Endocrinology — MCQs

A 64-year-old woman with type 2 diabetes for 10 years presents with increasing fatigue, dyspnea, and pedal edema. On examination, her blood pressure is 165/90 mmHg, pulse is 90/min, JVP is 4 cm, heart sounds are normal, lungs are clear, and there is 3+ pedal edema. Her urinalysis is positive for 3 gm/L of protein and shows no casts or red blood cells. An abdominal ultrasound reveals normal size kidneys and no hydronephrosis. Which of the following renal diseases is the most likely diagnosis in this patient?

Q867Easy

TSH is normal in which of the following conditions?

Q868Medium

Which of the following statements is true regarding thyroglobulin?

Q869Easy

Hyperpigmentation is seen with which of the following hormones?

Q870Medium

Ectopic ACTH production is most commonly seen in which of the following conditions?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 861: Decreased radioiodine uptake is seen in which of the following conditions?

A. Toxic multinodular goiter
B. Graves' disease
C. Subacute thyroiditis (Correct Answer)
D. Autonomous nodular goitre

Explanation: **Explanation:** The Radioactive Iodine Uptake (RAIU) test measures the thyroid gland's ability to trap and organify iodine to produce new hormones. [2] **Why Subacute Thyroiditis is correct:** In **Subacute Thyroiditis** (De Quervain’s), there is an inflammatory destruction of thyroid follicles. This leads to the "leakage" of preformed thyroid hormones into the bloodstream, causing thyrotoxicosis. Because the gland is damaged and the high levels of circulating T3/T4 suppress TSH (via negative feedback), the thyroid's machinery for iodine uptake is shut down. [1] Therefore, RAIU is **characteristically low/decreased** (<5%). **Why the other options are incorrect:** * **Graves' Disease (B):** This is caused by TSH-receptor antibodies that stimulate the gland to overproduce hormone. It shows **diffusely increased** RAIU. * **Toxic Multinodular Goiter (A) and Autonomous Nodular Goiter (D):** These involve hyperfunctioning nodules that act independently of TSH. They show **increased RAIU**, typically with a "patchy" or localized distribution. **High-Yield Clinical Pearls for NEET-PG:** * **Low RAIU Thyrotoxicosis:** Remember the mnemonic **"S-I-F-T"**: **S**ubacute thyroiditis, **I**atrogenic/Factitious (exogenous intake), **F**ollicular CA (metastatic), and **T**hyroiditis (Silent/Postpartum). [2] * **Painful vs. Painless:** Subacute thyroiditis is typically painful with a high ESR, whereas Silent/Postpartum thyroiditis is painless with a normal ESR; both have low RAIU. [1] * **Amiodarone:** Can cause both high (Type 1) and low (Type 2) RAIU depending on the mechanism of toxicity.

Question 862: What is the leading cause of adrenal insufficiency?

A. Autoimmune adrenalitis
B. Tuberculosis of the adrenals
C. X-linked Adrenoleukodystrophy
D. Hypothalamic-pituitary disease (Correct Answer)

Explanation: **Explanation:** The correct answer is **Hypothalamic-pituitary disease** because the question asks for the leading cause of adrenal insufficiency in general, without specifying "Primary" (Addison’s disease). 1. **Why D is correct:** Adrenal insufficiency is classified into Primary (adrenal gland failure) and Secondary/Tertiary (pituitary or hypothalamic failure) [4]. Globally, **Secondary adrenal insufficiency** (due to pituitary disease or exogenous steroid suppression) is significantly more common than primary adrenal failure [1]. Exogenous steroid use is the most frequent cause of suppressed ACTH, but among pathological lesions, hypothalamic-pituitary tumors and their treatment are the leading causes. 2. **Why the other options are incorrect:** * **A. Autoimmune adrenalitis:** This is the most common cause of **Primary** adrenal insufficiency (Addison’s disease) in **developed countries** (approx. 80% of cases) [3]. * **B. Tuberculosis:** This remains the most common cause of **Primary** adrenal insufficiency in **developing countries**, including India [2], [3]. However, it is not the leading cause of adrenal insufficiency overall. * **C. X-linked Adrenoleukodystrophy:** This is the most common **enzymatic/genetic** cause of adrenal insufficiency in young males but is rare in the general population. **NEET-PG High-Yield Pearls:** * **Most common cause of Primary AI (Global/Developed):** Autoimmune adrenalitis. * **Most common cause of Primary AI (India):** Tuberculosis. * **Most common cause of AI overall:** Exogenous steroid withdrawal (leading to secondary AI). * **Clinical Distinction:** Hyperpigmentation and hyperkalemia occur **only** in Primary AI (due to high ACTH and mineralocorticoid deficiency, respectively) [1]. These are absent in Secondary/Tertiary AI.

Question 863: A young hypertensive patient has serum K+ 2.8 meq/L and elevated plasma aldosterone level with suppressed plasma renin activity. What is the likely cause?

A. Renal artery stenosis
B. Ectopic ACTH syndrome
C. Diuretic therapy
D. Conn's syndrome (Correct Answer)

Explanation: ### Explanation The clinical presentation of **hypertension, hypokalemia (K+ 2.8 mEq/L), and a high Aldosterone-to-Renin Ratio (ARR)** is the classic triad of **Primary Hyperaldosteronism**, of which **Conn’s Syndrome** (aldosterone-producing adenoma) is a leading cause. **1. Why Conn’s Syndrome is correct:** In Primary Hyperaldosteronism, the adrenal cortex autonomously secretes excess aldosterone. Aldosterone acts on the distal tubules to retain sodium and water (causing hypertension) and excrete potassium (causing hypokalemia) and hydrogen ions [2]. The resulting volume expansion and high blood pressure provide negative feedback to the juxtaglomerular apparatus, leading to **suppressed Plasma Renin Activity (PRA)**. **2. Why the other options are incorrect:** * **Renal Artery Stenosis:** This causes *Secondary* Hyperaldosteronism. Decreased renal perfusion activates the Renin-Angiotensin-Aldosterone System (RAAS), leading to **elevated renin** and elevated aldosterone [3]. * **Ectopic ACTH Syndrome:** This causes mineralocorticoid excess due to high cortisol levels saturating the 11β-HSD2 enzyme. While it causes hypertension and hypokalemia, both **renin AND aldosterone are suppressed** (Pseudohyperaldosteronism). * **Diuretic Therapy:** While diuretics (like thiazides or loops) cause hypokalemia, they typically cause volume depletion, which **increases renin** levels. **3. High-Yield Pearls for NEET-PG:** * **Screening Test:** Aldosterone-to-Renin Ratio (ARR). An ARR > 20–30 with aldosterone > 15 ng/dL is highly suggestive. * **Confirmatory Test:** Saline infusion test (failure to suppress aldosterone) or Oral Salt Loading test. * **Localization:** Adrenal CT is the first step; **Adrenal Venous Sampling (AVS)** is the gold standard to differentiate unilateral adenoma (Conn's) from bilateral hyperplasia [1]. * **Management:** Surgical resection for Conn’s; Medical management (Spironolactone/Eplerenone) for bilateral adrenal hyperplasia.

Question 864: What is the primary drug of choice for Addison's disease?

A. Hydrocortisone (Correct Answer)
B. Betamethasone
C. Prednisolone
D. Deoxycorticosterone acetate (DOCA)

Explanation: **Explanation:** **Addison’s disease (Primary Adrenocortical Insufficiency)** is characterized by the destruction of the adrenal cortex, leading to a deficiency of both glucocorticoids (cortisol) and mineralocorticoids (aldosterone) [1]. **Why Hydrocortisone is the Correct Answer:** Hydrocortisone is the drug of choice because it is the **pharmacological equivalent of endogenous cortisol**. It possesses both glucocorticoid and significant mineralocorticoid activity, closely mimicking the natural secretion pattern of the adrenal gland. It has a short half-life, allowing for split dosing (typically two-thirds in the morning and one-third in the afternoon) to simulate the physiological diurnal rhythm. **Analysis of Incorrect Options:** * **Betamethasone:** This is a potent, long-acting synthetic glucocorticoid with **zero mineralocorticoid activity**. It is unsuitable for primary adrenal insufficiency as it fails to address the aldosterone deficiency and makes dose titration difficult. * **Prednisolone:** While it has some mineralocorticoid activity, it is 4–5 times more potent than hydrocortisone and has a longer duration of action. It is generally reserved as a second-line agent if hydrocortisone is unavailable or for patients with poor compliance. * **Deoxycorticosterone acetate (DOCA):** This is a pure mineralocorticoid. While it helps with salt retention, it provides no glucocorticoid replacement, which is essential for metabolic function and stress response. **NEET-PG High-Yield Pearls:** * **Standard Regimen:** Hydrocortisone (15–25 mg/day) + Fludrocortisone (0.05–0.2 mg/day for mineralocorticoid replacement) [1]. * **Stress Dosing:** In cases of minor illness or surgery, the dose of hydrocortisone must be doubled or tripled ("Sick day rules"). * **Adrenal Crisis:** The immediate treatment is IV bolus of **100 mg Hydrocortisone** followed by saline infusion [1]. * **Monitoring:** Clinical response (weight, BP, electrolytes) is more reliable than ACTH levels for monitoring therapy.

Question 865: A 30-year-old man presents with recurrent flushing, diarrhea, and weight loss. His examination is normal. Lab investigations reveal an elevated urinary 5-hydroxyindoleacetic acid. Which of the following is the most likely diagnosis?

A. phenylketonuria
B. alkaptonuria
C. malignant melanoma
D. carcinoid syndrome (Correct Answer)

Explanation: **Explanation:** The clinical triad of **recurrent flushing, secretory diarrhea, and weight loss**, combined with elevated urinary **5-hydroxyindoleacetic acid (5-HIAA)**, is the classic presentation of **Carcinoid Syndrome**. **1. Why Carcinoid Syndrome is Correct:** Carcinoid tumors (neuroendocrine tumors) most commonly arise in the gastrointestinal tract or lungs [1]. These tumors secrete excessive amounts of **serotonin (5-HT)**. Serotonin is metabolized by monoamine oxidase (MAO) in the liver and lungs into **5-HIAA**, which is then excreted in the urine. Elevated 24-hour urinary 5-HIAA is the gold-standard diagnostic marker. Note that symptoms typically occur only after the tumor has metastasized to the **liver**, bypassing the first-pass metabolism of serotonin [1]. **2. Why Other Options are Incorrect:** * **Phenylketonuria (PKU):** A deficiency of phenylalanine hydroxylase leading to intellectual disability and a "mousy" odor, not flushing or elevated 5-HIAA. * **Alkaptonuria:** A deficiency of homogentisic acid dioxygenase characterized by dark urine (on standing), ochronosis (pigmentation), and arthritis. * **Malignant Melanoma:** While melanoma involves melanocytes (derived from neural crest cells), it presents with skin lesions or metastatic systemic symptoms, but does not produce 5-HIAA. **NEET-PG High-Yield Pearls:** * **Most common site:** The ileum is the most common site for carcinoid tumors leading to the syndrome. * **Carcinoid Heart Disease:** Look for **Tricuspid Regurgitation** and Pulmonary Stenosis (right-sided lesions) due to endocardial fibrosis. Left-sided lesions are rare as serotonin is inactivated in the lungs. * **Pellagra Risk:** Excessive serotonin synthesis depletes **Tryptophan** stores, leading to **Niacin (Vitamin B3) deficiency** (Dermatitis, Diarrhea, Dementia). * **Treatment:** **Octreotide** (Somatostatin analog) is used to manage symptoms.

Question 866: A 64-year-old woman with type 2 diabetes for 10 years presents with increasing fatigue, dyspnea, and pedal edema. On examination, her blood pressure is 165/90 mmHg, pulse is 90/min, JVP is 4 cm, heart sounds are normal, lungs are clear, and there is 3+ pedal edema. Her urinalysis is positive for 3 gm/L of protein and shows no casts or red blood cells. An abdominal ultrasound reveals normal size kidneys and no hydronephrosis. Which of the following renal diseases is the most likely diagnosis in this patient?

A. Acute glomerulonephritis
B. Obstructive uropathy
C. Glomerulosclerosis with mesangial thickening (Correct Answer)
D. Renal infarction

Explanation: ### Explanation **Correct Option: C. Glomerulosclerosis with mesangial thickening** The patient presents with a long-standing history of Type 2 Diabetes Mellitus (10 years), hypertension, and nephrotic-range proteinuria (3 gm/L) leading to edema. This classic triad in a diabetic patient strongly suggests **Diabetic Nephropathy (DN)**. [2] The hallmark histopathological changes of DN include: 1. **Diffuse Glomerulosclerosis:** The most common finding, characterized by **mesangial matrix expansion and thickening** of the glomerular basement membrane (GBM). [2] [4] 2. **Nodular Glomerulosclerosis (Kimmelstiel-Wilson lesions):** Pathognomonic for DN, though present in only 15-30% of cases. [2] 3. **Renal Size:** Unlike most chronic kidney diseases, kidneys in diabetic nephropathy are typically **normal or enlarged** in size due to hyperfiltration and hypertrophy, matching this patient's ultrasound findings. **Why Incorrect Options are Wrong:** * **A. Acute Glomerulonephritis:** Typically presents with hematuria (RBC casts) and "active" urinary sediment, which are absent here. [1] [3] * **B. Obstructive Uropathy:** Would show hydronephrosis on ultrasound and usually presents with flank pain or fluctuating urine output rather than isolated heavy proteinuria. * **D. Renal Infarction:** Presents with acute onset flank pain, hematuria, and LDH elevation; it does not cause chronic nephrotic-range proteinuria. **NEET-PG High-Yield Pearls:** * **Earliest Clinical Sign of DN:** Microalbuminuria (30–300 mg/day). [2] * **Earliest Histological Change:** Thickening of the Glomerular Basement Membrane (GBM). [2] * **Pathognomonic Lesion:** Kimmelstiel-Wilson (KW) nodules (Ovoid, hyaline, PAS-positive nodules in the periphery of the glomerulus). [2] * **Management:** ACE inhibitors or ARBs are the first-line treatment as they reduce intraglomerular pressure by dilating the efferent arteriole.

Question 867: TSH is normal in which of the following conditions?

A. Hyperthyroid
B. Euthyroid (Correct Answer)
C. Hypothyroid
D. Graves' disease

Explanation: **Explanation:** The thyroid-stimulating hormone (TSH), secreted by the anterior pituitary, is the most sensitive marker for assessing thyroid function due to the negative feedback loop of the hypothalamic-pituitary-thyroid (HPT) axis [1]. **1. Why "Euthyroid" is correct:** The term **"Euthyroid"** refers to a state of normal thyroid function. In this state, the thyroid gland produces physiological levels of Thyroxine (T4) and Triiodothyronine (T3), which provide appropriate feedback to the pituitary, resulting in a **TSH level within the reference range** (typically 0.4 to 4.0 mIU/L). **2. Why other options are incorrect:** * **Hyperthyroid:** In primary hyperthyroidism, excessive production of T3/T4 suppresses the pituitary, leading to a **low or undetectable TSH** [1]. * **Hypothyroid:** In primary hypothyroidism, the lack of T3/T4 removes the negative feedback inhibition, causing the pituitary to secrete **elevated levels of TSH** to stimulate the failing gland [1]. * **Graves' Disease:** This is an autoimmune form of primary hyperthyroidism caused by TSH-receptor antibodies (TRAb). These antibodies mimic TSH, leading to high T4/T3 and consequently **suppressed TSH**. **High-Yield Clinical Pearls for NEET-PG:** * **Best Screening Test:** Serum TSH is the single best initial screening test for thyroid dysfunction in the general population. * **Subclinical States:** * *Subclinical Hypothyroidism:* Elevated TSH with **Normal** T4 [2]. * *Subclinical Hyperthyroidism:* Low TSH with **Normal** T4/T3. * **The Exception:** In **Secondary (Central) Hypothyroidism** (pituitary/hypothalamic disease), TSH may be low, "normal," or slightly elevated, but it is biologically inactive [2]. Diagnosis here relies on Free T4.

Question 868: Which of the following statements is true regarding thyroglobulin?

A. It is a specific marker for anaplastic carcinoma.
B. Elevation after complete therapy suggests recurrence in well-differentiated thyroid malignancies. (Correct Answer)
C. Preoperative elevation always suggests thyroidal disease.
D. Intraoperative estimation from thyroid veins is very useful for prognosis.

Explanation: **Explanation:** Thyroglobulin (Tg) is a large glycoprotein synthesized exclusively by follicular cells of the thyroid gland. Understanding its role as a tumor marker is crucial for NEET-PG. **Why Option B is Correct:** In patients with well-differentiated thyroid cancer (DTC), such as papillary or follicular carcinoma, the primary treatment is total thyroidectomy followed by radioactive iodine (RAI) ablation. Once all thyroid tissue is removed, serum Tg levels should ideally become undetectable. Therefore, a **rising or detectable Tg level during follow-up** is a highly sensitive and specific indicator of **recurrent or metastatic disease**. **Why Other Options are Incorrect:** * **Option A:** Anaplastic carcinoma is undifferentiated and typically does not produce thyroglobulin. Tg is a marker for **well-differentiated** thyroid cancers only. * **Option C:** Serum Tg can be elevated in various non-malignant conditions, including Graves' disease, toxic multinodular goiter, and thyroiditis. Thus, a preoperative elevation is **non-specific** and cannot be used to diagnose malignancy. * **Option D:** Intraoperative Tg estimation from thyroid veins has no established clinical utility or prognostic value. Tg is used for long-term surveillance, not acute surgical decision-making. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-Tg Antibodies:** Always measure Tg antibodies (TgAb) alongside Tg. If TgAb is present, it can falsely lower the measured Tg level, leading to a false-negative result. * **Stimulated Tg:** Tg levels are most sensitive when TSH is high (either by stopping levothyroxine or giving recombinant human TSH). * **Calcitonin:** Remember that Calcitonin (not Tg) is the tumor marker for **Medullary Thyroid Carcinoma**.

Question 869: Hyperpigmentation is seen with which of the following hormones?

A. FSH
B. LH
C. ACTH (Correct Answer)
D. TSH

Explanation: ### Explanation The correct answer is **C. ACTH**. [1] **Mechanism of Hyperpigmentation:** The primary reason ACTH causes hyperpigmentation is due to its structural similarity to **Melanocyte-Stimulating Hormone (MSH)**. Both ACTH and MSH are derived from a common precursor molecule called **Pro-opiomelanocortin (POMC)**. When ACTH levels are pathologically elevated (as seen in Addison’s disease or Nelson syndrome), the excess ACTH acts as a weak agonist on the **Melanocortin-1 receptors (MC1R)** located on melanocytes in the skin. [2] This stimulates the production of melanin, leading to the characteristic "bronzing" of the skin, particularly in sun-exposed areas, skin creases, and mucous membranes. **Analysis of Incorrect Options:** * **A & B (FSH and LH):** These are gonadotropins. While they share a common alpha-subunit with TSH and hCG, they do not share the POMC lineage and have no effect on melanocytes. [1] * **D (TSH):** Although TSH shares a common alpha-subunit with other glycoprotein hormones, it does not interact with melanocortin receptors. [1] Hyperpigmentation is not a feature of thyroid disorders unless they are part of a polyglandular autoimmune syndrome involving the adrenals. **High-Yield Clinical Pearls for NEET-PG:** * **Addison’s Disease (Primary Adrenal Insufficiency):** Characterized by **high ACTH** and **hyperpigmentation**. [2] * **Secondary Adrenal Insufficiency (Pituitary cause):** Characterized by **low ACTH** and **no hyperpigmentation** (skin appears pale). [2] * **Nelson Syndrome:** Rapid enlargement of an ACTH-secreting pituitary adenoma following bilateral adrenalectomy, leading to extreme hyperpigmentation. * **Cushing’s Disease:** May show mild hyperpigmentation, but it is much more prominent in **Ectopic ACTH syndrome** (e.g., Small Cell Lung Cancer). [3]

Question 870: Ectopic ACTH production is most commonly seen in which of the following conditions?

A. Small cell carcinoma of the lung (Correct Answer)
B. Anaplastic carcinoma of the lung
C. Squamous cell carcinoma of the lung
D. Adenocarcinoma of the cerebellum

Explanation: ### Explanation **Correct Option: A. Small cell carcinoma of the lung** Ectopic ACTH syndrome occurs when non-pituitary tumors secrete adrenocorticotropic hormone, leading to hypercortisolism (Cushing’s syndrome) [1]. **Small cell carcinoma of the lung (SCLC)** is the most common cause, accounting for approximately 50% of all ectopic ACTH cases [2]. SCLC is a neuroendocrine tumor derived from Kulchitsky cells, which possess the biochemical machinery to synthesize and secrete polypeptide hormones like ACTH and ADH [2]. **Analysis of Incorrect Options:** * **B & C (Anaplastic and Squamous cell carcinoma):** While these are types of lung cancer, they are not typically associated with ACTH production. Squamous cell carcinoma is famously associated with the production of **PTHrP** (Parathyroid Hormone-related Protein), leading to hypercalcemia, rather than ACTH [2]. * **D (Adenocarcinoma of the cerebellum):** This is not a recognized clinical entity associated with ectopic hormone production. However, cerebellar **hemangioblastomas** can sometimes produce erythropoietin (EPO), leading to polycythemia [2]. **NEET-PG High-Yield Pearls:** 1. **Clinical Presentation:** Patients with ectopic ACTH from SCLC often present with rapid-onset hypertension, profound hypokalemia, and hyperpigmentation (due to MSH-like activity), rather than the classic "buffalo hump" or "moon facies" seen in pituitary Cushing’s. 2. **Dexamethasone Suppression Test (DST):** Unlike Cushing’s disease (pituitary adenoma), ectopic ACTH production from SCLC is **not suppressed** by high-dose dexamethasone. 3. **Other Causes:** Other neuroendocrine tumors causing ectopic ACTH include bronchial carcinoids, thymic carcinoids, and pancreatic islet cell tumors. 4. **Key Association:** SCLC = ACTH (Cushing’s) and ADH (SIADH). Squamous Cell = PTHrP (Hypercalcemia) [2].

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

Pituitary Disorders

Practice Questions

Calcium and Bone Metabolism

Practice Questions

Reproductive Endocrinology

Practice Questions

Lipid Disorders

Practice Questions

Endocrine Hypertension

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Neuroendocrine Tumors

Practice Questions

Endocrine Emergencies

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free