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IM23.1-12,IM24.1-5 | Mineral Fluid Electrolyte Acid Base and Nutrition — Practice Quiz
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A 55-year-old woman is found to have a serum calcium of 3.1 mmol/L on a routine panel. She reports polyuria, polydipsia, and constipation for 3 months. PTH is 98 pg/mL (normal 10–65). Serum phosphate is low. Which of the following is the MOST likely diagnosis?
Correct. The elevated PTH in the context of hypercalcaemia is the hallmark of PTH-mediated hypercalcaemia. In primary hyperparathyroidism, PTH is inappropriately elevated (not suppressed) for the degree of calcium elevation. PTHrP from malignancy would suppress PTH. Sarcoidosis, vitamin D toxicity, and milk-alkali syndrome all suppress PTH due to non-PTH-mediated calcium release.
Normal calcium is 2.1–2.6 mmol/L. In hypercalcaemia, measuring simultaneous PTH divides causes into PTH-mediated (PTH elevated or unsuppressed: primary hyperparathyroidism, familial hypocalciuric hypercalcaemia) versus non-PTH-mediated (PTH suppressed: malignancy, granulomatous disease, vitamin D excess).
The key discriminator is the PTH level: in primary hyperparathyroidism, PTH is elevated or inappropriately normal despite hypercalcaemia. All non-PTH-mediated causes (malignancy, sarcoidosis, vitamin D toxicity) suppress PTH. Always interpret PTH in the context of the calcium — a PTH of 98 with calcium of 3.1 is clearly inappropriate and confirms PTH-driven hypercalcaemia.
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A 62-year-old man with a known parathyroid adenoma has a corrected serum calcium of 3.6 mmol/L, is confused, and has a GCS of 13. He is euvolaemic. What is the FIRST step in immediate management?
Correct. Intravenous normal saline is the cornerstone of acute hypercalcaemia management. Volume expansion increases glomerular filtration rate and inhibits proximal tubular sodium (and calcium) reabsorption, promoting calciuresis. Furosemide should only be added after adequate hydration and is no longer recommended routinely. Bisphosphonates (e.g., zoledronic acid) take 2–4 days to work and follow initial hydration. Calcitonin acts rapidly but has a ceiling effect and tachyphylaxis develops within 48 hours.
Acute management of hypercalcaemia: (1) IV normal saline 200–300 mL/hr — cornerstone; (2) IV bisphosphonates (zoledronic acid 4 mg) — definitive, onset 2–4 days; (3) SC calcitonin — rapid but tachyphylaxis limits to 48 hours; (4) steroids — for granulomatous disease and vitamin D toxicity; (5) haemodialysis — refractory cases with renal failure.
In acute severe hypercalcaemia, the first step is IV normal saline to restore volume and increase renal calcium excretion. Furosemide is not given until hydration is established and euvolaemia confirmed. Bisphosphonates are effective but take 48–72 hours; they follow, not replace, initial saline. Parathyroidectomy is definitive but is never the acute first step.
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A 42-year-old woman presents with nausea, headache, and generalised weakness. Serum sodium is 121 mmol/L. Serum osmolality is 248 mOsm/kg. She is clinically euvolaemic. Urine sodium is 45 mmol/L and urine osmolality is 520 mOsm/kg. Which of the following is the MOST likely cause?
Correct. The combination of hypo-osmolar hyponatraemia, euvolaemia, concentrated urine (urine osmolality >100 mOsm/kg and well above plasma osmolality), and elevated urine sodium (>20 mmol/L) in the absence of adrenal or thyroid insufficiency is diagnostic of SIADH. In psychogenic polydipsia, urine is maximally dilute. CHF and nephrotic syndrome present with hypervolaemia and low urine sodium.
The diagnostic algorithm for hyponatraemia: (1) serum osmolality — exclude pseudohyponatraemia and hypertonic causes; (2) volume status — hypovolaemic vs euvolaemic vs hypervolaemic; (3) urine sodium — in euvolaemic hyponatraemia, urine Na >20 suggests SIADH/hypothyroidism/adrenal insufficiency; urine Na <20 is unusual. SIADH criteria: hypo-osmolar hyponatraemia, urine osmolality >100 mOsm/kg, urine Na >20, euvolaemia, normal thyroid and adrenal function.
SIADH produces euvolaemic hypo-osmolar hyponatraemia with inappropriately concentrated urine (urine osmolality >100, usually >300 mOsm/kg) and elevated urine sodium (>20 mmol/L) because ADH-driven water retention is the mechanism. Psychogenic polydipsia produces dilute urine. CHF and nephrotic syndrome are hypervolaemic with low urine sodium due to avid sodium retention.
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A 68-year-old woman with chronic hyponatraemia (Na 118 mmol/L for several days) is started on IV 3% saline for symptomatic deterioration. After 24 hours her sodium has risen to 134 mmol/L — a correction of 16 mmol/L in 24 hours. What is the MOST serious complication of this rate of correction?
Correct. Osmotic demyelination syndrome (ODS), previously called central pontine myelinolysis, results from overly rapid correction of chronic hyponatraemia. The brain adapts to chronic hyponatraemia by extruding osmolytes (taurine, myoinositol). Rapid correction creates a hyperosmolar environment that the brain cannot re-adapt to quickly, causing demyelination of oligodendrocytes — most commonly in the pons. Safe correction limit: no more than 8–10 mmol/L in 24 hours (10–12 mmol/L in the first 24 hours in severe symptomatic cases). This patient's correction of 16 mmol/L far exceeds the safe limit.
Correction rate limits in hyponatraemia: do NOT exceed 8–10 mmol/L per 24 hours for chronic hyponatraemia (duration >48 hours or unknown). If overcorrection occurs, give DDAVP 2 mcg IV + D5W to lower sodium back. High-risk groups for ODS: alcoholism, malnutrition, advanced liver disease, hypokalaemia.
Osmotic demyelination syndrome (ODS) is the feared complication of overly rapid correction of chronic hyponatraemia. The safe upper limit is 8–10 mmol/L per 24 hours (some authorities allow up to 12 mmol/L in the first 24 hours only for severe symptoms). A correction of 16 mmol/L in 24 hours significantly exceeds this. Cerebral oedema is the risk of under-correcting acute hyponatraemia; ODS is the risk of over-correcting chronic hyponatraemia.
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A 28-year-old man presents with muscle weakness and palpitations. ECG shows flattened T waves, prominent U waves, and a prolonged QU interval. Serum potassium is 2.4 mmol/L. He is taking furosemide for heart failure. What is the BEST initial IV replacement strategy?
Correct. For symptomatic hypokalaemia (ECG changes, weakness) with potassium 2.4 mmol/L, IV replacement is indicated. The safe rate via peripheral IV is 10–20 mmol/hour in normal saline (not dextrose — insulin in dextrose drives K into cells further). Cardiac monitoring is mandatory. Rapid bolus IV potassium causes fatal arrhythmias. Rates above 20 mmol/hour require central venous access. Also check and correct magnesium — hypomagnesaemia causes refractory hypokalaemia because magnesium is required for renal potassium conservation.
Hypokalaemia ECG sequence (in order): flattened T waves → prominent U waves → ST depression → QU prolongation → ventricular arrhythmias. Management: KCl 10–20 mmol/hr peripherally; always in saline not dextrose; correct Mg simultaneously (Mg deficiency prevents renal K conservation).
IV potassium for symptomatic hypokalaemia must NEVER be given as a bolus (fatal arrhythmia risk). The safe peripheral IV rate is 10–20 mmol/hour in normal saline with cardiac monitoring. Rates above 20 mmol/hour require central access. Always check magnesium — uncorrected hypomagnesaemia causes refractory hypokalaemia.
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A 60-year-old man with CKD stage 4 (eGFR 22 mL/min) presents with generalised weakness. ECG shows peaked (tall, narrow, symmetrical) T waves and a widened QRS of 160 ms. Potassium is 7.2 mmol/L. What is the FIRST priority in emergency management?
Correct. The presence of ECG changes (peaked T waves, widened QRS) indicates imminent cardiac toxicity. The FIRST and most urgent step is IV calcium to stabilise (membrane-protect) the myocardium — calcium gluconate 10 mL of 10% over 2–3 minutes (calcium chloride 10 mL of 10% if central access available, provides three times the ionised calcium). Calcium does NOT lower serum potassium; it raises the threshold potential, widening the safety margin between resting and threshold potential. Shifting agents (insulin-glucose, salbutamol, bicarbonate) and removal agents (resonium, dialysis) come next.
Hyperkalaemia ECG sequence: peaked T waves → PR prolongation → P wave loss → sine wave → VF/asystole. Management sequence: (1) Cardiac membrane stabilisation: IV calcium gluconate (ECG changes present); (2) Shift into cells: insulin 10 U + 50 mL 50% dextrose (onset 20 min); salbutamol 10–20 mg nebulised; NaHCO3 if acidotic; (3) Remove from body: furosemide, calcium resonium, dialysis.
When hyperkalaemia causes ECG changes (peaked T waves, QRS widening), the first priority is to protect the heart — IV calcium gluconate stabilises the myocardium immediately. It does not lower potassium; that is the role of shifting agents (insulin-glucose = first-line shift) and removal agents (resonium, loop diuretic, dialysis). Calcium must come first when there are ECG changes.
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A 45-year-old man with chronic alcohol use is admitted with severe vomiting for 5 days. ABG shows: pH 7.52, PaCO2 48 mmHg, HCO3 38 mmol/L. Serum chloride is 82 mmol/L. Which acid-base disorder does this ABG represent?
Correct. pH >7.45 = alkalosis. HCO3 38 mmol/L elevated = primary metabolic alkalosis. Expected compensatory PaCO2 = 40 + (0.7 × [HCO3 − 24]) = 40 + (0.7 × 14) = 40 + 9.8 = 49.8 mmHg. Measured PaCO2 is 48 mmHg — within the expected range (within 2 mmHg), confirming appropriate respiratory compensation, not a second disorder. Prolonged vomiting causes loss of HCl → hypochloraemic metabolic alkalosis, with renal bicarbonate retention to maintain electroneutrality.
Metabolic alkalosis compensation formula: expected PaCO2 = 40 + 0.7 × (HCO3 − 24), maximum ~55 mmHg. Causes: vomiting (HCl loss), diuretics (K/H loss), hyperaldosteronism, alkali ingestion. If measured PaCO2 > expected: concurrent respiratory acidosis. If measured PaCO2 < expected: concurrent respiratory alkalosis.
This is metabolic alkalosis with appropriate respiratory compensation. The primary disorder is the elevated HCO3 (38 mmol/L) producing alkaline pH. Expected compensation for metabolic alkalosis: PaCO2 = 40 + 0.7 × (HCO3 − 24) = approximately 50 mmHg. Measured PaCO2 of 48 mmHg falls within the expected range → appropriate compensation, not a second disorder. Chronic vomiting causes HCl loss → hypochloraemic, hypokalaemic metabolic alkalosis.
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A 22-year-old woman with type 1 diabetes is admitted unconscious. ABG: pH 7.08, PaCO2 18 mmHg, HCO3 5 mmol/L. Na 138, Cl 98, K 5.2 mmol/L. Anion gap = 138 − (98 + 5) = 35 mmol/L. Applying Winter's formula, the expected PaCO2 is approximately:
Correct. Winter's formula: expected PaCO2 = 1.5 × HCO3 + 8 (± 2) = 1.5 × 5 + 8 = 7.5 + 8 = 15.5 ± 2 = range 13.5–17.5 mmHg. The measured PaCO2 of 18 mmHg is just within this range (borderline high end), confirming the respiratory compensation is appropriate for the degree of metabolic acidosis. There is no concurrent respiratory disorder. This is pure high anion-gap metabolic acidosis (DKA), with appropriate Kussmaul breathing.
Winter's formula: expected PaCO2 = 1.5 × HCO3 + 8 ± 2. If measured PaCO2 > expected: concurrent respiratory acidosis. If measured PaCO2 < expected: concurrent respiratory alkalosis. Anion gap = Na − (Cl + HCO3); normal = 8–12 mmol/L. High AG causes: MUDPILES — Methanol, Uraemia, DKA, Propylene glycol/Paracetamol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates.
Winter's formula for metabolic acidosis: expected PaCO2 = (1.5 × HCO3) + 8 ± 2. With HCO3 of 5 mmol/L: 1.5 × 5 + 8 = 15.5 ± 2 = 13.5–17.5 mmHg. Measured PaCO2 of 18 falls at the borderline upper limit — compatible with appropriate compensation. If measured PaCO2 were significantly above 17.5 (e.g., >20), a concurrent respiratory acidosis would be present. Winter's formula is essential for every metabolic acidosis ABG.
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A 35-year-old man with anorexia nervosa (BMI 14.2 kg/m2, 3-month near-total starvation) is admitted and started on enteral feeding at 30 kcal/kg/day. On day 3 he develops generalised weakness, paraesthesiae, and respiratory distress. Serum phosphate is 0.4 mmol/L (normal 0.8–1.4 mmol/L). What is the MOST likely diagnosis?
Correct. Refeeding syndrome occurs when nutrition is reintroduced after prolonged starvation. The reintroduction of carbohydrates stimulates insulin release, driving phosphate (and also potassium and magnesium) into cells for anabolic processes. Critically, phosphate is required for ATP and 2,3-DPG synthesis — a profound fall causes ATP depletion manifesting as muscle weakness (including respiratory muscles), cardiac failure, haemolysis, neurological dysfunction, and death. Risk factors: BMI <16, >5 days minimal intake, significant weight loss. Prevention: start at 10–15 kcal/kg/day (not full calories), give prophylactic phosphate, thiamine, and multivitamins before and during initiation.
Refeeding syndrome: risk factors include BMI <16, >10% weight loss in 6 months, negligible intake >5 days, history of alcohol excess or chemotherapy. Key deficiencies: phosphate (most critical), potassium, magnesium, thiamine. Management: start at 10 kcal/kg/day, supplement phosphate/K/Mg before starting feeds, give IV thiamine (before any glucose) in high-risk patients.
Refeeding syndrome is caused by insulin-driven intracellular shift of phosphate (also K, Mg) when carbohydrates are reintroduced to a starved patient. Severe hypophosphataemia (phosphate <0.4 mmol/L) causes ATP depletion, impaired diaphragmatic function, cardiac arrhythmias, and haemolysis. Prevention: start slowly at 10 kcal/kg/day, pre-treat with phosphate and thiamine. Wernicke's is also a risk in alcoholic/malnourished patients but presents with the triad of ophthalmoplegia, ataxia, and confusion — not respiratory failure and hypophosphataemia.
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A 55-year-old man with advanced hepatocellular carcinoma and poor oral intake is assessed for nutritional support. He has no gag reflex impairment; his GCS is 15. Intestinal motility is intact. Which route of nutritional support is MOST appropriate?
Correct. The fundamental rule of artificial nutrition support is: if the gut works, use it. Enteral nutrition (EN) via nasogastric tube is preferred over parenteral nutrition when the gastrointestinal tract is functional because EN preserves gut mucosal integrity, maintains the intestinal immune barrier, is associated with lower rates of infection and complications, and is less expensive. Total parenteral nutrition (TPN) is indicated only when the gut cannot be used (bowel obstruction, high-output fistula, severe malabsorption, ileus). In this patient, GI motility is intact, making NG enteral feeding the correct choice.
Indications for parenteral nutrition: bowel obstruction, short bowel syndrome, high-output proximal intestinal fistula, severe malabsorption, prolonged ileus. Complications of TPN: line sepsis (most common), metabolic complications (hyperglycaemia, electrolyte shifts, refeeding if malnourished), liver steatosis (prolonged TPN), venous thrombosis.
The fundamental principle of nutritional support: enteral is always preferred over parenteral when the gut is functional. Enteral nutrition preserves intestinal mucosal integrity and immune function. TPN is reserved for patients where the gut cannot be used (obstruction, ileus, high-output proximal fistula). Malignancy alone is not an indication for parenteral nutrition.
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