Endocrinology Practice Questions

Q: Which of the following is NOT a feature of thyrotoxicosis?

Diastolic murmur. Thyrotoxicosis represents a hypermetabolic state caused by excess circulating thyroid hormones ($T_{3}$ and $T_{4}$). These hormones increase the expression of $\beta$-adrenergic receptors and exert direct chronotropic and inotropic effects on the myocardium. [3] **Why "Diastolic Murmur" is the Correct Answer:** Thyrotoxicosis is a classic **high-output state**. The increased stroke volume and rapid blood flow across the heart valves typically result in a **systolic flow murmur** (ejection systolic). Diastolic murmurs are generally associated with structural valvular disease (like Mitral Stenosis or Aortic Regurgitation) and are **not** a feature of thyrotoxicosis. **Analysis of Incorrect Options:** * **Tremors:** Excess thyroid hormone increases $\beta$-adrenergic activity. This manifests as a characteristic **fine, rapid, distal tremor** (best seen when the patient extends their hands). [3] * **Irregularly Irregular Pulse:** Thyrotoxicosis is a leading cause of **Atrial Fibrillation (AF)**, especially in elderly patients. [1] AF presents clinically as an irregularly irregular pulse. * **Osteoporosis:** Thyroid hormones directly stimulate osteoclast activity. Chronic thyrotoxicosis leads to increased bone resorption, hypercalciuria, and a reduction in bone mineral density, eventually causing osteoporosis. [2] **NEET-PG High-Yield Pearls:** * **Means-Lerman Scratch:** A mid-systolic scratching sound heard at the left second intercostal space during expiration, caused by the rubbing of the hyperdynamic heart against the pleura. * **Pulse Pressure:** Thyrotoxicosis causes **widened pulse pressure** (increased systolic BP due to stroke volume and decreased diastolic BP due to peripheral vasodilation). [3] * **Apathetic Hyperthyroidism:** In the elderly, typical signs like tremors may be absent; they may present only with AF or weight loss.

Q: Which one of the following features may not be seen in hypothyroidism?

Pretibial myxedema. Explanation: The correct answer is **Pretibial myxedema**. This is a classic "trap" question in NEET-PG, as it tests the distinction between hypothyroidism and Graves' disease. **Why Pretibial Myxedema is the correct answer:** Pretibial myxedema (localized dermopathy) is a characteristic feature of **Graves' disease (Hyperthyroidism)**, not hypothyroidism [1]. It occurs due to the deposition of glycosaminoglycans in the dermis, triggered by the same autoimmune process (TSH-receptor antibodies) that causes Graves' ophthalmopathy. While "myxedema" is a term used to describe the generalized non-pitting edema of severe hypothyroidism, the specific *pretibial* distribution is unique to Graves' disease [1]. **Analysis of incorrect options:** * **Cold intolerance:** A hallmark of hypothyroidism. Low levels of thyroid hormone decrease the basal metabolic rate (BMR) and thermogenesis, making patients sensitive to cold. * **Deafness:** Sensorineural or conductive hearing loss can occur in hypothyroidism. It is notably seen in **Pendred syndrome** (congenital hypothyroidism with goiter and deafness). * **Pericardial effusion:** Hypothyroidism causes increased capillary permeability and decreased lymphatic drainage, leading to protein-rich fluid accumulation in serous cavities (pleural, pericardial, or peritoneal). It is usually asymptomatic as it accumulates slowly. **High-Yield Clinical Pearls for NEET-PG:** * **Wolff-Chaikoff Effect:** Inhibition of thyroid hormone synthesis by high iodine levels (can lead to hypothyroidism). * **Most common cause:** Hashimoto’s thyroiditis (in iodine-sufficient areas). * **ECG in Hypothyroidism:** Low voltage complexes, sinus bradycardia, and flattened T-waves. * **Myxedema Coma:** The most severe form of hypothyroidism, characterized by hypothermia, bradycardia, and altered mental status.

Q: All of the following are true about Cushing's syndrome except?

Hyperkalemia. **Explanation:** The correct answer is **C (Hyperkalemia)** because Cushing’s syndrome is characterized by **Hypokalemia**, not hyperkalemia. **Medical Concept:** In Cushing’s syndrome, excess cortisol exerts a "mineralocorticoid effect" when present in high concentrations. Cortisol binds to mineralocorticoid receptors in the renal distal tubules, acting like aldosterone [3]. This leads to increased sodium reabsorption and increased secretion of potassium ($K^+$) and hydrogen ions ($H^+$) into the urine [3]. Consequently, patients develop **hypokalemia** and **metabolic alkalosis**. **Analysis of Options:** * **A. Hyperpigmentation:** This occurs specifically in **ACTH-dependent** Cushing’s (like Cushing’s Disease or Ectopic ACTH syndrome). * **B. Purplish striae:** A classic sign caused by cortisol-induced inhibition of fibroblasts, leading to loss of collagen and thinning of the dermis [1]. These are typically >1 cm wide and reddish-purple. * **D. Metabolic alkalosis:** As explained above, the mineralocorticoid effect of excess cortisol causes the kidneys to excrete $H^+$ ions, resulting in a systemic alkalotic state [3]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common cause of Cushing’s syndrome:** Exogenous steroid use. 2. **Most common endogenous cause:** Cushing’s Disease (Pituitary adenoma) [1]. 3. **Severe Hypokalemia:** If a patient has Cushing’s features with profound hypokalemia, suspect **Ectopic ACTH secretion** (e.g., Small Cell Carcinoma of the Lung). 4. **Screening Tests:** 24-hour urinary free cortisol, Low-dose dexamethasone suppression test (LDDST), or late-night salivary cortisol [2].

Q: According to the American Diabetes Association, what is the target HbA1c level for diabetes patients under good control?

<7%. The **American Diabetes Association (ADA)** recommends a glycemic target of **HbA1c <7%** for most non-pregnant adults with diabetes. This target is based on landmark trials like the **UKPDS** and **DCCT**, which demonstrated that maintaining an HbA1c below 7% significantly reduces the risk of microvascular complications (retinopathy, nephropathy, and neuropathy) [1]. HbA1c reflects the average blood glucose over the preceding 2-3 months (the lifespan of an erythrocyte). **Analysis of Options:** * **Option A (4-6%):** This is the normal physiological range for non-diabetic individuals. While ideal, targeting this range in diabetics often increases the risk of life-threatening hypoglycemia. * **Option B ( 8%):** These levels indicate suboptimal control. However, a less stringent goal (e.g., <8%) may be appropriate for patients with a history of severe hypoglycemia, limited life expectancy, or advanced macrovascular complications [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Individualization:** The ADA emphasizes "individualized" targets. Tight control (<6.5%) may be sought in young patients with short disease duration, while relaxed targets (<8%) are for the elderly or comorbid [1]. * **Diagnosis:** HbA1c **≥6.5%** is diagnostic for Diabetes Mellitus; **5.7-6.4%** is diagnostic for Pre-diabetes. * **Falsely Low HbA1c:** Seen in conditions with high red cell turnover (e.g., Hemolytic anemia, pregnancy, recent blood transfusion). * **Falsely High HbA1c:** Seen in Iron deficiency anemia (due to increased erythrocyte lifespan).

Q: All are features of Bartter syndrome, EXCEPT:

Hypertension. **Explanation:** **Bartter syndrome** is a group of autosomal recessive disorders caused by mutations in the ion transporters of the **Thick Ascending Limb (TAL)** of the Loop of Henle. It mimics the chronic use of loop diuretics (like Furosemide) [2]. **1. Why Hypertension is the Correct Answer:** The hallmark of Bartter syndrome is **normotension or hypotension**. The defect in NaCl reabsorption leads to salt wasting and volume depletion. This activates the Renin-Angiotensin-Aldosterone System (RAAS), leading to **Secondary Hyperaldosteronism** [1]. Despite high renin and aldosterone levels, patients remain non-hypertensive because the primary defect is salt loss, and there is often a resistance to the pressor effects of Angiotensin II [1]. **2. Why other options are incorrect:** * **Polyuria (A):** The defect in the TAL impairs the medullary osmotic gradient, leading to a loss of concentrating ability (nephrogenic diabetes insipidus-like effect), resulting in polyuria and polydipsia [2]. * **Metabolic Alkalosis (B):** Increased distal delivery of sodium and high aldosterone levels promote the secretion of H+ and K+ in the collecting duct, leading to hypokalemic metabolic alkalosis [1]. * **Periodic Paralysis (C):** Severe hypokalemia (due to renal potassium wasting) can manifest clinically as muscle weakness or even hypokalemic periodic paralysis [1]. **Clinical Pearls for NEET-PG:** * **Bartter vs. Gitelman:** Bartter syndrome usually presents in infancy/childhood with **Hypercalciuria** (stones), whereas Gitelman syndrome presents in adolescence/adulthood with **Hypocalciuria** and hypomagnesemia. * **Mnemonic:** **B**artter = **B**oop (Loop diuretics/TAL); **G**itelman = **G**reen (Thiazide diuretics/DCT). * Both syndromes present with **Low/Normal BP**, distinguishing them from Liddle Syndrome (High BP).

Q: Hypercalcemia is seen in all of the following conditions EXCEPT?

Pseudohypoparathyroidism. **Explanation:** The correct answer is **Pseudohypoparathyroidism (PHP)** because it is characterized by **hypocalcemia**, not hypercalcemia [1]. **1. Why Pseudohypoparathyroidism is the correct answer:** PHP is a genetic disorder caused by **end-organ resistance to Parathyroid Hormone (PTH)** [2]. Although PTH levels are high, the kidneys and bones fail to respond to it. This leads to the biochemical triad of **hypocalcemia**, hyperphosphatemia, and elevated PTH [1]. Type 1A (Albright’s Hereditary Osteodystrophy) also presents with physical features like short stature and shortened 4th/5th metacarpals [2]. **2. Why the other options are incorrect:** * **Bone Metastasis:** This is a common cause of hypercalcemia of malignancy [1]. It occurs via direct osteolysis by tumor cells or the release of local cytokines (e.g., RANKL) that activate osteoclasts. * **Sarcoidosis:** Granulomatous diseases cause hypercalcemia because macrophages within the granulomas contain the enzyme **1-alpha-hydroxylase** [1]. This leads to uncontrolled conversion of Vitamin D to its active form (1,25-dihydroxyvitamin D), increasing intestinal calcium absorption. * **Hyperparathyroidism:** Primary hyperparathyroidism (usually due to a parathyroid adenoma) involves autonomous secretion of PTH, which directly increases bone resorption and renal calcium reabsorption, leading to hypercalcemia [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of hypercalcemia:** Outpatients = Primary Hyperparathyroidism; Inpatients = Malignancy [1]. * **PTHrP (PTH-related protein):** The most common cause of hypercalcemia in non-metastatic solid tumors (e.g., Squamous cell carcinoma of the lung). * **Pseudopseudohypoparathyroidism (PPHP):** Has the physical features of Albright’s but **normal** calcium and PTH levels (due to paternal imprinting) [2]. * **ECG in Hypercalcemia:** Look for a **shortened QT interval**.

Q: What are the diagnostic criteria for diabetes mellitus?

HbA1c greater than 6.5%. The diagnosis of Diabetes Mellitus (DM) is based on specific glycemic thresholds established by the ADA (American Diabetes Association) and WHO. [1] ### **Explanation of the Correct Answer** **Option D (HbA1c ≥ 6.5%)** is a primary diagnostic criterion. HbA1c reflects the average blood glucose over the preceding 2–3 months by measuring the glycation of hemoglobin. A value of **≥ 6.5%** is diagnostic of diabetes. This test is advantageous as it does not require fasting and has low day-to-day variability. ### **Analysis of Incorrect Options** * **Option A & B:** These values fall into the **Pre-diabetes** or normal range. For a diagnosis of DM, the Fasting Plasma Glucose (FPG) must be **≥ 126 mg/dL** [1] and the 2-hour Plasma Glucose during an Oral Glucose Tolerance Test (OGTT) must be **≥ 200 mg/dL**. Option B (125/199 mg/dL) specifically describes the upper limit of Impaired Fasting Glucose and Impaired Glucose Tolerance. [1] * **Option C:** Insulin levels are not used to diagnose diabetes. While Type 2 DM often features initial hyperinsulinemia (insulin resistance) and Type 1 DM features hypoinsulinemia, these levels vary significantly and do not define the disease clinically. [1] ### **High-Yield NEET-PG Pearls** * **Diagnostic Criteria Summary:** 1. **HbA1c ≥ 6.5%** 2. **Fasting Plasma Glucose (FPG) ≥ 126 mg/dL** (Fasting = no caloric intake for ≥ 8 hours) [1] 3. **2-hour Post-load Glucose ≥ 200 mg/dL** (during 75g OGTT) 4. **Random Plasma Glucose ≥ 200 mg/dL** in a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, weight loss). [1] * **Pre-diabetes Ranges:** HbA1c: 5.7–6.4%; FPG: 100–125 mg/dL; 2-hr OGTT: 140–199 mg/dL. [1] * **Note:** Unless there is clear clinical exhaustion (symptoms + random glucose > 200), a diagnosis requires **two abnormal test results** from the same sample or two separate test samples.

Q: What is a characteristic physical finding of prolactinoma, besides galactorrhea?

Bitemporal hemianopia. ### Explanation **Correct Option: A. Bitemporal hemianopia** **Medical Concept:** The pituitary gland sits in the **sella turcica**, located directly beneath the **optic chiasm**. Prolactinomas, particularly **macroadenomas** (size >10 mm), can expand superiorly out of the sella [1]. This upward extension causes mechanical compression of the decussating nasal fibers of the optic nerves at the optic chiasm [2]. Since these fibers carry visual information from the temporal fields, the classic physical finding is **bitemporal hemianopia** (loss of the outer half of the visual field in both eyes) [1]. **Why the other options are incorrect:** * **B, C, and D (Anovulatory cycles, Amenorrhea, Infertility):** While these are classic clinical manifestations of hyperprolactinemia in females, they are **symptoms** (subjective complaints) rather than **physical findings** (objective signs detected by a clinician during an examination). High prolactin inhibits the pulsatile release of GnRH, leading to low LH/FSH and subsequent hypogonadism. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common:** Prolactinoma is the most common secretory tumor of the anterior pituitary. * **Size vs. Gender:** Microadenomas ( 10 mm) are more common in males (presenting late with mass effect symptoms like headache and visual field defects) [1]. * **Hook Effect:** In extremely high prolactin levels, lab assays may show falsely low levels; serial dilution is required for accurate diagnosis. * **Drug of Choice:** **Cabergoline** (a dopamine agonist) is the first-line treatment for both micro and macroadenomas, unlike most other pituitary tumors which require surgery [2].

Q: Which of the following is NOT a sign of thyrotoxicosis?

Stridor on gently pressing the lobes of the thyroid. **Explanation:** The correct answer is **D. Stridor on gently pressing the lobes of the thyroid.** This clinical finding is known as **Pemberton’s Sign**, which indicates superior vena cava syndrome or thoracic inlet obstruction, typically caused by a large retrosternal goiter. It is a mechanical complication of an enlarged thyroid gland rather than a physiological sign of thyrotoxicosis (excess thyroid hormone). **Analysis of Options:** * **A. Infrequent blinking (Stellwag’s Sign):** This is a classic ocular sign of thyrotoxicosis caused by sympathetic overactivity of the superior tarsal (Müller’s) muscle, leading to a "staring" appearance. * **B. Inability to converge the eyeballs (Moebius Sign):** This occurs due to weakness of the medial rectus muscles, a common finding in Graves' ophthalmopathy associated with thyrotoxicosis [2]. * **C. Visible upper sclera on looking straight (Dalrymple’s Sign):** This refers to widened palpebral fissures due to lid retraction [2]. In a normal individual, the upper eyelid covers the superior limbus; in thyrotoxicosis, the sclera above the iris becomes visible. **NEET-PG High-Yield Pearls:** * **Graves’ Specificity:** While lid retraction (Dalrymple’s) can occur in any cause of thyrotoxicosis due to sympathetic overactivity, **exophthalmos** (proptosis) and **extraocular muscle palsy** are specific to Graves' Disease (autoimmune mediated) [1], [2]. * **Lid Lag:** Known as **von Graefe’s Sign**, it is the failure of the upper eyelid to move downward smoothly with the eyeball on downward gaze [2]. * **Joffroy’s Sign:** Absence of forehead wrinkling on upward gaze. * **Pemberton’s Sign:** Positive if facial flushing, cyanosis, or respiratory distress (stridor) occurs when the patient raises both arms above the head (clogging the thoracic inlet).

Question 1

Which of the following is NOT a feature of thyrotoxicosis?

Accepted Answer

Diastolic murmur

Answer

Tremors

Answer

Irregularly irregular pulse

Answer

Osteoporosis

Question 2

Which one of the following features may not be seen in hypothyroidism?

Accepted Answer

Pretibial myxedema

Answer

Cold intolerance

Answer

Deafness

Answer

Pericardial effusion

Question 3

All of the following are true about Cushing's syndrome except?

Accepted Answer

Hyperkalemia

Answer

Hyperpigmentation

Answer

Purplish striae

Answer

Metabolic alkalosis

Question 4

According to the American Diabetes Association, what is the target HbA1c level for diabetes patients under good control?

Accepted Answer

<7%

Answer

4-6%

Answer

8%

Answer

>8%

Question 5

All are features of Bartter syndrome, EXCEPT:

Accepted Answer

Hypertension

Answer

Polyuria

Answer

Metabolic alkalosis

Answer

Periodic paralysis

Question 6

Hypercalcemia is seen in all of the following conditions EXCEPT?

Accepted Answer

Pseudohypoparathyroidism

Answer

Bone metastasis

Answer

Sarcoidosis

Answer

Hyperparathyroidism

Question 7

What are the diagnostic criteria for diabetes mellitus?

Accepted Answer

HbA1c greater than 6.5%

Answer

Fasting blood glucose of 100 mg/dL and postprandial blood glucose of 140 mg/dL

Answer

Fasting blood glucose of 125 mg/dL and 2-hour postprandial blood glucose of 199 mg/dL

Answer

Elevated insulin levels

Question 8

What is a characteristic physical finding of prolactinoma, besides galactorrhea?

Accepted Answer

Bitemporal hemianopia

Answer

Anovulatory cycles

Answer

Amenorrhea

Answer

Infertility

Question 9

A large toxic retrosternal goiter is best treated by?

Accepted Answer

Surgical resection

Answer

Antithyroid drugs

Answer

Radioiodine therapy

Answer

Lugol's iodine

Question 10

Which of the following is NOT a sign of thyrotoxicosis?

Accepted Answer

Stridor on gently pressing the lobes of the thyroid

Answer

Infrequent blinking

Answer

Inability to converge the eyeballs

Answer

Visible upper sclera on looking straight

Endocrinology — MCQs

Endocrinology — MCQs

On this page

Practice by Chapter

Want unlimited practice?