Adrenal Incidentalomas — MCQs
VMA is elevated in which of the following condition?
In a patient diagnosed with pheochromocytoma, what is the appropriate preoperative pharmacological management to control hypertension before surgery?
What is the correct sequence of medication administration for pre-operative prophylaxis in pheochromocytoma?
What is the most common adrenal incidentaloma?
Investigation of choice in pheochromocytoma is:
Where is a bruit typically heard in the thyroid gland?
Thyroxine is used in the treatment of which thyroid cancer?
During bilateral adrenalectomy, what is the appropriate timing for intra-operative hydrocortisone administration?
A 32-year-old male presents with a painless cervical lymph node. Lymph node biopsy reveals normal thyroid gland features, and the thyroid is clinically normal on palpation. What is the most likely diagnosis?
Which of the following statements is FALSE regarding medullary cancer of the thyroid?
Adrenal Incidentalomas Indian Medical PG Practice Questions and MCQs
Question 1: VMA is elevated in which of the following condition?
- A. Tuberous sclerosis
- B. Addison disease
- C. Pheochromocytoma (Correct Answer)
- D. Conn Syndrome
Explanation: Pheochromocytoma - Pheochromocytoma is a tumor of the adrenal medulla that secretes excessive amounts of catecholamines (epinephrine and norepinephrine). - Vanillylmandelic acid (VMA) is a breakdown product of these catecholamines [1], so its levels are elevated in the urine of patients with pheochromocytoma. Tuberous sclerosis - Tuberous sclerosis is a genetic disorder characterized by the growth of numerous non-cancerous tumors in various organs. - While it can be associated with renal angiomyolipomas or brain lesions, it does not directly cause elevated VMA levels. Addison disease - Addison disease is characterized by adrenal insufficiency [2], meaning the adrenal glands produce insufficient amounts of hormones like cortisol and aldosterone. - This condition is not associated with the overproduction of catecholamines or elevated VMA. Conn Syndrome - Conn syndrome (primary hyperaldosteronism) is due to an overproduction of aldosterone by the adrenal glands, often caused by an adrenal adenoma [3]. - Aldosterone is a mineralocorticoid, and its overproduction does not lead to increased catecholamine metabolism or elevated VMA levels.
Question 2: In a patient diagnosed with pheochromocytoma, what is the appropriate preoperative pharmacological management to control hypertension before surgery?
- A. Phenoxybenzamine and propranolol (Correct Answer)
- B. Propranolol
- C. Nitroglycerine
- D. Phentolamine
Explanation: ***Phenoxybenzamine and propranolol*** - **Phenoxybenzamine** (an **irreversible** non-selective **alpha-blocker**) is initiated first to prevent hypertensive crises during surgery by blocking the effects of catecholamines on blood vessels. - **Propranolol** (a **beta-blocker**) is added after adequate alpha-blockade to control **tachycardia** and arrhythmias, as blocking only alpha-receptors can lead to unopposed beta-adrenergic stimulation. *Phentolamine (short-acting alpha blocker)* - While **phentolamine** is an alpha-blocker, it is typically used for **intraoperative management** of hypertensive crises or for short-term control, not as the primary preoperative preparation. - It is a **reversible** blocker and does not provide the sustained, robust alpha-blockade required for safe preoperative management of pheochromocytoma. *Propranolol (beta-blocker)* - **Beta-blockers** alone should **never be started first** in pheochromocytoma because blocking beta-2 receptors (which mediate vasodilation) in the presence of high circulating catecholamines can lead to **unopposed alpha-adrenergic vasoconstriction**, causing a dangerous hypertensive crisis. - It is only added after adequate alpha-blockade has been achieved to manage **tachycardia**. *Nitroglycerine (vasodilator)* - **Nitroglycerine** is primarily a **venodilator** and is used to relieve angina or manage acute hypertensive emergencies, not for the chronic preoperative management of pheochromocytoma. - It does not address the underlying pathophysiology of excessive catecholamine release and can lead to reflex **tachycardia**.
Question 3: What is the correct sequence of medication administration for pre-operative prophylaxis in pheochromocytoma?
- A. Beta blockade followed by alpha blockade
- B. Simultaneous alpha and beta blockade
- C. Alpha blockade followed by beta blockade (Correct Answer)
- D. Alpha blockade only
Explanation: ***Alpha blockade followed by beta blockade*** - **Alpha blockade** should always be initiated first to control **hypertension** and prevent a **hypertensive crisis** during surgery. This is critical because pheochromocytoma causes excessive catecholamine release, leading to profound vasoconstriction. - **Beta blockade** is then added only after adequate alpha blockade has been achieved to control **tachycardia** and arrhythmias, preventing **unopposed alpha-adrenergic stimulation** which could paradoxically worsen hypertension. *Simultaneous alpha and beta blockade* - Administering both simultaneously is dangerous because **beta blockade** can mask the effects of inadequate alpha blockade. - This can lead to **unopposed alpha-adrenergic stimulation** after beta blockade, causing severe **vasoconstriction** and hypertensive crisis. *Beta blockade followed by alpha blockade* - Initiating with **beta blockade** without prior **alpha blockade** is absolutely contraindicated in pheochromocytoma. - This can lead to severe and potentially fatal **hypertension** due to **unopposed alpha-adrenergic stimulation** as beta blockade prevents vasodilation. *Alpha blockade only* - While essential for initial management, **alpha blockade alone** might not fully control all symptoms, especially **tachycardia** and **arrhythmias** caused by high circulating catecholamine levels. - Adding a **beta blocker** after achieving adequate alpha blockade helps in controlling these cardiac effects, optimizing patient preparation for surgery.
Question 4: What is the most common adrenal incidentaloma?
- A. Aldosterone producing
- B. Pheochromocytoma
- C. Endocrine inactive tumors (Correct Answer)
- D. Cortisol producing
Explanation: ***Endocrine inactive tumors*** - The majority, about **70-85%**, of adrenal incidentalomas are **benign, non-secretory adenomas**, which are often referred to as endocrine inactive tumors. [1] - These tumors do not produce excess hormones and are typically discovered incidentally on imaging performed for other reasons. *Cortisol producing* - While **cortisol-producing adenomas** are a type of functional adrenal tumor, they represent a smaller percentage of incidentalomas, usually less than 10%. - These can lead to **Cushing's syndrome**, but most incidentalomas causing hypercortisolism are subclinical. *Aldosterone producing* - **Aldosterone-producing adenomas**, which cause primary aldosteronism, are also less common than inactive tumors, accounting for about 1-5% of incidentalomas. [1] - They are typically associated with **hypertension** and **hypokalemia**. *Pheochromocytoma* - **Pheochromocytomas**, which secrete catecholamines, are rare adrenal incidentalomas, making up less than 5% of cases. - These tumors can cause **hypertension**, **tachycardia**, and other symptoms related to catecholamine excess. [1]
Question 5: Investigation of choice in pheochromocytoma is:
- A. CT scan
- B. Urinary catecholamines (Correct Answer)
- C. MIBG scan
- D. MRI Scan
Explanation: ***Urinary catecholamines*** - Measurement of **24-hour urinary fractionated metanephrines and catecholamines** is the initial **biochemical test of choice**. - These biochemical tests are preferred over plasma levels due to the **episodic release** of hormones from a pheochromocytoma, which can lead to high false-negative rates in single plasma measurements. *CT scan* - While a **CT scan** is a crucial **imaging modality** for localizing a pheochromocytoma once the biochemical diagnosis is established [1], it is not the *initial* diagnostic investigation. - Imaging should be performed only after **biochemical confirmation** to avoid unnecessary investigations of incidental adrenal masses [1]. *MIBG scan* - An **MIBG scan** (metaiodobenzylguanidine scan) is a **functional imaging study** used primarily for **localizing metastatic pheochromocytomas** [1] or for cases where CT/MRI is equivocal. - It is not the initial investigation but rather a **secondary imaging test** [1]. *MRI Scan* - **MRI** is an alternative **imaging modality** to CT for localizing pheochromocytomas [1], especially in pregnant women or when radiation exposure is a concern. - Like CT, it serves as a **localization tool** after biochemical confirmation, not the diagnostic test itself.
Question 6: Where is a bruit typically heard in the thyroid gland?
- A. Upper pole (Correct Answer)
- B. Lower pole
- C. Middle part
- D. Lateral aspect
Explanation: **Explanation:** The presence of a thyroid bruit is a classic clinical sign of **Graves' disease** (toxic diffuse goiter). It occurs due to the hyperdynamic circulation and significantly increased vascularity of the gland. **Why the Upper Pole is Correct:** The bruit is most commonly heard over the **upper pole** of the thyroid gland. This is because the **superior thyroid artery**, a direct branch of the external carotid artery, enters the gland at the upper pole. Due to its proximity to a major high-pressure arterial trunk and its relatively superficial location, the turbulent blood flow (hypervascularity) is most audible at this site. **Analysis of Incorrect Options:** * **Lower Pole:** While the inferior thyroid artery (from the thyrocervical trunk) supplies the lower pole, it is situated deeper and has a more tortuous course, making a bruit less likely to be localized here compared to the superior pole. * **Middle Part & Lateral Aspect:** These areas represent the body of the lobes. While vascularity is increased throughout in Graves' disease, the primary inflow points (the poles) are the high-yield areas for auscultation. **High-Yield Clinical Pearls for NEET-PG:** 1. **Bruit vs. Thrill:** A bruit is an auditory sign (auscultation), whereas a **thrill** is its tactile equivalent (palpation). Both indicate Graves' disease. 2. **Differential Diagnosis:** A thyroid bruit must be distinguished from a **venous hum** (disappears with pressure over the internal jugular vein) and a **carotid bruit** (heard lateral to the gland). 3. **Significance:** The presence of a bruit is highly specific for Graves' disease and helps differentiate it from other causes of thyrotoxicosis, such as toxic multinodular goiter or thyroiditis.
Question 7: Thyroxine is used in the treatment of which thyroid cancer?
- A. Medullary
- B. Radiation induced
- C. Anaplastic
- D. Papillary (Correct Answer)
Explanation: **Explanation:** The correct answer is **Papillary Thyroid Carcinoma (PTC)**. **Why Papillary is Correct:** Papillary and Follicular thyroid cancers are **Differentiated Thyroid Cancers (DTC)**. These tumor cells retain receptors for **Thyroid Stimulating Hormone (TSH)**. TSH acts as a growth factor for these cells; elevated levels can promote tumor recurrence or progression. By administering exogenous **Thyroxine (L-Thyroxine)** in supra-physiological doses, we initiate a negative feedback loop that suppresses pituitary TSH secretion. This "TSH Suppression Therapy" deprives the residual cancer cells of their growth stimulus, thereby reducing recurrence rates and improving survival. **Why other options are incorrect:** * **Medullary Thyroid Cancer (MTC):** Arises from parafollicular C-cells (which produce calcitonin), not follicular cells. These cells do not have TSH receptors; therefore, TSH suppression with thyroxine has no therapeutic effect on the tumor itself. * **Anaplastic Thyroid Cancer:** This is an undifferentiated, highly aggressive tumor. The cells have lost all functional characteristics of normal thyroid tissue, including TSH receptors, making thyroxine therapy ineffective. * **Radiation-induced:** While radiation is a major risk factor for Papillary carcinoma, the term describes the etiology rather than the pathological type. The treatment depends on the resulting histology (usually Papillary). **High-Yield Clinical Pearls for NEET-PG:** * **Target TSH levels:** For high-risk DTC patients, the target TSH is usually **<0.1 mU/L**. For low-risk patients, it is **0.1–0.5 mU/L**. * **Side Effects:** Long-term TSH suppression can lead to **osteoporosis** (especially in post-menopausal women) and **atrial fibrillation**. * **Follow-up:** Serum **Thyroglobulin (Tg)** is used as a tumor marker for DTC follow-up after total thyroidectomy.
Question 8: During bilateral adrenalectomy, what is the appropriate timing for intra-operative hydrocortisone administration?
- A. After opening the abdomen
- B. After ligation of the left adrenal vein
- C. After ligation of the right adrenal vein
- D. After excision of both adrenal glands (Correct Answer)
Explanation: **Explanation:** The primary goal of perioperative steroid management in bilateral adrenalectomy is to prevent **acute adrenal crisis** while ensuring the body has sufficient glucocorticoids to handle surgical stress. **Why Option D is Correct:** During a bilateral adrenalectomy, the body can still produce endogenous cortisol as long as one gland (or a portion of it) remains vascularized and functional. The critical point of "surgical Addisonian state" occurs only after **both** glands have been completely devascularized or removed. Therefore, the full replacement dose of intra-operative hydrocortisone (typically 100mg IV) is administered immediately **after the excision of both adrenal glands**. This timing ensures a seamless transition from endogenous production to exogenous replacement. **Why Other Options are Incorrect:** * **Option A:** Administering steroids upon opening the abdomen is premature, as the patient’s own glands are still functioning and responding to the stress of surgery. * **Options B & C:** Ligation of only one adrenal vein (left or right) leaves the contralateral gland intact. The remaining gland is capable of maintaining physiological cortisol levels under the stimulus of ACTH; thus, replacement is not yet mandatory. **High-Yield Clinical Pearls for NEET-PG:** * **Steroid Cover:** Patients undergoing bilateral adrenalectomy require lifelong glucocorticoid and mineralocorticoid replacement. * **Post-Op Regimen:** After the initial intra-operative bolus, hydrocortisone is typically continued at 100mg every 8 hours for the first 24 hours, then tapered. * **Nelson’s Syndrome:** Watch for this post-bilateral adrenalectomy complication, characterized by a pituitary adenoma enlarging due to loss of cortisol feedback, leading to hyperpigmentation and high ACTH levels. * **Conn’s vs. Cushing’s:** In unilateral adrenalectomy for Conn’s syndrome, post-op steroids are usually not needed, whereas, in Cushing’s, they are vital due to contralateral gland suppression.
Question 9: A 32-year-old male presents with a painless cervical lymph node. Lymph node biopsy reveals normal thyroid gland features, and the thyroid is clinically normal on palpation. What is the most likely diagnosis?
- A. Lateral aberrant thyroid
- B. Papillary carcinoma thyroid (Correct Answer)
- C. Follicular carcinoma thyroid with metastatic lymph nodes
- D. Anaplastic carcinoma
Explanation: **Explanation:** The clinical presentation of a cervical lymph node containing normal-looking thyroid tissue, even when the thyroid gland itself feels normal, is a classic "red flag" for **Papillary Carcinoma of the Thyroid (PTC)**. **1. Why Papillary Carcinoma is Correct:** The concept of "Lateral Aberrant Thyroid" is now considered a misnomer. In modern surgery, any thyroid tissue found in a cervical lymph node is considered a **metastatic deposit** from an occult (hidden) papillary carcinoma until proven otherwise. PTC is highly lymphophilic; it frequently spreads to regional lymph nodes (Level II-V) while the primary tumor remains small and non-palpable (occult). Histologically, these metastases can sometimes appear surprisingly well-differentiated, mimicking normal thyroid tissue. **2. Why other options are incorrect:** * **Lateral Aberrant Thyroid:** This was an older theory suggesting that thyroid tissue could embryologically develop in the lateral neck. This theory is now obsolete; such findings are almost always metastatic PTC. * **Follicular Carcinoma:** This variant typically spreads via the **hematogenous route** (bloodstream) to bones and lungs, rather than through the lymphatic system. Lymph node involvement is rare in follicular carcinoma. * **Anaplastic Carcinoma:** This is an extremely aggressive tumor usually seen in elderly patients (60+ years). It presents as a rapidly enlarging, painful, and hard neck mass, not a painless "normal-looking" node in a 32-year-old. **Clinical Pearls for NEET-PG:** * **Psammoma bodies:** Characteristic laminated calcifications often seen in PTC. * **Orphan Annie Eye nuclei:** The pathognomonic nuclear feature of PTC. * **Investigation of Choice:** Ultrasound-guided Fine Needle Aspiration Cytology (FNAC) of both the node and the thyroid gland. * **Treatment:** Total thyroidectomy with therapeutic neck dissection.
Question 10: Which of the following statements is FALSE regarding medullary cancer of the thyroid?
- A. Secrete Calcitonin
- B. 20-25% are familial
- C. Diarrhea is seen in 30%
- D. These cancers take up Radioactive Iodine (Correct Answer)
Explanation: ### Explanation **Medullary Thyroid Carcinoma (MTC)** arises from the **parafollicular C-cells**, which are neuroendocrine cells derived from the neural crest. This fundamental embryological origin is the key to understanding its clinical behavior and management. **Why Option D is the Correct (False) Statement:** Radioactive Iodine (RAI) uptake depends on the expression of the Sodium-Iodide Symporter (NIS), which is exclusive to follicular epithelial cells. Since MTC originates from C-cells (not follicular cells), these tumors **do not take up radioactive iodine**. Consequently, RAI ablation is not a therapeutic option for MTC, unlike papillary or follicular thyroid cancers. **Analysis of Other Options:** * **Option A (True):** C-cells naturally produce **Calcitonin**. Elevated serum calcitonin is a highly sensitive and specific tumor marker for MTC, used for both diagnosis and monitoring recurrence. * **Option B (True):** Approximately **20–25%** of MTC cases are familial, occurring as part of **MEN 2A, MEN 2B**, or Familial MTC (FMTC) syndromes, usually due to germline **RET proto-oncogene** mutations. The remaining 75–80% are sporadic. * **Option C (True):** Diarrhea occurs in about **30%** of patients, particularly in advanced or metastatic disease. It is caused by the hypersecretion of calcitonin, prostaglandins, or serotonin, which increases intestinal motility. **High-Yield Clinical Pearls for NEET-PG:** * **Amyloid Stroma:** Histologically, MTC is characterized by nests of cells separated by amyloid deposits (stained by Congo Red). * **CEA:** Carcinoembryonic Antigen is another important tumor marker for MTC. * **Screening:** All patients diagnosed with MTC must be screened for **RET mutations** and **Pheochromocytoma** (before surgery) to rule out MEN 2. * **Treatment:** The primary treatment is Total Thyroidectomy with central compartment neck dissection.
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