Endocrine & Metabolic
Adrenal, thyroid, diabetes, electrolyte disturbances, acid-base, hypercalcemia, hyperkalemia, glucose management. ← Back to Q-Bank
Q1. Stress dose steroids
A patient on prednisone 30 mg/day for 8 weeks presents for hip replacement. Stress dose steroid coverage:
A. Not needed for any surgery
B. Hydrocortisone 100 mg IV at induction, then 50 mg q8h × 24 hr for major surgery
C. Triple the patient's home dose for 1 week
D. Cortisol 1 g IV bolus
E. Methylprednisolone 1 g
Show answer
Answer: B. HPA suppression is presumed with >20 mg/day prednisone × ≥3 weeks (or equivalent). Coverage: minor surgery — home dose; moderate — 50–75 mg hydrocortisone day of surgery; major — 100–150 mg hydrocortisone day of surgery + taper. Normal adrenal output ~30 mg cortisol/day, rises to 75–150 mg in major surgery.
Q2. Pheochromocytoma preoperative
Preoperative management of pheochromocytoma requires:
A. β-blockade alone
B. α-blockade (phenoxybenzamine or doxazosin) for 7–14 days, then β-blockade if needed, plus volume repletion
C. ACE inhibition
D. Glucagon infusion
E. No specific preparation
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Answer: B. Sequence matters: α before β. Unopposed α-stimulation from β-blockade in untreated pheo → hypertensive crisis. Phenoxybenzamine (irreversible) or doxazosin (selective α1). β-blocker only after α to control reflex tachycardia. Metyrosine (inhibits tyrosine hydroxylase) for refractory cases. Volume repletion crucial — chronic vasoconstriction → hypovolemia.
Q3. Pheochromocytoma intraoperative crisis
During tumor manipulation in pheo resection, BP rises to 240/130. The most appropriate treatment is:
A. Esmolol
B. Phenylephrine
C. Nicardipine or nitroprusside; phentolamine for reversible α-blockade
D. Hydralazine
E. Norepinephrine
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Answer: C. Pre-resection: control HTN with nicardipine, nitroprusside, or phentolamine; control tachycardia with esmolol (β1-selective, short half-life). After tumor vein ligated, hypotension often profound — give fluids, norepinephrine, vasopressin. Hypoglycemia can occur post-resection from rebound insulin.
Q4. Thyroid storm
A patient with untreated hyperthyroidism develops hyperthermia, tachycardia, AMS during surgery. The mainstay of treatment is:
A. Acetaminophen alone
B. PTU + propranolol + hydrocortisone + iodine (Lugol's, given >1 hr after PTU)
C. Methimazole alone
D. β-blocker alone
E. Cooling blankets only
Show answer
Answer: B. Thyroid storm: PTU (blocks synthesis + peripheral T4→T3 conversion) before iodine; propranolol (blocks β + inhibits T4→T3); hydrocortisone (treats relative adrenal insufficiency, inhibits T4→T3); iodine (Lugol's or potassium iodide — Wolff-Chaikoff effect, blocks hormone release) ≥1 hr after PTU to avoid substrate for new synthesis.
Q5. Hypothyroidism anesthesia
A severely hypothyroid patient has anesthesia considerations including:
A. Hypotension, blunted reflexes, hyponatremia, decreased MAC, anemia, possible difficult airway from macroglossia
B. Hyperthermia and hypertension
C. Hyperkalemia and decreased reflexes
D. Diuresis and polydipsia
E. Decreased oxygen consumption only
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Answer: A. Decompensated hypothyroidism (myxedema coma): hypothermia, hypotension, hyponatremia, hypoglycemia, decreased MAC. Elective surgery should be postponed in severe disease. Mild-moderate untreated hypothyroidism is not an absolute contraindication to surgery.
Q6. Carcinoid syndrome pretreatment
Preoperative prep for carcinoid tumor resection includes:
A. β-blocker
B. Octreotide 100 mcg subq TID × several days, plus infusion intraoperatively
C. Phenoxybenzamine
D. Steroids
E. Insulin
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Answer: B. Octreotide blunts release of vasoactive mediators (serotonin, histamine, kallikrein, bradykinin). Avoid catecholamines (ephedrine, epinephrine) — paradoxically worsens hypotension via kallikrein release. Avoid histamine-releasing drugs (morphine, atracurium). Symptoms only with hepatic mets or non-portal-drained tumors. Right-sided valvular fibrosis (lung metabolizes serotonin so left side spared).
Q7. Acute intermittent porphyria triggers
A patient with acute intermittent porphyria requires general anesthesia. Avoid:
A. Propofol
B. Barbiturates, etomidate, sulfonamides, ergotamine
C. Fentanyl
D. Sevoflurane
E. Vecuronium
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Answer: B. Triggers induce ALA synthase → accumulate porphyrin precursors. Avoid: barbiturates (classic — thiopental contraindicated), etomidate, sulfonamides, ergotamine, alcohol, OCPs, valproate. Safe: propofol, opioids, volatile anesthetics (except enflurane/halothane), benzodiazepines, succinylcholine, NMBDs, droperidol. Manage with IV glucose, possibly heme arginate.
Q8. Perioperative glucose target
Periop glucose target in non-cardiac surgery is:
A. <110 mg/dL
B. 140–180 mg/dL
C. 180–220 mg/dL
D. <80 mg/dL
E. <250 mg/dL only
Show answer
Answer: B. ACE/SCCM/ASA recommend 140–180 mg/dL. NICE-SUGAR trial showed tight glycemic control (80–110) increased mortality from hypoglycemia. Cardiac surgery may target 110–150 mg/dL.
Q9. Insulin pump intraoperative
A patient with an insulin pump for type 1 DM presents for surgery. The most appropriate strategy is:
A. Discontinue pump preoperatively, switch to subcutaneous regimen
B. Continue pump at basal rate; monitor glucose q1h; have IV insulin and dextrose available
C. Bolus insulin at induction
D. Remove pump immediately after induction
E. Increase basal rate
Show answer
Answer: B. For short cases (<2 hr), continue basal infusion; monitor glucose. For longer cases or hyperglycemia, transition to IV insulin infusion. Don't bolus insulin at induction. Communicate with patient and endocrinology preoperatively. Avoid pump electrodiathermy interference.
Q10. SGLT2 inhibitor perioperative
Sodium-glucose cotransporter-2 inhibitors (canagliflozin, empagliflozin, dapagliflozin) should be held perioperatively because of:
A. Risk of hyperkalemia
B. Risk of euglycemic diabetic ketoacidosis
C. Drug interactions with anesthetic agents
D. Hypotension during induction
E. Renal protection lost
Show answer
Answer: B. SGLT2 inhibitors → euglycemic DKA in catabolic stress states (surgery, infection, fasting). Hold 3–4 days before surgery. If new metabolic acidosis develops postoperatively with normal/mildly elevated glucose, check ketones.
Q11. Hyperkalemia treatment
Severe hyperkalemia (K 7.2 with peaked T waves) is initially managed with:
A. Kayexalate alone
B. Calcium chloride 1 g IV (or calcium gluconate 3 g), then insulin 10 U + D50, then β2-agonist, then removal therapy
C. Hemodialysis as first step
D. Furosemide alone
E. Sodium bicarbonate alone
Show answer
Answer: B. Sequence: stabilize membrane (calcium) → shift intracellularly (insulin+glucose, β2-agonist, bicarbonate if acidotic) → remove (loop diuretic if making urine, sodium zirconium cyclosilicate, patiromer, hemodialysis). Sodium polystyrene sulfonate (Kayexalate) has fallen out of favor (slow, association with bowel necrosis).
Q12. Hypocalcemia signs
Chvostek and Trousseau signs are seen in:
A. Hypercalcemia
B. Hypocalcemia
C. Hyperkalemia
D. Hypokalemia
E. Hypomagnesemia
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Answer: B. Hypocalcemia: Chvostek (facial twitch with tap), Trousseau (carpal spasm with cuff inflation), prolonged QT, tetany, seizures, laryngospasm. Causes: post-thyroidectomy/parathyroidectomy, citrate during massive transfusion, alkalosis (shifts to bound form), pancreatitis, rhabdomyolysis, hypomagnesemia (functional hypoPTH).
Q13. Diabetes insipidus posterior pituitary surgery
After transsphenoidal hypophysectomy, a patient develops polyuria (>500 mL/hr), Na 152, urine osm 80, serum osm 320. The most appropriate treatment is:
A. Fluid restriction
B. DDAVP (desmopressin) 1–2 mcg IV
C. Hypertonic saline
D. Lasix
E. Tolvaptan
Show answer
Answer: B. Central DI (no ADH): DDAVP. Lab triad: hypernatremia + hyposthenuric urine (low osm) + dilute urine. Treat hypernatremia with free water replacement, DDAVP. Triphasic response after pituitary surgery: DI day 1 → SIADH days 5–7 → permanent DI possible.
Q14. Hypermagnesemia toxicity
A preeclamptic patient on magnesium infusion loses patellar reflexes. The corresponding magnesium level is:
A. 3 mg/dL
B. 5 mg/dL
C. 8–10 mg/dL
D. 15 mg/dL
E. 20 mg/dL
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Answer: C. Therapeutic 5–9 mg/dL. Loss of DTRs >10 mg/dL. Respiratory paralysis 15–20. Cardiac arrest >25. Antidote: calcium gluconate 1 g IV. Magnesium potentiates NDNMBDs.
Q15. Conn syndrome electrolytes
Primary hyperaldosteronism (Conn syndrome) classically shows:
A. Hyperkalemia and metabolic acidosis
B. Hypertension, hypokalemia, metabolic alkalosis, mildly elevated sodium
C. Hypocalcemia
D. Hypoglycemia
E. Hypernatremia and respiratory acidosis
Show answer
Answer: B. Conn syndrome: aldosterone excess → Na/K exchange in DCT → K wasting + H wasting + Na retention → HTN, hypokalemia, metabolic alkalosis. Plasma aldosterone/renin ratio >20 = screening test. Treat with spironolactone, eplerenone, or adrenalectomy.
Q16. Adrenal insufficiency
A patient on chronic steroids fails to respond to vasopressors after induction. The most appropriate treatment is:
A. Increase phenylephrine
B. Hydrocortisone 100 mg IV (stress dose)
C. Glucagon
D. Octreotide
E. Bicarbonate
Show answer
Answer: B. Suspected acute adrenal crisis: hydrocortisone 100 mg IV bolus, then 50 mg q6h. Concurrent fluid resuscitation. Diagnostic: random cortisol + cosyntropin stimulation. Common precipitants: steroid taper, infection, surgery, trauma.
Q17. Liddle syndrome
Liddle syndrome causes hypertension via:
A. Aldosterone overproduction
B. Gain-of-function mutation of ENaC channel → constitutive Na reabsorption with K loss
C. Renin overproduction
D. Cortisol overproduction
E. ACE deficiency
Show answer
Answer: B. Liddle syndrome: constitutively active ENaC → HTN, hypokalemia, metabolic alkalosis, low aldosterone (vs. Conn syndrome). Treat with amiloride or triamterene (block ENaC).
Q18. Apparent mineralocorticoid excess
Eating large quantities of licorice can cause hypertension via:
A. Direct vasoconstriction
B. Glycyrrhizic acid inhibits 11β-HSD2 → cortisol activates mineralocorticoid receptor
C. Renin overproduction
D. Sodium loading
E. Direct ENaC activation
Show answer
Answer: B. Apparent mineralocorticoid excess: 11β-HSD2 normally converts cortisol → cortisone before mineralocorticoid receptor → cortisol activates receptor → HTN, hypokalemia, metabolic alkalosis. Caused by licorice (glycyrrhizic acid blocks the enzyme), or genetic 11β-HSD2 deficiency.
Q19. Refeeding hypophosphatemia
In refeeding syndrome, hypophosphatemia causes:
A. Skin rash
B. Decreased cardiac contractility, arrhythmias, weakness, left-shift of oxyhemoglobin curve (decreased 2,3-DPG), AMS
C. Hypertension
D. Bradycardia
E. Hypothermia
Show answer
Answer: B. Severe hypophosphatemia (<1 mg/dL): cardiac dysfunction, rhabdomyolysis, hemolysis, respiratory weakness, AMS, seizures, central pontine myelinolysis. Replace with potassium phosphate or sodium phosphate.
Q20. Hyperventilation electrolyte effects
Acute respiratory alkalosis from hyperventilation causes which electrolyte changes?
A. Hyperkalemia, hypercalcemia, hyperphosphatemia
B. Hypokalemia, hypocalcemia (ionized), hypophosphatemia
C. Hyperkalemia, hypocalcemia
D. Hyponatremia, hypocalcemia
E. No changes
Show answer
Answer: B. Alkalosis: K shifts into cells (hypokalemia), albumin binds more Ca²⁺ (↓ionized Ca → paresthesias, tetany), glycolysis stimulated → ↑phosphate uptake (hypophosphatemia). Reverses with rebreathing.
Q21. Causes of normal anion gap metabolic acidosis
A patient has normal anion gap metabolic acidosis. Causes include all EXCEPT:
A. Diarrhea
B. Renal tubular acidosis
C. Hyperalimentation
D. Methanol ingestion
E. Acetazolamide
Show answer
Answer: D. Methanol = elevated anion gap (MUDPILES). Normal AG metabolic acidosis = HARDASS or FUSEDCARS: Hyperalimentation, Addison disease, RTA, Diarrhea, Acetazolamide, Spironolactone, Saline (large volume), ureteroenterostomy.
Q22. Methanol vs ethylene glycol
Differentiating methanol from ethylene glycol toxicity:
A. Methanol — calcium oxalate crystals; ethylene glycol — optic neuritis
B. Methanol — optic neuritis and blindness; ethylene glycol — calcium oxalate crystals in urine and renal failure
C. Both indistinguishable
D. Both cause hyperkalemia
E. Both spare the eyes
Show answer
Answer: B. Methanol → formic acid → optic nerve damage (blindness, snowy vision). Ethylene glycol → glycolic acid → renal tubular damage; oxalic acid → calcium oxalate crystalluria. Treatment for both: fomepizole (alcohol dehydrogenase inhibitor) or ethanol; dialysis for severe cases. Anion-gap + osmolar-gap acidosis.
Q23. PCC for warfarin reversal indications
Prothrombin complex concentrate (PCC) for emergent warfarin reversal includes which factors?
A. II, VII, IX, X (4-factor PCC includes all four)
B. V, VIII, IX
C. VII alone
D. Fibrinogen + VIII
E. Antithrombin + plasminogen
Show answer
Answer: A. 4-factor PCC: II, VII, IX, X (Kcentra, Beriplex). 3-factor PCC: II, IX, X (low VII). FDA-approved for urgent warfarin reversal. Faster than FFP, lower volume, no allergic/TRALI risk. Always with vitamin K (PCC effect lasts only 6–8 hr).
Q24. Magnesium replacement target
In a patient with torsades de pointes and hypomagnesemia, magnesium replacement is:
A. 1 g over 24 hr
B. 1–2 g IV bolus over 5–15 min, repeat as needed
C. 5 g IV over 1 hour
D. 10 g IM
E. PO only
Show answer
Answer: B. Magnesium sulfate 1–2 g IV bolus for torsades, even with normal Mg level. Refractory: continuous infusion. Mg stabilizes the membrane and is recommended in ACLS for polymorphic VT with long QT.
Q25. Salicylate toxicity acid-base
Adult aspirin overdose classically produces:
A. Anion gap metabolic acidosis alone
B. Respiratory alkalosis followed by mixed anion-gap metabolic acidosis + respiratory alkalosis
C. Pure respiratory acidosis
D. Hypochloremic metabolic alkalosis
E. Normal anion gap acidosis
Show answer
Answer: B. Salicylates directly stimulate respiratory center → respiratory alkalosis. Then anion-gap metabolic acidosis (lactic + ketoacids). pH often near normal because of the mix. Treatment: glucose, alkalinize urine with bicarbonate (traps salicylate in urine), hemodialysis for severe (>100 mg/dL, AMS, renal failure).
Q26. Hypercalcemia of malignancy
The most common mechanism of hypercalcemia in metastatic cancer is:
A. Direct osteolysis
B. PTHrP (parathyroid hormone-related peptide) secretion by tumor
C. Vitamin D excess
D. Hyperparathyroidism
E. Sarcoidosis-like granulomas
Show answer
Answer: B. PTHrP-mediated humoral hypercalcemia: squamous cell carcinomas (lung, head/neck), renal cell, breast. Osteolytic mets second most common (breast, multiple myeloma). Calcitriol excess in lymphoma. PTH is low in malignancy-related hypercalcemia (suppressed). Treat: NS, calcitonin (fast), bisphosphonate (durable).