Endocrinology — MCQs
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A 75-year-old woman presents with mild congestive heart failure 6 weeks after a myocardial infarction. She has a past history of neck surgery for parathyroid adenoma 5 years ago. Her EKG shows slow atrial fibrillation. Serum calcium is 13.0 mg/dL and urinary calcium is 300 mg/24 hr. On examination, there is a small mass in the paratracheal position behind the right clavicle. What is the appropriate management at this time?
Vitamin D-resistant rickets is associated with all of the following, except?
Which of the following conditions is most likely to be associated with the clinical findings shown in the image?
Galactorrhea may be associated with the use of all the following drugs except?
In hyperparathyroidism, which of the following is not typically seen?
Hypophosphatemia is seen in which of the following conditions?
What fasting blood glucose level is indicative of diabetes mellitus?
What is the immediate treatment of hypercalcemia of malignancy?
All of the following occur in adrenal deficiency except?
Dilutional hyponatremia is seen in which of the following conditions or agents?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 1181: A 75-year-old woman presents with mild congestive heart failure 6 weeks after a myocardial infarction. She has a past history of neck surgery for parathyroid adenoma 5 years ago. Her EKG shows slow atrial fibrillation. Serum calcium is 13.0 mg/dL and urinary calcium is 300 mg/24 hr. On examination, there is a small mass in the paratracheal position behind the right clavicle. What is the appropriate management at this time?
- A. Repeat neck surgery
- B. Treatment with Technetium-99
- C. Observation and repeat serum calcium in two months
- D. Ultrasound-guided alcohol injection of the mass (Correct Answer)
Explanation: The patient presents with symptomatic **recurrent primary hyperparathyroidism** (Calcium 13.0 mg/dL) and a localized paratracheal mass, likely representing a recurrent parathyroid adenoma or ectopic tissue. **1. Why Option D is Correct:** The patient is a **high-risk surgical candidate** due to two critical factors: * **Recent Myocardial Infarction (6 weeks ago):** Major elective surgery is generally contraindicated within 6 months of an MI due to high perioperative cardiovascular risk. * **Previous Neck Surgery:** Re-exploration of the neck is technically difficult, carries a higher risk of complications (e.g., recurrent laryngeal nerve injury), and has a lower success rate. **Ultrasound-guided alcohol (ethanol) injection** is a minimally invasive "chemical parathyroidectomy" used for patients who are symptomatic but unfit for surgery. It causes coagulative necrosis of the adenoma, effectively lowering PTH and calcium levels without general anesthesia. **2. Why Incorrect Options are Wrong:** * **A. Repeat neck surgery:** While surgery is the definitive treatment for primary hyperparathyroidism, it is contraindicated here due to the recent MI and the risks associated with re-operation. * **B. Treatment with Technetium-99:** Tc-99m Sestamibi is a **diagnostic imaging modality** used to localize parathyroid adenomas; it is not a therapeutic agent [1]. * **C. Observation:** A serum calcium of 13.0 mg/dL is significantly elevated (normal 8.5–10.5 mg/dL) and is likely exacerbating her congestive heart failure and atrial fibrillation. Observation is unsafe [1]. **Clinical Pearls for NEET-PG:** * **Surgical Criteria (AACE/AAES):** Surgery is indicated if Calcium is >1 mg/dL above normal, age <50, T-score <-2.5, or creatinine clearance <60 mL/min [1]. * **Localization:** Sestamibi scan is the gold standard for localizing ectopic/recurrent adenomas [1]. * **EKG Findings:** Hypercalcemia typically causes a **shortened QT interval**. However, this patient has AFib, which can be triggered by electrolyte imbalances and hypercalcemia. * **Post-op Complication:** "Hungry Bone Syndrome" (profound hypocalcemia) is a common post-surgical concern in severe cases.
Question 1182: Vitamin D-resistant rickets is associated with all of the following, except?
- A. Hypophosphatemia
- B. Increased calcium absorption
- C. Osteomalacia
- D. Osteoporosis (Correct Answer)
Explanation: **Explanation:** **Vitamin D-Resistant Rickets (VDRR)**, most commonly inherited as X-linked Hypophosphatemic Rickets, is characterized by a defect in renal phosphate handling and impaired vitamin D metabolism. **Why Osteoporosis is the Correct Answer:** Osteoporosis is a **quantitative** defect where the bone density is low, but the mineralization of the remaining bone matrix is normal. In contrast, VDRR is a **qualitative** defect of mineralization [1]. In VDRR, the primary pathology is the failure to mineralize the osteoid (bone matrix) due to low phosphate levels, leading to "soft bones" rather than "porous bones." **Analysis of Other Options:** * **Hypophosphatemia:** This is the hallmark of VDRR [1]. Mutations (e.g., in the *PHEX* gene) lead to increased levels of FGF-23, which causes renal phosphate wasting and inhibits the 1-alpha-hydroxylase enzyme. * **Osteomalacia:** This is the adult manifestation of defective mineralization [1]. While children get rickets (affecting growth plates), adults with VDRR develop osteomalacia, characterized by bone pain and pseudofractures. * **Increased calcium absorption:** This is the **incorrect** statement regarding the pathophysiology of VDRR, but it is often listed as a distractor. In VDRR, there is actually **decreased** intestinal calcium and phosphate absorption due to low 1,25(OH)₂D levels. However, in the context of this "Except" question, Osteoporosis is the most definitive pathological mismatch. **Clinical Pearls for NEET-PG:** * **Biochemical Profile:** Low Serum Phosphate, Normal Serum Calcium, Normal/Low 1,25(OH)₂D, and **Elevated Alkaline Phosphatase (ALP)**. * **Key Difference:** Unlike nutritional rickets, VDRR does **not** respond to physiological doses of Vitamin D. Treatment requires oral phosphate supplements and Calcitriol. * **Radiology:** Look for "Looser’s zones" (pseudofractures) in osteomalacia and widening of the epiphyseal plates in rickets [1].
Question 1183: Which of the following conditions is most likely to be associated with the clinical findings shown in the image?
- A. Hypothyroidism (Correct Answer)
- B. Acromegaly
- C. Cushing syndrome
- D. Graves' disease
Explanation: ***Hypothyroidism*** - The image demonstrates classic **myxedematous facies** with **periorbital puffiness**, **dry coarse skin**, and **loss of outer third of eyebrows**. - The **dull facial expression** and overall appearance are characteristic of **severe hypothyroidism** (myxedema). *Acromegaly* - Features **coarse facial features** with **enlarged nose**, **thick lips**, and **prognathism** (protruding jaw), which are not present here. - Associated with **macroglossia** and **enlarged hands and feet** due to excess **growth hormone**. *Cushing syndrome* - Characterized by **moon face** with **central facial plethora** and **hirsutism**, contrasting with the pale, puffy appearance seen. - Often presents with **purple striae**, **buffalo hump**, and **truncal obesity** due to excess **cortisol**. *Graves' disease* - Typically shows **exophthalmos** (bulging eyes) and **lid retraction** with a **staring appearance**. - Associated with **hyperthyroid features** like **weight loss**, **tremor**, and **goiter**, opposite to the findings shown.
Question 1184: Galactorrhea may be associated with the use of all the following drugs except?
- A. Methyldopa
- B. Tricyclic antidepressants
- C. Pyridoxine (Correct Answer)
- D. Phenothiazine
Explanation: The regulation of prolactin is primarily under the **inhibitory control of Dopamine** (Prolactin Inhibiting Factor). Any drug that decreases dopamine levels or blocks dopamine receptors will lead to hyperprolactinemia and subsequent galactorrhea [1]. **Why Pyridoxine is the correct answer:** **Pyridoxine (Vitamin B6)** is a cofactor in the synthesis of dopamine (it aids the conversion of L-Dopa to Dopamine). By increasing central dopamine levels, pyridoxine actually **inhibits** prolactin secretion. In fact, high doses of Pyridoxine have historically been used to suppress lactation, making it the "except" in this list. **Analysis of incorrect options:** * **Methyldopa (Option A):** This centrally acting antihypertensive acts as a false neurotransmitter and depletes central dopamine stores, leading to increased prolactin. * **Tricyclic Antidepressants (Option B):** TCAs (like Amitriptyline) can cause galactorrhea by inhibiting dopamine reuptake or through mild serotonergic stimulation, which stimulates prolactin release. * **Phenothiazines (Option D):** These are typical antipsychotics (e.g., Chlorpromazine) that act as potent **D2 receptor antagonists** in the tuberoinfundibular pathway, frequently causing significant hyperprolactinemia [1]. **NEET-PG High-Yield Pearls:** 1. **Metoclopramide and Domperidone** (anti-emetics) are common causes of drug-induced galactorrhea due to D2 blockade [1]. 2. **Verapamil** is a unique calcium channel blocker known to cause galactorrhea by interfering with dopamine synthesis. 3. **Hypothyroidism** can cause galactorrhea because increased TRH (Thyrotropin-Releasing Hormone) acts as a prolactin-releasing factor [1]. 4. **Bromocriptine and Cabergoline** (Dopamine agonists) are the treatments of choice for pathological hyperprolactinemia.
Question 1185: In hyperparathyroidism, which of the following is not typically seen?
- A. Normal alkaline phosphatase
- B. Decreased phosphate in urine (Correct Answer)
- C. Increased calcium
- D. Hypophosphatemia
Explanation: In **Primary Hyperparathyroidism (PHPT)**, the fundamental pathology is the autonomous overproduction of Parathyroid Hormone (PTH), usually due to a parathyroid adenoma [1]. ### Why "Decreased phosphate in urine" is the correct answer: PTH has a potent **phosphaturic effect**. It acts on the proximal convoluted tubules of the kidney to inhibit the sodium-phosphate cotransporter (NaPi-2a), thereby decreasing phosphate reabsorption [2]. This leads to **increased phosphate excretion in the urine (Hyperphosphaturia)**. Therefore, "decreased phosphate in urine" is the incorrect statement regarding the typical presentation of hyperparathyroidism. ### Explanation of other options: * **A. Normal alkaline phosphatase:** In many mild or early cases of PHPT, Alkaline Phosphatase (ALP) remains within the normal range. It only rises significantly when there is extensive bone involvement (Osteitis fibrosa cystica). * **C. Increased calcium:** Hypercalcemia is the hallmark of PHPT [1]. PTH increases serum calcium by enhancing bone resorption, increasing renal distal tubule calcium reabsorption, and stimulating Vitamin D activation (which increases intestinal absorption) [2]. * **D. Hypophosphatemia:** Due to the phosphaturic effect mentioned above, the kidneys "waste" phosphate, leading to low serum phosphate levels [1], [2]. ### NEET-PG High-Yield Pearls: * **Classic Triad:** Hypercalcemia, Hypophosphatemia, and Hyperphosphaturia. * **Urinary cAMP:** PTH increases urinary cyclic AMP; this is a classic biochemical marker. * **Radiology:** Look for "subperiosteal resorption" (pathognomonic), especially on the radial aspect of the middle phalanges, and "salt and pepper" appearance of the skull. * **Mnemonic for symptoms:** "Stones (renal), bones (aches), abdominal groans (peptic ulcers/pancreatitis), and psychic overtones (depression)" [3].
Question 1186: Hypophosphatemia is seen in which of the following conditions?
- A. Pseudohypoparathyroidism
- B. Chronic renal failure (CRF)
- C. Rickets (Correct Answer)
- D. Hyperparathyroidism
Explanation: **Explanation:** **Correct Answer: C. Rickets** The primary mechanism in Rickets (Vitamin D deficiency) is the failure of mineralization of the osteoid matrix [1]. Vitamin D deficiency leads to decreased intestinal absorption of calcium and phosphorus. The resulting hypocalcemia triggers a compensatory rise in **Parathyroid Hormone (PTH)**—a condition known as secondary hyperparathyroidism. PTH acts on the kidneys to increase phosphate excretion (phosphaturia) while attempting to normalize calcium, leading to the characteristic **hypophosphatemia** seen in these patients [2]. **Analysis of Incorrect Options:** * **A. Pseudohypoparathyroidism:** This is characterized by end-organ resistance to PTH. Since the kidneys cannot respond to PTH, phosphate excretion is impaired, leading to **hyperphosphatemia** and hypocalcemia. * **B. Chronic Renal Failure (CRF):** In CRF, the declining Glomerular Filtration Rate (GFR) leads to the retention of phosphate. This results in **hyperphosphatemia**, which further contributes to secondary hyperparathyroidism and renal osteodystrophy. * **D. Hyperparathyroidism:** While primary hyperparathyroidism *does* cause hypophosphatemia due to PTH-induced phosphaturia [2], **Rickets** is a more classic and frequently tested association for profound hypophosphatemia in the context of pediatric bone disease and Vitamin D metabolism. *(Note: In some exam patterns, both C and D could be technically correct, but Rickets is the prioritized answer in the context of metabolic bone disease pathology).* **NEET-PG High-Yield Pearls:** * **PTH Effect:** "P" for PTH stands for **P**hosphate **T**hrashing (it dumps phosphate in the urine) [2]. * **FGF-23:** A key hormone in phosphate homeostasis; elevated levels (as seen in oncogenic osteomalacia or X-linked hypophosphatemic rickets) also cause hypophosphatemia [2]. * **Refeeding Syndrome:** A common clinical cause of severe hypophosphatemia due to an insulin-driven shift of phosphate into cells [2].
Question 1187: What fasting blood glucose level is indicative of diabetes mellitus?
- A. 126 mg/dl (Correct Answer)
- B. 140 mg/dl
- C. 100 mg/dl
- D. 200 mg/dl
Explanation: **Explanation:** The diagnosis of Diabetes Mellitus (DM) is based on specific glycemic thresholds defined by the American Diabetes Association (ADA). **1. Why Option A is correct:** According to current diagnostic criteria, a **Fasting Plasma Glucose (FPG) level ≥ 126 mg/dl (7.0 mmol/L)** is indicative of Diabetes Mellitus [1]. "Fasting" is defined as no caloric intake for at least 8 hours. This threshold is chosen because it correlates with a significantly increased risk of developing microvascular complications, particularly diabetic retinopathy [1]. **2. Analysis of Incorrect Options:** * **Option B (140 mg/dl):** While this value is diagnostic of diabetes (as it is >126 mg/dl), it is not the *minimum* threshold. Additionally, 140 mg/dl is the cutoff for the 2-hour post-load glucose in **Impaired Glucose Tolerance (IGT)**. * **Option C (100 mg/dl):** This is the upper limit of normal. An FPG between **100–125 mg/dl** is categorized as **Impaired Fasting Glucose (IFG)**, a state of pre-diabetes [1]. * **Option D (200 mg/dl):** This is the diagnostic threshold for a **Random Plasma Glucose** (in a symptomatic patient) or a **2-hour Plasma Glucose** during an Oral Glucose Tolerance Test (OGTT). **High-Yield Clinical Pearls for NEET-PG:** * **HbA1c Criteria:** A level of **≥ 6.5%** is diagnostic for DM; **5.7–6.4%** indicates pre-diabetes. * **Confirmatory Testing:** Unless there is clear clinical hyperglycemia (polyuria, polydipsia, weight loss) with a random glucose ≥ 200 mg/dl, the diagnosis requires **two abnormal test results** from the same sample or two separate test samples. * **Gold Standard:** The OGTT is considered the most sensitive test for diagnosis, though FPG and HbA1c are more commonly used in clinical practice.
Question 1188: What is the immediate treatment of hypercalcemia of malignancy?
- A. IV fluids (Correct Answer)
- B. Bisphosphonates
- C. Calcitonin
- D. Glucocorticoids
Explanation: **Explanation:** The management of severe hypercalcemia (typically >14 mg/dL) or symptomatic hypercalcemia of malignancy follows a prioritized sequence. **Why IV Fluids are the correct answer:** The **immediate** and most critical step is aggressive volume expansion with **0.9% Normal Saline** [1]. Patients with hypercalcemia are almost always severely dehydrated due to polyuria (nephrogenic diabetes insipidus) and vomiting. Rehydration restores intravascular volume, increases the glomerular filtration rate (GFR), and promotes the renal excretion of calcium [1]. This is the only intervention that works within minutes to hours. **Analysis of Incorrect Options:** * **Bisphosphonates (e.g., Zoledronic acid):** While these are the most effective long-term treatment for malignancy-associated hypercalcemia (by inhibiting osteoclasts), they have a delayed onset of action (24–72 hours). They are not the "immediate" choice [1]. * **Calcitonin:** This works quickly (within 4–6 hours) by inhibiting bone resorption and increasing renal excretion. However, its effect is mild, transient (due to tachyphylaxis), and it is used as an *adjunct* to IV fluids, not as the primary first-line therapy. * **Glucocorticoids:** These are primarily effective in hypercalcemia caused by Vitamin D toxicity, sarcoidosis, or certain lymphomas. They are not the first-line treatment for general malignancy-induced hypercalcemia. **Clinical Pearls for NEET-PG:** * **Target:** Aim for a urine output of 100–150 mL/h during rehydration. * **Loop Diuretics (Furosemide):** These are **no longer** used routinely unless the patient develops fluid overload/heart failure. * **Mechanism:** Most cases of hypercalcemia of malignancy are caused by **PTHrP** (Parathyroid Hormone-related Protein) secretion, most commonly seen in Squamous Cell Carcinoma of the lung. * **Refractory Cases:** Hemodialysis is the treatment of choice for patients with severe hypercalcemia and renal failure.
Question 1189: All of the following occur in adrenal deficiency except?
- A. Hypoglycemia
- B. Hypocalcemia (Correct Answer)
- C. Hypotension
- D. Hyponatremia
Explanation: In adrenal insufficiency (Addison’s disease), the primary pathology is the deficiency of cortisol and aldosterone [1]. **Why Hypocalcemia is the Correct Answer:** Adrenal deficiency actually causes **Hypercalcemia**, not hypocalcemia. Cortisol normally antagonizes Vitamin D action and promotes renal calcium excretion. When cortisol is deficient, there is increased renal tubular reabsorption of calcium and increased sensitivity to Vitamin D, leading to elevated serum calcium levels in about 10-20% of patients. **Explanation of Incorrect Options:** * **Hypoglycemia:** Cortisol is a counter-regulatory (diabetogenic) hormone that stimulates gluconeogenesis. Its absence leads to decreased glucose production and increased insulin sensitivity, resulting in low blood sugar. * **Hypotension:** This occurs due to two mechanisms: (1) Aldosterone deficiency leads to sodium and water wasting (volume depletion) [1], and (2) Cortisol is required to maintain the pressor response of blood vessels to catecholamines. * **Hyponatremia:** This is the most common electrolyte abnormality. It results from the loss of sodium in urine (due to low aldosterone) and the "inappropriate" secretion of ADH (cortisol normally inhibits ADH release) [2]. **NEET-PG High-Yield Pearls:** * **Classic Electrolyte Triad:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis (due to aldosterone deficiency). * **Hyperpigmentation:** Seen only in *Primary* adrenal insufficiency due to increased ACTH/POMC levels (MSH-like activity). * **Diagnosis:** The gold standard is the **ACTH Stimulation Test** (Cosyntropin test) [2]. * **Eosinophilia:** A common but often overlooked hematological finding in Addison’s disease.
Question 1190: Dilutional hyponatremia is seen in which of the following conditions or agents?
- A. Addison's disease
- B. Vincristine (Correct Answer)
- C. Diuretic therapy
- D. Craniphyrangioma
Explanation: **Explanation** The correct answer is **Vincristine**. **1. Why Vincristine is Correct:** Vincristine (a vinca alkaloid used in chemotherapy) is a well-known cause of **SIADH (Syndrome of Inappropriate Antidiuretic Hormone secretion)**. It exerts a neurotoxic effect on the hypothalamus and posterior pituitary, leading to the excessive release of ADH. High levels of ADH cause water reabsorption in the renal collecting ducts [1], leading to water retention and **dilutional hyponatremia** (euvolemic hyponatremia) [2]. **2. Analysis of Incorrect Options:** * **Addison’s Disease:** This causes **hypovolemic hyponatremia**. The deficiency of aldosterone leads to "salt wasting" (loss of sodium and water), but the sodium loss exceeds water loss [2]. * **Diuretic Therapy:** Thiazides and loop diuretics cause hyponatremia primarily through the depletion of total body sodium and water (**hypovolemic hyponatremia**) [2], not through primary water retention. * **Craniopharyngioma:** This tumor typically destroys the posterior pituitary or hypothalamus, leading to a *deficiency* of ADH, resulting in **Diabetes Insipidus** (hypernatremia due to excessive water loss), rather than hyponatremia [3]. **3. NEET-PG High-Yield Pearls:** * **Drugs causing SIADH:** Remember the mnemonic **"S-C-V-C"**: **S**SRIs, **C**yclophosphamide/Carbamazepine, **V**incristine/Vinblastine, **C**hlorpropamide. * **Diagnostic Criteria for SIADH:** Euvolemic status [2], low serum osmolality (<275 mOsm/kg), and inappropriately high urine osmolality (>100 mOsm/kg). * **Management:** The first-line treatment for SIADH is **fluid restriction**. For severe symptomatic cases, hypertonic saline (3%) is used, but must be administered carefully to avoid Central Pontine Myelinolysis.
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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