Endocrinology — MCQs

A 38-year-old woman presents with new symptoms of palpitations, weight loss, and heat intolerance. On physical examination, she has a mild tremor of her outstretched hands, an enlarged thyroid, and resting tachycardia (heart rate 110/min). Biochemical tests confirm the diagnosis and she is started on methimazole. Which of the following is the most likely mechanism of this drug?

Q895Medium

Which of the following is NOT typically seen in diabetic ketoacidosis?

Q896Medium

A 55-year-old man has had a foot ulcer for 2 months that has not healed. Physical examination shows a 2-cm shallow, nonhealing ulceration of the left medial malleolus. There is symmetric decreased sensation in the distal regions of the lower extremities. He has a history of multiple urinary tract infections resulting from difficulty in completely emptying the bladder. He is impotent. Which of the following pathologic findings is most likely to be present in the peripheral nerves?

Q897Easy

All of the following are associated with Multiple Endocrine Neoplasia type 2 (MEN-2) except:

Q898Easy

What is the treatment for myxedema coma?

Q899Easy

According to ADA guidelines, the diagnosis of diabetes is made when the fasting blood glucose is more than?

Q900Easy

All of the following conditions are known to cause diabetes insipidus except?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 891: Palpation of the costovertebral angle produces pain and tenderness in acute adrenal insufficiency. This is termed as:

A. Osler's sign
B. Rotch's sign
C. Rogoff's sign (Correct Answer)
D. Rossolimo's sign

Explanation: ### Explanation **Rogoff’s Sign** is a clinical finding characterized by pain and tenderness upon deep palpation of the **costovertebral angle** (the area overlying the adrenal glands). In the context of **acute adrenal insufficiency** (Addisonian crisis), the adrenal glands may become congested or inflamed, leading to localized tenderness at this anatomical site. While not pathognomonic, it is a classic physical sign taught in endocrine semiology. #### Analysis of Incorrect Options: * **Osler’s Sign:** This term refers to two distinct findings: (1) **Osler’s nodes**, which are painful, erythematous nodules on the pads of fingers/toes in infective endocarditis; and (2) **Pseudohypertension**, where the radial artery remains palpable despite the blood pressure cuff being inflated above systolic pressure. * **Rotch’s Sign:** This is a sign of **pericardial effusion**, characterized by dullness to percussion in the right 5th intercostal space (at the cardio-hepatic angle). * **Rossolimo’s Sign:** A neurological sign indicating a **pyramidal tract lesion**. It involves percussion of the plantar surface of the toes, resulting in abnormal flexion of the toes. #### NEET-PG High-Yield Pearls: * **Acute Adrenal Insufficiency:** Most commonly caused by sudden withdrawal of long-term steroid therapy. * **Clinical Presentation:** Refractory hypotension (shock not responding to vasopressors), abdominal pain (mimicking acute abdomen), hyponatremia, and hyperkalemia. * **Management:** Immediate administration of **IV Hydrocortisone** (100mg bolus) and aggressive fluid resuscitation with normal saline. Do not wait for ACTH stimulation test results if the patient is unstable.

Question 892: Which of the following statements is true regarding thyrotoxicosis?

A. In Graves' disease, antibodies are formed against TSH receptors, leading to excessive thyroxine secretion. (Correct Answer)
B. Hashimoto's thyroiditis typically occurs in young males.
C. In primary hypothyroidism, decreased TSH levels are observed.
D. In Graves' disease, no antibodies are formed against TSH receptors, resulting in decreased thyroxine secretion.

Explanation: **Explanation:** **Correct Option (A):** Graves' disease is the most common cause of hyperthyroidism [1], [2]. It is an autoimmune disorder characterized by the production of **Thyroid Stimulating Immunoglobulins (TSI)** [1]. These are IgG antibodies that bind to and activate the **TSH receptors** on thyroid follicular cells [1], [2]. This mimics the action of TSH, leading to autonomous, excessive synthesis and secretion of thyroid hormones (T4 and T3), resulting in thyrotoxicosis. **Incorrect Options:** * **Option B:** Hashimoto's thyroiditis, like most autoimmune thyroid disorders, shows a strong **female predilection** (ratio approx. 10:1) and typically presents in middle-aged women, not young males [1]. * **Option C:** In **primary hypothyroidism**, the thyroid gland fails to produce enough hormones. Due to the loss of negative feedback on the pituitary, **TSH levels are characteristically elevated**, not decreased [3]. * **Option D:** This is the opposite of the pathophysiology of Graves' disease. Antibodies (TSI) are indeed formed, and they lead to increased (not decreased) thyroxine secretion [2]. **NEET-PG High-Yield Pearls:** * **Triad of Graves':** Hyperthyroidism with diffuse goiter, Ophthalmopathy (Exophthalmos), and Dermopathy (Pretibial myxedema) [2]. * **Diagnosis:** Low TSH, high Free T4/T3, and diffuse uptake on Radioactive Iodine Uptake (RAIU) scan [2]. * **Specific Marker:** TSH Receptor Antibodies (TRAb) are highly specific for Graves' [1]. * **Wolff-Chaikoff Effect:** A reduction in thyroid hormone levels caused by the administration of a large amount of iodine.

Question 893: Addison disease is commonly associated with which of the following?

A. Autoimmune adrenalitis (Correct Answer)
B. Adrenocortical carcinoma
C. Hypernephroma
D. Medullary carcinoma of the thyroid

Explanation: **Explanation:** **Addison’s disease** (Primary Adrenocortical Insufficiency) results from the progressive destruction of the adrenal cortex, leading to a deficiency of cortisol, aldosterone, and androgens [1]. **1. Why Autoimmune Adrenalitis is Correct:** In developed countries and increasingly worldwide, **autoimmune adrenalitis** is the most common cause of Addison’s disease (accounting for ~80% of cases). It involves the production of antibodies against the enzyme **21-hydroxylase**, leading to lymphocytic infiltration and atrophy of the adrenal cortex. In patients with suspected autoimmune failure, adrenal autoantibodies are frequently positive [2]. In developing nations, tuberculosis remains a significant infectious cause; tuberculosis often causes adrenal calcification visible on imaging [2]. **2. Analysis of Incorrect Options:** * **Adrenocortical Carcinoma:** This is a rare malignancy that typically presents with **hormone excess** (e.g., Cushing’s syndrome or virilization) rather than insufficiency. * **Hypernephroma (Renal Cell Carcinoma):** This is a primary tumor of the kidney parenchyma. While it may metastasize, it does not characteristically cause adrenal insufficiency unless there is massive bilateral destruction. * **Medullary Carcinoma of the Thyroid (MTC):** MTC is associated with **MEN 2A and 2B** syndromes. While these syndromes involve the adrenal gland, they are associated with **Pheochromocytoma** (medullary tumor), not cortical insufficiency. **3. NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Hyperpigmentation (due to high ACTH/POMC), hypotension, hyponatremia, and hyperkalemia [1]. Vitiligo also occurs in 10–20% of patients with autoimmune Addison's [2]. * **Diagnosis:** The gold standard is the **ACTH Stimulation Test** (Cosyntropin test); a subnormal cortisol response confirms the diagnosis [2]. * **Autoimmune Association:** Often occurs as part of **Autoimmune Polyendocrine Syndromes (APS)** Type 1 or Type 2 (Schmidt Syndrome). Patients should be screened for other autoimmune diseases like thyroid disease or type 1 diabetes [2]. * **Radiology:** In autoimmune disease, adrenals are **atrophic**; in TB or metastatic disease, they are often **enlarged/calcified** [2].

Question 894: A 38-year-old woman presents with new symptoms of palpitations, weight loss, and heat intolerance. On physical examination, she has a mild tremor of her outstretched hands, an enlarged thyroid, and resting tachycardia (heart rate 110/min). Biochemical tests confirm the diagnosis and she is started on methimazole. Which of the following is the most likely mechanism of this drug?

A. Inhibition of iodine uptake
B. Inhibition of thyroidal organic binding and coupling reactions (Correct Answer)
C. Lowering serum calcium
D. Adrenal suppression

Explanation: **Explanation:** The patient presents with classic symptoms of hyperthyroidism (palpitations, weight loss, heat intolerance, and tachycardia) [1]. Methimazole is a **Thionamide** used as a first-line antithyroid medication [2]. **1. Why Option B is Correct:** Methimazole acts by inhibiting the enzyme **Thyroid Peroxidase (TPO)**. This enzyme is crucial for two major steps in thyroid hormone synthesis: * **Organification:** The binding of oxidized iodine to tyrosine residues on thyroglobulin to form Monoiodotyrosine (MIT) and Diiodotyrosine (DIT). * **Coupling:** The joining of MIT and DIT to form $T_3$ and $T_4$. By blocking these steps, methimazole prevents the synthesis of new thyroid hormones. **2. Why Other Options are Incorrect:** * **Option A:** Inhibition of iodine uptake is the mechanism of **anionic inhibitors** like perchlorate or thiocyanate, which competitively inhibit the sodium-iodide symporter (NIS). * **Option C:** Lowering serum calcium is a function of **Calcitonin** or bisphosphonates, unrelated to thyroid hormone synthesis. * **Option D:** Adrenal suppression is a side effect of long-term **Glucocorticoid** therapy or drugs like Ketoconazole/Etomidate, not methimazole. **3. NEET-PG High-Yield Pearls:** * **PTU vs. Methimazole:** While both inhibit TPO, **Propylthiouracil (PTU)** has the additional mechanism of inhibiting the **peripheral conversion** of $T_4$ to $T_3$ (via 5'-deiodinase inhibition). * **Pregnancy:** Methimazole is generally avoided in the **1st trimester** due to the risk of *Aplasia Cutis* and *Choanal Atresia*. PTU is preferred in the 1st trimester. * **Side Effects:** The most dreaded side effect of thionamides is **Agraulocytosis** (presents as fever and sore throat). Methimazole is also associated with cholestatic jaundice.

Question 895: Which of the following is NOT typically seen in diabetic ketoacidosis?

A. Normal serum potassium (Correct Answer)
B. Plasma osmolality of 320 mosm/kg
C. Urine Rothera test positive
D. Urine Benedict's test positive

Explanation: In Diabetic Ketoacidosis (DKA), the hallmark electrolyte abnormality regarding potassium is a **total body potassium deficit** despite serum levels appearing normal or even elevated [1], [2]. ### **Explanation of Options** * **A. Normal serum potassium (Correct):** While serum potassium can occasionally be normal [2], it is **not typically** the expected finding. Most patients present with **hyperkalemia** (elevated serum potassium). This occurs because insulin deficiency and metabolic acidosis cause potassium to shift from the intracellular to the extracellular space [2]. However, due to osmotic diuresis, the patient actually has a massive total body deficit [1]. A "normal" level in DKA is a warning sign of severe depletion. * **B. Plasma osmolality of 320 mosm/kg:** This is a typical finding. While Hyperosmolar Hyperglycemic State (HHS) has higher osmolality (>320), DKA patients frequently present with moderate elevations (usually <320, but 320 is within the possible range) due to hyperglycemia and dehydration. * **C. Urine Rothera test positive:** This test detects **acetone and acetoacetate** [1]. Since DKA is characterized by the overproduction of ketone bodies, this test will be strongly positive. * **D. Urine Benedict's test positive:** This test detects reducing sugars (glucose). In DKA, blood glucose levels typically exceed 250 mg/dL, surpassing the renal threshold and resulting in significant glucosuria. ### **High-Yield Clinical Pearls for NEET-PG** * **The Potassium Paradox:** Always remember: *Serum K+ is high, but Total Body K+ is low.* [2] * **Management Priority:** Never start insulin if serum potassium is **<3.3 mEq/L**, as insulin will drive potassium into cells and may cause fatal arrhythmias. * **Anion Gap:** DKA is a classic cause of **High Anion Gap Metabolic Acidosis (HAGMA)**. * **Ketone Monitoring:** Serum beta-hydroxybutyrate is a more reliable marker for monitoring DKA resolution than urine ketones (Rothera test).

Question 896: A 55-year-old man has had a foot ulcer for 2 months that has not healed. Physical examination shows a 2-cm shallow, nonhealing ulceration of the left medial malleolus. There is symmetric decreased sensation in the distal regions of the lower extremities. He has a history of multiple urinary tract infections resulting from difficulty in completely emptying the bladder. He is impotent. Which of the following pathologic findings is most likely to be present in the peripheral nerves?

A. Acute inflammation
B. Axonal neuropathy
C. Onion bulb formation
D. Segmental demyelination (Correct Answer)

Explanation: ### Explanation The clinical presentation of a non-healing foot ulcer, distal symmetric sensory loss, neurogenic bladder (difficulty emptying), and impotence in a 55-year-old man is classic for **Diabetic Polyneuropathy**. **Why Segmental Demyelination is Correct:** In Diabetes Mellitus, chronic hyperglycemia leads to the formation of Advanced Glycation End-products (AGEs) and increased polyol pathway activity (sorbitol accumulation). This causes oxidative stress and microvascular injury (vasa nervorum ischemia). The hallmark pathologic change in diabetic neuropathy is a combination of **segmental demyelination** and axonal degeneration [1]. Segmental demyelination occurs due to the dysfunction of Schwann cells and the breakdown of myelin sheaths in specific segments, leading to slowed nerve conduction velocities. **Analysis of Incorrect Options:** * **A. Acute inflammation:** This is characteristic of infectious processes (like leprosy) or acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barré Syndrome), not chronic metabolic conditions like diabetes. * **B. Axonal neuropathy:** While axonal loss occurs in late-stage diabetes, the initial and most characteristic pathological description often tested in exams for the underlying process of nerve damage in metabolic syndromes is segmental demyelination [1]. * **C. Onion bulb formation:** This represents repetitive cycles of demyelination and remyelination, classically seen in hereditary neuropathies like **Charcot-Marie-Tooth (CMT) disease** or Chronic Inflammatory Demyelinating Polyneuropathy (CIDP). **NEET-PG High-Yield Pearls:** * **Most common type of Diabetic Neuropathy:** Distal Symmetric Sensorimotor Polyneuropathy ("Glove and Stocking" distribution) [1]. * **Autonomic involvement:** Leads to gastroparesis, orthostatic hypotension, and neurogenic bladder (overflow incontinence) [1]. * **Pathology:** Look for "Soribitol accumulation" and "Non-enzymatic glycosylation of proteins" as the biochemical triggers. * **First sensation lost:** Vibration and position sense (large fiber) or pain and temperature (small fiber) depending on the subtype, but usually, small fiber damage (pain/burning) precedes large fiber damage [1].

Question 897: All of the following are associated with Multiple Endocrine Neoplasia type 2 (MEN-2) except:

A. Pheochromocytoma
B. Islet cell hyperplasia (Correct Answer)
C. Medullary carcinoma of the thyroid
D. Parathyroid adenoma

Explanation: **Explanation:** The Multiple Endocrine Neoplasia (MEN) syndromes are autosomal dominant conditions characterized by tumors involving two or more endocrine glands. The key to answering this question lies in distinguishing between **MEN-1 (Wermer Syndrome)** and **MEN-2 (Sipple Syndrome)**. **Why "Islet cell hyperplasia" is the correct answer:** Islet cell hyperplasia (and pancreatic endocrine tumors like gastrinomas or insulinomas) is a hallmark of **MEN-1**, not MEN-2. The "3 Ps" of MEN-1 are **P**arathyroid hyperplasia, **P**ituitary adenoma, and **P**ancreatic/Islet cell tumors. **Analysis of incorrect options (Features of MEN-2):** * **Medullary Carcinoma of Thyroid (MCT):** This is the most consistent feature of MEN-2 (occurring in >90% of cases). It arises from parafollicular C-cells. * **Pheochromocytoma:** Seen in approximately 50% of patients with MEN-2A and 2B. They are often bilateral and occur within the adrenal medulla. * **Parathyroid Adenoma/Hyperplasia:** This occurs in about 20-30% of patients with **MEN-2A**. Note: It is *absent* in MEN-2B. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** MEN-2 is associated with a germline mutation in the **RET proto-oncogene** (Chromosome 10). MEN-1 is associated with the **MENIN gene** (Chromosome 11). * **MEN-2B vs. 2A:** MEN-2B includes MCT and Pheochromocytoma (like 2A) but is distinguished by **Mucosal neuromas**, **Marfanoid habitus**, and the *absence* of parathyroid involvement. * **Prophylaxis:** Due to the high penetrance of MCT, prophylactic thyroidectomy is often recommended for RET mutation carriers.

Question 898: What is the treatment for myxedema coma?

A. Hydrocortisone
B. Liothyronine
C. Levothyroxine
D. All of the above (Correct Answer)

Explanation: ### Explanation Myxedema coma is a life-threatening emergency characterized by severe hypothyroidism, altered mental status, and hypothermia. The management requires a multi-pronged approach to address hormonal deficiencies and prevent adrenal crisis. **Why "All of the above" is correct:** 1. **Levothyroxine (T4):** This is the mainstay of therapy. A loading dose (200–400 µg IV) is given to saturate thyroid-binding globulin, followed by daily maintenance doses. 2. **Liothyronine (T3):** Since the peripheral conversion of T4 to T3 is often impaired in critically ill patients, adding IV T3 (5–20 µg loading dose) provides a faster metabolic response and is often recommended alongside T4. 3. **Hydrocortisone:** **Crucially, corticosteroids must be administered BEFORE thyroid hormone replacement.** Severe hypothyroidism can mask co-existing adrenal insufficiency or pituitary failure. Starting thyroid hormones alone can precipitate an acute adrenal crisis by increasing the metabolic clearance of cortisol. **Analysis of Options:** * **A, B, and C** are all essential components of the treatment protocol. Selecting only one would result in incomplete management of the patient. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence of Treatment:** Always give IV Hydrocortisone (100 mg every 8 hours) **first**, then IV Levothyroxine. * **Precipitating Factors:** Most common triggers include infections (pneumonia, UTI), cold exposure, MI, or sedative drugs. * **Cardinal Signs:** Hypothermia (often <35°C), bradycardia, hyponatremia (due to SIADH), and hypercapnia (respiratory failure). * **Supportive Care:** Passive rewarming (not active) is preferred to avoid peripheral vasodilation and worsening hypotension.

Question 899: According to ADA guidelines, the diagnosis of diabetes is made when the fasting blood glucose is more than?

A. 126 mg/dl (Correct Answer)
B. 100 mg/dl
C. 140 mg/dl
D. 200 mg/dl

Explanation: The diagnosis of Diabetes Mellitus (DM) is based on specific glycemic thresholds established by the American Diabetes Association (ADA) to identify patients at high risk for microvascular complications, particularly retinopathy [1]. **Explanation of the Correct Answer:** * **A. 126 mg/dl:** According to ADA guidelines, a **Fasting Plasma Glucose (FPG) ≥ 126 mg/dL** (7.0 mmol/L) is diagnostic of diabetes [1]. "Fasting" is defined as no caloric intake for at least 8 hours. In the absence of unequivocal hyperglycemia, the diagnosis must be confirmed by a repeat test on a subsequent day. **Explanation of Incorrect Options:** * **B. 100 mg/dl:** This is the upper limit of normal. An FPG between **100–125 mg/dL** is categorized as **Impaired Fasting Glucose (IFG)**, which is a state of "Prediabetes" [1]. * **C. 140 mg/dl:** This value is significant in the 2-hour Oral Glucose Tolerance Test (OGTT). A 2-hour post-load glucose **< 140 mg/dL** is normal, while **140–199 mg/dL** indicates Impaired Glucose Tolerance (IGT). * **D. 200 mg/dl:** This is the diagnostic threshold for diabetes when using a **Random Plasma Glucose** (in a symptomatic patient) or a **2-hour OGTT** value. **High-Yield Clinical Pearls for NEET-PG:** * **HbA1c Criteria:** An HbA1c **≥ 6.5%** is also diagnostic of diabetes. * **Prediabetes Range:** HbA1c of **5.7% to 6.4%** or FPG of **100–125 mg/dL** [1]. * **Gold Standard:** While FPG is commonly used in practice, the **75g OGTT** is considered the most sensitive diagnostic test. * **Screening:** In asymptomatic adults, screening should begin at age 35 (revised from 45) or earlier if the BMI is ≥ 25 kg/m² with additional risk factors.

Question 900: All of the following conditions are known to cause diabetes insipidus except?

A. Multiple sclerosis (Correct Answer)
B. Head injury
C. Histiocytosis
D. Viral encephalitis

Explanation: Diabetes Insipidus (DI) results from either a deficiency of Antidiuretic Hormone (ADH/Vasopressin) due to hypothalamic-pituitary pathology (**Central DI**) or resistance to its action in the kidneys (**Nephrogenic DI**). **Why Multiple Sclerosis (Option A) is the correct answer:** Multiple Sclerosis is a demyelinating disease primarily affecting the white matter of the brain and spinal cord. While it can involve various CNS regions, it **rarely, if ever**, involves the hypothalamic-pituitary axis significantly enough to cause Diabetes Insipidus. Clinical manifestations are typically sensory, motor, or visual (optic neuritis), making it the "odd one out" in this list. **Why the other options are incorrect:** * **Head Injury (Option B):** Traumatic brain injury is a leading cause of Central DI. [1] Shearing forces can damage the pituitary stalk or the hypothalamic nuclei (supraoptic and paraventricular), disrupting ADH production or transport. * **Histiocytosis (Option C):** Langerhans Cell Histiocytosis (LCH) is a classic infiltrative cause of Central DI. [1] It often involves the pituitary stalk, leading to thickening and subsequent ADH deficiency. * **Viral Encephalitis (Option D):** Inflammatory and infectious processes (like encephalitis or meningitis) can cause transient or permanent damage to the hypothalamus or posterior pituitary, resulting in Central DI. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Central DI:** Idiopathic (30-50%), followed by neurosurgery and trauma. * **Triad of Hand-Schüller-Christian disease (a form of LCH):** Diabetes insipidus, exophthalmos, and lytic bone lesions. * **Diagnosis:** The **Water Deprivation Test** is the gold standard. [2] Central DI shows a >50% increase in urine osmolality after exogenous desmopressin administration, whereas Nephrogenic DI shows little to no response. * **Drug of Choice:** Desmopressin (DDAVP) for Central DI; [2] Thiazide diuretics for Nephrogenic DI.

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