Endocrinology Practice Questions

Q: The insulin preparation of choice in diabetic ketoacidosis is

Regular insulin. **Explanation:** **1. Why Regular Insulin is the Correct Choice:** Regular (Short-acting) insulin is the gold standard for managing Diabetic Ketoacidosis (DKA) because of its **pharmacokinetic profile**. When administered intravenously (IV), it has an immediate onset of action and a short half-life (approx. 5–10 minutes). This allows for rapid titration and precise control over blood glucose and ketone suppression [1]. In DKA, the goal is to inhibit lipolysis and ketogenesis quickly; Regular insulin is the only preparation that can be safely administered via continuous IV infusion, which is the preferred route in acute emergencies [3]. **2. Why the Other Options are Incorrect:** * **Lente and Isophane (NPH) Insulin:** These are intermediate-acting insulins. They contain additives (like zinc or protamine) to delay absorption, making them unsuitable for IV use [2]. Their slow onset and prolonged duration of action make them impossible to titrate rapidly during a metabolic crisis. * **30:70 Mixture:** This is a premixed combination of Regular and NPH insulin. While it contains some short-acting insulin, the NPH component makes it inappropriate for IV administration and acute management. **3. Clinical Pearls for NEET-PG:** * **Route of Choice:** In DKA, the IV route is preferred over subcutaneous because of poor peripheral perfusion in dehydrated patients. * **Standard Dose:** The standard protocol involves an initial bolus (0.1 U/kg) followed by a continuous infusion (0.1 U/kg/hr) [1]. * **The "Rule of 50":** When blood glucose reaches **200–250 mg/dL**, 5% Dextrose should be added to the IV fluids to prevent hypoglycemia while continuing insulin to resolve the ketosis [4]. * **Potassium Warning:** Never start insulin if serum potassium is **<3.3 mEq/L**, as insulin will shift potassium intracellularly, potentially causing fatal arrhythmias [2].

Q: In Sipple syndrome (MEN 2A), which of the following is typically absent?

Pituitary hyperplasia. Explanation: The correct answer is Pituitary hyperplasia because it is a classic feature of MEN 1 (Wermer Syndrome), not MEN 2A (Sipple Syndrome). Both syndromes are autosomal dominant neuroendocrine disorders, but they involve different genetic mutations and organ systems. 1. Why Pituitary Hyperplasia is the correct answer: MEN 2A is caused by a germline mutation in the RET proto-oncogene. Its clinical spectrum is strictly limited to the "MPH" triad: Medullary thyroid carcinoma, Pheochromocytoma, and Hyperparathyroidism. Pituitary adenomas or hyperplasia are characteristic of MEN 1 (the "3 Ps": Pituitary, Parathyroid, and Pancreas). 2. Analysis of Incorrect Options: * Pheochromocytoma (Option A): Present in approximately 50% of MEN 2A cases. They are often bilateral and almost always occur within the adrenal gland. * Medullary Carcinoma of Thyroid (MTC) (Option C): This is the most common feature (nearly 100% penetrance) and usually the first manifestation of MEN 2A. It arises from calcitonin-secreting C-cells. * Parathyroid Hyperplasia (Option D): Occurs in about 20-30% of MEN 2A patients, leading to primary hyperparathyroidism. High-Yield Clinical Pearls for NEET-PG: * MEN 2A (Sipple): MTC + Pheochromocytoma + Parathyroid hyperplasia. * MEN 2B (Williams): MTC + Pheochromocytoma + Mucosal neuromas + Marfanoid habitus (Note: Parathyroid involvement is rare in 2B). * Screening: For MEN 2A/2B, genetic testing for RET mutations is the gold standard. Prophylactic thyroidectomy is often indicated in childhood based on the specific codon mutation. * Rule of Thumb: Always rule out Pheochromocytoma (via plasma metanephrines) before performing surgery for MTC or Hyperparathyroidism to prevent a hypertensive crisis.

Q: Which of the following is NOT a cause of fasting hypoglycemia?

Excess glucagon. **Explanation:** The core physiological mechanism of fasting hypoglycemia involves an inability to maintain blood glucose levels during periods of starvation, usually due to defects in glycogenolysis, gluconeogenesis, or hormonal regulation [3]. **Why Option A is correct:** **Glucagon** is a counter-regulatory hormone produced by the alpha cells of the pancreas. Its primary function is to **increase** blood glucose levels by stimulating glycogenolysis and gluconeogenesis in the liver [1]. Therefore, an **excess of glucagon** (as seen in a Glucagonoma) would lead to **hyperglycemia**, not hypoglycemia. **Why the other options are incorrect:** * **B. Glucose-6-phosphatase deficiency (Von Gierke Disease):** This is Type I Glycogen Storage Disease (GSD). This enzyme is essential for the final step of both glycogenolysis and gluconeogenesis [2]. Its absence leads to severe fasting hypoglycemia because the liver cannot release free glucose into the blood. * **C. Uremia:** Chronic kidney disease/uremia causes hypoglycemia through multiple mechanisms, including reduced renal gluconeogenesis (the kidney contributes ~20% of glucose production), impaired insulin clearance, and malnutrition. * **D. Glycogen synthase deficiency:** Known as Type 0 GSD, this condition prevents the liver from storing glycogen [3]. Without glycogen stores to draw upon during a fast, patients develop ketotic hypoglycemia. **High-Yield NEET-PG Pearls:** * **Whipple’s Triad for Hypoglycemia:** 1. Symptoms of hypoglycemia, 2. Low plasma glucose (<55 mg/dL), 3. Relief of symptoms after glucose administration. * **Common causes of fasting hypoglycemia:** Insulinoma, exogenous insulin (factitious), adrenal insufficiency (Addison’s), and severe liver disease. * **Glucagonoma Clinical Triad:** Hyperglycemia (Diabetes), Necrolytic Migratory Erythema (NME), and weight loss.

Q: What is the most likely diagnosis in a patient with generalized weakness and the given cutaneous finding?

Diffuse melanosis cutis. ***Diffuse melanosis cutis*** - Generalized weakness combined with diffuse cutaneous hyperpigmentation suggests **Addison's disease** (primary adrenal insufficiency) causing excess **ACTH and MSH** stimulation. - The **melanosis cutis** results from increased melanin deposition due to elevated **melanocyte-stimulating hormone** levels when cortisol feedback is lost. *Lichen planus pigmentosus* - Presents with **localized hyperpigmented patches** rather than generalized melanosis, typically following inflammatory lichen planus lesions. - Does not cause **systemic weakness** or constitutional symptoms like adrenal insufficiency. *Smoker's melanosis* - Characterized by **localized oral mucosal pigmentation** from chronic smoking, not generalized cutaneous involvement. - Associated with **tobacco use** and does not cause generalized weakness or systemic symptoms. *Cushing's disease* - Typically causes **central obesity**, **purple striae**, and **moon facies** rather than generalized hyperpigmentation. - Results in **hyperglycemia** and **hypertension**, not the weakness and hyperpigmentation seen in adrenal insufficiency.

Q: Liddle syndrome is characterized by

Hypokalemic metabolic alkalosis with hypertension. **Explanation:** **Liddle Syndrome** is an autosomal dominant genetic disorder caused by a **gain-of-function mutation** in the genes encoding the **ENaC (Epithelial Sodium Channel)** in the collecting tubules of the kidney. 1. **Why Option B is Correct:** The overactive ENaC leads to constitutive (unregulated) reabsorption of sodium, regardless of aldosterone levels. This causes: * **Hypertension:** Due to excessive sodium and water retention (volume expansion). * **Hypokalemic Metabolic Alkalosis:** Increased sodium reabsorption creates a negative luminal potential, which forces the secretion of Potassium ($K^+$) and Hydrogen ions ($H^+$) into the urine [1]. [2]. 2. **Why Other Options are Incorrect:** * **Option A:** Hypotension is seen in "salt-wasting" syndromes like Bartter or Gitelman syndrome, not Liddle. * **Options C & D:** Hyperkalemia and acidosis are characteristic of **Hypoaldosteronism** or **Type 4 Renal Tubular Acidosis (RTA)** [1]. Liddle syndrome mimics *excess* mineralocorticoid activity, leading to the opposite (hypokalemia/alkalosis) [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Pseudo-hyperaldosteronism:** Liddle syndrome presents like primary hyperaldosteronism (Conn’s syndrome) but with **Low Renin** and **Low Aldosterone** levels (due to feedback suppression by volume expansion) [2]. * **Treatment:** It does **not** respond to Spironolactone (as the defect is distal to the aldosterone receptor). It is treated with ENaC blockers like **Amiloride** or **Triamterene**. * **Mnemonic:** "Liddle behaves like **Little** Aldosterone is present, but the channel is actually **Large** (overactive)."

Q: A patient presents with symptoms of hypoglycemia. Investigations reveal decreased blood glucose and increased insulin levels. A C-peptide assay shows normal levels of C-peptide. What is the most likely diagnosis?

Accidental exogenous insulin administration. ### Explanation The key to solving this clinical scenario lies in understanding the synthesis of endogenous insulin. Insulin is synthesized as **proinsulin**, which is cleaved into equal molar amounts of **active insulin** and **C-peptide** before being released into the bloodstream. **1. Why Option C is Correct:** In **exogenous insulin administration**, the patient injects pre-formed, purified insulin. This commercial insulin does not contain C-peptide. Therefore, the patient will present with the biochemical triad of: * **Low Blood Glucose** (Hypoglycemia) [3] * **High Insulin** (Exogenous) * **Low/Normal C-peptide** (Endogenous production is actually suppressed due to negative feedback from hypoglycemia) [1]. **2. Why the other options are incorrect:** * **Insulinoma (A):** This is an insulin-secreting tumor of the pancreas. Since it produces endogenous insulin, both **Insulin and C-peptide levels will be elevated** [1]. * **Sulfonylurea Ingestion (B):** Sulfonylureas are secretagogues that stimulate the pancreas to release its own insulin [2]. Consequently, both **Insulin and C-peptide levels will be elevated**, mimicking an insulinoma [1]. * **Metformin Ingestion (D):** Metformin works by increasing insulin sensitivity and decreasing hepatic glucose production; it does not increase insulin secretion and typically does not cause hypoglycemia in isolation. **3. NEET-PG High-Yield Pearls:** * **Factitious Hypoglycemia:** Suspect this in healthcare workers or relatives of diabetics. [1] * **Differential Diagnosis:** To differentiate Insulinoma from Sulfonylurea abuse (as both have high C-peptide), a **Screening for Oral Hypoglycemic Agents** in the urine or plasma is required [1]. * **Whipple’s Triad:** 1. Symptoms of hypoglycemia, 2. Low plasma glucose, 3. Relief of symptoms after glucose administration. This triad confirms a hypoglycemic disorder.

Q: Hypocalcemia is seen with which of the following conditions?

Acute pancreatitis. Hypocalcemia is a classic metabolic complication of acute pancreatitis [2]. The primary mechanism is saponification: during pancreatic inflammation, released lipases break down peripancreatic fat into free fatty acids. These fatty acids bind to circulating ionized calcium, forming insoluble calcium soaps (salts) in the retroperitoneum. Additionally, a transient "parathyroid hormone (PTH) resistance" and hypomagnesemia may contribute to the decline in serum calcium levels [2]. In the Ranson Criteria, a fall in serum calcium (<8 mg/dL) within 48 hours is a marker of severe disease and poor prognosis. **Incorrect Options:** * **A. Thyrotoxicosis:** Excess thyroid hormone increases bone turnover by stimulating osteoclastic activity, which typically leads to **mild hypercalcemia** and hypercalciuria [1]. * **B. Hyperparathyroidism:** Primary hyperparathyroidism is characterized by the "classic triad" of **hypercalcemia**, hypophosphatemia, and elevated PTH [1]. * **D. Addison Disease:** Adrenal insufficiency is associated with **hypercalcemia** [1]. This occurs due to decreased renal calcium excretion and increased bone resorption, though the exact mechanism remains multifactorial. **High-Yield Clinical Pearls for NEET-PG:** * **Chvostek sign** (facial twitching on tapping the facial nerve) and **Trousseau sign** (carpal spasm on BP cuff inflation) are clinical markers of hypocalcemia. * **ECG finding:** The hallmark of hypocalcemia is **QT interval prolongation** (specifically the ST segment) [2]. * **Correction:** Always check serum albumin; for every 1 g/dL drop in albumin below 4 g/dL, add 0.8 mg/dL to the measured calcium to get the "corrected calcium" [2].

Q: De Quervain's disease is:

Subacute thyroiditis.. **Explanation:** **De Quervain’s thyroiditis**, also known as **Subacute Granulomatous Thyroiditis**, is the correct answer (Option C). It is a self-limiting inflammatory condition of the thyroid gland, typically triggered by a **viral infection** (e.g., Coxsackievirus, Mumps, or Adenovirus). It classically presents in middle-aged women following an upper respiratory tract infection. **Why Option C is correct:** The underlying pathology involves the destruction of thyroid follicles and the formation of **multinucleated giant cells (granulomas)**. This leads to a characteristic clinical triad: 1. **Exquisite thyroid pain and tenderness** (often radiating to the jaw or ears). 2. **Transient hyperthyroidism** (due to the release of preformed hormones), followed by hypothyroidism, and eventual recovery [1]. 3. **Systemic symptoms** like fever and malaise. **Why other options are incorrect:** * **Option A (Acute Suppurative Thyroiditis):** This is a rare **bacterial infection** (usually *Staph* or *Strep*) characterized by abscess formation and high fever. It is distinct from the viral/granulomatous nature of De Quervain’s. * **Option B (Autoimmune Thyroiditis):** This refers to conditions like **Hashimoto’s thyroiditis**, which is typically painless and characterized by goiter and positive anti-TPO antibodies [1]. **High-Yield Clinical Pearls for NEET-PG:** * **ESR:** Characteristically **very high** (>50–100 mm/hr) [1]. * **Radioactive Iodine Uptake (RAIU):** Characteristically **low/depressed** (due to follicular damage), despite the patient being in a thyrotoxic state [1]. * **Treatment:** NSAIDs for mild cases; **Corticosteroids** for severe pain [1]. Antithyroid drugs (PTU/Methimazole) are **not** indicated as there is no new hormone synthesis [1].

Question 1

How is hyperthyroidism diagnosed?

Accepted Answer

Triiodothyronine (T3), Thyroxine (T4), and Thyroid Stimulating Hormone (TSH)

Answer

Triiodothyronine (T3) and Thyroxine (T4)

Answer

Triiodothyronine (T3), Thyroxine (T4), and Radioactive Iodine Uptake (RAI)

Answer

Triiodothyronine (T3), Thyroxine (T4), Radioactive Iodine Uptake (RAI), and TSH

Question 2

The insulin preparation of choice in diabetic ketoacidosis is

Accepted Answer

Regular insulin

Answer

Lente insulin

Answer

Isophane insulin

Answer

A 30:70 mixture of plain and isophane insulin

Question 3

In Sipple syndrome (MEN 2A), which of the following is typically absent?

Accepted Answer

Pituitary hyperplasia

Answer

Pheochromocytoma

Answer

Medullary carcinoma of the thyroid

Answer

Parathyroid hyperplasia

Question 4

The goals of therapy for type 1 or type 2 diabetes mellitus are all except?

Accepted Answer

Restore the function of Beta cells

Answer

Eliminate symptoms related to hyperglycemia

Answer

Reduce or eliminate the long-term microvascular and macrovascular complications of DM

Answer

Allow the patient to achieve as normal a lifestyle as possible

Question 5

Which of the following is NOT a cause of fasting hypoglycemia?

Accepted Answer

Excess glucagon

Answer

Glucose-6-phosphatase deficiency

Answer

Uremia

Answer

Glycogen synthase deficiency

Question 6

What is the most likely diagnosis in a patient with generalized weakness and the given cutaneous finding?

Accepted Answer

Diffuse melanosis cutis

Answer

Lichen planus pigmentosus

Answer

Smoker's melanosis

Answer

Cushing's disease

Question 7

Liddle syndrome is characterized by

Accepted Answer

Hypokalemic metabolic alkalosis with hypertension

Answer

Hypokalemic metabolic alkalosis with hypotension

Answer

Hyperkalemic metabolic acidosis with hypotension

Answer

Hyperkalemic metabolic acidosis with hypertension

Question 8

A patient presents with symptoms of hypoglycemia. Investigations reveal decreased blood glucose and increased insulin levels. A C-peptide assay shows normal levels of C-peptide. What is the most likely diagnosis?

Accepted Answer

Accidental exogenous insulin administration

Answer

Insulinoma

Answer

Accidental sulfonylurea ingestion

Answer

Accidental metformin ingestion

Question 9

Hypocalcemia is seen with which of the following conditions?

Accepted Answer

Acute pancreatitis

Answer

Thyrotoxicosis

Answer

Hyperparathyroidism

Answer

Addison disease

Question 10

De Quervain's disease is:

Accepted Answer

Subacute thyroiditis.

Answer

Acute suppurative thyroiditis.

Answer

Autoimmune thyroiditis.

Answer

None.

Endocrinology — MCQs

Endocrinology — MCQs

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