Endocrinology Practice Questions

Q: An 18-year-old girl presents with weakness. She reports high stress levels due to academic demands, with most of her time dedicated to studying, dieting, and exercising. Physical examination reveals a height of 5'8", a weight of 85 lbs, and she appears unwell. Her blood pressure is 85/70 mm Hg, heart rate is 50/min, and there is prominent muscle wasting. What is this patient most likely at risk for?

Ventricular tachyarrhythmias. ### Explanation This clinical presentation is classic for **Anorexia Nervosa (AN)**. The patient exhibits a low BMI (approx. 12.9 kg/m²), bradycardia, hypotension, and a preoccupation with dieting/exercise despite being severely underweight [2]. **1. Why Ventricular Tachyarrhythmias is Correct:** The most common cause of death in patients with severe Anorexia Nervosa is **cardiac complications**. Chronic starvation leads to the depletion of cardiac muscle mass (myocardial atrophy), resulting in a **prolonged QTc interval** [2]. This electrical instability, often exacerbated by electrolyte imbalances (like hypokalemia or hypomagnesemia from purging or malnutrition), predisposes the patient to life-threatening **ventricular tachyarrhythmias**, such as Torsades de Pointes, and sudden cardiac death. **2. Why the Other Options are Incorrect:** * **Renal Failure:** While dehydration can cause pre-renal azotemia, acute renal failure is a less common cause of immediate mortality compared to cardiac arrest in AN. * **Diabetes Mellitus:** Anorexia is associated with **hypoglycemia** due to depleted glycogen stores and lack of precursors for gluconeogenesis [3], not hyperglycemia or diabetes. * **Hyperthermia:** Patients with AN typically suffer from **hypothermia** due to the loss of insulating adipose tissue and a lowered basal metabolic rate [1], which is a compensatory mechanism for starvation. **Clinical Pearls for NEET-PG:** * **Refeeding Syndrome:** The most dangerous complication during treatment. It is characterized by **Hypophosphatemia**, which can lead to heart failure and seizures. * **Hormonal Profile in AN:** Low GnRH, low LH/FSH (Hypogonadotropic hypogonadism), and normal to high Cortisol. * **Physical Sign:** Look for **Lanugo hair** (fine, downy hair) and **Russell’s sign** (calluses on knuckles from self-induced vomiting).

Q: Which of the following is not involved in Multiple Endocrine Neoplasia type 2 (MEN II) syndrome?

Pituitary tumor. Multiple Endocrine Neoplasia (MEN) syndromes are autosomal dominant disorders characterized by tumors involving two or more endocrine glands [1]. To answer this question correctly, one must distinguish between the components of MEN 1 and MEN 2. **Why Pituitary Tumor is the correct answer:** Pituitary tumors (most commonly prolactinomas) are a hallmark of **MEN 1 (Wermer’s Syndrome)**, often remembered by the "3 Ps": **P**ituitary, **P**arathyroid, and **P**ancreas. They are **not** a component of MEN 2. **Analysis of incorrect options (Components of MEN 2):** * **Medullary Carcinoma of Thyroid (MTC):** This is the most consistent feature of MEN 2 (occurring in nearly 100% of cases). It arises from parafollicular C-cells. * **Pheochromocytoma:** Found in approximately 50% of patients with MEN 2A and 2B. They are frequently bilateral and occur in the adrenal medulla. * **Parathyroid Adenoma/Hyperplasia:** This is seen in **MEN 2A** (Sipple Syndrome) but is notably absent in MEN 2B. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Mutation:** MEN 1 is caused by a mutation in the *MEN1* gene (Menin protein), while MEN 2 (both 2A and 2B) is caused by a gain-of-function mutation in the **RET proto-oncogene**. * **MEN 2B vs. 2A:** MEN 2B is characterized by MTC and Pheochromocytoma (like 2A) but includes **Mucosal neuromas** and a **Marfanoid habitus** instead of parathyroid involvement. * **Screening:** In patients with a known *RET* mutation, prophylactic thyroidectomy is often indicated due to the high virulence of MTC.

Q: Which of the following conditions can lead to increased T4 levels?

X-linked TBG deficiency. The concentration of total T4 in the blood is dependent on two factors: the amount of hormone produced by the thyroid gland and the concentration of thyroid-binding proteins (primarily **Thyroid-Binding Globulin or TBG**) [1]. **Why Option B is Correct:** In **X-linked TBG deficiency**, there is a genetic decrease in the levels of TBG. Since >99% of T4 is protein-bound, a decrease in binding proteins leads to a **decrease in Total T4** levels [1]. However, the free T4 (fT4) and TSH levels remain normal, and the patient remains euthyroid [1]. *(Note: The question asks which condition leads to increased T4; however, based on standard medical physiology, TBG deficiency leads to **decreased** total T4. If the provided key marks B as correct, it likely refers to a scenario where the

Q: Which of the following is an anti-androgenic drug?

Bicalutamide. ### Explanation **Correct Option: A. Bicalutamide** Bicalutamide is a potent, non-steroidal **androgen receptor antagonist** [1]. It works by competitively inhibiting the binding of dihydrotestosterone (DHT) and testosterone to their receptors [1]. In clinical practice, it is primarily used in the management of metastatic prostate cancer, often combined with GnRH analogues to prevent the "testosterone flare" phenomenon. **Analysis of Incorrect Options:** * **B. Oxymetholone:** This is a synthetic **androgen/anabolic steroid** [2]. Instead of blocking androgens, it mimics them. It is clinically used to treat certain types of anemia (by stimulating erythropoietin) and muscle-wasting conditions [2]. * **C. Raloxifene:** This is a **Selective Estrogen Receptor Modulator (SERM)**. It acts as an estrogen agonist in the bone (preventing osteoporosis) and an antagonist in the breast and uterus. It has no direct activity on androgen receptors. * **D. Stanozolol:** Similar to oxymetholone, this is an **anabolic steroid** (derived from DHT) [2]. It is often discussed in the context of performance-enhancing drug abuse and the treatment of hereditary angioedema. **NEET-PG High-Yield Pearls:** * **Classification of Anti-androgens:** 1. **Receptor Antagonists:** Flutamide, Bicalutamide (longer half-life, less hepatotoxic), Enzalutamide, and Spironolactone [1]. 2. **5-alpha Reductase Inhibitors:** Finasteride, Dutasteride (used in BPH and male pattern baldness). 3. **Synthesis Inhibitors:** Ketoconazole, Abiraterone. * **Clinical Note:** Bicalutamide is preferred over Flutamide due to its once-daily dosing and significantly lower risk of hepatotoxicity [1]. * **Side Effects:** Common side effects of anti-androgens include gynecomastia, hot flashes, and decreased libido.

Q: Which of the following findings is FALSE regarding primary adrenal hyperplasia?

Hyponatremia. Primary adrenal hyperplasia (a form of **Primary Hyperaldosteronism** or Conn’s syndrome) is characterized by the autonomous overproduction of aldosterone from the adrenal cortex. To answer this question, one must understand the physiological actions of aldosterone on the distal convoluted tubule and collecting ducts of the kidney. **Why Hyponatremia is FALSE (The Correct Answer):** Aldosterone acts on the principal cells to increase the reabsorption of sodium ($Na^+$) and the secretion of potassium ($K^+$) and hydrogen ions ($H^+$) [2]. Consequently, primary hyperaldosteronism leads to **hypernatremia** (or high-normal sodium levels), not hyponatremia [3]. Therefore, Option A is the false statement. **Analysis of Other Options:** * **B. Hypernatremia:** This is a classic finding due to excessive sodium retention mediated by the ENaC channels [2]. * **C. Water Retention:** Sodium reabsorption creates an osmotic gradient that pulls water into the intravascular compartment. This leads to ECF volume expansion and hypertension [1]. (Note: Clinically, edema is usually absent due to the "Aldosterone Escape" phenomenon) [1]. * **D. Hypokalemia:** Excessive aldosterone causes profound renal potassium wasting, which is a hallmark of the disease, often presenting as muscle weakness or cardiac arrhythmias [2]. **NEET-PG High-Yield Pearls:** 1. **Aldosterone Escape:** Despite water retention, patients with primary hyperaldosteronism do not typically have edema because increased stretch in the atria releases **ANP (Atrial Natriuretic Peptide)**, which promotes secondary natriuresis [1]. 2. **Metabolic Profile:** Look for the triad of **Hypertension, Hypokalemia, and Metabolic Alkalosis** [3]. 3. **Screening:** The best initial test is the **Aldosterone-to-Renin Ratio (ARR)**. In primary disease, Aldosterone is high, and Renin is suppressed. 4. **Spironolactone:** This is the medical treatment of choice as it acts as a direct aldosterone antagonist.

Q: Which of the following is a feature of primary hyperaldosteronism?

Hypertension. **Primary Hyperaldosteronism (Conn’s Syndrome)** is characterized by the autonomous overproduction of aldosterone from the adrenal cortex, leading to increased sodium reabsorption and potassium excretion [1]. ### **Explanation of the Correct Answer** **D. Hypertension:** This is the hallmark of the condition. Excess aldosterone acts on the mineralocorticoid receptors in the distal convoluted tubule and collecting ducts, increasing the activity of ENaC channels [2]. This leads to **sodium and water retention**, expanding the extracellular fluid volume and increasing peripheral vascular resistance, resulting in secondary hypertension. ### **Explanation of Incorrect Options** * **A. Pedal Edema:** Despite sodium and water retention, clinically significant edema is typically **absent** due to the **"Aldosterone Escape" phenomenon** [1]. Increased atrial natriuretic peptide (ANP) levels and pressure natriuresis lead to the excretion of excess sodium, preventing overt volume overload. * **B. Polyuria:** While chronic hypokalemia can cause nephrogenic diabetes insipidus leading to polyuria, it is a secondary complication rather than a primary diagnostic feature. Hypertension is the more consistent and defining clinical finding. * **C. Hyperkalemia:** This is incorrect because aldosterone promotes **potassium secretion** into the urine [2]. Therefore, **hypokalemia** (not hyperkalemia) is the classic biochemical finding [1], often associated with metabolic alkalosis. ### **NEET-PG High-Yield Pearls** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A **PAC:PRA ratio > 20-30** is highly suggestive. * **Confirmatory Test:** Oral or Intravenous Saline Suppression Test (failure to suppress aldosterone levels). * **Most Common Cause:** Adrenal Adenoma (Conn’s Syndrome), followed by Bilateral Adrenal Hyperplasia. * **Triad:** Hypertension, Hypokalemia, and Metabolic Alkalosis [1].

Q: A 30-year-old patient presents with intermittent, severe headaches accompanied by perspiration, palpitations, and pallor. Blood pressure on initial examination was within normal limits, but when the patient came in later with a headache, it was 180/135 mm Hg. Urinary vanillylmandelic acid (VMA) levels were elevated. Roughly, what percentage of the tumors causing this pattern is malignant?

10%. ### Explanation The clinical presentation of paroxysmal hypertension, headache, perspiration, and palpitations (the classic triad) strongly suggests **Pheochromocytoma**, a catecholamine-secreting tumor of the adrenal medulla. The diagnosis is further supported by elevated urinary vanillylmandelic acid (VMA) levels. **Why 10% is Correct:** Pheochromocytoma is famously known as the **"10% Tumor"** because it historically follows a specific rule of percentages. According to this rule, approximately **10% of pheochromocytomas are malignant**. Malignancy is defined not by histology, but by the presence of chromaffin tissue in non-chromaffin sites (e.g., bones, liver, or lymph nodes). **Analysis of Incorrect Options:** * **A (1%):** This is too low. While some rare endocrine syndromes have lower malignancy rates, 10% is the established figure for pheochromocytoma. * **C (50%):** This is incorrect for adrenal pheochromocytoma. However, it is worth noting that the risk of malignancy is significantly higher (up to 35-40%) in extra-adrenal paragangliomas. * **D (90%):** This is incorrect; the vast majority (90%) of these tumors are benign. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of 10" for Pheochromocytoma:** * 10% are Malignant. * 10% are Bilateral (more common in familial cases like MEN 2A/2B). * 10% are Extra-adrenal (Paragangliomas; most common site is the **Organ of Zuckerkandl**). * 10% occur in Children. * 10% are Familial (though modern genetics suggests this may be as high as 30-40%). * **Diagnosis:** The most sensitive screening test is **plasma free metanephrines**. * **Management:** Always start **Alpha-blockade (Phenoxybenzamine)** before Beta-blockade to prevent a hypertensive crisis caused by unopposed alpha-receptor stimulation.

Question 1

The occurrence of hyperthyroidism following administration of supplemental iodine to subjects with endemic iodine deficiency goiter is known as what?

Accepted Answer

Jod-Basedow effect

Answer

Wolff-Chaokoff effect

Answer

Thyrotoxicosis factitia

Answer

De Quervain's thyroiditis

Question 2

An 18-year-old girl presents with weakness. She reports high stress levels due to academic demands, with most of her time dedicated to studying, dieting, and exercising. Physical examination reveals a height of 5'8", a weight of 85 lbs, and she appears unwell. Her blood pressure is 85/70 mm Hg, heart rate is 50/min, and there is prominent muscle wasting. What is this patient most likely at risk for?

Accepted Answer

Ventricular tachyarrhythmias

Answer

Renal failure

Answer

Diabetes Mellitus

Answer

Hyperthermia

Question 3

Which of the following is not involved in Multiple Endocrine Neoplasia type 2 (MEN II) syndrome?

Accepted Answer

Pituitary tumor

Answer

Medullary carcinoma of the thyroid

Answer

Pheochromocytoma

Answer

Parathyroid adenoma

Question 4

Which of the following conditions can lead to increased T4 levels?

Accepted Answer

X-linked TBG deficiency

Answer

Hyperparathyroidism

Answer

Familial dysalbuminemic hyperthyroxinemia

Answer

Low T3 syndrome

Question 5

Which of the following is an anti-androgenic drug?

Accepted Answer

Bicalutamide

Answer

Oxymetholone

Answer

Raloxifene

Answer

Stanozolol

Question 6

Which of the following findings is FALSE regarding primary adrenal hyperplasia?

Accepted Answer

Hyponatremia

Answer

Hypernatremia

Answer

Water retention

Answer

Hypokalemia

Question 7

A 56-year-old man is diagnosed with the metabolic syndrome, which consists of hypertension, insulin resistance, dyslipidemia, and abdominal obesity. He has no prior history of cardiac or vascular disease and is otherwise well. His fasting T-chol is 270 mg/dL, HDL 50 mg/dL, LDL 150 mg/dL, and triglycerides 150 mg/dL. His Framingham risk calculation approximates a 10-year risk for cardiac events of 10%-20%. For the above patient with dyslipidemia, select the most appropriate treatment.

Accepted Answer

Hepatic hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (lovastatin, simvastatin, pravastatin)

Answer

Fibric acid derivatives (clofibrate, gemfibrozil)

Answer

Nicotinic acid

Answer

Bile acid-binding resins (cholestyramine, colestipol)

Question 8

Which of the following is a feature of primary hyperaldosteronism?

Accepted Answer

Hypertension

Answer

Pedal edema

Answer

Polyuria

Answer

Hyperkalemia

Question 9

Which of the following is NOT true of Verner Morrison syndrome (WDHA syndrome)?

Accepted Answer

It is associated with hyperkalemia.

Answer

It is associated with Vipoma.

Answer

It presents with secretory diarrhea.

Answer

It can be associated with ganglioneuroblastoma.

Question 10

A 30-year-old patient presents with intermittent, severe headaches accompanied by perspiration, palpitations, and pallor. Blood pressure on initial examination was within normal limits, but when the patient came in later with a headache, it was 180/135 mm Hg. Urinary vanillylmandelic acid (VMA) levels were elevated. Roughly, what percentage of the tumors causing this pattern is malignant?

Accepted Answer

10%

Answer

1%

Answer

50%

Answer

90%

Endocrinology — MCQs

Endocrinology — MCQs

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