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IM23.1-12,IM24.1-5 | Mineral Fluid Electrolyte Acid Base and Nutrition — Graded Quiz
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A 58-year-old woman undergoing investigation for nephrolithiasis has a serum calcium of 2.9 mmol/L and PTH of 72 pg/mL (normal 10–65). Her 24-hour urinary calcium is 450 mg (normal <300 mg). A DEXA scan shows osteoporosis at the lumbar spine (T-score −2.8). Which factor, if present, would be the STRONGEST indication for surgical parathyroidectomy?
Correct. This patient has symptomatic primary hyperparathyroidism — active nephrolithiasis, hypercalciuria, AND osteoporosis (T-score −2.8, below the −2.5 threshold). The current guidelines (Fourth International Workshop on Asymptomatic PHPT) recommend parathyroidectomy when ANY of the following criteria are met: (1) serum calcium >1 mg/dL (0.25 mmol/L) above normal upper limit; (2) creatinine clearance <60 mL/min OR 24-hour urinary calcium >400 mg/day with nephrolithiasis/nephrocalcinosis; (3) BMD T-score ≤−2.5 at any site or vertebral fracture on imaging; (4) age <50 years. In this patient, criteria 2 and 3 are both met — but the single strongest indication that combines end-organ damage from both targets (bone AND kidney) is the combination of symptomatic stones with T-score below −2.5.
Surgical indications for asymptomatic primary hyperparathyroidism: calcium >0.25 mmol/L above normal; eGFR <60 mL/min or nephrolithiasis or nephrocalcinosis or urinary calcium >400 mg/day with hypercalciuric stone risk; T-score ≤−2.5 or vertebral fracture; age <50. If no criteria met: surveillance every 1–2 years (calcium, renal function, DEXA). Definitive cure: minimally invasive parathyroidectomy.
Surgery for primary hyperparathyroidism is indicated by end-organ damage criteria: calcium >0.25 mmol/L above normal, T-score ≤−2.5, symptomatic nephrolithiasis with hypercalciuria >400 mg/day, CrCl <60 mL/min, or age <50 years. This patient meets both the bone criterion (T-score −2.8) and the kidney criterion (symptomatic stones, hypercalciuria) — making parathyroidectomy clearly indicated. Elevated PTH alone, without meeting any end-organ criterion, is not itself a surgical indication.
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A 70-year-old woman with a 2-week history of progressive confusion, nausea, and reduced oral intake is brought to the emergency department. Her daughter reports she is on chlorpropamide (an oral hypoglycaemic) and hydrochlorothiazide. On examination she is euvolaemic, GCS 12/15. Lab results: Na 108 mmol/L, serum osmolality 225 mOsm/kg, urine osmolality 610 mOsm/kg, urine Na 55 mmol/L. What is the SINGLE most important initial treatment decision?
Correct. This is severe symptomatic chronic hyponatraemia (Na 108 mmol/L, GCS 12, duration >48 hours implied by the 2-week history). The pattern (euvolaemic, concentrated urine, elevated urine Na, two drugs known to cause SIADH — chlorpropamide augments ADH action, HCTZ causes hypovolaemia/SIADH) confirms SIADH. Management of severe symptomatic chronic hyponatraemia: small bolus of 3% saline (100–150 mL over 20 minutes, repeat once or twice if seizures/coma continue) to raise Na by ~5 mmol/L and relieve acute symptoms; then LIMIT total correction to 8–10 mmol/L/24h to prevent osmotic demyelination. Rapid full correction in chronic hyponatraemia causes ODS — the osmolyte-depleted brain cannot re-adapt. Stop causative drugs. Free water restriction alone is too slow for acute symptomatic cases.
Treatment of severe symptomatic chronic SIADH hyponatraemia: 3% saline 100–150 mL bolus to raise Na ~5 mmol/L acutely (symptom relief); cap total correction at 8–10 mmol/L/24h. If overcorrection occurs: DDAVP 2 mcg IV + D5W to lower Na back. Remove offending drug. Long-term: fluid restriction, demeclocycline (unavailable in India), vaptans (tolvaptan) where available.
In symptomatic chronic hyponatraemia, the goal is to relieve dangerous symptoms (seizures, coma) with a small initial rise of ~5 mmol/L using 3% saline, then limit total 24-hour correction to 8–10 mmol/L. Attempting rapid correction to normal will cause osmotic demyelination. Stop the offending drugs (chlorpropamide, thiazide). Free water restriction is the long-term treatment once stability is achieved.
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A 19-year-old medical student presents to the ED with severe perioral tingling, carpopedal spasm, and a positive Trousseau's sign. She reports anxiety and hyperventilation for the past 30 minutes after learning her exam results. ABG: pH 7.58, PaCO2 22 mmHg, HCO3 20 mmol/L. Serum calcium is 2.3 mmol/L. What is the BEST explanation for her neuromuscular symptoms?
Correct. This is respiratory alkalosis from acute hyperventilation (pH 7.58, low PaCO2 22, HCO3 minimally decreased suggesting acute not chronic). The expected HCO3 compensation for acute respiratory alkalosis is a fall of 2 mmol/L per 10 mmHg fall in PaCO2: fall in PaCO2 = 40 − 22 = 18 mmHg → expected HCO3 fall = 18/10 × 2 = 3.6 mmol/L → expected HCO3 ≈ 20.4 mmol/L, consistent with the measured 20 (acute, appropriate compensation). Alkalosis increases the binding of ionised calcium to albumin, decreasing ionised (physiologically active) calcium without changing total calcium. The result is functional hypocalcaemia — tetany, carpopedal spasm, perioral tingling — despite a normal total serum calcium.
Acute respiratory alkalosis: expected HCO3 fall = 2 mmol/L per 10 mmHg fall in PaCO2. Ionised calcium falls in alkalosis (increased albumin binding) → tetany and carpopedal spasm. Signs of hypocalcaemia: Chvostek (facial nerve tap → ipsilateral facial twitch), Trousseau (BP cuff → carpopedal spasm within 3 minutes). Treat hyperventilation respiratory alkalosis with rebreathing; do not administer IV calcium unless ionised Ca is truly low.
In respiratory alkalosis, the raised pH increases protein binding of ionised calcium — total calcium is unchanged but ionised calcium falls, causing functional hypocalcaemia. Trousseau's sign (carpal spasm when brachial artery occluded by BP cuff) and Chvostek's sign reflect neuromuscular excitability from low ionised calcium. Treatment: rebreathing into a paper bag to raise PaCO2; address the anxiety precipitant. This mechanism also explains why hyperventilation during labour can cause tetany.
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A 55-year-old man with type 2 diabetes and hypertension is admitted with a 4-day history of diarrhoea. ABG: pH 7.30, PaCO2 30 mmHg, HCO3 14 mmol/L. Na 140, Cl 118, K 3.2, creatinine 130 mmol/L. Anion gap = 140 − (118 + 14) = 8 mmol/L. What is the PRIMARY acid-base disorder and its MOST likely cause?
Correct. The anion gap is 8 mmol/L — normal (normal range 8–12 mmol/L). This is a normal anion-gap metabolic acidosis (NAGMA), also called hyperchloraemic metabolic acidosis. In NAGMA, every bicarbonate lost is replaced by a chloride ion (to maintain electroneutrality), so chloride rises while AG stays normal. The most common causes: diarrhoea (pancreatic secretions and intestinal fluid are bicarbonate-rich — diarrhoea directly removes HCO3), renal tubular acidosis (failure to excrete acid), saline infusion (dilutional), urinary diversion (uretero-sigmoid or ileal conduit). In this patient, 4 days of diarrhoea is the clear cause. The compensation is appropriate: expected PaCO2 = 1.5 × 14 + 8 = 21 + 8 = 29 ± 2 = 27–31, measured 30 — appropriate.
NAGMA vs HAGMA: key distinction is the anion gap. NAGMA causes: DURHAM — Diarrhoea, Ureteric diversion, RTA, High chloride loads (saline), Adrenal insufficiency, drugs (acetazolamide), Mineralocorticoid deficiency. In NAGMA from diarrhoea: check urine anion gap (UAG = urine Na + K − Cl); UAG negative (net positive ammonium excretion) = GI cause; UAG positive = renal cause (RTA, impaired ammoniagenesis).
A normal anion gap of 8 mmol/L identifies this as NAGMA (normal AG metabolic acidosis, hyperchloraemic). NAGMA causes: diarrhoea (HCO3-rich pancreatic/intestinal fluid loss), RTA, saline overload, carbonic anhydrase inhibitors, urinary diversion. High-AG causes (MUDPILES) include DKA, lactic acidosis, uraemia, toxins — but the anion gap must be elevated for these. This patient's diarrhoea × 4 days with normal AG and elevated chloride confirms gastrointestinal HCO3 loss.
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A 38-year-old woman with Crohn's disease has a BMI of 17.2 kg/m2, bilateral pitting oedema to mid-shin, and generalised muscle wasting but relatively preserved subcutaneous fat. Serum albumin is 18 g/L. Her hair is sparse and easily plucked. She has no angular stomatitis or glossitis. Which nutritional syndrome does this picture BEST represent?
Correct. Kwashiorkor is characterised by protein deficiency in the setting of relatively adequate energy intake. The clinical hallmarks are: oedema (from hypoalbuminaemia reducing oncotic pressure), hypoalbuminaemia (<25 g/L typically), muscle wasting with PRESERVED subcutaneous fat, sparse easily-plucked hair (flag sign in severe cases), skin changes (hyperpigmentation, 'flaky paint' dermatosis). In marasmus, there is severe total energy-protein deficiency — both fat and muscle are severely depleted, with a 'wizened old person' appearance but NO oedema. Marasmic-kwashiorkor has features of both. This patient's preserved fat, oedema, and very low albumin = kwashiorkor.
Marasmus vs kwashiorkor: Marasmus — severe total calorie deficiency, no oedema, 'aged-appearing' child/adult, severely depleted fat and muscle, relatively preserved serum albumin for degree of wasting. Kwashiorkor — protein deficiency ± adequate energy, bilateral oedema, hypoalbuminaemia <25 g/L, 'flag sign' (alternating light/dark bands in hair), moon face, skin 'flaky paint', hepatomegaly (fatty liver). Hospital malnutrition = often mixed. MUST, MNA, NRS-2002, SNAQ are validated screening tools.
Kwashiorkor = protein deficiency: oedema (hypoalbuminaemia), preserved fat, muscle wasting, hypoalbuminaemia, hair and skin changes. Marasmus = energy+protein deficiency: severe wasting of both fat and muscle, no oedema, 'old-person' cachexia. The key discriminator here is OEDEMA with PRESERVED FAT — that combination points to kwashiorkor. Albumin 18 g/L confirms severe hypoproteinaemia.
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A 60-year-old man is admitted with pneumonia. His ABG on room air: pH 7.32, PaCO2 55 mmHg, HCO3 27 mmol/L. He is on no medications affecting acid-base. Which of the following BEST describes the acid-base status?
Correct. pH 7.32 = acidosis. PaCO2 55 = elevated → primary respiratory acidosis. HCO3 27 = mildly elevated. For ACUTE respiratory acidosis, expected HCO3 compensation = 24 + 1 × (PaCO2 − 40)/10 = 24 + 1 × 1.5 = 25.5 mmol/L. Measured HCO3 is 27 — slightly above expected for acute (25.5) but well below the chronic compensation: expected HCO3 for CHRONIC respiratory acidosis = 24 + 3.5 × (PaCO2 − 40)/10 = 24 + 3.5 × 1.5 = 24 + 5.25 = 29.25. Measured 27 falls between acute (25.5) and chronic (29.25) expected values, consistent with an acute (or acute-on-chronic) respiratory acidosis with partial metabolic compensation developing. Context (acute pneumonia) supports acute/subacute presentation.
Respiratory acidosis compensation: Acute — HCO3 rises 1 mmol/L per 10 mmHg PaCO2 rise. Chronic — HCO3 rises 3.5 mmol/L per 10 mmHg. If HCO3 > expected: concurrent metabolic alkalosis. If HCO3 < expected: concurrent metabolic acidosis. Causes of respiratory acidosis: COPD, asthma, severe pneumonia, neuromuscular disease (GBS, MG), chest wall disorders, central hypoventilation (narcotics, brainstem lesion).
The primary disorder is elevated PaCO2 → respiratory acidosis. For acute respiratory acidosis: expected HCO3 rises by 1 mmol/L per 10 mmHg PaCO2 rise above 40. For chronic: expected rise is 3.5 mmol/L per 10 mmHg. This patient's HCO3 (27) is between the acute (25.5) and chronic (29.25) expected values — indicating partial/incomplete metabolic compensation, consistent with an acute presentation of respiratory acidosis. The context of acute pneumonia confirms the acuity.
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A 45-year-old woman with known hypothyroidism (on subtherapeutic levothyroxine) presents with lethargy and mild confusion. Serum Na 128 mmol/L, osmolality 265 mOsm/kg, urine osmolality 380 mOsm/kg, urine Na 28 mmol/L. She is euvolaemic. TSH is 48 mIU/L. Which pathophysiological mechanism BEST explains her hyponatraemia?
Correct. Hypothyroidism causes a SIADH-like state by impairing free water excretion. Thyroid hormone is required for normal cardiac output and therefore normal renal perfusion. In hypothyroidism, reduced cardiac output and reduced peripheral vascular resistance lead to non-osmotic stimulation of ADH release (the same mechanism as heart failure, but more subtle). Additionally, decreased GFR reduces diluting capacity. The net result is concentrated urine (inappropriately, given the low plasma osmolality) and hyponatraemia — biochemically indistinguishable from SIADH. Treatment: levothyroxine replacement corrects the hyponatraemia; do not aggressively correct sodium before identifying and treating the underlying hypothyroidism.
SIADH diagnostic criteria require exclusion of hypothyroidism and adrenal insufficiency — both produce identical biochemical pictures. Hypothyroidism: impaired free water excretion via non-osmotic ADH stimulation + reduced GFR. Adrenal insufficiency (Addison's): cortisol deficiency also increases ADH. In both, treating the underlying cause normalises sodium. Never attribute hyponatraemia to SIADH without first checking TSH and morning cortisol.
Hypothyroidism-associated hyponatraemia results from non-osmotic ADH stimulation secondary to reduced cardiac output — producing a SIADH-like picture: euvolaemia, low plasma osmolality, inappropriately concentrated urine, and urine Na >20 mmol/L. Treatment: levothyroxine replacement, not aggressive hypertonic saline. Always exclude hypothyroidism and adrenal insufficiency before diagnosing SIADH.
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A patient with multiple myeloma has a serum sodium of 128 mmol/L reported by the laboratory. A simultaneously measured serum osmolality is 298 mOsm/kg (normal 285–295). Urine osmolality is 620 mOsm/kg. The patient is clinically euvolaemic and asymptomatic. What is the CORRECT interpretation?
Correct. Pseudohyponatraemia occurs when massively elevated proteins (paraproteinaemia, severe hypertriglyceridaemia) occupy plasma volume, reducing the water fraction. Older flame photometry methods (and many modern indirect ISE methods) measure sodium per unit of total plasma volume, not per unit of plasma water — so if proteins are elevated, the reported sodium is falsely low. The key diagnostic clue: serum osmolality (measured directly by freezing-point depression) is NORMAL at 298 mOsm/kg. True hyponatraemia is always accompanied by low plasma osmolality (<280 mOsm/kg). Normal osmolality + low sodium = pseudohyponatraemia. Treatment: none for the sodium; treat the myeloma. Do NOT fluid-restrict or give hypertonic saline.
Step 1 in hyponatraemia algorithm: measure plasma osmolality. Low (<280) = true hypo-osmolar hyponatraemia → proceed to volume status. Normal (285–295) = pseudohyponatraemia (protein/lipid artefact). High (>295) = hypertonic hyponatraemia (glucose, mannitol, glycine) — osmole drawing water from cells. This step alone avoids treating patients who do not need treatment.
Pseudohyponatraemia: sodium is artefactually low but osmolality is normal. Seen with marked hyperproteinaemia (myeloma) or severe hypertriglyceridaemia. The discriminating test is measured plasma osmolality — true hyponatraemia always causes low osmolality (<280 mOsm/kg). Normal osmolality + low sodium = pseudohyponatraemia; no treatment needed for the sodium per se. Direct ISE (blood gas analyser measuring undiluted sample) gives the correct sodium.
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A 32-year-old man with poorly controlled type 1 diabetes is admitted with DKA. Initial ABG: pH 7.14, PaCO2 20 mmHg, HCO3 6 mmol/L. Na 134, K 5.8, Cl 96. Calculated anion gap = 134 − (96 + 6) = 32 mmol/L. Delta-delta calculation: delta AG = 32 − 12 = 20; delta HCO3 = 24 − 6 = 18. Delta-delta ratio = 20/18 = 1.1. What does this ratio indicate?
Correct. The delta-delta (delta ratio) = (measured AG − normal AG) / (normal HCO3 − measured HCO3) = 20/18 = 1.1. Interpretation: ratio 1–2 = pure high-AG metabolic acidosis (the rise in unmeasured anions accounts for approximately the same fall in bicarbonate). Ratio <1: some of the bicarbonate loss is from a concurrent NAGMA (HCO3 falls more than the AG rises). Ratio >2: concurrent metabolic alkalosis (bicarbonate has not fallen as far as expected — an alkalaemic process is 'hiding' bicarbonate). This patient's ratio of 1.1 confirms a pure HAGMA — DKA without a concurrent acid-base disturbance.
Delta-delta (gap-gap) ratio = (AG − 12) / (24 − HCO3). Interpretation: <1 = concurrent NAGMA; 1–2 = pure HAGMA; >2 = concurrent metabolic alkalosis. Clinical use: a vomiting DKA patient on diuretics might have delta-delta >2 (metabolic alkalosis from vomiting offsetting the DKA metabolic acidosis). Delta-delta detects hidden concurrent disorders in complex ABG interpretation.
Delta-delta interpretation: ratio = delta AG / delta HCO3. Less than 1: concurrent NAGMA (extra bicarbonate loss beyond what the anion gap accounts for). 1–2: pure HAGMA. Greater than 2: concurrent metabolic alkalosis (less bicarbonate loss than expected from the anion gap rise — an alkalotic process is protecting bicarbonate). This patient's ratio of 1.1 is firmly in the 'pure HAGMA' range — consistent with uncomplicated DKA.
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A 65-year-old woman with a 5 kg intentional weight loss over 12 months, BMI 18.5 kg/m2, is scheduled for elective colorectal resection. Pre-operative nutritional assessment reveals serum albumin 30 g/L, prealbumin 14 mg/dL, triceps skinfold 8 mm, and grip strength below the 10th percentile. What is the SINGLE MOST appropriate nutritional intervention BEFORE surgery?
Correct. This patient has moderate-to-severe preoperative malnutrition (recent significant weight loss, low BMI, low albumin, reduced muscle function). Evidence from ESPEN and ASPEN guidelines strongly supports preoperative nutritional optimisation in malnourished surgical patients: 7–14 days of oral nutritional supplements (ONS) or enteral feeding before elective surgery reduces postoperative infections, anastomotic leaks, and length of hospital stay. Enteral is preferred over TPN in patients with a functional gut. TPN is reserved for severe malnutrition where enteral feeding is not feasible or tolerated. Immediate surgery in a malnourished patient increases perioperative morbidity significantly.
Nutritional assessment tools: NRS-2002 (ESPEN recommended for hospitalised patients), MUST (community/outpatient), NutriSTEP/MNA (elderly). Pre-operative malnutrition indicators: BMI <18.5, >10% weight loss in 6 months, albumin <30 g/L. ESPEN recommends 7–14 days preoperative nutritional support for severe malnutrition. Immune-enhancing formulas (arginine, omega-3, glutamine) have evidence for elective GI surgery patients.
Preoperative nutritional optimisation for 7–14 days is strongly recommended for malnourished patients before elective major surgery. Oral nutritional supplements or enteral feeding (gut is functional) reduce postoperative complications. TPN before surgery is only used when enteral feeding is not feasible. Proceeding straight to surgery in this patient significantly increases the risk of anastomotic dehiscence, infection, and poor wound healing.
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A 50-year-old woman with a history of alcohol use disorder and poor oral intake presents with ataxia, bilateral lateral rectus palsy, and confusion (GCS 13). Blood glucose is 3.8 mmol/L. The intern plans to start IV dextrose immediately to prevent worsening hypoglycaemia. What SHOULD be given BEFORE the dextrose?
Correct. This patient has the classic triad of Wernicke's encephalopathy: ophthalmoplegia (lateral rectus palsy), ataxia, and confusion. Wernicke's is caused by thiamine (vitamin B1) deficiency — common in alcohol use disorder, prolonged starvation, hyperemesis gravidarum. Administering glucose without thiamine precipitates Wernicke's by consuming the last reserves of thiamine used in the Krebs cycle. The rule: THIAMINE BEFORE GLUCOSE in ANY malnourished/alcoholic patient requiring IV fluids. IV thiamine 200–500 mg (Pabrinex in UK; individual ampoules in India) should be given before or simultaneously with dextrose. Wernicke's must be treated immediately — if untreated it progresses to Korsakoff psychosis (irreversible anterograde amnesia) in up to 80% of cases.
Wernicke's encephalopathy triad: ophthalmoplegia (lateral rectus palsy/nystagmus), ataxia, confusion. Only 16% of cases have all three — treat empirically. Thiamine BEFORE glucose: rule applies in all alcoholic, malnourished, hyperemesis, post-bariatric surgery, and prolonged IV fluid patients. Dose: IV thiamine 200–500 mg (Pabrinex 2 pairs IM 3× daily for 3 days in UK). Prevention of Korsakoff (permanent anterograde amnesia, confabulation) depends on prompt thiamine administration.
Thiamine (vitamin B1) MUST be given before dextrose in any malnourished, alcoholic, or chronically starved patient. Glucose drives the Krebs cycle, consuming the last reserves of thiamine, precipitating Wernicke's encephalopathy — even in patients who have not yet developed it. The triad (ophthalmoplegia, ataxia, confusion) indicates Wernicke's is already present — IV thiamine 200–500 mg is an emergency. Untreated Wernicke's → Korsakoff syndrome (irreversible amnesia).
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