multiple Endocrine Neoplasia Type 1 (MEN 1), also known as **Wermer’s Syndrome**, is an autosomal dominant disorder caused by a mutation in the *MEN1* gene (encoding the protein Menin). It is classically characterized by the **"3 Ps"**: Parathyroid, Pancreas, and Pituitary. **Why Medullary Carcinoma of the Thyroid (MTC) is the correct answer:** MTC is a hallmark feature of **MEN 2A and MEN 2B**, not MEN 1. MTC arises from the parafollicular C-cells of the thyroid and is associated with mutations in the *RET* proto-oncogene. Its presence in a clinical vignette should immediately point toward MEN 2. **Analysis of Incorrect Options:** * **Parathyroid Adenoma:** This is the most common manifestation of MEN 1 (occurring in >95% of patients). It typically presents as multiglandular hyperplasia leading to primary hyperparathyroidism. * **Pancreatic Tumors:** These are the second most common feature. Gastrinomas (Zollinger-Ellison Syndrome) are the most frequent, followed by Insulinomas. * **Anterior Pituitary Adenomas:** These occur in about 30-40% of cases. Prolactinomas are the most common subtype, followed by GH-secreting adenomas (Acromegaly). **High-Yield Clinical Pearls for NEET-PG:** * **MEN 1 (Wermer’s):** 3 Ps (Parathyroid, Pancreas, Pituitary). Also associated with adrenal cortical tumors, facial angiofibromas, and lipomas. * **MEN 2A (Sipple’s):** 1 P (Parathyroid), 1 M (MTC), 1 P (Pheochromocytoma). * **MEN 2B (Williams):** 1 M (MTC), 1 P (Pheochromocytoma), Marfanoid habitus, and Mucosal neuromas. (Note: No Parathyroid involvement in 2B). * **Screening:** The first biochemical abnormality usually detected in MEN 1 is hypercalcemia due to hyperparathyroidism.

Q: Which of the following tests is used to distinguish primary hyperparathyroidism from familial benign hypercalcemia?

Urinary calcium levels. **Explanation:** The clinical distinction between **Primary Hyperparathyroidism (PHPT)** and **Familial Hypocalciuric Hypercalcemia (FHH)**—also known as familial benign hypercalcemia—is critical because PHPT requires surgery, while FHH is a benign condition where surgery is ineffective. **Why Urinary Calcium is the Correct Answer:** The underlying pathophysiology of FHH involves an inactivating mutation in the **Calcium-Sensing Receptor (CaSR)**. This leads to a higher "set-point" for calcium, causing the kidneys to reabsorb calcium excessively despite high serum levels. * **FHH:** Characterized by **low urinary calcium excretion** (Hypocalciuria). The Calcium-to-Creatinine Clearance Ratio (**CCCR**) is typically ** 0.02**. **Analysis of Incorrect Options:** * **A. Serum PTH levels:** Both conditions present with elevated or inappropriately normal PTH levels, making this test non-discriminatory. * **B. Serum calcium levels:** Both conditions present with hypercalcemia. * **D. Serum phosphorus levels:** Both conditions can present with low or low-normal serum phosphorus due to the phosphaturic effects of PTH. **NEET-PG High-Yield Pearls:** * **CCCR Formula:** (Urinary Ca × Serum Cr) / (Serum Ca × Urinary Cr). * **FHH Inheritance:** Autosomal Dominant. * **Clinical Clue:** If a patient has asymptomatic hypercalcemia, a family history of "failed" parathyroid surgeries, and low urinary calcium, suspect FHH. * **Management:** PHPT often requires parathyroidectomy; FHH requires no treatment (it is "benign").

Question 1

Which of the following is a symptom of hypothyroidism?

Accepted Answer

Hair loss

Answer

Hyperactivity

Answer

Palpitation

Answer

Diarrhoea

Question 2

What is the drug of choice for post-menopausal osteoporosis?

Accepted Answer

Alendronate

Answer

Raloxifene

Answer

Tamoxifene

Answer

Estrogen

Question 3

Which of the following are monogenic and autosomal dominant causes of hypertension?

Accepted Answer

Familial Conn's syndrome and Glucocorticoid-remediable hyperaldosteronism

Answer

Pregnancy-induced hypertension and Familial Conn's syndrome

Answer

Familial Conn's syndrome and 17-α hydroxylase deficiency

Answer

Glucocorticoid-remediable hyperaldosteronism and 17-α hydroxylase deficiency

Question 4

Calcification in basal ganglia is seen in which of the following conditions?

Accepted Answer

Hypoparathyroidism

Answer

Hypothyroidism

Answer

Hypopituitarism

Answer

Hypoaldosteronism

Question 5

A 53-year-old woman with a past medical history of chronic kidney disease due to diabetic nephropathy is noted to have hyperphosphatemia and hypocalcemia on routine electrolyte measurement. The disturbance is likely a result of metabolic bone disease seen in patients with chronic kidney disease. Which of the following findings is most likely associated with this electrolyte disturbance?

Accepted Answer

Neuromuscular irritability

Answer

Lethargy

Answer

Anorexia

Answer

Tachyarrhythmias

Question 6

What is the treatment for neurogenic diabetes insipidus?

Accepted Answer

Desmopressin

Answer

Vasopressin

Answer

Terlipressin

Answer

Amiodarone

Question 7

All of the following are features of pheochromocytoma except?

Accepted Answer

Wheezing

Answer

Hypertensive paroxysm

Answer

Headache

Answer

Orthostatic hypotension

Question 8

Hypogonadotropic hypogonadism with diabetes mellitus is seen in which of the following conditions?

Accepted Answer

Prader-Willi Syndrome

Answer

Kallman Syndrome

Answer

Hypothalamic hamartoma

Answer

Granulomatous hypophysitis

Question 9

MEN 1 syndrome is associated with all EXCEPT:

Accepted Answer

Medullary carcinoma of the thyroid

Answer

Pancreatic tumors

Answer

Anterior pituitary adenomas

Answer

Parathyroid adenoma

Question 10

Which of the following tests is used to distinguish primary hyperparathyroidism from familial benign hypercalcemia?

Accepted Answer

Urinary calcium levels

Answer

Serum PTH levels

Answer

Serum calcium levels

Answer

Serum phosphorus levels

Endocrinology — MCQs

Endocrinology — MCQs

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