Endocrine & Metabolic
Adrenal, thyroid, diabetes, electrolyte disturbances, acid-base, hypercalcemia, hyperkalemia, glucose management. ← All topics
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 because patient's endogenous cortisol production remains adequate for surgical stress
B. Hydrocortisone 100 mg IV at induction, then 50 mg every 8 hours for 24 hours
C. Triple the patient's usual prednisone dose starting the day before surgery for one week
D. Hydrocortisone 25 mg IV at induction with no additional dosing required postoperatively for hip surgery
E. Methylprednisolone 125 mg IV at induction, then 60 mg every 6 hours for 24 hours
Show answer
Answer: B. HPA axis suppression is presumed with prednisone >20 mg/day for ≥3 weeks (or equivalent glucocorticoid doses). This patient meets criteria and requires stress-dose coverage. For major surgery such as hip replacement, the recommended regimen is hydrocortisone 100–150 mg on the day of surgery (typically 100 mg IV at induction followed by 50 mg every 8 hours for 24 hours), then taper over 1–2 days. Normal adrenal cortisol output is approximately 30 mg/day but increases to 75–150 mg during major surgical stress. Minor surgery requires only the patient's usual home dose, while moderate surgery requires 50–75 mg hydrocortisone on the day of surgery. Cortisol 1 g IV would be excessive and potentially harmful. Methylprednisolone can be used but at equivalent doses (approximately 1:5 ratio with hydrocortisone).
Q2. Pheochromocytoma preoperative
Preoperative management of pheochromocytoma requires:
A. β-blockade alone for 7–14 days with volume repletion to prevent intraoperative hypertensive crisis
B. α-blockade for 7–14 days, then β-blockade if needed for tachycardia, plus volume repletion
C. ACE inhibition for 7–14 days with volume repletion to control catecholamine-induced hypertension
D. Glucagon infusion for 7–14 days with volume repletion to stabilize hemodynamics preoperatively
E. No specific pharmacologic preparation required if blood pressure is controlled on admission day
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Answer: B. Preoperative management of pheochromocytoma requires α-blockade first, followed by β-blockade only if needed. The sequence is critical: giving β-blockade before or without α-blockade can cause unopposed α-stimulation, leading to severe hypertensive crisis. α-blockade is typically administered for 7–14 days using phenoxybenzamine (irreversible, nonselective) or doxazosin (selective α1-blocker). β-blockers are added only after adequate α-blockade is established, primarily to control reflex tachycardia. Volume repletion is crucial because chronic catecholamine-induced vasoconstriction leads to significant hypovolemia that becomes apparent once α-blockade is initiated. For refractory cases, metyrosine (which inhibits tyrosine hydroxylase, the rate-limiting enzyme in catecholamine synthesis) may be added. ACE inhibitors, glucagon, and β-blockade alone are not appropriate primary management strategies.
Q3. Pheochromocytoma intraoperative crisis
During tumor manipulation in pheo resection, BP rises to 240/130. The most appropriate treatment is:
A. Esmolol for selective beta-1 blockade and control of reflex tachycardia during hypertensive crisis
B. Phenylephrine for alpha-1 agonism to counteract vasodilation and stabilize systemic vascular resistance
C. Nicardipine or nitroprusside for vasodilation; phentolamine for reversible competitive alpha-blockade during manipulation
D. Hydralazine for direct arteriolar smooth muscle relaxation and reduction of systemic vascular resistance
E. Norepinephrine for combined alpha and beta agonism to maintain perfusion pressure and cardiac output
Show answer
Answer: C. During pheochromocytoma resection, tumor manipulation causes massive catecholamine release leading to severe hypertension. The most appropriate treatment is nicardipine, nitroprusside, or phentolamine to control blood pressure. Phentolamine provides reversible competitive alpha-blockade, which is ideal for this situation. Esmolol (beta-1 selective with short half-life) should only be used after alpha-blockade is established to control reflex tachycardia; using beta-blockers first can worsen hypertension by leaving alpha-receptors unopposed. After the tumor's venous drainage is ligated, catecholamine levels drop precipitously and profound hypotension often occurs, requiring aggressive fluid resuscitation and vasopressors such as norepinephrine or vasopressin. Hypoglycemia can occur post-resection due to rebound insulin secretion once catecholamine suppression is removed.
Q4. Thyroid storm
A patient with untreated hyperthyroidism develops hyperthermia, tachycardia, AMS during surgery. The mainstay of treatment is:
A. Acetaminophen for hyperthermia plus external cooling measures and supportive care with fluids
B. PTU plus propranolol plus hydrocortisone plus iodine given at least one hour after PTU
C. Methimazole to block thyroid hormone synthesis plus supportive care with fluids and cooling
D. Beta-blocker to control tachycardia and hypertension plus acetaminophen for temperature control and fluids
E. Cooling blankets with ice packs and antipyretics plus intravenous fluids for hemodynamic support
Show answer
Answer: B. Thyroid storm requires multimodal treatment. PTU is preferred over methimazole because it blocks both thyroid hormone synthesis and peripheral conversion of T4 to T3. Propranolol provides beta-blockade and also inhibits peripheral T4 to T3 conversion. Hydrocortisone treats relative adrenal insufficiency and inhibits T4 to T3 conversion. Iodine (Lugol's solution or potassium iodide) exploits the Wolff-Chaikoff effect to block thyroid hormone release, but must be given at least one hour after PTU to avoid providing substrate for new hormone synthesis. Monotherapy with any single agent is insufficient for thyroid storm. Supportive care including cooling and fluids is important but not sufficient as sole therapy.
Q5. Hypothyroidism anesthesia
A severely hypothyroid patient has anesthesia considerations including:
A. Hypotension, blunted reflexes, hyponatremia, decreased MAC, anemia, and possible difficult airway from macroglossia
B. Hypertension, tachycardia, hyperreflexia, increased MAC, thrombocytosis, and possible difficult airway from thyromegaly
C. Hyperkalemia, decreased reflexes, hypernatremia, increased MAC, polycythemia, and possible difficult airway from neck mass
D. Hypokalemia, increased reflexes, hyponatremia, normal MAC, leukopenia, and possible difficult airway from laryngeal edema
E. Normotension, normal reflexes, normonatremia, normal MAC, normal hemoglobin, and decreased oxygen consumption only
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Answer: A. Severely hypothyroid patients present significant anesthetic challenges. Key considerations include hypotension from decreased cardiac output and blunted baroreceptor reflexes, hyponatremia from impaired free water clearance, decreased minimum alveolar concentration (MAC) due to reduced metabolic rate, anemia (typically normocytic), and potential difficult airway from macroglossia or myxedematous changes. Additional features of decompensated hypothyroidism (myxedema coma) include hypothermia and hypoglycemia. Elective surgery should be postponed in severe disease to optimize thyroid function first. Mild to moderate untreated hypothyroidism is not an absolute contraindication to surgery, though vigilance for perioperative complications remains important.
Q6. Carcinoid syndrome pretreatment
Preoperative prep for carcinoid tumor resection includes:
A. β-blocker administered orally for several days preoperatively, then continued intraoperatively as needed
B. Octreotide 100 mcg subq TID for several days preoperatively, then infusion continued intraoperatively
C. Phenoxybenzamine administered orally for several days preoperatively, then discontinued on day of surgery
D. Steroids administered intravenously for several days preoperatively, then continued as stress-dose intraoperatively
E. Insulin administered subcutaneously for several days preoperatively, then infusion titrated intraoperatively as needed
Show answer
Answer: B. Octreotide is the key preoperative medication for carcinoid tumor resection, given at 100 mcg subcutaneously three times daily for several days before surgery, with an intraoperative infusion continued during the procedure. Octreotide is a somatostatin analog that blunts the release of vasoactive mediators including serotonin, histamine, kallikrein, and bradykinin. During anesthesia, avoid catecholamines such as ephedrine and epinephrine, as they paradoxically worsen hypotension via kallikrein release. Also avoid histamine-releasing drugs like morphine and atracurium. Carcinoid syndrome symptoms typically occur only when hepatic metastases are present or when the tumor drains outside the portal circulation. Right-sided valvular fibrosis is characteristic because the lungs metabolize serotonin, sparing the left-sided valves.
Q7. Acute intermittent porphyria triggers
A patient with acute intermittent porphyria requires general anesthesia. Avoid:
A. Propofol, fentanyl, sevoflurane, and vecuronium
B. Barbiturates, etomidate, sulfonamides, and ergotamine
C. Fentanyl, remifentanil, morphine, and hydromorphone
D. Sevoflurane, desflurane, isoflurane, and nitrous oxide
E. Vecuronium, rocuronium, cisatracurium, and atracurium
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Answer: B. Acute intermittent porphyria triggers induce ALA synthase, leading to accumulation of toxic porphyrin precursors. Barbiturates are the classic trigger and thiopental is absolutely contraindicated. Other important triggers to avoid include etomidate, sulfonamides, ergotamine, alcohol, oral contraceptive pills, and valproate. Safe agents for anesthesia include propofol, all opioids (fentanyl, remifentanil, morphine), modern volatile anesthetics (sevoflurane, desflurane, isoflurane), benzodiazepines, all nondepolarizing neuromuscular blocking drugs (vecuronium, rocuronium, cisatracurium), succinylcholine, and droperidol. Older volatile agents enflurane and halothane should be avoided. Acute attacks are managed with intravenous glucose and possibly heme arginate.
Q8. Perioperative glucose target
Periop glucose target in non-cardiac surgery is:
A. 80–110 mg/dL
B. 140–180 mg/dL
C. 180–220 mg/dL
D. 110–150 mg/dL
E. 200–250 mg/dL
Show answer
Answer: B. The recommended perioperative glucose target in non-cardiac surgery is 140–180 mg/dL according to ACE/SCCM/ASA guidelines. The NICE-SUGAR trial demonstrated that tight glycemic control (80–110 mg/dL) increased mortality due to hypoglycemia, leading to abandonment of this approach in critically ill patients. Cardiac surgery may use a slightly lower target range of 110–150 mg/dL. Ranges above 180 mg/dL are associated with increased infection risk and poor wound healing, while targets below 110 mg/dL carry unacceptable hypoglycemia risk in the perioperative setting.
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 and switch to subcutaneous insulin regimen with scheduled dosing
B. Continue pump at basal rate with hourly glucose monitoring and IV insulin available
C. Bolus insulin at induction and maintain pump at increased basal rate throughout case
D. Remove pump immediately after induction and transition to intravenous insulin infusion protocol
E. Increase basal rate by fifty percent and monitor glucose every two hours intraoperatively
Show answer
Answer: B. For short surgical cases (less than 2 hours), the insulin pump should be continued at the basal rate with hourly glucose monitoring. IV insulin and dextrose should be readily available for management of hypo- or hyperglycemia. For longer cases or if hyperglycemia develops, transition to IV insulin infusion is appropriate. Insulin should not be bolused at induction as this risks intraoperative hypoglycemia. Preoperative communication with the patient and endocrinology team is essential. The pump should be positioned away from the surgical field to avoid interference from electrocautery. Discontinuing the pump or switching regimens preoperatively is unnecessary for short cases and increases complexity. Increasing the basal rate without indication risks hypoglycemia in the fasting, unstressed patient.
Q10. SGLT2 inhibitor perioperative
Sodium-glucose cotransporter-2 inhibitors (canagliflozin, empagliflozin, dapagliflozin) should be held perioperatively because of:
A. Risk of intraoperative hyperkalemia from impaired renal potassium excretion
B. Risk of euglycemic diabetic ketoacidosis in the perioperative catabolic state
C. Drug interactions with volatile anesthetic agents causing prolonged emergence
D. Hypotension during induction from intravascular volume depletion and vasoplegia
E. Loss of renal protection leading to acute kidney injury
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Answer: B. SGLT2 inhibitors increase the risk of euglycemic diabetic ketoacidosis in catabolic stress states such as surgery, infection, and fasting. The mechanism involves increased glucagon secretion, decreased insulin levels, and enhanced ketogenesis while glucose remains normal or only mildly elevated due to the drug's glucose-lowering effect. These medications should be held 3–4 days before elective surgery. If new metabolic acidosis develops postoperatively with normal or mildly elevated glucose, check serum and urine ketones to evaluate for this complication.
Q11. Hyperkalemia treatment
Severe hyperkalemia (K 7.2 with peaked T waves) is initially managed with:
A. Kayexalate orally or rectally as monotherapy to remove potassium from the body
B. Calcium chloride 1 g IV to stabilize membrane, then insulin with glucose and albuterol
C. Hemodialysis immediately as first-line therapy before any other pharmacologic intervention
D. Furosemide 40-80 mg IV as monotherapy to enhance renal potassium excretion
E. Sodium bicarbonate 50-100 mEq IV as monotherapy to shift potassium intracellularly
Show answer
Answer: B. The correct sequence for severe hyperkalemia with ECG changes is: (1) stabilize the cardiac membrane with calcium (calcium chloride 1 g IV or calcium gluconate 3 g IV), (2) shift potassium intracellularly with insulin 10 units plus dextrose 50% (D50), beta-2 agonists like albuterol, and sodium bicarbonate if acidotic, then (3) remove potassium from the body with loop diuretics if the patient is making urine, newer agents like sodium zirconium cyclosilicate or patiromer, or hemodialysis. Sodium polystyrene sulfonate (Kayexalate) has fallen out of favor due to slow onset and association with bowel necrosis. Monotherapy with any single agent is inadequate for life-threatening hyperkalemia with ECG changes.
Q12. Hypocalcemia signs
Chvostek and Trousseau signs are seen in:
A. Hypercalcemia with elevated serum calcium levels
B. Hypocalcemia with decreased serum calcium levels
C. Hyperkalemia with elevated serum potassium levels
D. Hypokalemia with decreased serum potassium levels
E. Hypomagnesemia with decreased serum magnesium levels
Show answer
Answer: B. Chvostek and Trousseau signs are classic physical examination findings in hypocalcemia. Chvostek sign is elicited by tapping the facial nerve anterior to the ear, causing ipsilateral facial muscle twitching. Trousseau sign is carpal spasm induced by inflating a blood pressure cuff above systolic pressure for 3 minutes. Other manifestations of hypocalcemia include prolonged QT interval on ECG, tetany, seizures, and laryngospasm. Common causes include post-thyroidectomy or parathyroidectomy (hypoparathyroidism), citrate toxicity during massive transfusion, respiratory or metabolic alkalosis (shifts calcium to protein-bound form), acute pancreatitis, rhabdomyolysis, and hypomagnesemia (causes functional hypoparathyroidism). While severe hypomagnesemia can present with similar neuromuscular irritability, the classic teaching associates Chvostek and Trousseau signs specifically with hypocalcemia.
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 to reduce urine output and allow endogenous ADH recovery
B. DDAVP (desmopressin) 1–2 mcg IV to replace absent ADH and concentrate urine
C. Hypertonic saline infusion to correct the serum sodium and osmolality acutely
D. Lasix (furosemide) to promote diuresis and normalize the elevated serum sodium
E. Tolvaptan (vasopressin antagonist) to block remaining ADH receptors and increase excretion
Show answer
Answer: B. This patient has central diabetes insipidus following transsphenoidal hypophysectomy, characterized by the classic triad: hypernatremia (Na 152), hyposthenuric urine (urine osm 80), and high serum osmolality (320). The absence of ADH leads to massive free water loss. Treatment requires DDAVP (desmopressin) 1–2 mcg IV to replace the missing ADH and allow the kidneys to concentrate urine. Hypernatremia should also be corrected with free water replacement. Fluid restriction would worsen hypernatremia. Hypertonic saline would dangerously increase sodium further. Lasix would exacerbate volume depletion. Tolvaptan is a vasopressin antagonist used for SIADH, the opposite condition. After pituitary surgery, watch for the triphasic response: DI on day 1, SIADH on days 5–7, then possible permanent DI.
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. Loss of deep tendon reflexes (DTRs), including patellar reflexes, occurs at magnesium levels greater than 10 mg/dL, typically in the 8–10 mg/dL range. The therapeutic range for magnesium in preeclampsia is 5–9 mg/dL. As toxicity progresses, respiratory paralysis occurs at 15–20 mg/dL, and cardiac arrest occurs at levels greater than 25 mg/dL. The antidote for magnesium toxicity is calcium gluconate 1 g IV. Magnesium also potentiates nondepolarizing neuromuscular blocking drugs (NDNMBDs), which is clinically important during anesthesia.
Q15. Conn syndrome electrolytes
Primary hyperaldosteronism (Conn syndrome) classically shows:
A. Hyperkalemia, metabolic acidosis, hypotension, and low sodium levels
B. Hypertension, hypokalemia, metabolic alkalosis, and mildly elevated sodium levels
C. Hypocalcemia, hyperphosphatemia, metabolic acidosis, and normal potassium levels
D. Hypoglycemia, hyponatremia, metabolic acidosis, and elevated potassium levels
E. Hypernatremia, respiratory acidosis, hyperkalemia, and elevated bicarbonate levels
Show answer
Answer: B. Conn syndrome results from aldosterone excess, which causes increased sodium-potassium exchange in the distal convoluted tubule. This leads to potassium wasting, hydrogen ion wasting, and sodium retention, producing the classic tetrad of hypertension, hypokalemia, metabolic alkalosis, and mildly elevated sodium. The plasma aldosterone to renin ratio greater than 20 is the screening test of choice. Treatment options include mineralocorticoid receptor antagonists such as spironolactone or eplerenone, or surgical adrenalectomy for adenomas.
Q16. Adrenal insufficiency
A patient on chronic steroids fails to respond to vasopressors after induction. The most appropriate treatment is:
A. Increase phenylephrine infusion rate to overcome vasodilatory shock
B. Hydrocortisone 100 mg IV bolus for suspected acute adrenal crisis
C. Glucagon bolus to increase cardiac contractility and vascular tone
D. Octreotide infusion to counteract refractory distributive hypotension
E. Sodium bicarbonate bolus to correct metabolic acidosis from hypoperfusion
Show answer
Answer: B. This patient on chronic steroids with vasopressor-refractory hypotension after induction has suspected acute adrenal crisis. The appropriate treatment is hydrocortisone 100 mg IV bolus, followed by 50 mg every 6 hours, with concurrent aggressive fluid resuscitation. Diagnostic workup includes random cortisol level and cosyntropin stimulation test. Common precipitants of adrenal crisis include steroid taper, infection, surgery, and trauma. Chronic steroid use suppresses the hypothalamic-pituitary-adrenal axis, preventing adequate endogenous cortisol response to surgical stress. Simply increasing vasopressors will not address the underlying glucocorticoid deficiency causing the refractory hypotension.
Q17. Liddle syndrome
Liddle syndrome causes hypertension via:
A. Aldosterone overproduction leading to increased sodium reabsorption and potassium loss
B. Gain-of-function mutation of ENaC channel causing constitutive sodium reabsorption with potassium loss
C. Renin overproduction leading to increased angiotensin II and aldosterone-mediated sodium retention
D. Cortisol overproduction causing mineralocorticoid receptor activation and increased sodium reabsorption
E. ACE deficiency leading to impaired degradation of bradykinin and altered sodium handling
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Answer: B. Liddle syndrome results from a gain-of-function mutation in the epithelial sodium channel (ENaC), leading to constitutively active sodium reabsorption in the collecting duct. This causes hypertension, hypokalemia, and metabolic alkalosis. Importantly, aldosterone levels are low (distinguishing it from Conn syndrome, which has high aldosterone). The mechanism bypasses the renin-angiotensin-aldosterone system entirely. Treatment is with potassium-sparing diuretics that directly block ENaC, specifically amiloride or triamterene, rather than aldosterone antagonists like spironolactone which would be ineffective since aldosterone is already suppressed.
Q18. Apparent mineralocorticoid excess
Eating large quantities of licorice can cause hypertension via:
A. Direct vasoconstriction through smooth muscle calcium channel activation
B. Glycyrrhizic acid inhibits 11β-HSD2 allowing cortisol to activate mineralocorticoid receptor
C. Renin overproduction from juxtaglomerular apparatus stimulation by glycyrrhizic acid
D. Sodium loading from high salt content in commercial licorice preparations
E. Direct ENaC activation in the collecting duct by glycyrrhizic acid
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Answer: B. Apparent mineralocorticoid excess occurs when 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is inhibited. This enzyme normally converts cortisol to cortisone in the kidney, preventing cortisol from activating the mineralocorticoid receptor. Glycyrrhizic acid in licorice blocks 11β-HSD2, allowing cortisol to bind and activate the mineralocorticoid receptor. This produces the clinical syndrome of hypertension, hypokalemia, and metabolic alkalosis with suppressed renin and aldosterone levels. The same syndrome can occur from genetic 11β-HSD2 deficiency. The mechanism is indirect mineralocorticoid receptor activation by cortisol, not direct effects on vascular smooth muscle, renin production, sodium content, or epithelial sodium channels.
Q19. Refeeding hypophosphatemia
In refeeding syndrome, hypophosphatemia causes:
A. Skin rash, pruritus, urticaria, angioedema, and peripheral edema
B. Decreased cardiac contractility, arrhythmias, weakness, left-shift of oxyhemoglobin curve, and altered mental status
C. Hypertension, tachycardia, increased systemic vascular resistance, headache, and visual changes
D. Bradycardia, heart block, prolonged QT interval, hypotension, and syncope
E. Hypothermia, shivering, decreased metabolic rate, vasoconstriction, and cold intolerance
Show answer
Answer: B. Severe hypophosphatemia (less than 1 mg/dL) in refeeding syndrome causes decreased cardiac contractility, arrhythmias, skeletal muscle weakness, and altered mental status. The left-shift of the oxyhemoglobin dissociation curve occurs due to decreased 2,3-DPG production, impairing oxygen delivery to tissues. Additional manifestations include cardiac dysfunction, rhabdomyolysis, hemolysis, respiratory muscle weakness, seizures, and central pontine myelinolysis. Treatment involves replacement with potassium phosphate or sodium phosphate, with careful monitoring to avoid overcorrection.
Q20. Hyperventilation electrolyte effects
Acute respiratory alkalosis from hyperventilation causes which electrolyte changes?
A. Hyperkalemia, hypercalcemia, hyperphosphatemia
B. Hypokalemia, hypocalcemia, hypophosphatemia
C. Hyperkalemia, hypocalcemia, hyperphosphatemia
D. Hyponatremia, hypocalcemia, hypophosphatemia
E. Hypokalemia, hypercalcemia, hyperphosphatemia
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Answer: B. Acute respiratory alkalosis from hyperventilation causes hypokalemia, hypocalcemia, and hypophosphatemia. The alkalotic state causes potassium to shift intracellularly, lowering serum potassium. Increased pH causes albumin and other proteins to bind more calcium, reducing ionized (free) calcium levels, which can manifest as paresthesias and tetany. Alkalosis stimulates glycolysis, increasing cellular phosphate uptake and lowering serum phosphate. These electrolyte changes reverse with rebreathing or correction of the alkalosis.
Q21. Causes of normal anion gap metabolic acidosis
A patient has normal anion gap metabolic acidosis. Causes include all EXCEPT:
A. Diarrhea causing bicarbonate loss through gastrointestinal secretions
B. Renal tubular acidosis causing impaired renal bicarbonate reabsorption
C. Hyperalimentation causing increased chloride load from amino acids
D. Methanol ingestion causing formic acid accumulation and toxicity
E. Acetazolamide causing carbonic anhydrase inhibition in renal tubules
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Answer: D. Methanol ingestion causes an elevated anion gap metabolic acidosis through accumulation of formic acid, making it part of the MUDPILES mnemonic (Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol/Paraldehyde, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates). Normal anion gap metabolic acidosis is caused by conditions that result in bicarbonate loss or impaired bicarbonate handling without accumulation of unmeasured anions. These causes are remembered by the mnemonics HARDASS or FUSEDCARS: Hyperalimentation, Addison disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline (large volume infusion), Fistula (pancreatic), Ureteroenterostomy, Small bowel fistula, Extra chloride, and Carbonic anhydrase inhibitors. Diarrhea causes direct bicarbonate loss in stool. Renal tubular acidosis involves defective renal acid handling. Hyperalimentation provides excess chloride from amino acid solutions. Acetazolamide inhibits carbonic anhydrase, leading to renal bicarbonate wasting.
Q22. Methanol vs ethylene glycol
Differentiating methanol from ethylene glycol toxicity:
A. Methanol causes calcium oxalate crystals in urine and renal failure; ethylene glycol causes optic neuritis and blindness
B. Methanol causes optic neuritis and blindness; ethylene glycol causes calcium oxalate crystals in urine and renal failure
C. Methanol causes hyperkalemia and renal tubular acidosis; ethylene glycol causes hypokalemia and metabolic alkalosis
D. Methanol causes hypocalcemia and seizures; ethylene glycol causes hypercalcemia and cardiac arrhythmias
E. Methanol causes hepatic necrosis and coagulopathy; ethylene glycol causes pulmonary edema and respiratory failure
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Answer: B. Methanol is metabolized to formic acid, which causes optic nerve damage leading to blindness and characteristic snowy vision. Ethylene glycol is metabolized to glycolic acid (causing renal tubular damage) and oxalic acid (which precipitates with calcium to form calcium oxalate crystals in the urine, leading to renal failure). Both toxicities present with anion-gap metabolic acidosis and an elevated osmolar gap. Treatment for both includes fomepizole (an alcohol dehydrogenase inhibitor) or ethanol as competitive substrates, and hemodialysis for severe cases to remove the parent compound and toxic metabolites.
Q23. PCC for warfarin reversal indications
Prothrombin complex concentrate (PCC) for emergent warfarin reversal includes which factors?
A. Factors II, VII, IX, and X
B. Factors V, VIII, and IX
C. Factor VII as monotherapy
D. Fibrinogen plus factor VIII
E. Antithrombin plus plasminogen
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Answer: A. 4-factor PCC contains factors II, VII, IX, and X (brand names Kcentra and Beriplex). This formulation includes all four vitamin K-dependent clotting factors inhibited by warfarin. In contrast, 3-factor PCC contains factors II, IX, and X with low levels of factor VII. 4-factor PCC is FDA-approved for urgent warfarin reversal and offers advantages over fresh frozen plasma including faster administration, lower volume, and reduced risk of allergic reactions and transfusion-related acute lung injury (TRALI). PCC should always be given with vitamin K because the effect of PCC lasts only 6 to 8 hours, while vitamin K provides sustained reversal.
Q24. Magnesium replacement target
In a patient with torsades de pointes and hypomagnesemia, magnesium replacement is:
A. 1–2 g IV bolus over 5–15 min, repeat as needed
B. 1 g IV infusion continuously over 24 hours
C. 5 g IV bolus over 1 hour, single dose
D. 10 g IM divided into multiple injection sites
E. Oral magnesium oxide 400 mg every 6 hours
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Answer: A. Magnesium sulfate 1–2 g IV bolus over 5–15 minutes is the correct treatment for torsades de pointes, even when serum magnesium levels are normal. The dose can be repeated as needed. For refractory cases, a continuous infusion may be required. Magnesium stabilizes the cardiac membrane and is recommended in ACLS guidelines for polymorphic ventricular tachycardia associated with prolonged QT interval. The rapid bolus administration is critical in this emergency situation to terminate the arrhythmia quickly.
Q25. Salicylate toxicity acid-base
Adult aspirin overdose classically produces:
A. Anion gap metabolic acidosis alone without any respiratory compensation or alkalosis
B. Respiratory alkalosis followed by mixed anion-gap metabolic acidosis plus respiratory alkalosis
C. Pure respiratory acidosis without metabolic derangement or any compensatory alkalosis
D. Hypochloremic metabolic alkalosis without anion gap elevation or respiratory acidosis
E. Normal anion gap metabolic acidosis without respiratory alkalosis or ketoacid accumulation
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Answer: B. Salicylates directly stimulate the respiratory center, causing initial respiratory alkalosis. This is followed by anion-gap metabolic acidosis from accumulation of lactic acid and ketoacids. The classic presentation is a mixed disorder with both respiratory alkalosis and anion-gap metabolic acidosis occurring simultaneously. The arterial pH is often near normal because the two opposing processes partially offset each other. Treatment includes glucose administration, urinary alkalinization with bicarbonate (which traps ionized salicylate in the urine and prevents reabsorption), and hemodialysis for severe cases (salicylate level >100 mg/dL, altered mental status, or renal failure).
Q26. Hypercalcemia of malignancy
The most common mechanism of hypercalcemia in metastatic cancer is:
A. Direct osteolysis from metastatic bone lesions causing local calcium release
B. PTHrP secretion by tumor causing humoral hypercalcemia of malignancy
C. Vitamin D excess from ectopic calcitriol production by tumor
D. Hyperparathyroidism from concurrent primary parathyroid adenoma or hyperplasia
E. Sarcoidosis-like granulomas producing calcitriol within tumor microenvironment
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Answer: B. PTHrP-mediated humoral hypercalcemia of malignancy is the most common mechanism, accounting for approximately 80% of cases. It is classically seen with squamous cell carcinomas of the lung, head and neck, renal cell carcinoma, and breast cancer. PTHrP binds to PTH receptors, increasing renal calcium reabsorption and bone resorption. Direct osteolytic metastases are the second most common mechanism, particularly with breast cancer and multiple myeloma. Calcitriol excess occurs rarely in lymphomas. In malignancy-related hypercalcemia, PTH is suppressed (low), distinguishing it from primary hyperparathyroidism. Treatment includes normal saline hydration, calcitonin for rapid effect, and bisphosphonates for durable control.