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SU23.1-3,SU24.1-3 | Adrenal and Pancreatic Surgery — Practice Quiz
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A 42-year-old man with resistant hypertension is found to have a 4 cm right adrenal mass. He reports episodic palpitations, sweating, and throbbing headaches. Which initial biochemical test is most appropriate to confirm the suspected diagnosis?
Correct. The triad of episodic palpitations, sweating, and headache with hypertension and an adrenal mass suggests phaeochromocytoma. Plasma free metanephrines (or 24-hour urinary fractionated metanephrines) is the most sensitive screening test because catecholamine secretion is episodic but metanephrine production is continuous.
Phaeochromocytoma is screened with plasma free or urinary fractionated metanephrines (continuously produced), not raw catecholamines (episodic).
Reconsider the clinical triad. Episodic palpitations, sweating, and headache point to a catecholamine-secreting tumour, which is confirmed biochemically by metanephrines, not by cortisol or aldosterone testing.
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A patient with biochemically confirmed phaeochromocytoma is scheduled for adrenalectomy. What is the most important preoperative pharmacological preparation?
Correct. Alpha-blockade (e.g. phenoxybenzamine) must be established FIRST to control hypertension and allow volume re-expansion. Beta-blockade is added only afterwards to control reflex tachycardia. Giving beta-blockade first causes unopposed alpha-mediated vasoconstriction and a hypertensive crisis.
Always alpha-block before beta-block in phaeochromocytoma; reverse order risks unopposed alpha vasoconstriction and crisis.
The cardinal rule of phaeochromocytoma preparation is ALPHA-before-BETA. Unopposed alpha stimulation from premature beta-blockade can precipitate a hypertensive crisis.
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A 38-year-old woman has hypertension with persistent hypokalaemia despite no diuretic use. Aldosterone is elevated and renin is suppressed. Which diagnosis does this pattern indicate?
Correct. Hypertension with hypokalaemia, high aldosterone and suppressed renin (raised aldosterone-to-renin ratio) is the classic biochemical signature of Conn's syndrome (primary hyperaldosteronism), usually from an aldosterone-producing adenoma or bilateral hyperplasia.
Conn's syndrome = hypertension + hypokalaemia + raised aldosterone-to-renin ratio (high aldosterone, suppressed renin).
The key pattern is hypertension + hypokalaemia + high aldosterone + LOW renin. This is primary hyperaldosteronism (Conn's), where autonomous aldosterone suppresses renin.
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An incidentally discovered 2 cm adrenal mass shows abundant intracytoplasmic lipid on imaging with low Hounsfield units on non-contrast CT and rapid contrast washout. Hormonal work-up is negative. What is the most likely diagnosis?
Correct. A small (<4 cm), lipid-rich mass with low non-contrast attenuation (<10 HU) and rapid contrast washout, with a negative hormonal screen, has the classic imaging phenotype of a benign non-functioning adenoma. These are managed conservatively with surveillance.
Benign adrenal adenomas are lipid-rich (<10 HU on non-contrast CT) with rapid washout; size >4 cm and lipid-poor heterogeneity raise concern for carcinoma.
Lipid-rich content, low Hounsfield units (<10 HU) and rapid washout are reassuring benign features. Adrenocortical carcinoma is typically large, heterogeneous, and lipid-poor.
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A 50-year-old man presents with severe epigastric pain radiating to the back, vomiting, and a serum amylase five times the upper limit of normal. He drinks alcohol heavily. Beyond alcohol, which is the other most common aetiology of acute pancreatitis you must actively exclude?
Correct. Gallstones and alcohol together account for the large majority of acute pancreatitis (the 'GET SMASHED' mnemonic lists Gallstones and Ethanol first). An abdominal ultrasound to look for gallstones is mandatory in every case of acute pancreatitis.
Gallstones and alcohol are the two leading causes of acute pancreatitis (GET SMASHED); always image the biliary tree.
The two dominant causes of acute pancreatitis are gallstones and alcohol. Even in a heavy drinker, gallstones must be actively excluded with ultrasound because it changes management.
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A patient with mild acute pancreatitis (no organ failure, no necrosis) is admitted. Regarding antibiotic use, which management principle is correct?
Correct. Prophylactic antibiotics are NOT recommended in mild acute pancreatitis; they are reserved for proven or strongly suspected infected necrosis or extra-pancreatic infection. Mainstay management is aggressive fluid resuscitation, analgesia, and early enteral nutrition.
No routine prophylactic antibiotics in mild acute pancreatitis; reserve for proven infected necrosis. Cornerstone = fluids, analgesia, early enteral feeding.
Routine prophylactic antibiotics are not indicated in mild acute pancreatitis. They are reserved for documented infection (e.g. infected necrosis). Supportive care with fluids and analgesia is the foundation.
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A 35-year-old woman has recurrent episodes of confusion and sweating after fasting, relieved by eating. During a supervised fast she develops documented hypoglycaemia with inappropriately high insulin AND high C-peptide. What is the most likely diagnosis?
Correct. Whipple's triad (symptoms of hypoglycaemia, documented low glucose, relief with glucose) plus inappropriately high insulin AND high C-peptide indicates endogenous hyperinsulinism from an insulinoma. The raised C-peptide is what distinguishes it from exogenous insulin (where C-peptide is suppressed).
Insulinoma: Whipple's triad + hypoglycaemia with high insulin and HIGH C-peptide. Suppressed C-peptide implies exogenous insulin.
Endogenous insulin is co-secreted with C-peptide. High insulin WITH high C-peptide during hypoglycaemia indicates an insulinoma. Exogenous insulin would show suppressed C-peptide.
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A patient has recurrent, multiple, treatment-refractory peptic ulcers including in the distal duodenum, with chronic diarrhoea. Fasting serum gastrin is markedly elevated. Which condition does this represent, and with what syndrome is it commonly associated?
Correct. Multiple refractory peptic ulcers in unusual locations with diarrhoea and markedly raised gastrin is Zollinger-Ellison syndrome from a gastrinoma. Gastrinomas (and other pancreatic neuroendocrine tumours) are a recognised component of MEN-1 (with parathyroid and pituitary tumours).
Gastrinoma causes Zollinger-Ellison syndrome (refractory multiple ulcers, high gastrin) and is associated with MEN-1 (parathyroid, pituitary, pancreas).
Refractory multiple ulcers + diarrhoea + high gastrin = Zollinger-Ellison syndrome (gastrinoma). Pancreatic neuroendocrine tumours including gastrinoma are part of MEN-1, not MEN-2.
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