Endocrinology Practice Questions

Q: All of the following are associated with pheochromocytoma except:

Hypotension. **Explanation:** Pheochromocytoma is a catecholamine-secreting tumor arising from the chromaffin cells of the adrenal medulla. The clinical manifestations are primarily driven by the excessive release of epinephrine and norepinephrine [3]. **Why Hypotension is the Correct Answer:** The hallmark of pheochromocytoma is **Hypertension** (persistent in 60% and paroxysmal in 40% of cases). Hypotension is highly atypical and usually only occurs in specific scenarios, such as sudden catecholamine withdrawal, severe volume depletion, or a switch to a purely epinephrine-secreting tumor (causing beta-2 mediated vasodilation). Therefore, it is not a standard association. **Analysis of Other Options:** * **Ventricular Arrhythmias:** Excess catecholamines overstimulate $\beta_1$ receptors in the heart, leading to palpitations, tachycardia, and potentially fatal ventricular arrhythmias [3]. * **Interstitial Fibrosis:** Chronic exposure to high catecholamine levels causes "Catecholamine Cardiomyopathy." This leads to focal myocardial necrosis, inflammatory cell infiltration, and eventually **interstitial fibrosis**, which can progress to heart failure. * **Ectopic ACTH Production:** Pheochromocytoma is a known cause of ectopic ACTH syndrome [2], [4]. These tumors can co-secrete peptides like ACTH or CRH, leading to Cushing’s syndrome features alongside hypertensive crises. **NEET-PG High-Yield Pearls:** 1. **Rule of 10s:** 10% bilateral, 10% malignant, 10% extra-adrenal (Paraganglioma), 10% pediatric, and 10% familial [1]. 2. **Genetic Associations:** MEN 2A, MEN 2B, von Hippel-Lindau (VHL) syndrome, and NF-1 [1]. 3. **Diagnosis:** Best initial screening test is **24-hour urinary fractionated metanephrines** or plasma free metanephrines. 4. **Management:** Always give **Alpha-blockers first** (e.g., Phenoxybenzamine) followed by Beta-blockers to avoid an unopposed alpha-mediated hypertensive crisis [1].

Q: An overweight 48-year-old male presents with complaints of increased thirst and frequent urination. Laboratory examination reveals a blood glucose level of 180 mg/dL. The patient's past medical history is unremarkable, except for an anaphylactic reaction that occurred one year ago when he was given trimethoprim-sulfamethoxazole for a sinus infection. Based on this information, which of the following agents should be prescribed?

Metformin. The patient presents with classic symptoms of Type 2 Diabetes Mellitus (polyuria, polydipsia) and a blood glucose level of 180 mg/dL. According to current clinical guidelines, **Metformin** is the first-line pharmacological therapy for Type 2 Diabetes, especially in overweight patients, due to its efficacy, weight-neutrality (or modest weight loss), and low risk of hypoglycemia [1]. **Why the other options are incorrect:** * **Chlorpropamide & Glipizide (Options A & B):** These are **Sulfonylureas**. The patient has a documented history of an **anaphylactic reaction to trimethoprim-sulfamethoxazole**. Sulfonylureas contain a sulfonamide moiety; while cross-reactivity between antibiotic sulfonamides and non-antibiotic sulfonamides is debated, it is generally contraindicated or used with extreme caution in patients with a history of severe (anaphylactic) sulfa allergies. Furthermore, Metformin remains the preferred initial agent over sulfonylureas [1]. * **Glucagon (Option C):** Glucagon is used to treat severe hypoglycemia. Prescribing it to a patient with hyperglycemia (180 mg/dL) would worsen their clinical state. **NEET-PG High-Yield Pearls:** * **Mechanism of Action (Metformin):** Primarily inhibits hepatic gluconeogenesis by activating AMP-activated protein kinase (AMPK) [1]. * **Side Effects:** Most common are GI upset (diarrhea, nausea) [1]. The most serious, though rare, is **Lactic Acidosis**. * **Contraindications:** Metformin should be avoided in patients with significant renal impairment (eGFR <30 mL/min/1.73m²) due to the risk of lactic acidosis. * **Sulfa Allergy Cross-reactivity:** Always be cautious with Sulfonylureas, Carbonic anhydrase inhibitors (Acetazolamide), and Loop diuretics (Furosemide) in patients with severe sulfa allergies.

Q: When the patient is asked to look upwards with the head fixed, there is an absence of wrinkling on the forehead. This clinical finding is known as:

Joffroy's sign. The clinical finding described is **Joffroy’s sign**, a characteristic ocular manifestation of **Graves' ophthalmopathy** (Thyroid Eye Disease). **1. Why Joffroy’s Sign is Correct:** In patients with hyperthyroidism, there is often a combination of sympathetic overactivity and infiltrative changes in the extraocular muscles [1]. Joffroy’s sign refers to the **absence of forehead wrinkling** when the patient attempts to look upward with the head fixed. This occurs because the patient relies on the superior rectus muscle rather than the frontalis muscle, or due to the inherent muscle weakness/rigidity associated with thyrotoxicosis. **2. Analysis of Incorrect Options:** * **Von Graefe’s sign:** This refers to **lid lag**. When the patient is asked to look slowly downward, the upper eyelid lags behind the movement of the globe, exposing the white sclera above the cornea. * **Moebius sign:** This is the **inability to maintain convergence** of the eyes when looking at a near object, resulting from weakness of the medial rectus muscles. * **Dalrymple’s sign:** This is the **widening of the palpebral fissures** (staring look) caused by the retraction of the upper eyelids in the primary position of gaze. **3. High-Yield Clinical Pearls for NEET-PG:** * **Stellwag’s sign:** Infrequent or incomplete blinking. * **Enroth’s sign:** Edema of the eyelids. * **Pathophysiology:** These signs are primarily due to overactivity of the **Müller’s muscle** (sympathetic stimulation) and autoimmune-mediated inflammation of orbital tissues [2]. * **Diagnosis:** While these signs suggest thyrotoxicosis, the most specific sign for Graves' disease (vs. other causes of hyperthyroidism) is **Exophthalmos** (proptosis) [1].

Q: Which of the following is NOT typically seen in myxedema coma?

Tachycardia. **Explanation:** Myxedema coma is a life-threatening complication of severe, untreated hypothyroidism. It is characterized by a global slowing of metabolic processes. **1. Why Tachycardia is the correct answer:** In severe hypothyroidism, there is a marked decrease in metabolic rate and sympathetic activity. This leads to **bradycardia** (slow heart rate), not tachycardia [1]. The heart muscle also suffers from decreased contractility and reduced stroke volume. Therefore, tachycardia is inconsistent with the clinical presentation of myxedema coma. **2. Why the other options are wrong:** * **Hypothermia (A):** This is a hallmark feature. Due to the lack of thyroid hormone, thermogenesis is impaired. Patients often present with temperatures below 35°C (95°F). * **Hypotension (C):** Reduced cardiac output and decreased vascular tone lead to low blood pressure. This can progress to shock if not treated promptly. * **Hyponatremia (D):** This is frequently seen due to an increase in Antidiuretic Hormone (ADH) secretion (SIADH-like picture) and reduced free water clearance by the kidneys. **Clinical Pearls for NEET-PG:** * **Precipitating Factors:** Sepsis, cold exposure, myocardial infarction, or sedative use. * **Classic Triad:** Altered mental status (coma/lethargy), hypothermia, and a precipitating event. * **Treatment:** Immediate IV Levothyroxine (T4) and/or Liothyronine (T3). **Crucial:** Always administer **IV Hydrocortisone** before thyroid hormone replacement to avoid precipitating an adrenal crisis (as the patient may have concomitant adrenal insufficiency). * **Lab findings:** High TSH, low Free T4, and often hypoglycemia.

Q: What is the treatment of Diabetes Insipidus?

Antidiuretic Hormone (ADH). Diabetes Insipidus (DI) is characterized by the inability to concentrate urine due to either a deficiency of **Antidiuretic Hormone (ADH/Vasopressin)** from the posterior pituitary (Central DI) or resistance to its action in the kidneys (Nephrogenic DI) [3]. **Why Option A is Correct:** The primary treatment for Central DI is hormone replacement. **Desmopressin (dDAVP)**, a synthetic analogue of ADH, is the drug of choice [1]. It acts on V2 receptors in the renal collecting ducts to increase water reabsorption, thereby reducing polyuria and correcting hypernatremia [3]. **Why Other Options are Incorrect:** * **B. Thiazide Diuretics:** While used in *Nephrogenic* DI to create a mild hypovolemia-induced increase in proximal sodium/water reabsorption, they are not the primary physiological replacement for the underlying hormone deficiency. * **C. Loop Diuretics:** These (e.g., Furosemide) inhibit water reabsorption in the Thick Ascending Limb and would worsen the polyuria and dehydration seen in DI. * **D. Insulin:** This is the treatment for Diabetes Mellitus (hyperglycemia), which is pathophysiologically unrelated to Diabetes Insipidus [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Water Deprivation Test:** The gold standard for diagnosis [1]. If urine osmolality increases >50% after exogenous ADH administration, it confirms **Central DI**. If there is little to no response, it is **Nephrogenic DI**. * **Drug-Induced Nephrogenic DI:** Most commonly caused by **Lithium**. * **Treatment of Nephrogenic DI:** Amiloride (especially for Lithium-induced cases), Thiazides, and NSAIDs (which inhibit prostaglandins that antagonize ADH).

Q: Chvostek sign is seen in:

Hypothyroidism. **Explanation:** The **Chvostek sign** is a clinical indicator of hyperexcitability of the facial nerve, typically associated with **hypocalcemia**. In the context of this question, **Hypothyroidism** is the correct answer because it is frequently associated with **Hypoparathyroidism** (either due to autoimmune destruction or as a post-surgical complication of thyroidectomy). A deficiency in Parathyroid Hormone (PTH) leads to low serum calcium levels, which decreases the threshold for nerve depolarization [1]. * **Mechanism:** Tapping the facial nerve at the angle of the jaw (anterior to the tragus) causes ipsilateral twitching of the facial muscles (nose or lips). **Analysis of Options:** * **Hypothyroidism (Correct):** Often co-exists with hypocalcemia via associated hypoparathyroidism or as part of polyglandular autoimmune syndromes. * **Hypercalcemia (Incorrect):** High calcium levels actually stabilize neuronal membranes, leading to decreased excitability and diminished reflexes. * **Insulinoma & Diabetes Mellitus (Incorrect):** These are disorders of glucose metabolism and do not typically affect serum ionized calcium levels or neuromuscular irritability. **NEET-PG High-Yield Pearls:** 1. **Trousseau Sign:** Carpopedal spasm induced by inflating a BP cuff above systolic pressure for 3 minutes. It is **more sensitive and specific** than Chvostek sign for latent tetany. 2. **Other causes of Chvostek Sign:** Hypomagnesemia, metabolic alkalosis (which decreases ionized calcium), and hyperventilation. 3. **False Positives:** Approximately 10% of healthy individuals with normal calcium levels may exhibit a positive Chvostek sign. 4. **ECG in Hypocalcemia:** Look for **prolonged QT interval**, a classic exam favorite [1].

Q: Which of the following is not a feature of Sipple syndrome?

Hyperthyroidism. **Explanation:** Sipple Syndrome, also known as **Multiple Endocrine Neoplasia Type 2A (MEN 2A)**, is an autosomal dominant disorder caused by a germline mutation in the **RET proto-oncogene** [1]. It is characterized by a specific triad of endocrine tumors. **Why Hyperthyroidism is the Correct Answer:** Hyperthyroidism is **not** a component of MEN 2A [2]. While patients with Sipple syndrome develop thyroid pathology, it is specifically **Medullary Thyroid Carcinoma (MTC)**, which arises from the parafollicular C-cells (secreting calcitonin) rather than the follicular cells. Therefore, it does not typically result in a hypermetabolic thyrotoxic state. **Analysis of Incorrect Options:** * **Medullary Carcinoma Thyroid (MTC):** This is the most common feature (seen in >90% of cases) and is often the first manifestation. It is usually bilateral and multicentric. * **Pheochromocytoma:** Occurs in approximately 50% of patients [2]. It is frequently bilateral and usually develops after the thyroid pathology. * **Hyperparathyroidism:** Seen in about 10–20% of patients, typically due to parathyroid hyperplasia rather than a single adenoma [3]. **High-Yield Clinical Pearls for NEET-PG:** * **MEN 2A (Sipple Syndrome):** MTC + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN 2B (Wermer-Morrison):** MTC + Pheochromocytoma + Mucosal Neuromas + Marfanoid Habitus (Note: No Parathyroid involvement). * **Screening:** All first-degree relatives of a patient with MTC should be screened for the **RET mutation** [3]. * **Prophylactic Thyroidectomy:** Recommended in children carrying the RET mutation to prevent the inevitable development of MTC [3].

Q: Vitamin D resistant rickets occurs due to all EXCEPT:

Alpha-1-hydroxylase deficiency. **Explanation:** The term **Vitamin D Resistant Rickets (VDRR)** refers to conditions where rickets occurs despite normal or high intake of Vitamin D, typically due to defects in phosphate metabolism or end-organ resistance [1]. **Why Option A is the Correct Answer:** **Alpha-1-hydroxylase deficiency** is the underlying cause of **Vitamin D Dependent Rickets (VDDR) Type 1**, not Vitamin D *Resistant* Rickets. In this condition, the body cannot convert 25(OH)D into its active form, 1,25(OH)₂D. It is classified as "dependent" because it can be successfully treated with physiological doses of active Vitamin D (Calcitriol). **Analysis of Incorrect Options:** * **Renal Tubular Acidosis (RTA):** Distal (Type 1) and Proximal (Type 2) RTA cause chronic metabolic acidosis, which leads to hypercalciuria and phosphate wasting. This results in rickets that does not respond to standard Vitamin D therapy, classifying it as a "resistant" form. * **Fanconi Syndrome:** This is a generalized dysfunction of the proximal tubule leading to phosphaturia. The resulting hypophosphatemia causes rickets that is resistant to Vitamin D alone and requires phosphate supplementation. * **Drugs:** Long-term use of certain drugs, most notably **Anticonvulsants** (like Phenytoin or Phenobarbital), induces hepatic cytochrome P450 enzymes. This accelerates the catabolism of Vitamin D into inactive metabolites, leading to a resistant state. **High-Yield Clinical Pearls for NEET-PG:** * **X-linked Hypophosphatemic Rickets:** The most common cause of Vitamin D Resistant Rickets (due to PHEX gene mutation and increased FGF-23) [1]. * **VDDR Type 2:** Caused by a mutation in the **Vitamin D Receptor (VDR)**; often presents with **alopecia**. * **Biochemical Hallmark of VDRR:** Low serum phosphate with normal serum calcium and normal/high 1,25(OH)₂D (except in FGF-23 mediated types).

Question 1

All of the following are associated with pheochromocytoma except:

Accepted Answer

Hypotension

Answer

Ventricular arrhythmias

Answer

Interstitial fibrosis

Answer

Ectopic ACTH production

Question 2

An overweight 48-year-old male presents with complaints of increased thirst and frequent urination. Laboratory examination reveals a blood glucose level of 180 mg/dL. The patient's past medical history is unremarkable, except for an anaphylactic reaction that occurred one year ago when he was given trimethoprim-sulfamethoxazole for a sinus infection. Based on this information, which of the following agents should be prescribed?

Accepted Answer

Metformin

Answer

Chlorpropamide

Answer

Glipizide

Answer

Glucagon

Question 3

When the patient is asked to look upwards with the head fixed, there is an absence of wrinkling on the forehead. This clinical finding is known as:

Accepted Answer

Joffroy's sign

Answer

Von Graefe's sign

Answer

Moebius sign

Answer

Dalrymple's sign

Question 4

Which of the following is NOT typically seen in myxedema coma?

Accepted Answer

Tachycardia

Answer

Hypothermia

Answer

Hypotension

Answer

Hyponatremia

Question 5

A 60-year-old male presented with skin hyperpigmentation, central obesity, violet striae, and proximal myopathy. His blood pressure is 160/90 mmHg. Lab studies show hypokalemic metabolic alkalosis. Which of the following statements is true regarding this condition?

Accepted Answer

Serum potassium level <3.3 mmol/L is suggestive of ectopic ACTH production.

Answer

Basal ACTH level is likely to be low.

Answer

Circulating corticotropin-releasing hormone is likely to be elevated.

Answer

Pituitary magnetic resonance imaging (MRI) will visualize all ACTH-secreting tumors.

Question 6

What is the treatment of Diabetes Insipidus?

Accepted Answer

Antidiuretic Hormone (ADH)

Answer

Thiazide diuretics

Answer

Loop diuretics

Answer

Insulin

Question 7

In diabetes mellitus, which of the following complications are NOT found?

Accepted Answer

Encephalopathy, myelopathy, and myopathy

Answer

Encephalopathy, retinopathy, and diabetes

Answer

Myelopathy, retinopathy, and diabetes

Answer

Encephalopathy and myelopathy

Question 8

Chvostek sign is seen in:

Accepted Answer

Hypothyroidism

Answer

Hypercalcemia

Answer

Insulinoma

Answer

Diabetes mellitus

Question 9

Which of the following is not a feature of Sipple syndrome?

Accepted Answer

Hyperthyroidism

Answer

Pheochromocytoma

Answer

Medullary carcinoma thyroid

Answer

Hyperparathyroidism

Question 10

Vitamin D resistant rickets occurs due to all EXCEPT:

Accepted Answer

Alpha-1-hydroxylase deficiency

Answer

Renal tubular acidosis

Answer

Fanconi syndrome

Answer

Drugs

Endocrinology — MCQs

Endocrinology — MCQs

On this page

Practice by Chapter

Want unlimited practice?