Endocrinology Practice Questions

Q: Which diagnostic procedure is not typically performed in cases of pheochromocytoma?

Fine Needle Aspiration Cytology (FNAC). **Explanation:** The correct answer is **C. Fine Needle Aspiration Cytology (FNAC)**. In cases of suspected pheochromocytoma, FNAC is strictly **contraindicated**. This is because the mechanical trauma of the needle can trigger a massive, uncontrolled release of catecholamines from the tumor. This "catecholamine storm" can lead to a life-threatening hypertensive crisis, cardiac arrhythmias, or hemorrhage within the tumor. Diagnosis is primarily biochemical (metanephrines) followed by imaging; biopsy is never required for diagnosis and is dangerous. **Why other options are incorrect:** * **A. CT Scan:** This is the initial imaging modality of choice for localizing the tumor due to its excellent spatial resolution. Pheochromocytomas typically appear as hypervascular masses with high attenuation (>10 HU) on non-contrast CT. * **B. MRI:** Highly sensitive for detecting pheochromocytomas. On T2-weighted images, these tumors often exhibit a characteristic "light bulb" appearance (hyperintensity). MRI is preferred in children, pregnant women, or patients with contrast allergies. * **D. MIBG Scan:** Metaiodobenzylguanidine (MIBG) is a functional imaging study used to detect extra-adrenal (paragangliomas) or metastatic disease that may be missed by CT/MRI. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 10s:** 10% are bilateral, 10% are malignant, 10% are extra-adrenal, and 10% are familial. * **Biochemical Screening:** 24-hour urinary fractionated metanephrines or plasma free metanephrines are the first-line tests. * **Pre-operative Management:** Always start **Alpha-blockers first** (e.g., Phenoxybenzamine) followed by Beta-blockers to avoid an unopposed alpha-mediated hypertensive crisis.

Q: A 40-year-old man presents with nausea, vomiting, diarrhea, and cramping abdominal pain. His temperature is 38°C, blood pressure is 90/60 mm Hg, and pulse rate is 90/minute. Physical examination reveals dehydration with sunken eyeballs, dry tongue, and poor skin turgor. Hyperpigmentation is noted in the palmar creases and the gingival margins. Laboratory results include fasting serum glucose of 62 mg/dL, BUN of 27 mg/dL, Na of 122 mEq/L, and K of 6.5 mEq/L. What is the most likely cause of this patient's symptoms?

Autoimmunity. **Explanation:** The clinical presentation of hypotension, dehydration, hypoglycemia, hyponatremia, and hyperkalemia, combined with hyperpigmentation, is classic for **Primary Adrenal Insufficiency (Addison’s Disease)** [2]. The patient is currently in an **Addisonian Crisis**, likely precipitated by an acute stressor [1]. 1. **Why Autoimmunity is Correct:** In developed countries and increasingly in urban India, **Autoimmune Adrenalitis** (either isolated or as part of Polyglandular Autoimmune Syndromes) is the **most common cause** of primary adrenal insufficiency (responsible for ~80% of cases) [3]. It involves the destruction of the adrenal cortex, leading to a deficiency of cortisol (causing hypoglycemia and hypotension) and aldosterone (causing hyponatremia and hyperkalemia). The hyperpigmentation occurs because low cortisol triggers a compensatory increase in ACTH; the precursor molecule (POMC) also produces Melanocyte-Stimulating Hormone (MSH). 2. **Why Incorrect Options are Wrong:** * **Amyloidosis and Sarcoidosis:** These are infiltrative diseases that can involve the adrenal glands, but they are rare causes of clinical adrenal insufficiency compared to autoimmunity. * **Metastatic Cancer:** While cancers (especially lung and breast) frequently metastasize to the adrenals, they rarely destroy >90% of the gland required to cause symptomatic insufficiency [3]. **NEET-PG High-Yield Pearls:** * **Most common cause worldwide:** Autoimmunity (formerly Tuberculosis). * **Most common cause in developing countries/India:** Tuberculosis (look for adrenal calcification on CT) [3]. * **Electrolyte Hallmark:** Hyponatremia + Hyperkalemia + Metabolic Acidosis (Non-gap). * **Diagnosis:** Best initial test is the **ACTH Stimulation Test** (Cosyntropin test) [1]. * **Management of Crisis:** Immediate IV fluids (Normal Saline) and high-dose **IV Hydrocortisone**. Do not wait for lab confirmation [1].

Q: A 59-year-old man with type 2 diabetes presents for a screening eye examination. The ophthalmologist reports the development of non-proliferative retinopathy. For this patient with a complication of diabetes, select the most likely findings.

Microaneurysms and hemorrhage (dot and blot). **Explanation:** Diabetic Retinopathy (DR) is a leading cause of blindness and is categorized into Non-Proliferative (NPDR) and Proliferative (PDR) stages. **Why Option A is Correct:** The earliest clinical sign of NPDR is the formation of **microaneurysms**, which appear as small red dots due to capillary wall outpouching [1]. As these capillaries leak or rupture within the deeper layers of the retina (inner nuclear and outer plexiform layers), they create **"dot and blot" hemorrhages**. Other features of NPDR include hard exudates (lipid leaks) and cotton wool spots (nerve fiber layer infarcts). **Analysis of Incorrect Options:** * **B. Vitreous hemorrhage:** This is a hallmark of **Proliferative Diabetic Retinopathy (PDR)** [1]. It occurs when fragile new vessels (neovascularization) bleed into the vitreous cavity [1]. * **C. Dilated veins:** While venous "beading" or loops can occur in severe NPDR, simple dilated veins are more characteristic of Central Retinal Vein Occlusion (CRVO) or early hypertensive changes rather than the primary screening finding for NPDR. * **D. Open-angle glaucoma:** While diabetics have a higher risk of glaucoma, it is a separate pathological entity and not a diagnostic feature of non-proliferative retinopathy. **High-Yield NEET-PG Pearls:** * **Earliest Sign:** Microaneurysms (seen on Fundus Fluorescein Angiography) [1]. * **NPDR vs. PDR:** The defining feature of PDR is **Neovascularization** (NVD/NVE) driven by VEGF [1]. * **Macular Edema:** Can occur at *any* stage of DR and is the most common cause of vision loss in NPDR [1]. * **Screening:** Type 2 DM patients need a fundus exam **at the time of diagnosis**, whereas Type 1 DM patients should be screened **5 years after diagnosis**.

Q: A 20-year-old girl presents with a 9-month history of neck swelling and thyrotoxicosis symptoms. Investigations revealed increased T4 and decreased TSH with a palpable 2 cm nodule. What is the next investigation?

Thyroid scan. The patient presents with clinical and biochemical evidence of **hyperthyroidism** (↑T4, ↓TSH) associated with a **palpable thyroid nodule**. In the management of a thyroid nodule, the first step is always checking the serum TSH [1]. **1. Why Thyroid Scan is the correct answer:** When TSH is suppressed (low), the priority is to determine if the nodule is "functioning" (autonomously producing hormone) [1]. A **Thyroid Scan (Radionuclide Scanning)** using Technetium-99m or Iodine-123 is the gold standard for this [1][2]. * If the nodule is **"Hot"** (increased uptake), it confirms a Toxic Adenoma. Hot nodules are almost never malignant, so Fine Needle Aspiration (FNA) is not required [1]. * If the nodule is **"Cold"** (no uptake), the risk of malignancy is higher, and the next step would be USG-guided FNA [1]. **2. Why other options are incorrect:** * **A. Ultrasound (USG):** While USG is the first-line imaging for a *euthyroid* nodule, in a *hyperthyroid* patient, the functional status (Scan) takes precedence to avoid unnecessary biopsies of hot nodules [1]. * **C. Radioactive Iodine Uptake (RAIU):** This measures the percentage of iodine trapped by the *entire* gland to differentiate causes of thyrotoxicosis (e.g., Graves' vs. Thyroiditis) [2]. It does not provide the anatomical localization needed to evaluate a specific nodule. * **D. CT Scan:** CT is not used for the initial evaluation of thyroid function or nodules and can interfere with future radioiodine therapy due to iodinated contrast [3]. ### Clinical Pearls for NEET-PG * **Algorithm:** Low TSH → Thyroid Scan; Normal/High TSH → USG followed by FNA (based on TIRADS) [1]. * **Toxic Adenoma (Plummer Disease):** Usually presents as a single "Hot" nodule with suppression of the rest of the gland. * **Rule of Thumb:** "Hot" nodules are safe (benign); "Cold" nodules need biopsy [1].

Q: Which of the following symptoms is NOT typically seen in hyponatremia?

Delusion. Hyponatremia (Serum Sodium <135 mEq/L) primarily manifests through gastrointestinal and neurological symptoms due to cerebral edema and increased intracranial pressure [1]. **Explanation of the Correct Answer:** **B. Delusion** is the correct answer because it is a fixed, false belief typically associated with primary psychiatric disorders (like schizophrenia) or chronic organic brain syndromes. While hyponatremia causes significant neurological impairment, it presents as **Delirium** (acute encephalopathy, confusion, or altered sensorium) rather than structured delusions. In severe cases, patients progress from lethargy and disorientation to seizures and coma, but not typically to isolated delusional thinking. **Explanation of Incorrect Options:** * **A & C. Nausea and Vomiting:** These are among the earliest and most common symptoms of hyponatremia [1]. They occur due to cerebral edema affecting the postrema (chemoreceptor trigger zone) and increased intracranial pressure. * **D. Anorexia:** Loss of appetite is a classic non-specific early symptom of electrolyte imbalance, particularly hyponatremia, often preceding more severe neurological decline. **High-Yield Clinical Pearls for NEET-PG:** 1. **Symptom Severity:** Symptoms depend more on the **rate of fall** of sodium rather than the absolute value. 2. **Neurological Spectrum:** Mild (130–135 mEq/L): Asymptomatic; Moderate (125–129 mEq/L): Nausea, headache, confusion; Severe ( 10–12 mEq/L in 24 hours) can lead to Central Pontine Myelinolysis [2]. Remember: *"From Low to High, your Pons will die."* 4. **SIADH:** A common cause of euvolemic hyponatremia; look for low serum osmolality with inappropriately high urine osmolality (>100 mOsm/kg) [1].

Q: Which drug is used in the management of severe hypercalcemia?

All of the above. **Explanation:** The management of severe hypercalcemia (typically defined as Serum Calcium >14 mg/dL) requires a multi-pronged approach aimed at increasing urinary excretion, inhibiting bone resorption, and addressing the underlying cause. **Why "All of the above" is correct:** 1. **Pamidronate (Bisphosphonates):** These are the **mainstay of treatment** for severe hypercalcemia, especially when malignancy-associated. They work by inhibiting osteoclast-mediated bone resorption. While they are highly effective, they have a delayed onset of action (24–72 hours). 2. **Furosemide (Loop Diuretics):** Once the patient is adequately rehydrated with IV Normal Saline, loop diuretics are used to promote "calciuresis" (urinary calcium excretion) by inhibiting the Na-K-2Cl symporter in the thick ascending limb of the Loop of Henle. *Note: Thiazides are contraindicated as they increase calcium reabsorption.* 3. **Prednisolone (Glucocorticoids):** These are specifically effective in hypercalcemia caused by Vitamin D toxicity, sarcoidosis, or lymphomas. They act by decreasing intestinal calcium absorption and inhibiting 1-alpha-hydroxylase activity. **Clinical Pearls for NEET-PG:** * **Immediate First Step:** The most crucial initial step in managing severe hypercalcemia is **aggressive IV hydration with 0.9% Normal Saline** to restore volume and enhance calcium excretion. * **Calcitonin:** Used for rapid reduction of calcium (works within hours) but is limited by **tachyphylaxis** (effect wears off after 48 hours). * **Cinacalcet:** A calcimimetic used specifically in secondary hyperparathyroidism (CKD) or parathyroid carcinoma. * **Denosumab:** A RANKL inhibitor used in refractory hypercalcemia of malignancy. * **Hemodialysis:** The treatment of choice for patients with severe hypercalcemia and concomitant heart failure or renal failure who cannot tolerate aggressive hydration.

Q: Syndrome X is not found in which of the following?

Weight loss. Explanation: **Syndrome X**, now more commonly known as **Metabolic Syndrome** (or Insulin Resistance Syndrome), is a cluster of metabolic abnormalities that significantly increase the risk of cardiovascular disease and Type II Diabetes Mellitus. [1] **Why Weight Loss is the Correct Answer:** The hallmark of Metabolic Syndrome is **central (android) obesity** and insulin resistance. [1] Weight loss is actually a therapeutic goal and a protective factor, whereas **weight gain** (specifically an increased waist circumference) is a core diagnostic criterion. Therefore, weight loss is not a component of the syndrome. **Analysis of Incorrect Options:** * **Diabetes Mellitus Type II (Option A):** Insulin resistance is the pathophysiological backbone of Syndrome X. This leads to impaired glucose tolerance and eventually overt Type II Diabetes. [1] * **Dyslipidemia (Option B):** This is a broad term covering the lipid abnormalities found in the syndrome, characterized by a pro-atherogenic profile. * **High Triglycerides (Option C):** This is a specific diagnostic criterion (≥150 mg/dL). It is typically accompanied by **Low HDL** levels. **NEET-PG High-Yield Pearls:** To diagnose Metabolic Syndrome (per NCEP ATP III criteria), 3 out of the following 5 must be present: 1. **Waist Circumference:** >102 cm (M) or >88 cm (W). *Note: For Indians (Modified), it is >90 cm (M) and >80 cm (W).* 2. **Triglycerides:** ≥150 mg/dL. 3. **HDL Cholesterol:** <40 mg/dL (M) or <50 mg/dL (W). 4. **Blood Pressure:** ≥130/85 mmHg. 5. **Fasting Glucose:** ≥100 mg/dL. *Distinction:* Do not confuse "Syndrome X" (Metabolic) with **"Cardiac Syndrome X"** (Microvascular angina with normal epicardial coronaries).

Question 1

Which diagnostic procedure is not typically performed in cases of pheochromocytoma?

Accepted Answer

Fine Needle Aspiration Cytology (FNAC)

Answer

CT scan

Answer

MRI

Answer

MIBG scan

Question 2

Which of the following statements regarding obesity syndromes are true or false?

Accepted Answer

Prader-Willi syndrome has normal stature with truncal obesity; Laurence-Moon-Biedl is autosomal with polydactyly; Ahlstrom's syndrome patients have moderate mental retardation; Cohen's syndrome patients have craniofacial anomalies and delayed puberty; Carpenter's syndrome have secondary hypogonadism are all true, except Prader-Willi syndrome and Ahlstrom's syndrome are false.

Answer

Prader-Willi syndrome has normal stature with truncal obesity; Laurence-Moon-Biedl is autosomal with polydactyly; Ahlstrom's syndrome patients have moderate mental retardation; Cohen's syndrome patients have craniofacial anomalies and delayed puberty; Carpenter's syndrome have secondary hypogonadism are all true, except Laurence-Moon-Biedl is false.

Answer

Prader-Willi syndrome has normal stature with truncal obesity; Laurence-Moon-Biedl is autosomal with polydactyly; Ahlstrom's syndrome patients have moderate mental retardation; Cohen's syndrome patients have craniofacial anomalies and delayed puberty; Carpenter's syndrome have secondary hypogonadism are all true, except Prader-Willi syndrome is false.

Answer

Prader-Willi syndrome has normal stature with truncal obesity; Laurence-Moon-Biedl is autosomal with polydactyly; Ahlstrom's syndrome patients have moderate mental retardation; Cohen's syndrome patients have craniofacial anomalies and delayed puberty; Carpenter's syndrome have secondary hypogonadism are all true, except Prader-Willi syndrome and Carpenter's syndrome are false.

Question 3

A 40-year-old man presents with nausea, vomiting, diarrhea, and cramping abdominal pain. His temperature is 38°C, blood pressure is 90/60 mm Hg, and pulse rate is 90/minute. Physical examination reveals dehydration with sunken eyeballs, dry tongue, and poor skin turgor. Hyperpigmentation is noted in the palmar creases and the gingival margins. Laboratory results include fasting serum glucose of 62 mg/dL, BUN of 27 mg/dL, Na of 122 mEq/L, and K of 6.5 mEq/L. What is the most likely cause of this patient's symptoms?

Accepted Answer

Autoimmunity

Answer

Amyloidosis

Answer

Metastatic cancer

Answer

Sarcoidosis

Question 4

A 59-year-old man with type 2 diabetes presents for a screening eye examination. The ophthalmologist reports the development of non-proliferative retinopathy. For this patient with a complication of diabetes, select the most likely findings.

Accepted Answer

Microaneurysms and hemorrhage (dot and blot)

Answer

Vitreous hemorrhage

Answer

Dilated veins

Answer

Open-angle glaucoma

Question 5

A 20-year-old girl presents with a 9-month history of neck swelling and thyrotoxicosis symptoms. Investigations revealed increased T4 and decreased TSH with a palpable 2 cm nodule. What is the next investigation?

Accepted Answer

Thyroid scan

Answer

Ultrasound (USG) of the thyroid

Answer

Radioactive iodine uptake

Answer

CT scan

Question 6

Which of the following statements about Cushing's disease is true?

Accepted Answer

A pituitary microadenoma usually is present

Answer

Serum adrenocorticotropic hormone (ACTH) levels usually are high

Answer

There is a low incidence of nonendocrine tumors

Answer

Suppression of cortisol production by the high-dose dexamethasone suppression test is a characteristic finding

Question 7

A patient presents with bilateral proptosis, heat intolerance, and palpitations. Which of the following is the most unlikely diagnosis?

Accepted Answer

Riedel's thyroiditis

Answer

Hashimoto's thyroiditis

Answer

Thyroid adenoma

Answer

Diffuse thyroid goiter

Question 8

Which of the following symptoms is NOT typically seen in hyponatremia?

Accepted Answer

Delusion

Answer

Nausea

Answer

Vomiting

Answer

Anorexia

Question 9

Which drug is used in the management of severe hypercalcemia?

Accepted Answer

All of the above

Answer

Furosemide

Answer

Prednisolone

Answer

Pamidronate

Question 10

Syndrome X is not found in which of the following?

Accepted Answer

Weight loss

Answer

Diabetes Mellitus Type II

Answer

Dyslipidemia

Answer

High triglycerides

Endocrinology — MCQs

Endocrinology — MCQs

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