Endocrinology — MCQs
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Which of the following statements is not true regarding Hashimoto's thyroiditis?
What laboratory test is most appropriate for this patient?
In osteoporosis, what change occurs?
A 68-year-old patient, postoperative from thyroidectomy, presents with muscle cramps. Chvostek's and Trousseau's signs are noted on examination. What is the most likely finding on electrocardiogram?
All of the following statements about Pseudohypoparathyroidism are true, except?
Which of the following is true for Klinefelter's syndrome?
Which of the following is NOT a feature of Kallmann syndrome?
All of the following are helpful in the initial treatment of severe hypercalcemia associated with hyperparathyroidism except?
Weight gain is seen in all of the following conditions except?
Hypophosphatemia is seen in all except?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 1151: Which of the following statements is not true regarding Hashimoto's thyroiditis?
- A. More common in females
- B. HLA-B8 association
- C. Presents after 6-8 weeks of upper respiratory tract infection (Correct Answer)
- D. Can lead to thyroid lymphoma
Explanation: The correct answer is **C**, as this statement describes **Subacute Granulomatous (De Quervain’s) Thyroiditis**, not Hashimoto’s thyroiditis. De Quervain’s is a post-viral inflammatory condition that typically follows an upper respiratory tract infection (URTI) by 2–8 weeks and presents with a painful, tender thyroid [1]. In contrast, Hashimoto’s thyroiditis is a chronic autoimmune process characterized by painless goiter and gradual thyroid failure. **Analysis of Options:** * **Option A (More common in females):** This is true. Like most autoimmune diseases, Hashimoto’s shows a strong female predilection (ratio approx. 10:1 to 20:1). * **Option B (HLA-B8 association):** This is true. Hashimoto’s is associated with HLA-DR3, HLA-DR5, and **HLA-B8**. (Note: HLA-B8 is also linked to Graves' disease and Myasthenia Gravis). * **Option D (Can lead to thyroid lymphoma):** This is true. Patients with Hashimoto’s have a significantly increased risk (approx. 60–80 fold) of developing **Primary Thyroid Lymphoma** (usually B-cell MALT lymphoma). **High-Yield NEET-PG Pearls:** * **Most common cause** of hypothyroidism in iodine-sufficient areas. * **Pathology:** Characterized by intense lymphocytic infiltrate, **germinal centers**, and **Hürthle cells** (oxyphilic, granular eosinophilic cytoplasm). * **Antibodies:** Anti-TPO (95%) and Anti-Thyroglobulin (60%) [1]. * **Hashitoxicosis:** A transient thyrotoxic phase early in the disease due to follicular rupture and leak of preformed hormones [1].
Question 1152: What laboratory test is most appropriate for this patient?
- A. Alpha-fetoprotein
- B. Beta2-microglobulin
- C. Calcitonin (Correct Answer)
- D. Insulin-like growth factor-1
Explanation: ***Calcitonin*** - **Calcitonin** is the most specific tumor marker for **medullary thyroid carcinoma (MTC)**, produced by parafollicular **C-cells**. - Elevated serum calcitonin levels help diagnose MTC and monitor treatment response, especially in **MEN 2 syndrome** cases. *Alpha-fetoprotein* - **AFP** is primarily elevated in **hepatocellular carcinoma** and **germ cell tumors** (testicular/ovarian). - It has no association with **thyroid malignancies** and would not be useful for suspected MTC. *Beta2-microglobulin* - **Beta2-microglobulin** is elevated in **multiple myeloma**, **lymphomas**, and other hematologic malignancies. - It is not a marker for **thyroid cancer** and lacks specificity for MTC diagnosis. *Insulin-like growth factor-1* - **IGF-1** is used to diagnose **acromegaly** caused by **growth hormone excess** from pituitary adenomas. - It has no role in thyroid cancer evaluation and is unrelated to **C-cell tumors**.
Question 1153: In osteoporosis, what change occurs?
- A. Decrease in absolute amount of bone mass (Correct Answer)
- B. More common in males
- C. Radiographs show normal bone density
- D. Hormonal replacement therapy
Explanation: Explanation: 1. Why Option A is Correct: Osteoporosis is defined as a systemic skeletal disorder characterized by low bone mass and micro-architectural deterioration of bone tissue [1]. The fundamental pathology is an imbalance between bone resorption (osteoclasts) and bone formation (osteoblasts), leading to a decrease in the absolute amount of bone mass [2]. Crucially, the chemical composition of the remaining bone remains normal (unlike osteomalacia, where mineralization is defective); there is simply "less bone" overall. 2. Why Other Options are Incorrect: * Option B: Osteoporosis is significantly more common in females [1], particularly post-menopausal women, due to the rapid decline in estrogen levels which leads to increased osteoclast activity. * Option C: Radiographs are insensitive for early diagnosis. A plain X-ray only shows decreased bone density (osteopenia) after 30-50% of bone mass has already been lost. The gold standard for diagnosis is the DEXA scan [2]. * Option D: While Hormone Replacement Therapy (HRT) was historically used, it is no longer the first-line treatment due to risks of breast cancer and cardiovascular events. Bisphosphonates (e.g., Alendronate) are the current mainstay of pharmacological management. High-Yield Clinical Pearls for NEET-PG: * WHO Diagnostic Criteria (DEXA): Osteoporosis is defined as a T-score ≤ -2.5 SD. A T-score between -1.0 and -2.5 is termed Osteopenia. * Most Common Fracture Site: The vertebral body (compression fractures) is the most common site, followed by the hip and distal radius (Colles’ fracture) [2]. * Biochemical Profile: In primary osteoporosis, serum Calcium, Phosphate, and PTH levels are typically normal. * Gold Standard Investigation: Dual-energy X-ray absorptiometry (DEXA).
Question 1154: A 68-year-old patient, postoperative from thyroidectomy, presents with muscle cramps. Chvostek's and Trousseau's signs are noted on examination. What is the most likely finding on electrocardiogram?
- A. Prolonged QT interval (Correct Answer)
- B. Short QT interval
- C. ST elevation
- D. ST depression
Explanation: ### Explanation **Correct Answer: A. Prolonged QT interval** **Concept:** The patient is presenting with signs of **hypocalcemia** (muscle cramps, Chvostek's sign, and Trousseau's sign) following a thyroidectomy. This is a classic complication caused by accidental removal or devascularization of the parathyroid glands, leading to **Hypoparathyroidism** [1]. Calcium ions play a critical role in the ventricular action potential. In hypocalcemia, there is a **prolongation of Phase 2 (the plateau phase)** of the action potential. Since the QT interval represents the total duration of ventricular depolarization and repolarization, a lengthened plateau phase manifests on the ECG as a **prolonged QT interval** [1]. **Analysis of Incorrect Options:** * **B. Short QT interval:** This is a characteristic finding in **Hypercalcemia**. High calcium levels shorten the plateau phase of the action potential. * **C & D. ST elevation/depression:** These are typically associated with myocardial ischemia, infarction, or electrolyte imbalances like hyperkalemia (ST depression), but are not the primary or classic findings of isolated hypocalcemia. **NEET-PG High-Yield Pearls:** * **Chvostek’s Sign:** Tapping the facial nerve (anterior to the ear) causes twitching of facial muscles. * **Trousseau’s Sign:** Carpal spasm induced by inflating a BP cuff above systolic pressure for 3 minutes (more sensitive than Chvostek’s). * **ECG in Hypocalcemia:** Specifically, it is the **ST segment** that prolongs, leading to a long QT [1]. The T-wave usually remains normal. * **Danger:** A prolonged QT interval can predispose patients to **Torsades de Pointes** (a form of polymorphic ventricular tachycardia) [2]. * **Management:** Acute symptomatic hypocalcemia is treated with **IV Calcium Gluconate**.
Question 1155: All of the following statements about Pseudohypoparathyroidism are true, except?
- A. Decreased serum PTH (Correct Answer)
- B. Decreased serum calcium
- C. Increased serum phosphate
- D. Albright's hereditary osteodystrophy
Explanation: **Explanation:** **Pseudohypoparathyroidism (PHP)** is a group of disorders characterized by **target organ resistance to Parathyroid Hormone (PTH)**. The underlying defect is typically a mutation in the *GNAS1* gene, which encodes the alpha subunit of the stimulatory G protein (Gsα) required for PTH signaling [1]. 1. **Why Option A is the Correct Answer (The "Except"):** In PHP, the body is resistant to PTH. Because the kidneys and bones do not respond to the hormone, the body perceives a deficiency. In an attempt to compensate, the parathyroid glands become hyperactive, leading to **Increased serum PTH** (Secondary Hyperparathyroidism). Therefore, "Decreased serum PTH" is incorrect and is the right choice for this "except" question. 2. **Analysis of Other Options:** * **Option B (Decreased serum calcium):** Since the kidneys cannot respond to PTH, there is decreased renal calcium reabsorption and impaired Vitamin D activation, leading to hypocalcemia [1]. * **Option C (Increased serum phosphate):** PTH normally promotes phosphate excretion (phosphaturia) [2]. Resistance to PTH leads to phosphate retention, resulting in hyperphosphatemia [1]. * **Option D (Albright's hereditary osteodystrophy):** This is the classic phenotypic presentation of PHP Type 1a, characterized by short stature, round face, obesity, and brachydactyly (shortening of the 4th and 5th metacarpals) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Pseudopseudohypoparathyroidism (PPHP):** Patients have the physical features of Albright's (AHO) but have **normal** biochemical levels (Normal Ca, PO4, and PTH) because the defect is inherited paternally [1]. * **Ellsworth-Howard Test:** Historically used to differentiate Hypoparathyroidism from PHP. In PHP, administration of exogenous PTH fails to increase urinary cAMP or phosphate. * **Short 4th Metacarpal:** Also known as **Archibald’s sign**, a classic radiological finding in AHO.
Question 1156: Which of the following is true for Klinefelter's syndrome?
- A. 45,X
- B. Increased arm span and height (Correct Answer)
- C. Attains puberty normally
- D. Normal testes and genitalia
Explanation: Explanation: **Klinefelter’s Syndrome (47,XXY)** is the most common sex chromosome disorder causing primary hypogonadism in males. **Why Option B is Correct:** Patients with Klinefelter’s syndrome exhibit **eunuchoid body proportions** [1]. This occurs because the deficiency in testosterone leads to delayed closure of the epiphyseal plates. Growth continues under the influence of growth hormone, specifically affecting the long bones. Consequently, the **arm span exceeds the total height** (usually by >2 cm), and the lower segment (pubis to floor) is longer than the upper segment (crown to pubis) [1]. **Analysis of Incorrect Options:** * **A (45,X):** This is the karyotype for **Turner Syndrome**, which presents in phenotypic females with short stature and streak ovaries [3, 5]. Klinefelter’s is typically **47,XXY**. * **C (Attains puberty normally):** While initial pubertal changes may begin, patients fail to complete maturation. They develop **hypergonadotropic hypogonadism** due to testicular failure, leading to poor development of secondary sexual characteristics [1, 4]. * **D (Normal testes and genitalia):** A hallmark of Klinefelter’s is **small, firm testes** (usually <2 cm or <6 mL volume) due to hyalinization and fibrosis of the seminiferous tubules [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Laboratory Findings:** Low Testosterone, **Increased LH and FSH** (due to loss of feedback inhibition), and Increased Estradiol [1]. * **Clinical Features:** Gynecomastia (increased risk of male breast cancer), infertility (azoospermia), and mild intellectual disability [1, 4]. * **Histology:** Absence of germ cells and **Leydig cell hyperplasia** (clumping). * **Barr Body:** Positive (due to the extra X chromosome).
Question 1157: Which of the following is NOT a feature of Kallmann syndrome?
- A. Micropenis
- B. Primary amenorrhea
- C. Mirror movements of the hands
- D. Mental retardation (Correct Answer)
Explanation: **Explanation:** **Kallmann Syndrome** is a form of **hypogonadotropic hypogonadism** (low FSH/LH) associated with **anosmia** (loss of smell). It results from the failure of GnRH-secreting neurons and olfactory neurons to migrate from the olfactory placode to the hypothalamus during development. **Why Mental Retardation is the Correct Answer:** Mental retardation is **not** a characteristic feature of Kallmann syndrome. While the condition involves developmental migration defects, cognitive function is typically preserved. If a patient presents with hypogonadotropic hypogonadism and mental retardation, clinicians should consider other syndromes like **Prader-Willi Syndrome** or **Laurence-Moon-Biedl Syndrome**. **Analysis of Incorrect Options:** * **Micropenis (A):** Due to low testosterone levels during the critical period of fetal development, males often present with a micropenis and cryptorchidism. * **Primary Amenorrhea (B):** In females, the lack of GnRH leads to low estrogen levels and a failure to initiate puberty, resulting in primary amenorrhea and absent secondary sexual characteristics. * **Mirror Movements (C):** Also known as **bimanual synkinesis**, these are involuntary movements of one hand that mimic the voluntary movements of the other. This is a recognized neurological association in Kallmann syndrome (often linked to *KAL1* gene mutations). **High-Yield Clinical Pearls for NEET-PG:** 1. **Inheritance:** Most commonly X-linked recessive (*KAL1* gene), but can be Autosomal Dominant (*FGFR1*) or Autosomal Recessive. 2. **Key Triad:** Hypogonadotropic hypogonadism + Anosmia/Hyposmia + Midline defects. 3. **Associated Features:** Renal agenesis (unilateral), cleft lip/palate, and sensorineural deafness. 4. **Diagnosis:** Low Testosterone/Estrogen with low or inappropriately normal FSH/LH; MRI may show absent/hypoplastic olfactory bulbs.
Question 1158: All of the following are helpful in the initial treatment of severe hypercalcemia associated with hyperparathyroidism except?
- A. Hydration with saline
- B. Forced diuresis with loop diuretics
- C. Glucocorticoids (Correct Answer)
- D. Pamidronate
Explanation: ### Explanation The management of severe hypercalcemia (Calcium >14 mg/dL) focuses on increasing urinary excretion and inhibiting bone resorption. **Why Glucocorticoids are the correct answer (Except):** Glucocorticoids (e.g., Prednisone) are highly effective in hypercalcemia caused by **Vitamin D toxicity, sarcoidosis (granulomatous diseases), and certain lymphomas** because they decrease intestinal calcium absorption and inhibit 1-alpha-hydroxylase [1]. However, they have **no significant role** in the acute management of hyperparathyroidism-induced hypercalcemia, as the underlying mechanism in PTH excess is increased bone resorption and renal reabsorption [2], which steroids do not acutely reverse. **Analysis of Incorrect Options:** * **Hydration with Saline (A):** This is the **first-step** in treatment. Isotonic saline restores extracellular volume and increases the glomerular filtration rate, promoting the passive excretion of calcium [1]. * **Forced Diuresis (B):** Loop diuretics (e.g., Furosemide) inhibit calcium reabsorption in the thick ascending limb of the Loop of Henle. They are used *after* adequate volume resuscitation to prevent fluid overload and further lower calcium levels. * **Pamidronate (D):** Intravenous bisphosphonates (Pamidronate/Zoledronate) are the **mainstay for long-term control**. They potent inhibitors of osteoclast-mediated bone resorption. While they take 48–72 hours to reach peak effect, they are standard in the initial management protocol for severe cases [1]. **NEET-PG High-Yield Pearls:** * **Drug of Choice for Acute Management:** IV Normal Saline (Initial) + IV Bisphosphonates (Potency) [1]. * **Most Potent Bisphosphonate:** Zoledronic acid. * **Calcitonin:** Used for rapid reduction (works within hours) but is limited by **tachyphylaxis** (effect wears off after 48 hours). * **Cinacalcet:** A calcimimetic used specifically in refractory cases of Primary Hyperparathyroidism or Parathyroid Carcinoma.
Question 1159: Weight gain is seen in all of the following conditions except?
- A. Cushing's syndrome
- B. Hypothyroidism
- C. Pheochromocytoma (Correct Answer)
- D. Insulinoma
Explanation: The correct answer is **Pheochromocytoma**. This condition is characterized by the hypersecretion of catecholamines (epinephrine and norepinephrine), which leads to a **hypermetabolic state**. Catecholamines stimulate glycogenolysis and lipolysis, significantly increasing the basal metabolic rate (BMR) [1]. Consequently, patients typically present with **weight loss** [2] despite a normal or increased appetite, alongside the classic triad of episodic headaches, sweating, and palpitations [2]. **Analysis of Incorrect Options:** * **Cushing’s Syndrome:** Excess cortisol leads to increased gluconeogenesis and adipogenesis. It causes characteristic **centripetal obesity** (moon facies, buffalo hump, and truncal weight gain) [2] due to the redistribution of fat. * **Hypothyroidism:** A deficiency in thyroid hormones leads to a **decreased BMR**. Weight gain in hypothyroidism [2] is common but usually modest, resulting from both fat accumulation and fluid retention (myxedema/glycosaminoglycan deposition). * **Insulinoma:** This neuroendocrine tumor secretes excessive insulin, leading to recurrent hypoglycemia. Patients often experience weight gain because they **overeat (hyperphagia)** to prevent or treat hypoglycemic symptoms, and insulin itself is a potent anabolic/lipogenic hormone. **NEET-PG High-Yield Pearls:** * **Pheochromocytoma Rule of 10s:** 10% bilateral, 10% malignant, 10% pediatric, 10% extra-adrenal (Paragangliomas), and 10% familial. * **MEN 2A/2B:** Always screen for Pheochromocytoma before performing surgery for Medullary Thyroid Carcinoma. * **Differential for Weight Loss with Increased Appetite:** Hyperthyroidism, Diabetes Mellitus (Type 1), Pheochromocytoma, and Malabsorption syndromes.
Question 1160: Hypophosphatemia is seen in all except?
- A. Acute renal failure (Correct Answer)
- B. Rickets
- C. Respiratory alkalosis/COPD
- D. Chronic alcoholism
Explanation: **Explanation:** The correct answer is **Acute Renal Failure (ARF)**. In ARF, particularly during the oliguric phase, the kidneys fail to excrete phosphate, leading to **Hyperphosphatemia**, not hypophosphatemia. This occurs due to a decreased Glomerular Filtration Rate (GFR), which causes phosphate retention in the blood. [1] **Analysis of Options:** * **Rickets (Option B):** Whether due to Vitamin D deficiency or Vitamin D-resistant types, Rickets leads to decreased intestinal absorption of calcium and phosphate. Secondary hyperparathyroidism (in response to low calcium) further increases renal phosphate excretion, causing **hypophosphatemia**. * **Respiratory Alkalosis/COPD (Option C):** Acute respiratory alkalosis (often seen in COPD patients during hyperventilation or treatment) triggers intracellular pH changes. This activates phosphofructokinase, stimulating glycolysis, which shifts inorganic phosphate from the extracellular space into the cells, resulting in **transcellular hypophosphatemia**. * **Chronic Alcoholism (Option D):** This is a classic cause of hypophosphatemia due to multiple factors: poor dietary intake, decreased intestinal absorption, and alcohol-induced tubular dysfunction leading to phosphaturia. **NEET-PG High-Yield Pearls:** 1. **Refeeding Syndrome:** A high-yield cause of severe hypophosphatemia. Insulin release causes a massive shift of phosphate into cells. [1] 2. **Hungry Bone Syndrome:** Seen post-parathyroidectomy; rapid bone mineralization "consumes" serum phosphate. 3. **Fanconi Syndrome:** Proximal tubular defect leading to significant renal phosphate wasting. [1] 4. **Rule of Thumb:** Renal failure is the most common cause of *high* phosphate; almost all other metabolic crises (alkalosis, malnutrition, Vitamin D deficiency) lead to *low* phosphate.
Practice by Chapter
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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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Multiple Endocrine Neoplasia
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Endocrine Emergencies
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