Endocrinology & Diabetes — MCQs

Endocrinology & Diabetes UK Medical PG Practice Questions and MCQs

Question 31: A 58-year-old woman presents with bone pain and fatigue. Blood tests show calcium 3.1 mmol/L, albumin 35 g/L, and creatinine 180 μmol/L. She has a history of breast cancer treated 5 years ago. What is the most likely cause of hypercalcemia?

A. Primary hyperparathyroidism
B. Malignancy (Correct Answer)
C. Sarcoidosis
D. Vitamin D toxicity
E. Milk-alkali syndrome

Explanation: ***Malignancy***- The history of **breast cancer**, which commonly metastasizes to bone, along with severe hypercalcemia (3.1 mmol/L) and **bone pain**, strongly points to malignancy-associated hypercalcemia.- **Hypercalcemia of malignancy** can occur due to **osseous metastases** or the secretion of **Parathyroid hormone-related peptide (PTHrP)**, leading to increased bone resorption and renal calcium reabsorption, and can cause **acute kidney injury** (creatinine 180 μmol/L).*Primary hyperparathyroidism*- This is typically associated with **milder, chronic hypercalcemia** and often a normal or only slightly elevated creatinine, not the severe hypercalcemia and significant renal dysfunction seen here.- While a common cause of hypercalcemia, the patient's history of **breast cancer** and the severity of symptoms make malignancy a more acute and likely cause.*Sarcoidosis*- Hypercalcemia in sarcoidosis is due to unregulated **1-alpha-hydroxylase activity** in activated macrophages, leading to increased **1,25-dihydroxyvitamin D** synthesis and calcium absorption.- This condition would typically present with other systemic features like **pulmonary disease** or lymphadenopathy, which are not described in the clinical picture.*Vitamin D toxicity*- This condition results from excessive intake of **exogenous vitamin D**, leading to increased intestinal absorption of calcium and severe hypercalcemia.- There is no mention of excessive vitamin D supplementation or overdose in the patient's history.*Milk-alkali syndrome*- This syndrome is caused by the ingestion of large amounts of **calcium and absorbable alkali**, leading to hypercalcemia, **metabolic alkalosis**, and renal insufficiency.- This etiology is not suggested by the patient's history and is less likely given the clear history of **breast cancer**.

Question 32: A 41-year-old man presents with recurrent kidney stones and peptic ulcers. Serum calcium is 2.9 mmol/L and gastrin is markedly elevated. CT shows a pancreatic mass. What is the most likely syndrome?

A. Zollinger-Ellison syndrome
B. Multiple endocrine neoplasia type 1 (Correct Answer)
C. Carcinoid syndrome
D. Glucagonoma syndrome
E. VIPoma syndrome

Explanation: ***Multiple endocrine neoplasia type 1*** - This syndrome is defined by tumors of the '3 Ps': **Parathyroid**, **Pituitary**, and **Pancreatic** (or duodenal) tumors. - The combination of **primary hyperparathyroidism** (leading to hypercalcemia and kidney stones) and a **gastrinoma** (leading to markedly elevated gastrin and peptic ulcers/Zollinger-Ellison syndrome) is pathognomonic for **MEN 1**. *Zollinger-Ellison syndrome* - While the patient certainly has features of **Zollinger-Ellison syndrome** (high gastrin, peptic ulcers, pancreatic mass), this diagnosis fails to explain the concurrent **hypercalcemia** and recurrent kidney stones. - Given the involvement of both the gastrointestinal tract and the parathyroid glands, **MEN 1** is the superior, overarching diagnosis. *Carcinoid syndrome* - This syndrome usually involves GI or bronchial tumors producing excessive **serotonin**, leading to cutaneous **flushing**, diarrhea, and carcinoid heart disease. - It does not cause primary **hypercalcemia** or a markedly elevated **gastrin** level leading to peptic ulcers. *Glucagonoma syndrome* - Characterized by overproduction of **glucagon**, presenting classically with **necrolytic migratory erythema**, diabetes mellitus, anemia, and weight loss. - This clinical picture does not include primary **hyperparathyroidism** or **Zollinger-Ellison syndrome** features. *VIPoma syndrome* - Caused by tumors secreting **Vasoactive Intestinal Peptide (VIP)**, resulting in the classic **WDHA syndrome** (Watery Diarrhea, Hypokalemia, Achlorhydria). - The main symptoms here (hypercalcemia and peptic ulcers) are inconsistent with the profound secretory diarrhea that defines a VIPoma.

Question 33: A 43-year-old woman presents with fatigue, muscle weakness, and hypertension. Blood was show hypokalemia and metabolic alkalosis. Plasma aldosterone is elevated with suppressed renin. What is the most likely diagnosis?

A. Primary hyperaldosteronism (Correct Answer)
B. Secondary hyperaldosteronism
C. Cushing's syndrome
D. Renal artery stenosis
E. Pheochromocytoma

Explanation: ***Primary hyperaldosteronism***- The combination of **hypertension**, **hypokalemia**, and **metabolic alkalosis** strongly suggests excess mineralocorticoid activity (aldosterone).- The key diagnostic findings are **elevated plasma aldosterone** coupled with **suppressed plasma renin activity** (PRA), indicating aldosterone production independent of the Renin-Angiotensin System. *Secondary hyperaldosteronism*- This condition is characterized by **elevated renin** activity, as aldosterone overproduction is a response to RAAS stimulation (e.g., renovascular disease or decreased effective circulating volume).- While it causes hypertension and hypokalemia, both renin and aldosterone levels would be **high**, contradicting the suppressed renin found in the patient. *Cushing's syndrome*- Cushing's involves excess **cortisol**, typically presenting with centripetal obesity, striae, and proximal myopathy, features not emphasized here.- While cortisol excess can cause hypertension and mild hypokalemia (via mineralocorticoid receptor activity), the primary endocrine abnormality in this patient is specific dysregulation of aldosterone and renin. *Renal artery stenosis*- This causes decreased renal perfusion, leading to activation of the **Renin-Angiotensin-Aldosterone System (RAAS)**.- It results in **secondary hyperaldosteronism**, characterized by both **elevated renin** and **elevated aldosterone**, inconsistent with the patient's suppressed renin. *Pheochromocytoma*- This tumor produces excess **catecholamines**, leading to symptoms like paroxysmal hypertension, headaches, palpitations, and excessive sweating.- It does not cause mineralocorticoid-driven findings like the profound **hypokalemia** and **metabolic alkalosis** typical of hyperaldosteronism.

Question 34: A 41-year-old woman presents with fatigue, muscle weakness, and hyperpigmentation of her knuckles and axillae. Blood glucose is $18.2\mathrm{mmol/L}$. BMI is $34\mathrm{kg/m^2}$. What is the most likely diagnosis?

A. Type 1 diabetes
B. Type 2 diabetes with acanthosis nigricans (Correct Answer)
C. Cushing's syndrome
D. Addison's disease
E. Hypothyroidism

Explanation: ***Type 2 diabetes with acanthosis nigricans***- The patient's **obesity (BMI 34 kg/m²)**, **marked hyperglycemia (blood glucose 18.2 mmol/L)**, fatigue, and muscle weakness are highly suggestive of **Type 2 diabetes mellitus**.- **Hyperpigmentation of the knuckles and axillae** is characteristic of **acanthosis nigricans**, a skin condition strongly associated with **insulin resistance** and Type 2 diabetes.*Type 1 diabetes*- **Type 1 diabetes** typically manifests in younger, non-obese individuals and is an **autoimmune condition** leading to absolute insulin deficiency, often with abrupt onset.- Although hyperglycemia is present, the patient's **obesity** and **acanthosis nigricans** are classic indicators of **insulin resistance**, making Type 2 diabetes more likely.*Cushing's syndrome*- **Cushing's syndrome** is characterized by **hypercortisolism**, leading to central obesity, moon facies, striae, and often hyperglycemia, but not typically **hyperpigmentation of knuckles and axillae**.- The hyperpigmentation in Cushing's, if present, is usually diffuse and due to high ACTH, but distinct from the friction-area pigmentation seen in acanthosis nigricans.*Addison's disease*- **Addison's disease (primary adrenal insufficiency)** causes diffuse **hyperpigmentation** (due to increased ACTH), fatigue, and muscle weakness, but typically leads to **hypoglycemia**, **hypotension**, and **hyponatremia**, not elevated blood glucose.- The combination of **obesity** and significant **hyperglycemia** makes Addison's disease an unlikely diagnosis.*Hypothyroidism*- **Hypothyroidism** presents with fatigue, weight gain, and muscle weakness, but is not directly associated with **hyperpigmentation of knuckles and axillae** or **severe hyperglycemia** as seen here.- While hypothyroidism can cause generalized skin changes (dryness, pallor), it doesn't manifest as acanthosis nigricans, and hyperglycemia is not a primary symptom.

Question 35: A 37-year-old woman presents with recurrent episodes of severe flushing and diarrhea triggered by alcohol and stress. CT shows multiple liver lesions. 24-hour urine 5-HIAA is markedly elevated. What is the most appropriate treatment for symptom control?

A. Octreotide (Correct Answer)
B. Ondansetron
C. Loperamide
D. Propranolol
E. Diphenhydramine

Explanation: ***Octreotide***- This is a **somatostatin analog** which inhibits the release of **serotonin** and other vasoactive peptides (like kinins) responsible for carcinoid syndrome symptoms (flushing, secretory diarrhea).- It is the **first-line therapy** for controlling symptoms in patients with metastatic **neuroendocrine tumors (NETs)**, which is strongly indicated by the elevated **5-HIAA** and liver lesions.*Ondansetron*- *Ondansetron* is a **5-HT3 receptor antagonist** primarily used as an **anti-emetic** to prevent nausea and vomiting.- It is ineffective against the severe **secretory diarrhea** and **flushing** characteristic of metastatic carcinoid syndrome mediated by excessive circulating hormones.*Loperamide*- *Loperamide* is an **opioid receptor agonist** that works by slowing gut motility to reduce the frequency of diarrhea.- It only provides general symptomatic relief for diarrhea but does not address the underlying pathology (excess **serotonin-mediated secretion**) or the associated severe flushing.*Propranolol*- *Propranolol* is a **beta-blocker** and is not the primary treatment for **serotonin-mediated flushing** seen in carcinoid syndrome.- It does not inhibit the high output of **vasoactive peptides** from the tumor, which are the main cause of the patient's symptoms.*Diphenhydramine*- *Diphenhydramine* is an **H1-antihistamine**; while histamine can occasionally contribute to atypical carcinoid syndrome, the standard severe flushing and diarrhea are driven mainly by **serotonin and kinins**.- Antihistamines are generally ineffective at decreasing the production or release of the primary hormones responsible for the patient's severe, systemic symptoms.

Question 36: A 59-year-old woman presents with bone pain and fatigue. Blood tests show calcium 3.2 mmol/L, phosphate 0.8 mmol/L, and PTH 180 pg/mL (markedly elevated). What is the most likely diagnosis?

A. Primary hyperparathyroidism (Correct Answer)
B. Secondary hyperparathyroidism
C. Malignancy
D. Sarcoidosis
E. Vitamin D intoxication

Explanation: ***Primary hyperparathyroidism***- The coexistence of **hypercalcemia** (Ca 3.2 mmol/L), low or low-normal phosphate (Phos 0.8 mmol/L), and **markedly elevated PTH** (180 pg/mL) is the classic biochemical triad defining primary hyperparathyroidism.- This condition is characterized by an inappropriate, autonomous overproduction of PTH, typically due to a **parathyroid adenoma**.*Secondary hyperparathyroidism*- This condition involves high PTH levels resulting as a compensatory response to chronic **hypocalcemia** or severe Vitamin D deficiency, often seen in **chronic kidney disease**.- While PTH is high, the overall calcium status in secondary hyperparathyroidism is typically normal or low, making the presentation of severe **hypercalcemia** unsuitable.*Malignancy*- Malignancy frequently causes hypercalcemia, often via **Humoral Hypercalcemia of Malignancy (HHOM)**, where tumor cells secrete **PTH-related peptide (PTHrP)**.- A key differentiating feature is that calcium elevation caused by malignancy or PTHrP leads to appropriate feedback, resulting in **suppressed** or low PTH levels.*Sarcoidosis*- Sarcoidosis produces hypercalcemia through the extrarenal, unregulated production of **1,25-dihydroxyvitamin D** (calcitriol) by activated macrophages in the granulomas.- The hypercalcemia induced by excessive calcitriol suppresses the parathyroid glands, leading to **low or suppressed PTH** levels.*Vitamin D intoxication*- Excessive intake of Vitamin D leads to increased intestinal absorption of calcium and phosphate, resulting in **hypercalcemia**.- Vitamin D intoxication also suppresses PTH production, resulting in **low PTH** levels and often concurrent **hyperphosphatemia**, which is not seen here.

Question 37: A 41-year-old man presents with recurrent episodes of severe flushing, diarrhea, and wheezing over 6 months. CT shows multiple liver lesions and a small bowel mass. What is the most appropriate biochemical test?

A. Serum gastrin
B. 24-hour urine 5-HIAA (Correct Answer)
C. Serum chromogranin A
D. Serum insulin
E. Serum glucagon

Explanation: ***24-hour urine 5-HIAA***- This test measures the urinary excretion of **5-hydroxyindoleacetic acid**, the primary metabolite of **serotonin**.- The triad of recurrent **flushing**, **diarrhea**, and **wheezing**, combined with **small bowel** and **liver metastases**, is highly characteristic of **carcinoid syndrome**, caused by excessive serotonin secretion.*Serum gastrin*- This hormone is the primary test for **Zollinger-Ellison syndrome** (ZES), which typically presents with severe, refractory **peptic ulcer disease** and diarrhea.- While ZES is a type of neuroendocrine tumor (NET), the defining features in this patient (**flushing** and **wheezing**) are distinct from typical ZES presentation.*Serum chromogranin A*- CgA is a general marker for **neuroendocrine tumors** (NETs) but is less specific than 5-HIAA for confirming active **carcinoid syndrome**.- It can be elevated in other conditions (e.g., renal failure, chronic atrophic gastritis) and is usually monitored for tumor burden rather than initial syndrome diagnosis.*Serum insulin*- This hormone is evaluated when an **insulinoma** is suspected, which presents primarily with symptoms of **hypoglycemia** (e.g., confusion, tremors, syncope).- The patient’s symptoms are related to hormonal excess (**serotonin**/kinins), not low blood glucose.*Serum glucagon*- This is the biochemical marker for a **glucagonoma**, a rare pancreatic NET.- Glucagonoma typically presents with **diabetes mellitus**, weight loss, and characteristic **necrolytic migratory erythema**, none of which describe this patient.

Question 38: A 39-year-old woman presents with recurrent episodes of severe abdominal pain, nausea, and confusion. During episodes, her urine turns dark. She has a family history of similar symptoms. What should be avoided during acute attacks?

A. Carbohydrates
B. Barbiturates (Correct Answer)
C. IV fluids
D. Analgesia
E. Antibiotics

Explanation: ***Barbiturates*** - **Barbiturates** are highly potent inducers of the hepatic **cytochrome P450 system**, which subsequently upregulates **\delta-aminolevulinic acid synthase (ALAS1)**, the rate-limiting enzyme in heme synthesis. - This increase in ALAS1 activity leads to an accumulation of neurotoxic porphyrin precursors (**aminolevulinic acid** and **porphobilinogen**), thereby triggering or markedly worsening an acute porphyria attack. *Carbohydrates* - High-dose **intravenous glucose** (IV dextrose) is a primary treatment modality for acute porphyria attacks as glucose suppresses ALAS1 activity and reduces porphyrin precursor production. - Adequate carbohydrate intake is essential, and avoiding them would be contraindicated as it can worsen the catabolic state, potentially precipitating an attack. *IV fluids* - Patients frequently experience **volume depletion** due to vomiting and sometimes **SIADH (syndrome of inappropriate ADH secretion)**, leading to hyponatremia. - **IV fluids** are necessary to maintain hydration and electrolyte balance, particularly managing potentially life-threatening **hyponatremia**. *Analgesia* - Severe **abdominal pain** is a major symptom of acute porphyria, and effective pain relief is crucial for management and patient comfort. - Safe analgesics, such as **opioids** (e.g., morphine), should be used; avoidance of all analgesia would result in unnecessary suffering. *Antibiotics* - While certain antibiotics (e.g., **sulfonamides**, griseofulvin) are strictly porphyrinogenic and must be avoided, many others (e.g., penicillins, cephalosporins) are safe. - Avoiding all antibiotics is unnecessary; appropriate, non-porphyrinogenic antibiotics are used if an **intercurrent infection** triggers the acute attack.

Question 39: A 46-year-old woman presents with fatigue, muscle weakness, and hypertension. Blood tests show hypokalemia, metabolic alkalosis, and elevated aldosterone with suppressed renin. What is the most appropriate initial investigation?

A. CT adrenals (Correct Answer)
B. Aldosterone suppression test
C. Renal artery imaging
D. 24-hour urine aldosterone
E. Adrenal vein sampling

Explanation: ***CT adrenals***- After biochemical confirmation of Primary Aldosteronism (hypertension, hypokalemia, elevated aldosterone, and **suppressed renin**), **CT imaging of the adrenals** is the most appropriate initial step for localization.- This investigation aims to differentiate between a unilateral **Aldosterone-Producing Adenoma (APA)**, which is surgically curable, and bilateral adrenal hyperplasia (BAH), which requires medical management.*Aldosterone suppression test*- This test is part of the **biochemical confirmation** of Primary Aldosteronism, used to confirm non-suppressible aldosterone secretion (e.g., with a saline infusion test).- The patient's presentation already provides strong biochemical evidence (elevated aldosterone with suppressed renin), making the next logical step **localization imaging** rather than further confirmatory tests.*Renal artery imaging*- This investigation is used to diagnose **renovascular hypertension**, a cause of Secondary Aldosteronism.- Secondary Aldosteronism is characterized by **elevated renin** due to decreased renal perfusion, which directly contradicts the patient's finding of **suppressed renin**.*24-hour urine aldosterone*- While a **24-hour urine aldosterone** collection can quantify aldosterone excretion, the initial screening and diagnosis of Primary Aldosteronism typically relies on the **plasma Aldosterone/Renin Ratio (ARR)**.- After biochemical diagnosis, the immediate priority shifts to **localization studies** like adrenal CT to determine the etiology (adenoma vs. hyperplasia), rather than further quantifying aldosterone excretion.*Adrenal vein sampling*- **Adrenal vein sampling (AVS)** is the gold standard for determining the *laterality* of aldosterone excess (unilateral vs. bilateral) and is essential for guiding surgical decisions.- However, AVS is an **invasive procedure** and is typically performed *after* initial non-invasive imaging (like CT adrenals) and often reserved for cases where CT is inconclusive or in older patients, making it not the initial investigation.

Question 40: A 45-year-old woman presents with recurrent episodes of severe headache, sweating, and palpitations. Episodes last 15-20 minutes and her BP during attacks reaches 200/120 mmHg. 24-hour urine metanephrines are elevated. What is the most appropriate preoperative management?

A. Beta-blockers alone
B. Alpha-blockers followed by beta-blockers (Correct Answer)
C. ACE inhibitor
D. Calcium channel blockers
E. No preoperative medication

Explanation: ***Alpha-blockers followed by beta-blockers***- Preoperative preparation for **pheochromocytoma** always begins with **alpha-adrenergic blockade** (e.g., *phenoxybenzamine*) to control blood pressure and allow for plasma volume expansion, which is essential to prevent severe hypotension after tumor removal.- **Beta-blockers** (e.g., *propranolol*) are only added *after* adequate alpha-blockade has been established, typically to manage catecholamine-induced tachycardia or arrhythmias.*Beta-blockers alone*- Using a beta-blocker before achieving adequate alpha-blockade is **contraindicated** because unopposed stimulation of **alpha-1 receptors** leads to severe vasoconstriction and a potentially fatal hypertensive crisis.- Beta-blockade controls heart rate but fails to manage the critical systemic peripheral resistance caused by excess **norepinephrine** and **epinephrine** acting on alpha-receptors.*ACE inhibitor*- **ACE inhibitors** are typically ineffective in managing the severe catecholamine-driven hypertension seen in a pheochromocytoma crisis because they do not directly block **alpha-adrenergic receptors**.- While they are used for essential hypertension, their mechanism (blocking *angiotensin II* production) is insufficiently potent or targeted for necessary preoperative control in this setting.*Calcium channel blockers*- **Calcium channel blockers** (CCBs) can be used as adjuvant therapy to control blood pressure or coronary vasospasm, but they are not the primary initial strategy for comprehensive **adrenergic blockade**.- The standard of care demands initial use of non-selective **alpha-blockers** (like phenoxybenzamine) to ensure both pressure control and necessary volume expansion.*No preoperative medication*- The surgical manipulation of a pheochromocytoma tumor triggers massive, life-threatening release of catecholamines, requiring mandatory preoperative medication to prevent a **hypertensive crisis** and arrhythmias.- This approach would result in extreme, uncontrolled hypertension (often >300/150 mmHg) and high risk of myocardial infarction, stroke, pulmonary edema, or death during surgery.

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Type 2 diabetes

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