Endocrinology Practice Questions

Q: Migratory necrolytic erythema is seen in which condition?

Glucagonoma syndrome. **Explanation:** **Migratory Necrolytic Erythema (MNE)** is the pathognomonic cutaneous manifestation of **Glucagonoma syndrome**, a rare neuroendocrine tumor of the pancreatic alpha cells [1]. 1. **Why Glucagonoma is correct:** MNE presents as pruritic, painful, erythematous plaques that blister and crust, typically involving the perineum, extremities, and perioral areas. The underlying mechanism involves hyperglucagonemia leading to increased gluconeogenesis and protein catabolism, resulting in hypoaminoacidemia. This nutritional deficiency, along with zinc and essential fatty acid depletion, is thought to trigger epidermal necrosis. 2. **Why other options are incorrect:** * **Peutz-Jeghers Syndrome:** Characterized by hamartomatous GI polyps and **mucocutaneous hyperpigmentation** (melanotic macules) on the lips and buccal mucosa. * **Sarcoidosis:** Classically associated with **Lupus Pernio** (violaceous plaques on the nose/cheeks) and Erythema Nodosum. * **Amyloidosis:** Skin findings typically include **waxy papules**, plaques, and "pinch purpura" (ecchymosis following minor trauma), especially in the periorbital area. **High-Yield Clinical Pearls for NEET-PG:** * **The "6Ds" of Glucagonoma:** **D**ermatitis (MNE), **D**iabetes (mild), **D**epression, **D**eclining weight, **D**eep vein thrombosis (DVT), and **D**iarrhea [1]. * **Diagnosis:** Markedly elevated fasting plasma glucagon levels (>1000 pg/mL). * **Treatment:** Surgical resection is definitive; Octreotide (somatostatin analog) is used to manage symptoms by inhibiting glucagon release.

Q: Conn's syndrome is characterized by diastolic hypertension without edema. Which of the following is a characteristic electrolyte imbalance seen in Conn's syndrome?

Hypokalemia. **Explanation:** **Conn’s Syndrome** (Primary Hyperaldosteronism) is caused by an aldosterone-secreting adenoma of the adrenal cortex. The pathophysiology revolves against the excessive action of aldosterone on the **principal cells** of the renal collecting ducts. 1. **Why Hypokalemia is correct:** Aldosterone increases the activity of the ENaC (epithelial sodium channels), leading to sodium reabsorption. To maintain electrochemical neutrality, the kidney must excrete positive ions, specifically **Potassium (K+)** and Hydrogen (H+) [1]. This results in excessive urinary potassium loss, leading to **hypokalemia** and metabolic alkalosis [3]. 2. **Analysis of Incorrect Options:** * **B. Hyperkalemia:** This is the opposite of the expected finding. Hyperkalemia is seen in Addison’s disease (adrenal insufficiency) or Hypoaldosteronism. * **C. Sodium retention:** While sodium is indeed retained, it is **not** an electrolyte imbalance typically measured as "hypernatremia." Due to the **"Aldosterone Escape"** phenomenon (where increased ANP and pressure natriuresis prevent fluid overload), sodium levels usually remain at the high end of the normal range, and clinical edema is absent [2]. * **D. Hypertension:** While hypertension is a hallmark clinical feature of Conn’s syndrome, the question specifically asks for a characteristic **electrolyte imbalance**. **High-Yield Clinical Pearls for NEET-PG:** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A ratio **>20-30** is suggestive. * **Confirmatory Test:** Saline infusion test or Oral salt loading test (failure to suppress aldosterone). * **Aldosterone Escape:** Explains why patients with Conn’s syndrome do not develop overt volume overload or edema despite sodium retention [2]. * **Triad:** Hypertension + Hypokalemia + Metabolic Alkalosis.

Q: Which of the following clinical features of diabetes insipidus is false?

Dehydration. **Explanation:** In Diabetes Insipidus (DI), the primary pathology is a deficiency of Antidiuretic Hormone (ADH) or resistance to its action. This leads to an inability of the kidneys to concentrate urine, resulting in massive polyuria. **Why "Dehydration" is the False Feature:** While patients with DI lose significant amounts of free water, **clinically significant dehydration is rare** in patients with an intact thirst mechanism and free access to water. These patients compensate for urinary losses by developing intense thirst (polydipsia). Dehydration only occurs if the patient is unable to communicate thirst (e.g., infants, elderly) or has a concomitant hypothalamic lesion affecting the thirst center (adipsic DI). **Analysis of Other Options:** * **A. Daily urine volume >50 mL/kg:** This is a diagnostic criterion for polyuria. In DI, urine output is typically massive, often ranging from 3 to 20 liters per day. * **B. Urine osmolarity 290 mOsm/kg). * **D. Enuresis:** Nocturia is almost universal in DI. In children, this frequently manifests as bedwetting (enuresis) and is often a presenting complaint. **High-Yield NEET-PG Pearls:** * **Water Deprivation Test:** The gold standard for diagnosis. Central DI shows a >50% increase in urine osmolarity after Desmopressin; Nephrogenic DI shows little to no response. * **Most common cause of Central DI:** Idiopathic (30-50%), followed by trauma/surgery and tumors (Craniopharyngioma). * **Drug-induced Nephrogenic DI:** Lithium is the most common cause. * **Treatment:** Desmopressin (DDAVP) is the drug of choice for Central DI. Thiazide diuretics are used for Nephrogenic DI.

Q: A 63-year-old woman with Type 2 diabetes is seen for follow-up after a fasting lipid profile. She has no other medical conditions and feels well. Her diabetes is well controlled and the last hemoglobin A1c value was 6.5%. Her total cholesterol is 240 mg/dL, HDL is 50 mg/dL, low-density lipoprotein is 160 mg/dL, and triglycerides are 150 mg/dL. For this patient with dyslipidemia, what is the most appropriate treatment?

HMG-CoA reductase inhibitors. **Explanation:** The correct answer is **D. HMG-CoA reductase inhibitors (Statins).** The primary goal in managing dyslipidemia in a patient with Type 2 Diabetes Mellitus (T2DM) is the reduction of cardiovascular risk. According to current clinical guidelines (ADA and AHA/ACC), **statins are the first-line therapy** for diabetic patients aged 40–75 years, regardless of their baseline lipid levels, provided their LDL-C is $\geq$ 70 mg/dL. This patient is 63 years old with an LDL of 160 mg/dL, placing her in a high-risk category where statins have been proven to significantly reduce major adverse cardiovascular events (MACE) [1]. **Why other options are incorrect:** * **A. Fibric acid derivatives:** These are primarily used to lower triglycerides [2]. While they can be used in T2DM, they are second-line and indicated mainly when triglycerides are severely elevated (>500 mg/dL) to prevent pancreatitis. * **B. Nicotinic acid:** Niacin can increase HDL and lower LDL, but it is rarely used now due to side effects (flushing, hyperglycemia) and a lack of evidence showing improved cardiovascular outcomes when added to statins. * **C. Bile acid-binding resins:** These are less potent than statins and can actually increase triglyceride levels, making them unfavorable for many diabetic patients [2]. **NEET-PG High-Yield Pearls:** * **Statin Benefit Groups:** T2DM patients aged 40–75 are a major "statin benefit group." * **Intensity:** Patients with T2DM and multiple risk factors or aged 50-75 usually require **High-Intensity Statins** (e.g., Atorvastatin 40–80 mg or Rosuvastatin 20–40 mg) [3]. * **Pleiotropic Effects:** Statins do more than lower LDL; they stabilize atherosclerotic plaques and have anti-inflammatory properties [1]. * **Rule of 6:** Each doubling of the statin dose leads to an additional 6% reduction in LDL-C.

Q: Which type of thyroiditis is also known as "Painless Thyroiditis"?

Subacute lymphocytic thyroiditis. **Explanation:** **Subacute lymphocytic thyroiditis** (Option A) is the correct answer. It is also known as **"Painless Thyroiditis"** or "Silent Thyroiditis." Pathologically, it is characterized by a lymphocytic infiltration of the thyroid gland. Clinically, it presents with a transient phase of thyrotoxicosis (due to the release of stored hormones from damaged follicles) followed by hypothyroidism, eventually returning to a euthyroid state [1]. Crucially, unlike other inflammatory thyroid conditions, there is **no thyroid tenderness** on palpation. **Why other options are incorrect:** * **Subacute granulomatous thyroiditis (de Quervain’s):** This is the most common cause of a **painful** thyroid gland. It typically follows a viral upper respiratory tract infection and presents with exquisite tenderness and an elevated ESR. * **Hashimoto's thyroiditis:** While it is a lymphocytic thyroiditis, it is chronic and typically presents with a firm, non-tender goiter and permanent hypothyroidism. It is not referred to as "painless thyroiditis" in clinical nomenclature. * **Riedel's thyroiditis:** This is a rare manifestation of IgG4-related disease characterized by dense fibrous replacement of the thyroid ("stony hard" thyroid). While painless, it presents with obstructive symptoms (dysphagia, hoarseness). **High-Yield NEET-PG Pearls:** * **Postpartum Thyroiditis:** A variant of subacute lymphocytic thyroiditis occurring within one year of delivery. * **Radioactive Iodine Uptake (RAIU):** In the thyrotoxic phase of painless thyroiditis, RAIU is **low** (distinguishing it from Graves' disease where RAIU is high) [1]. * **Treatment:** Since the thyrotoxicosis is due to "leakage" and not overproduction, antithyroid drugs (PTU/Methimazole) are **not** used; beta-blockers are used for symptomatic relief [1].

Q: A 60-year-old man with small cell carcinoma of the lung presents to the emergency room in a coma after a clonic-tonic seizure. His temperature is 37°C, blood pressure is 100/50 mm Hg, and pulse is 88 per minute. Laboratory studies show a serum sodium of 103 mmol/L, normal serum levels of BUN and creatinine, and a dilute but otherwise normal urine. A CT scan of the head is normal. What is the most likely cause of seizures in this patient?

Syndrome of inappropriate ADH secretion. The patient presents with severe hyponatremia (103 mmol/L) and neurological symptoms (coma, seizures) in the setting of Small Cell Carcinoma of the Lung (SCLC) [1]. This is a classic presentation of Syndrome of Inappropriate Antidiuretic Hormone (SIADH), a common paraneoplastic syndrome associated with SCLC [1]. Why SIADH is correct: In SIADH, ectopic production of ADH leads to excessive water reabsorption in the renal collecting ducts [4]. This results in euvolemic hyponatremia due to water retention and secondary natriuresis [3]. When serum sodium drops rapidly or falls below 120 mmol/L, it causes cerebral edema, leading to headache, confusion, seizures, and coma [2]. The normal BUN and creatinine levels support a non-renal, euvolemic state [3]. Why other options are incorrect: * Central Diabetes Insipidus: This involves a deficiency of ADH, leading to polyuria and hypernatremia, not hyponatremia. * Diabetes Mellitus: While severe hyperglycemia can cause osmotic diuresis or pseudohyponatremia, it would not typically present with a sodium level as low as 103 mmol/L without significant glucose elevation or ketoacidosis. * Renal Metastases: While possible in advanced cancer, they usually cause hematuria or renal failure (elevated BUN/Creatinine) rather than isolated, profound hyponatremia. NEET-PG High-Yield Pearls: * SCLC Associations: SIADH and Lambert-Eaton Myasthenic Syndrome are the most common paraneoplastic syndromes [1]. * Diagnosis of SIADH: Characterized by hyponatremia, low serum osmolality ( 100 mOsm/kg). * Management: For severe symptomatic hyponatremia (seizures/coma), the treatment of choice is Hypertonic Saline (3% NaCl). * Caution: Avoid rapid correction (>8–10 mmol/L in 24 hours) to prevent Osmotic Demyelination Syndrome (Central Pontine Myelinolysis) [5].

Q: Which of the following is NOT a complication arising out of the use of the medical device shown?

Molar ratio of insulin/C-peptide 1)**, not less than 1. - A **molar ratio < 1** suggests **insulinoma** where endogenous insulin and C-peptide are co-secreted in equimolar amounts, which is unrelated to insulin pump complications. *Lipo-hypertrophy* - **Repeated injections** at the same infusion site can cause **subcutaneous fat hypertrophy**, leading to lumpy skin areas. - This is a **common complication** of insulin pump therapy and affects **insulin absorption** at affected sites. *Neuro-glucopenia* - **Hypoglycemia** from insulin pump malfunction or incorrect dosing can cause **neuroglycopenic symptoms** like confusion, seizures, or coma. - This is a **serious complication** requiring immediate glucose administration and pump adjustment. *Pre-breakfast hyperglycemia* - Can result from **Dawn phenomenon** (physiological cortisol rise) or **Somogyi effect** (rebound hyperglycemia after nocturnal hypoglycemia). - **Insulin pump programming** may need adjustment to address these **circadian glucose variations**.

Q: Which of the following is NOT a recommended site for insulin administration?

Dorsum of hands. Explanation: Insulin must be administered into the **subcutaneous fat** layer to ensure predictable absorption and minimize pain [1]. **Why Option A is correct:** The **dorsum of the hands** is an inappropriate site because it lacks sufficient subcutaneous adipose tissue. Injecting here increases the risk of **intramuscular (IM) injection**, which leads to rapid, unpredictable absorption and severe hypoglycemia [1]. Furthermore, the presence of superficial tendons, nerves, and vessels makes it clinically unsafe. Examination of a patient with diabetes should always include checking insulin injection sites [2]. **Why the other options are incorrect:** * **Abdomen (Option D):** This is the preferred site for insulin administration. It offers the most rapid and consistent absorption rate. Patients are advised to inject at least 2 inches away from the umbilicus. * **Arms (Option B):** The posterior surface (triceps area) of the upper arm is a standard site with moderate absorption speed. * **Lateral Thigh (Option C):** The upper-outer aspect of the thigh is used for slower absorption, which can be beneficial for basal insulin. **High-Yield NEET-PG Pearls:** 1. **Absorption Speed:** Abdomen > Arms > Thighs > Buttocks. 2. **Lipohypertrophy:** Repeated injections in the exact same spot cause fatty lumps that delay insulin absorption. **Site rotation** is the most important preventive measure. 3. **Exercise Effect:** Injecting into a limb that is about to be exercised (e.g., thigh before running) increases blood flow and accelerates insulin absorption, risking hypoglycemia. 4. **Angle of Injection:** Usually 90 degrees with short needles (4-6mm); a 45-degree angle or skin fold may be used in very thin individuals to avoid IM injection [1].

Question 1

Migratory necrolytic erythema is seen in which condition?

Accepted Answer

Glucagonoma syndrome

Answer

Peutz-Jeghers syndrome

Answer

Sarcoidosis

Answer

Amyloidosis

Question 2

Conn's syndrome is characterized by diastolic hypertension without edema. Which of the following is a characteristic electrolyte imbalance seen in Conn's syndrome?

Accepted Answer

Hypokalemia

Answer

Hyperkalemia

Answer

Sodium retention

Answer

Hypertension

Question 3

Which of the following clinical features of diabetes insipidus is false?

Accepted Answer

Dehydration

Answer

Daily urine volume is >50 mL/kg body weight

Answer

Urine osmolarity is <300 mosmol/L

Answer

Enuresis

Question 4

A 63-year-old woman with Type 2 diabetes is seen for follow-up after a fasting lipid profile. She has no other medical conditions and feels well. Her diabetes is well controlled and the last hemoglobin A1c value was 6.5%. Her total cholesterol is 240 mg/dL, HDL is 50 mg/dL, low-density lipoprotein is 160 mg/dL, and triglycerides are 150 mg/dL. For this patient with dyslipidemia, what is the most appropriate treatment?

Accepted Answer

HMG-CoA reductase inhibitors

Answer

Fibric acid derivatives

Answer

Nicotinic acid

Answer

Bile acid-binding resins

Question 5

Which type of thyroiditis is also known as "Painless Thyroiditis"?

Accepted Answer

Subacute lymphocytic thyroiditis

Answer

Subacute granulomatous thyroiditis

Answer

Hashimoto's thyroiditis

Answer

Riedel's thyroiditis

Question 6

A 60-year-old man with small cell carcinoma of the lung presents to the emergency room in a coma after a clonic-tonic seizure. His temperature is 37°C, blood pressure is 100/50 mm Hg, and pulse is 88 per minute. Laboratory studies show a serum sodium of 103 mmol/L, normal serum levels of BUN and creatinine, and a dilute but otherwise normal urine. A CT scan of the head is normal. What is the most likely cause of seizures in this patient?

Accepted Answer

Syndrome of inappropriate ADH secretion

Answer

Central diabetes insipidus

Answer

Diabetes mellitus

Answer

Renal metastases

Question 7

A 40-year-old lady presents with weight loss and palpitations, having a heart rate of 110/min, BP 130/70 mmHg, bilateral proptosis, and warm, moist skin. Investigations show undetectable TSH and normal free T4. What is the next best step in diagnosis?

Accepted Answer

Free T3 levels

Answer

Radioactive iodine uptake scan

Answer

Thyroid peroxidase antibody screen

Answer

Thyroid stimulating antibody screen

Question 8

Which of the following is NOT a complication arising out of the use of the medical device shown?

Accepted Answer

Molar ratio of insulin/C-peptide < 1

Answer

Lipo-hypertrophy

Answer

Neuro-glucopenia

Answer

Pre-breakfast hyperglycemia

Question 9

Which of the following is NOT a recommended site for insulin administration?

Accepted Answer

Dorsum of hands

Answer

Arms

Answer

Lateral aspect of thigh

Answer

Abdomen around the umbilicus

Question 10

A 50-year-old man has had a nonhealing ulcer on the bottom of his foot for 2 months. On examination, the 2-cm ulcer overlies the right first metatarsal head. There is reduced sensation to pinprick in his feet, and his visual acuity is reduced bilaterally. His serum creatinine is 2.9 mg/dL. Which of the following laboratory test findings is he most likely to have?

Accepted Answer

Glucosuria

Answer

Hypoalbuminemia

Answer

Hypokalemia

Answer

Leukopenia

Endocrinology — MCQs

Endocrinology — MCQs

On this page

Practice by Chapter

Want unlimited practice?