Endocrinology — MCQs
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Which of the following is NOT a consequence of primary hyperaldosteronism?
A 35-year-old male with a history of severe bronchial asthma for several months now complains of weight gain and the development of purple stretch marks. Physical examination showed BP 149/95 mmHg, supraclavicular fullness, thinned skin with areas of bruising, and decreased strength in proximal muscles. Laboratory investigations showed reduced serum cortisol and reduced plasma ACTH. An electrolyte workup in this patient will most likely reveal?
Which of the following is seen in secondary hyperparathyroidism?
A couple has two children and is currently unable to conceive. The father is diagnosed with hypogonadotropic hypogonadism. Which of the following statements is false regarding his condition?
A patient presents with increased serum calcium and decreased serum phosphate. What is the most likely diagnosis?
Which of the following is NOT typically seen in hypothyroidism?
What is true about thyroid storm?
A patient with IDDM injects a mixture of NPH insulin and crystalline zinc (Regular) insulin before breakfast (at 7 AM) and before dinner (at 8 PM) each day. She reports the following average self-monitored RBS for the past week.
Which pituitary tumor is most responsive to medical therapy?
Which of the following is NOT a cause of hypercalcemia?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 951: Which of the following is NOT a consequence of primary hyperaldosteronism?
- A. Hyperkalemia (Correct Answer)
- B. Hypernatremia
- C. Hydrogen depletion and metabolic alkalosis
- D. Hypertension
Explanation: Explanation: Primary hyperaldosteronism (Conn’s Syndrome) is characterized by the autonomous overproduction of aldosterone from the adrenal cortex. To understand the consequences, one must recall the action of aldosterone on the **principal cells** and **alpha-intercalated cells** of the distal convoluted tubule and collecting duct [1]. **Why Option A is the Correct Answer:** Aldosterone increases the activity of the **ENaC (Epithelial Sodium Channels)** and the **ROMK (Renal Outer Medullary Potassium)** channels [4]. This leads to sodium reabsorption in exchange for potassium excretion. Therefore, primary hyperaldosteronism causes **hypokalemia**, not hyperkalemia [5]. Hyperkalemia is actually a stimulus for aldosterone release [1], but its presence suggests adrenal insufficiency (Addison’s) or hypoaldosteronism. **Analysis of Incorrect Options:** * **B. Hypernatremia:** Aldosterone promotes sodium reabsorption. While the "aldosterone escape" [2] mechanism prevents massive edema, patients typically maintain a high-normal or mildly elevated serum sodium level [5]. * **C. Hydrogen depletion and metabolic alkalosis:** Aldosterone stimulates the H+-ATPase pump in alpha-intercalated cells, leading to increased secretion of hydrogen ions into the urine [1]. The loss of H+ results in systemic metabolic alkalosis [3]. * **D. Hypertension:** Increased sodium reabsorption leads to volume expansion and increased peripheral resistance, making hypertension a hallmark clinical feature. **NEET-PG High-Yield Pearls:** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A ratio **>20-30** is highly suggestive. * **Confirmatory Test:** Oral or IV Saline Suppression Test (failure to suppress aldosterone). * **Aldosterone Escape:** This phenomenon explains why patients with Conn’s syndrome have hypertension but **rarely have overt edema**, as increased pressure natriuresis compensates for sodium retention [2]. * **Triad:** Hypertension + Hypokalemia + Metabolic Alkalosis [5].
Question 952: A 35-year-old male with a history of severe bronchial asthma for several months now complains of weight gain and the development of purple stretch marks. Physical examination showed BP 149/95 mmHg, supraclavicular fullness, thinned skin with areas of bruising, and decreased strength in proximal muscles. Laboratory investigations showed reduced serum cortisol and reduced plasma ACTH. An electrolyte workup in this patient will most likely reveal?
- A. Pituitary tumor
- B. Tumor of the adrenal cortex
- C. Iatrogenic cause (Correct Answer)
- D. Lung cancer
Explanation: ### Explanation **1. Why "Iatrogenic cause" is correct:** The patient presents with classic features of **Cushing’s Syndrome** (weight gain, purple striae, hypertension, supraclavicular fullness, and proximal myopathy) [1]. However, the laboratory findings show **reduced serum cortisol** and **reduced plasma ACTH**. This biochemical profile (Low ACTH + Low Cortisol) indicates **Secondary Adrenal Insufficiency**. In the context of severe bronchial asthma, the patient has likely been using long-term exogenous glucocorticoids (oral or inhaled). Exogenous steroids provide systemic glucocorticoid activity (causing the Cushingoid appearance) while simultaneously suppressing the Hypothalamic-Pituitary-Adrenal (HPA) axis via negative feedback. This leads to low endogenous cortisol and ACTH levels. In iatrogenic Cushing's syndrome, cortisol levels are low unless the patient is taking a corticosteroid like prednisolone that cross-reacts in immunoassays [2]. **2. Why other options are incorrect:** * **Pituitary tumor (Cushing’s Disease):** Would show **High ACTH** and **High Cortisol** [1]. * **Tumor of the adrenal cortex:** Would show **Low ACTH** (due to feedback) but **High endogenous Cortisol** [2]. * **Lung cancer (Ectopic ACTH):** Small cell lung cancer typically causes **High ACTH** and **High Cortisol**, often presenting with severe hypokalemia rather than classic fat redistribution. **3. NEET-PG Clinical Pearls:** * **Most common cause of Cushing’s Syndrome:** Iatrogenic (exogenous steroid use). * **Most common endogenous cause:** Cushing’s Disease (Pituitary adenoma). * **Proximal Myopathy:** A key clinical differentiator; Cushing’s causes muscle wasting, whereas simple obesity does not [1]. * **The "Paradox":** Iatrogenic Cushing’s is the only state where a patient looks "Cushingoid" but has low laboratory cortisol levels (unless the specific synthetic steroid used is cross-reactive in the assay) [2].
Question 953: Which of the following is seen in secondary hyperparathyroidism?
- A. Chronic hypercalcemia
- B. Chronic hypocalcemia (Correct Answer)
- C. Chronic hypomagnesemia
- D. Chronic hypermagnesemia
Explanation: ### Explanation **Secondary Hyperparathyroidism (sHPT)** is a compensatory physiological response where the parathyroid glands become overactive in an attempt to correct low serum calcium levels [1]. **1. Why Chronic Hypocalcemia is Correct:** The hallmark of sHPT is **chronic hypocalcemia** (or low-normal calcium) [2]. The most common cause is **Chronic Kidney Disease (CKD)** [1]. In CKD, the kidneys fail to excrete phosphate (leading to hyperphosphatemia) and fail to activate Vitamin D (1,25-dihydroxyvitamin D deficiency) [4]. Both low Vitamin D and high phosphate lead to low serum ionized calcium [4]. This persistent hypocalcemia acts as a potent stimulus for the parathyroid glands to secrete excessive **Parathyroid Hormone (PTH)** to restore calcium homeostasis [3]. **2. Analysis of Incorrect Options:** * **A. Chronic hypercalcemia:** This is the hallmark of **Primary Hyperparathyroidism** (usually due to an adenoma) or **Tertiary Hyperparathyroidism** (autonomous secretion after long-standing CKD) [1,4]. * **C & D. Magnesium levels:** While magnesium can influence PTH secretion (severe hypomagnesemia actually inhibits PTH release), it is not the primary driver or the characteristic finding used to define secondary hyperparathyroidism in standard clinical scenarios [2]. **3. NEET-PG High-Yield Pearls:** * **Primary HPT:** ↑ PTH, ↑ Calcium, ↓ Phosphate [1]. * **Secondary HPT:** ↑ PTH, **↓/Normal Calcium**, ↑ Phosphate (in CKD) or ↓ Phosphate (in Vitamin D deficiency/malabsorption) [2,4]. * **Tertiary HPT:** ↑↑ PTH, ↑ Calcium (seen in long-term dialysis patients where glands become autonomous) [4]. * **Key Radiology:** Look for "subperiosteal bone resorption" (especially in phalanges) and "Salt and Pepper" appearance of the skull (Osteitis Fibrosa Cystica) [4].
Question 954: A couple has two children and is currently unable to conceive. The father is diagnosed with hypogonadotropic hypogonadism. Which of the following statements is false regarding his condition?
- A. Low luteinizing hormone (LH) and follicle-stimulating hormone (FSH)
- B. Normal testosterone levels (Correct Answer)
- C. Oligospermia
- D. High prolactin levels
Explanation: **Explanation:** Hypogonadotropic hypogonadism (Secondary Hypogonadism) is characterized by a failure of the pituitary gland or hypothalamus to produce the gonadotropins required to stimulate the testes [1]. **Why Option B is the Correct Answer (The False Statement):** In hypogonadotropic hypogonadism, the primary defect lies in the low secretion of **LH and FSH**. Since LH is responsible for stimulating Leydig cells to produce testosterone, a deficiency in LH directly leads to **low testosterone levels** [2]. Therefore, stating that testosterone levels are "normal" is clinically incorrect. **Analysis of Other Options:** * **Option A (Low LH and FSH):** This is the hallmark of secondary hypogonadism. The "hypo-hypo" state implies that both the stimulatory hormones (gonadotropins) and the end-product (testosterone) are low [1]. * **Option C (Oligospermia):** FSH is essential for stimulating Sertoli cells and maintaining spermatogenesis. Low FSH leads to impaired sperm production, resulting in oligospermia or azoospermia, explaining the couple's secondary infertility [3]. * **Option D (High prolactin levels):** Hyperprolactinemia is a common cause of secondary hypogonadism. High prolactin inhibits the pulsatile release of GnRH from the hypothalamus, leading to decreased LH/FSH and subsequent hypogonadism [2]. **NEET-PG High-Yield Pearls:** * **Primary vs. Secondary:** In Primary Hypogonadism (e.g., Klinefelter syndrome), LH/FSH are **high** (Hypergonadotropic). In Secondary, they are **low/normal** (Hypotropic) [2]. * **Kallmann Syndrome:** A key differential for congenital hypogonadotropic hypogonadism, characterized by **anosmia** (loss of smell) due to failure of GnRH neuron migration. * **Initial Investigation:** The first step in evaluating a male with low testosterone and low LH/FSH is often checking **Serum Prolactin** and performing an **MRI of the sella** to rule out a pituitary adenoma [2].
Question 955: A patient presents with increased serum calcium and decreased serum phosphate. What is the most likely diagnosis?
- A. Primary hyperparathyroidism (Correct Answer)
- B. Secondary hyperparathyroidism due to Vitamin D deficiency
- C. Malignancy
- D. Osteoporosis
Explanation: ### Explanation The biochemical hallmark of **Primary Hyperparathyroidism (PHPT)** is the combination of **hypercalcemia** and **hypophosphatemia** [1, 2]. **Pathophysiology:** In PHPT, there is autonomous secretion of Parathyroid Hormone (PTH), usually due to a solitary parathyroid adenoma [2]. PTH increases serum calcium through three mechanisms: 1. **Bone:** Increases osteoclastic bone resorption [1]. 2. **Kidney:** Increases distal tubular reabsorption of calcium and **decreases proximal tubular reabsorption of phosphate** (phosphaturic effect) [1]. 3. **Intestine:** Indirectly increases calcium absorption by stimulating the synthesis of 1,25-(OH)₂ Vitamin D (Calcitriol) [1]. The inhibition of phosphate reabsorption in the kidneys leads to increased urinary phosphate excretion, resulting in low serum phosphate levels [1]. **Analysis of Incorrect Options:** * **Secondary Hyperparathyroidism:** This is a compensatory rise in PTH due to **hypocalcemia** (commonly from Vitamin D deficiency or Chronic Kidney Disease) [2]. Serum calcium is typically low or low-normal. * **Malignancy:** While malignancy is a common cause of hypercalcemia (often via PTHrP), serum phosphate is usually **normal or elevated** unless there is a specific co-existing tubular defect. * **Osteoporosis:** This is a disease of bone density; routine serum calcium, phosphate, and PTH levels are typically **normal**. **NEET-PG High-Yield Pearls:** * **Most common cause of PHPT:** Solitary Parathyroid Adenoma (85%). * **Classic Clinical Pentad:** "Stones (renal calculi), bones (osteitis fibrosa cystica), abdominal groans (peptic ulcers/pancreatitis), psychic moans (depression), and fatigue overtones." * **Biochemical Marker:** High PTH, High Ca²⁺, Low PO₄³⁻, and increased urinary cAMP. * **X-ray finding:** Subperiosteal bone resorption (most common in the radial aspect of middle phalanges) and "Salt and pepper" appearance of the skull.
Question 956: Which of the following is NOT typically seen in hypothyroidism?
- A. Weight gain
- B. Cold intolerance
- C. Diarrhoea (Correct Answer)
- D. Menorrhagia
Explanation: **Explanation:** Hypothyroidism is characterized by a generalized slowing of metabolic processes and sympathetic activity. The correct answer is **Diarrhoea**, as hypothyroidism typically causes **constipation** due to decreased gastrointestinal motility and slowed peristalsis [1]. Diarrhoea is instead a hallmark symptom of hyperthyroidism (due to hypermotility). **Analysis of Options:** * **A. Weight Gain:** This is a classic feature [1]. It occurs due to a lowered basal metabolic rate (BMR) and the accumulation of glycosaminoglycans (myxedema), which leads to water retention, rather than excessive fat deposition. * **B. Cold Intolerance:** Decreased thermogenesis (due to low BMR) makes patients highly sensitive to cold environments. * **D. Menorrhagia:** Hypothyroidism often leads to menstrual irregularities. Menorrhagia (heavy bleeding) is common because low thyroid hormone levels interfere with the coagulation cascade and alter the metabolism of estrogen and progesterone, leading to anovulatory cycles. **Clinical Pearls for NEET-PG:** * **Most Common Cause:** Worldwide, iodine deficiency is the leading cause; in iodine-sufficient areas, **Hashimoto’s Thyroiditis** (anti-TPO antibodies) is most common. * **Cardiac Findings:** Look for **bradycardia**, hypertension (diastolic), and pericardial effusion. * **Neuromuscular:** A high-yield physical sign is the **"hung-up" reflex** (delayed relaxation phase of the deep tendon reflexes, especially the ankle jerk) [2]. * **Lab Diagnosis:** Elevated TSH is the most sensitive initial screening test for primary hypothyroidism [3].
Question 957: What is true about thyroid storm?
- A. It is precipitated by infection in a hypothyroid patient.
- B. Treatment is delayed until thyroid function test results are known.
- C. Steroids should be withheld.
- D. It can be precipitated by surgery. (Correct Answer)
Explanation: **Explanation:** Thyroid storm is a life-threatening, hypermetabolic state caused by an acute surge in thyroid hormones. It is a clinical diagnosis, and management must be aggressive to prevent multi-organ failure. **Why Option D is Correct:** Thyroid storm is typically triggered by a precipitating event in a patient with pre-existing (often undiagnosed or poorly controlled) hyperthyroidism. **Surgery** (both thyroid and non-thyroid surgery) is a classic trigger due to the massive release of catecholamines and thyroid hormones into the circulation during physiological stress. Other triggers include trauma, myocardial infarction, and parturition. **Why the Other Options are Incorrect:** * **Option A:** Thyroid storm occurs in **hyperthyroid** patients (most commonly Graves' disease). A crisis in a hypothyroid patient is called Myxedema Coma. * **Option B:** Thyroid storm is a **clinical diagnosis** based on signs like hyperpyrexia, tachycardia, and agitation (Burch-Wartofsky Point Scale). Treatment must be started **immediately** based on clinical suspicion; waiting for lab results (TSH/T4) significantly increases mortality. * **Option C:** **Steroids (Dexamethasone or Hydrocortisone)** are a cornerstone of treatment. They inhibit the peripheral conversion of T4 to the more active T3 and help treat potential relative adrenal insufficiency associated with the hypermetabolic state. **High-Yield Clinical Pearls for NEET-PG:** * **Management Sequence:** 1. **Beta-blockers (Propranolol):** Control heart rate and inhibit T4 to T3 conversion. 2. **Thionamides (PTU is preferred over Methimazole):** PTU also inhibits peripheral T4 to T3 conversion. 3. **Iodine (Lugol’s iodine/SSKI):** Must be given **1 hour AFTER** thionamides to prevent the iodine from being used as substrate for new hormone synthesis (Wolff-Chaikoff effect). 4. **Glucocorticoids.** * **Burch-Wartofsky Point Scale:** A score ≥45 is highly suggestive of thyroid storm.
Question 958: A patient with IDDM injects a mixture of NPH insulin and crystalline zinc (Regular) insulin before breakfast (at 7 AM) and before dinner (at 8 PM) each day. She reports the following average self-monitored RBS for the past week.
- A. Increasing the 7 AM dose of NPH insulin
- B. Increasing both 7 AM and 8 PM doses of NPH insulin
- C. Increasing the 7 AM dose of regular insulin
- D. Increasing both the 7 AM and 8 PM doses of regular insulin (Correct Answer)
Explanation: ***Increasing both the 7 AM and 8 PM doses of regular insulin*** - **Regular insulin** peaks 2-4 hours after injection, directly controlling **postprandial glucose** after breakfast and dinner meals. - The elevated **post-breakfast** and **post-dinner** readings indicate inadequate regular insulin coverage for meal-related glucose spikes. *Increasing the 7 AM dose of NPH insulin* - **NPH insulin** has a longer duration (12-18 hours) and primarily controls **fasting glucose** and pre-meal readings, not postprandial spikes. - The **normal fasting** and **pre-dinner** glucose levels suggest adequate NPH coverage, making this adjustment inappropriate. *Increasing both 7 AM and 8 PM doses of NPH insulin* - **NPH insulin** from the morning dose peaks around **pre-dinner time**, while evening NPH controls **overnight** and **fasting glucose**. - Since **fasting** and **pre-dinner** readings are normal, increasing NPH would risk **hypoglycemia** during these periods. *Increasing the 7 AM dose of regular insulin* - This would only address the **post-breakfast hyperglycemia** but would not correct the elevated **post-dinner** glucose readings. - A **split-mixed regimen** requires adjustment of both regular insulin doses when postprandial control is inadequate at both meals.
Question 959: Which pituitary tumor is most responsive to medical therapy?
- A. Growth hormone secreting tumor
- B. ACTH secreting tumor
- C. Prolactinoma (Correct Answer)
- D. Thyrotropin secreting tumor
Explanation: **Explanation:** **Prolactinoma** is the correct answer because it is the only pituitary adenoma where **medical therapy is the first-line treatment** and is highly effective in both normalizing hormone levels and achieving significant tumor shrinkage [1]. **Why Prolactinoma is the most responsive:** Prolactinomas arise from lactotrophs, which are physiologically inhibited by dopamine. **Dopamine agonists (Cabergoline, Bromocriptine)** mimic this natural inhibition by binding to D2 receptors on the tumor cells [1]. This leads to a rapid decrease in prolactin synthesis and cellular autophagy, resulting in tumor mass reduction in over 80% of patients [1]. Surgery is reserved only for drug-resistant cases or acute complications like pituitary apoplexy [1]. **Why other options are less responsive:** * **Growth hormone (GH) secreting tumor:** While Somatostatin analogues (Octreotide) and GH-receptor antagonists (Pegvisomant) are used, **transsphenoidal surgery** remains the primary treatment of choice for a definitive cure [1]. * **ACTH secreting tumor (Cushing’s Disease):** Medical therapy (e.g., Ketoconazole, Pasireotide) is generally adjunctive or used when surgery fails. **Surgical resection** is the gold standard. * **Thyrotropin (TSH) secreting tumor:** These are rare and usually require **surgical excision** as the primary modality, though somatostatin analogues can be used to achieve euthyroidism pre-operatively. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Cabergoline is preferred over Bromocriptine due to higher efficacy and fewer side effects [1]. * **Hook Effect:** In extremely high prolactin levels, a lab artifact may show falsely low levels; serial dilution is required for diagnosis [1]. * **Micro vs. Macro:** Microadenomas are <10mm; Macroadenomas are >10mm. Both respond excellently to medical therapy [1].
Question 960: Which of the following is NOT a cause of hypercalcemia?
- A. Multiple myeloma
- B. Lytic skeletal metastasis
- C. Total parenteral nutrition
- D. Acute pancreatitis (Correct Answer)
Explanation: The correct answer is **Acute pancreatitis**, which is a classic cause of **hypocalcemia**, not hypercalcemia [1]. **1. Why Acute Pancreatitis causes Hypocalcemia:** The primary mechanism is **saponification**. During acute pancreatitis, released pancreatic lipases break down periapcreatic fat into free fatty acids [1]. These acids bind with circulating calcium ions to form insoluble calcium soaps in the retroperitoneum. Other contributing factors include hypomagnesemia and a transient resistance to parathyroid hormone (PTH) [1]. **2. Analysis of Incorrect Options (Causes of Hypercalcemia):** * **Multiple Myeloma:** Plasma cells produce Osteoclast Activating Factors (OAFs) like IL-6 and TNF-beta, leading to extensive bone resorption and hypercalcemia [2]. * **Lytic Skeletal Metastasis:** Tumors (e.g., breast, lung, renal cell carcinoma) metastasize to bone and cause local osteolysis through the release of cytokines and PTHrP, elevating serum calcium [2]. * **Total Parenteral Nutrition (TPN):** TPN can cause hypercalcemia due to excessive calcium/vitamin D supplementation in the mix, or as a result of "metabolic bone disease" associated with long-term parenteral feeding. **NEET-PG High-Yield Pearls:** * **Most common cause of hypercalcemia:** In outpatients, it is **Primary Hyperparathyroidism**; in hospitalized patients, it is **Malignancy** [2]. * **Ranson’s Criteria:** A fall in serum calcium (<8 mg/dL) within 48 hours of admission is a poor prognostic sign in acute pancreatitis. * **ECG Findings:** Hypercalcemia causes a **shortened QT interval**, whereas hypocalcemia causes **prolonged QT interval** [1]. * **Milk-Alkali Syndrome:** A triad of hypercalcemia, metabolic alkalosis, and renal insufficiency due to excessive ingestion of calcium and absorbable antacids [2].
Practice by Chapter
Diabetes Mellitus
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Thyroid Disorders
Practice Questions
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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