IM23.1-12,IM24.1-5 | Mineral Fluid Electrolyte Acid Base and Nutrition — Glossary

A worsening of chronic CO₂ retention beyond the compensated baseline; identified when HCO₃⁻ is below the expected chronic compensation level for the current PaCO₂; indicates an acute deterioration in a COPD or OHS patient and warrants urgent intervention (NIV, bronchodilators).

Calculated as Na⁺ − (Cl⁻ + HCO₃⁻); normal 8–12 mEq/L; represents unmeasured anions (albumin, phosphate, sulphate, organic anions); elevated in HAGMA when an organic acid accumulates; must be corrected for hypoalbuminaemia: add 2.5 mEq/L per 1 g/dL fall in albumin below 4.

Nonapeptide released from the posterior pituitary in response to rising plasma osmolality (>280 mOsm/kg) or falling blood volume; acts on V2 receptors in the renal collecting duct to insert aquaporin-2 water channels, increasing water reabsorption and concentrating urine.

The amount of strong acid (if positive) or base (if negative) required to titrate 1 litre of blood to pH 7.40 at normal PaCO₂ and temperature; normal −2 to +2 mEq/L; a base excess >+2 = metabolic alkalosis component; base excess <−2 = metabolic acidosis component; useful supplement to HCO₃⁻ in ABG interpretation but does not replace the anion gap calculation.

The active form of vitamin D produced by renal 1α-hydroxylation of 25-hydroxyvitamin D; stimulated by PTH; increases intestinal absorption of calcium and phosphate via TRPV6 channels and calbindin. Produced autonomously by macrophages in granulomatous disease.

10% calcium gluconate 10 mL IV over 3–5 minutes; first-line treatment in hyperkalaemia with ECG changes; raises the membrane depolarisation threshold, protecting cardiac cells from arrhythmia. Does NOT lower serum potassium. Acts within 1–3 minutes; duration approximately 30–60 minutes.

Calculated as (urine calcium × plasma creatinine) / (plasma calcium × urine creatinine); CCR <0.01 is diagnostic of familial hypocalciuric hypercalcaemia; CCR >0.02 is typical of primary hyperparathyroidism; essential test before parathyroid surgery.

See calcium SDL — listed here for cross-reference: the equivalent concept in K disorders is the transtubular potassium gradient (TTKG) or spot urine K-to-creatinine ratio, used to distinguish renal from extrarenal K losses.

G-protein-coupled receptor on parathyroid chief cells (and renal tubular cells) that detects the ionised calcium concentration; suppresses PTH secretion when calcium rises; loss-of-function mutations cause familial hypocalciuric hypercalcaemia.

The most important infectious complication of parenteral nutrition; caused by organisms colonising the central venous catheter (Staphylococcus aureus, coagulase-negative Staphylococci, Candida); prevented by strict asepsis during insertion and line care, use of a dedicated single-lumen catheter for PN, and daily review of catheter necessity.

A calcimimetic drug that allosterically sensitises the CaSR to calcium, suppressing PTH secretion and lowering serum calcium; used in patients with PHPT who are not surgical candidates, tertiary hyperparathyroidism, and parathyroid carcinoma; does not improve bone mineral density.

Adjusted serum calcium accounting for hypoalbuminaemia; formula: corrected Ca = measured Ca (mmol/L) + 0.02 × (40 − albumin in g/L); alternatively: corrected Ca (mg/dL) = measured Ca + 0.8 × (4 − albumin in g/dL). Necessary when albumin is low as total calcium underestimates ionised calcium.

Calculated as (measured AG − 12) / (24 − measured HCO₃⁻); compares the rise in AG to the fall in HCO₃⁻. DDR 1–2: pure HAGMA. DDR <1: concurrent NAGMA (HCO₃⁻ fell more than AG rose). DDR >2: concurrent metabolic alkalosis (HCO₃⁻ started higher than normal before the acidosis, masking the fall).

A disorder of urinary concentration causing hypotonic polyuria and polydipsia; central DI: ADH deficiency from posterior pituitary damage (responds to desmopressin); nephrogenic DI: renal resistance to ADH (causes include lithium, hypercalcaemia, hypokalaemia — does not respond to desmopressin).

Delivery of nutrients into the gastrointestinal tract via a feeding tube (NGT, nasoduodenal, nasojejunal, PEG, or jejunostomy); preferred over PN when the gut is functional; maintains gut mucosal integrity, reduces bacterial translocation, and has fewer infectious complications; indicated when oral intake is <50% of requirements for >3 days.

Autosomal dominant disorder from loss-of-function CaSR mutation; elevated calcium and PTH with LOW 24-hour urinary calcium and calcium-creatinine clearance ratio (CCR) <0.01; benign condition — parathyroidectomy is ineffective and contraindicated.

pH = 6.1 + log(HCO₃⁻ / (PaCO₂ × 0.03)); at normal values pH = 6.1 + log(24 / 1.2) = 6.1 + log(20) = 7.40. The ratio HCO₃⁻ / dissolved CO₂ is normally 20:1 — any change in this ratio changes pH.

Metabolic acidosis with AG >12 mEq/L (albumin-corrected); caused by accumulation of an unmeasured anion — ketones (DKA), lactate (lactic acidosis), uraemic anions, toxic alcohols (methanol, ethylene glycol), or salicylate. MUDPILES mnemonic.

Hypercalcaemia from tumour secretion of PTH-related protein (PTHrP), which binds the PTH-1 receptor and mimics PTH effects; PTH is suppressed; most common in squamous cell carcinoma of lung, head, neck, and oesophagus; renal cell and breast carcinoma.

Serum calcium above 2.6 mmol/L (10.5 mg/dL); classified as mild (2.6–3.0), moderate (3.0–3.5), and severe (>3.5 mmol/L); corrected for albumin in hypoalbuminaemic states.

Serum potassium >5.0 mmol/L; causes include reduced renal excretion (CKD, RAAS drugs), transcellular shift (acidosis, insulin deficiency, rhabdomyolysis), and pseudohyperkalaemia (haemolysis). ECG progression: peaked T waves → PR prolongation → wide QRS → sine wave → VF.

Serum sodium >145 mmol/L; always indicates a hyperosmolar state from free water deficit relative to sodium; occurs when water intake or renal conservation is inadequate (access to water impaired or thirst absent).

Sodium chloride 3% (513 mmol/L Na); used specifically for acute severe symptomatic hyponatraemia (seizures, coma) at 100 mL bolus IV over 10–15 minutes, repeated up to three times. The only indication for hypertonic saline in hyponatraemia — never for chronic asymptomatic hyponatraemia.

Serum potassium <3.5 mmol/L; classified by mechanism — transcellular shift (insulin, alkalosis, catecholamines), renal losses (diuretics, hyperaldosteronism, hypomagnesaemia — urine K >20 mmol/L), or extrarenal losses (GI — urine K <20 mmol/L).

Low serum magnesium (<0.70 mmol/L) causes renal K wasting by keeping ROMK channels open in the cortical collecting duct; hypokalaemia refractory to K replacement strongly suggests concurrent hypomagnesaemia; Mg must be corrected first (IV MgSO₄ 10–20 mmol over 30–60 min).

Serum sodium <135 mmol/L; reflects water excess relative to sodium (not necessarily sodium depletion); classified by serum osmolality (isotonic/hypertonic/hypotonic) and then by volume status (hypovolaemic/euvolaemic/hypervolaemic).

Rapid PTH assay (half-life 2–4 min) performed before and 10 minutes after parathyroid adenoma resection; a >50% fall in PTH level confirms complete removal of hyperfunctioning tissue (Miami criterion); guides minimally invasive parathyroidectomy.

Deep, regular, rapid breathing pattern seen in severe metabolic acidosis (especially DKA and uraemia); represents maximal compensatory hyperventilation blowing off CO₂ to reduce the respiratory component of the acid load; clinically the breath may be fruity (ketones) in DKA.

Severe protein deficiency with relatively adequate caloric intake; hallmark: hypoalbuminaemia causing protein-deficiency oedema (may mask wasting), 'flaky paint' dermatosis, hepatomegaly (fatty infiltration from absent VLDL synthesis), flag sign in hair, misery. Serum albumin severely low (<2.0 g/dL).

HAGMA from lactate accumulation; Type A: tissue hypoperfusion/hypoxia (shock, cardiac arrest, mesenteric ischaemia, severe anaemia); Type B: normal perfusion (metformin, antiretrovirals, liver failure, malignancy, B1 deficiency, cyanide). Diagnosis: serum lactate >4 mmol/L with HAGMA.

A validated three-parameter nutritional screening tool using BMI, unintentional weight loss percentage, and acute disease effect (no intake >5 days); scores 0 (low risk) to ≥2 (high risk); widely used in community and hospital settings.

Severe protein-calorie malnutrition with global nutrient depletion; clinical features: extreme wasting (fat and muscle), loose wrinkled skin, 'old man' facies, thin hair, no oedema; serum albumin preserved; BMI severely reduced; MUAC <11.5 cm in under-5 children.

Anaemia from impaired DNA synthesis in erythroid precursors due to B12 or folate deficiency; blood film shows macrocytosis (MCV >100 fL) and hypersegmented neutrophils (≥5 lobes); B12 deficiency additionally causes SACD; folate deficiency does not cause neurological disease.

Primary fall in HCO₃⁻ (<22 mmol/L) driving pH below 7.35; classified by anion gap into HAGMA (MUDPILES: methanol, uraemia, DKA, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates) and NAGMA (diarrhoea, RTA, saline infusion, hypoaldosteronism).

Primary rise in HCO₃⁻ (>26 mmol/L) driving pH above 7.45; generated by H⁺ loss (vomiting, diuretics) or HCO₃⁻ gain; maintained by Cl and volume depletion. Classified as chloride-responsive (urine Cl <20 mmol/L — treat with saline) or chloride-resistant (urine Cl >20 — hyperaldosteronism, severe hypokalaemia).

Autosomal dominant syndrome caused by MEN1 gene (menin) mutation; comprises parathyroid adenoma/hyperplasia (most common, >90%), anterior pituitary adenoma (prolactinoma most common), and pancreatic/duodenal neuroendocrine tumour (gastrinoma, insulinoma); PHPT is often the first manifestation.

Kidney stones occurring in ~10–20% of primary hyperparathyroidism patients, predominantly calcium oxalate or calcium phosphate; results from hypercalciuria and hyperphosphaturia; one of the standard surgical criteria (any stone on imaging warrants parathyroidectomy).

Measure of the difference between nitrogen intake (dietary protein) and nitrogen losses (urine, stool, skin); calculated as protein intake (g/day) ÷ 6.25 − (urinary urea nitrogen g/day + 4 g insensible losses); positive = anabolic state; negative = catabolic state; critical illness causes prolonged negative nitrogen balance.

Metabolic acidosis with normal AG (8–12 mEq/L), i.e., hyperchloraemic acidosis; caused by HCO₃⁻ loss (diarrhoea — urine AG negative) or impaired H⁺ excretion (RTA — urine AG positive); also caused by large-volume saline infusion (dilution and Cl⁻ excess).

Validated nutritional screening tool for hospitalised patients; combines a nutritional status score (recent weight loss, BMI, reduced intake) with a disease severity score; total ≥3 indicates nutritional risk and warrants active nutritional support and dietitian referral.

A neurological complication of overly rapid correction of chronic hyponatraemia; previously called central pontine myelinolysis; occurs when serum Na rises >12 mmol/L in 24 hours in a brain adapted to low sodium; presents 2–4 days after correction with dysarthria, dysphagia, quadriplegia, and coma; largely irreversible.

Severe skeletal manifestation of untreated primary hyperparathyroidism; characterised by subperiosteal bone resorption (most visible on radial aspect of middle phalanges), brown tumours, and bone cysts; now rare due to early biochemical diagnosis.

84-amino acid peptide secreted by parathyroid chief cells in response to low ionised calcium; raises serum calcium by stimulating osteoclast-mediated bone resorption, increasing renal distal tubule calcium reabsorption, promoting phosphaturia, and activating renal 1α-hydroxylase to produce calcitriol.

Intravenous delivery of nutrients (glucose, amino acids, lipid emulsion, electrolytes, vitamins, trace elements) directly into the bloodstream via central venous catheter; reserved for when the gut cannot be used; complications include CRBSI, hyperglycaemia, TPN-associated cholestasis, refeeding syndrome, and metabolic derangements.

Niacin (vitamin B3) deficiency syndrome; the 4 Ds: photosensitive Dermatitis (Casal necklace on the neck, glove-and-stocking on sun-exposed areas), Diarrhoea, Dementia, Death; classic in populations dependent on untreated maize (bound niacin + absent tryptophan); treated with oral nicotinamide.

Metabolic alkalosis occurring after rapid correction of chronic CO₂ retention (e.g., by mechanical ventilation); the kidneys have accumulated HCO₃⁻ as chronic compensation; when PaCO₂ is suddenly normalised by ventilation, HCO₃⁻ remains elevated until the kidney can excrete it (days); treat by weaning ventilation slowly and correcting chloride/potassium depletion.

Autonomous aldosterone secretion from an adrenal adenoma (60–70%) or bilateral adrenal hyperplasia (30–40%); causes hypertension, hypokalaemia (usually <3.0 mmol/L), and metabolic alkalosis. Screened by aldosterone-to-renin ratio >30 with aldosterone >15 ng/dL; confirmed by CT adrenal and adrenal vein sampling.

Autonomous overproduction of PTH most commonly from a single parathyroid adenoma (80–85%); biochemical hallmark is elevated calcium + elevated or inappropriately non-suppressed PTH + low phosphate; most commonly diagnosed incidentally on routine biochemistry.

A spectrum of undernutrition from mild inadequacy to severe marasmus and kwashiorkor; results from insufficient intake of calories and/or protein; causes wasting, immunosuppression, poor wound healing, and increased mortality; classified clinically as marasmus (wasting without oedema, preserved albumin) or kwashiorkor (oedema, low albumin, relatively preserved fat).

A protein sharing amino-terminal homology with PTH that binds the PTH-1 receptor; normally produced in many tissues for paracrine functions; when secreted in excess by tumours, causes humoral hypercalcaemia of malignancy; undetectable in primary hyperparathyroidism.

Metabolic complication of nutritional repletion after prolonged starvation; hallmark: hypophosphataemia (and hypokalaemia, hypomagnesaemia, thiamine depletion) when carbohydrate causes insulin surge driving electrolytes into cells; consequences: respiratory failure, cardiac arrhythmia, neuromuscular weakness; prevented by slow refeeding (5–10 kcal/kg/day) with prophylactic phosphate and thiamine supplementation.

A group of disorders impairing renal acid excretion: Type 1 (distal) — failure of H⁺ secretion in collecting duct → urine pH >5.5, severe hypokalaemia, nephrocalcinosis; Type 2 (proximal) — failure of HCO₃⁻ reabsorption; Type 4 (hyporeninaemic) — most common, from hypoaldosteronism in diabetic nephropathy → hyperkalaemia with NAGMA.

Primary rise in PaCO₂ (>45 mmHg) from reduced alveolar ventilation, causing pH <7.35; causes include COPD, opioid toxicity, neuromuscular disease, obesity hypoventilation; acute compensation: HCO₃⁻ +1 mmol/L per 10 mmHg PaCO₂ rise; chronic compensation: +3.5 mmol/L per 10 mmHg.

Primary fall in PaCO₂ (<35 mmHg) from hyperventilation, causing pH >7.45; causes include anxiety, hypoxaemia, sepsis, salicylate poisoning, pregnancy, hepatic encephalopathy; acute compensation: HCO₃⁻ −2 mmol/L per 10 mmHg fall; chronic: −5 mmol/L per 10 mmHg.

Classic mixed disorder: respiratory alkalosis (salicylate directly stimulates the respiratory centre, causing hyperventilation and CO₂ blow-off) + metabolic acidosis (uncoupling of oxidative phosphorylation, organic acid accumulation); seen especially in children at toxic levels; ABG shows low PaCO₂ + low HCO₃⁻.

Vitamin C (ascorbic acid) deficiency; impairs collagen synthesis (cofactor for prolyl and lysyl hydroxylase); clinical features: perifollicular haemorrhage (corkscrew hairs), gingival bleeding and ulceration, haemarthroses, poor wound healing, anaemia (reduced iron absorption); treated with vitamin C 300–500 mg/day.

Euvolaemic hypotonic hyponatraemia with inappropriately concentrated urine (>100 mOsm/kg) and elevated urine sodium (>40 mmol/L) in the absence of hypothyroidism, adrenal insufficiency, or diuretic use; caused by CNS disorders, pulmonary disease, drugs, or ectopic ADH from malignancy (especially SCLC).

Demyelination of the posterior columns (impaired vibration and proprioception) and lateral columns (upper motor neuron signs) from vitamin B12 deficiency; presenting features: peripheral neuropathy (glove-stocking), absent ankle jerks, positive Babinski, spastic paraparesis; absent in folate deficiency — the key distinguishing feature; treated with IM hydroxocobalamin.

A depolarising neuromuscular blocking agent that opens ACh-receptor-associated K channels; can cause a dangerous rise in serum K (0.5–1.0 mmol/L normal rise; potentially much larger in burns, crush injury, prolonged immobilisation, upper motor neuron lesions due to upregulated receptors); CONTRAINDICATED in these high-risk conditions.

Nuclear medicine imaging using technetium-99m sestamibi, which is preferentially retained in hyperfunctioning parathyroid tissue; used to localise single adenoma before minimally invasive parathyroidectomy; sensitivity ~80% for single adenoma; not used to diagnose PHPT.

A selective V2 receptor antagonist (vaptan) that blocks ADH action in the collecting duct, promoting free water excretion (aquaresis) without sodium loss; used for euvolaemic (SIADH) and hypervolaemic hyponatraemia refractory to fluid restriction; risk of overcorrection requires close monitoring.

Movement of potassium between the intracellular and extracellular compartments without change in total body K; caused by insulin (K into cells), catecholamines (K into cells), alkalosis (K into cells), acidosis (K out of cells); explains why serum K can change rapidly without K gain or loss.

A calculated index estimating the aldosterone-driven K secretion in the collecting duct; TTKG >4 in hypokalaemia = renal K wasting (aldosterone excess, diuretics); TTKG <2 in hyperkalaemia = insufficient renal K excretion (aldosterone deficiency, CKD).

Calculated as urine (Na + K − Cl); distinguishes NAGMA from diarrhoea vs RTA. In diarrhoea: kidneys excrete NH₄⁺ appropriately → UAG negative (NH₄⁺ counted as unmeasured cation lowers Cl compared to Na+K). In RTA: impaired NH₄⁺ excretion → UAG positive (Na+K exceeds Cl in urine).

25-OH vitamin D <30 nmol/L; most prevalent nutritional deficiency in India; causes rickets (children) and osteomalacia (adults) — impaired bone mineralisation, proximal myopathy, Looser zones on X-ray; biochemistry: low 25-OH vitamin D, raised PTH, raised alkaline phosphatase, low-normal calcium and phosphate; treated with cholecalciferol (D3) supplementation.

Formula for estimating free water deficit in hypernatraemia: Water deficit (L) = TBW × [(serum Na / 140) − 1]; TBW = 0.6 × weight (kg) in men or 0.5 × weight in women. Replacement uses hypotonic fluids (5% dextrose or 0.45% saline); correct no faster than 10–12 mmol/L Na per 24 hours.

Acute thiamine (B1) deficiency emergency characterised by the classic triad: confusion, ophthalmoplegia (any abnormal eye movement), and ataxia; seen in alcoholics and any malnourished patient; treated with IV thiamine (pabrinex) BEFORE glucose; if untreated, progresses to Korsakoff psychosis (anterograde amnesia, confabulation — largely irreversible).

Predicts the expected PaCO₂ response to metabolic acidosis: expected PaCO₂ = 1.5 × HCO₃⁻ + 8 ± 2 mmHg. If measured PaCO₂ is above the expected range, concurrent respiratory acidosis is present. If below, concurrent respiratory alkalosis. The most important compensation formula to memorise for clinical practice.

A potent nitrogen-containing bisphosphonate administered IV (4 mg over 15 minutes); inhibits osteoclast function by blocking farnesyl pyrophosphate synthase; first-line pharmacological treatment for moderate-severe hypercalcaemia; onset 24–48 hours; duration 2–4 weeks; dose-adjust for renal impairment.