BI9.1-3 | Minerals, electrolytes, Water and Acid base balance — Glossary

The most clinically important mineral; ~65% in haemoglobin; absorbed in duodenum via DMT1; stored as ferritin; regulated by hepcidin; deficiency is the leading nutritional disorder in India

The major intracellular iron storage protein; serum ferritin is the best marker of iron stores but is also an acute phase reactant (elevated in inflammation independent of iron status)

The plasma iron transport protein; each molecule carries 2 Fe3+ ions; serum levels rise in iron deficiency (increased TIBC) and fall in chronic disease

The master regulatory peptide hormone of iron homeostasis produced by the liver; binds and degrades ferroportin to block iron release from enterocytes and macrophages

The only known iron exporter on the basolateral membrane of enterocytes, macrophages, and hepatocytes; regulated by hepcidin binding and internalisation

The most common nutritional anaemia worldwide; characterised by microcytic hypochromic red cells, low ferritin, low transferrin saturation, and elevated TIBC

Hereditary iron overload disorder (HFE gene, C282Y mutation) with inappropriately low hepcidin leading to excessive iron deposition in liver, pancreas, heart, skin, and joints

The most abundant mineral in the body; 99% in bones as hydroxyapatite; ionised Ca2+ in blood tightly regulated at 4.5-5.5 mg/dL by PTH, calcitriol, and calcitonin

The hormone from parathyroid glands that raises serum calcium by increasing bone resorption, renal Ca reabsorption, and calcitriol production (via 1-alpha-hydroxylase)

A systemic skeletal disease characterised by low bone mineral density and microarchitectural deterioration, increasing fracture risk; diagnosed by DEXA T-score <-2.5

An autosomal recessive disorder of copper metabolism (ATP7B mutation) causing copper accumulation in liver, brain, and cornea (Kayser-Fleischer rings); diagnosed by low ceruloplasmin

A copper-containing plasma protein with ferroxidase activity; low levels are diagnostic of Wilson disease; also an acute phase reactant

Enlargement of the thyroid gland; endemic goitre is caused by iodine deficiency leading to compensatory TSH stimulation and thyroid hyperplasia

An ion in body fluids that carries an electrical charge; major cations (Na+, K+, Ca2+, Mg2+) and anions (Cl-, HCO3-, PO43-) maintain osmolality, pH, and membrane potential

Serum K+ >5.5 mEq/L; the most dangerous electrolyte disturbance due to risk of fatal cardiac arrhythmias; ECG shows peaked T waves progressing to sine wave and cardiac arrest

Serum Na+ <135 mEq/L; the most common electrolyte abnormality in hospitalised patients; causes cellular oedema, especially cerebral oedema → confusion, seizures

pH = pKa + log([A-]/[HA]); for the bicarbonate buffer: pH = 6.1 + log([HCO3-] / 0.03 × pCO2); the ratio of HCO3- to dissolved CO2 determines blood pH

The most important ECF buffer: H+ + HCO3- ⇌ H2CO3 ⇌ H2O + CO2; effective because CO2 is regulated by lungs and HCO3- by kidneys (open buffer system)

A primary decrease in blood HCO3- causing pH <7.35; classified by anion gap into high AG (added acid: DKA, lactic acidosis) and normal AG (HCO3- loss: diarrhoea, RTA)

Calculated as Na+ - (Cl- + HCO3-); normal 8-12 mEq/L; an elevated AG indicates accumulation of unmeasured anions (organic acids) in the blood

A life-threatening complication of diabetes characterised by hyperglycaemia, ketonaemia, and high anion gap metabolic acidosis due to insulin deficiency and excess ketone body production

Deep, rapid breathing pattern seen in metabolic acidosis (especially DKA); represents respiratory compensation — hyperventilation to blow off CO2 and raise pH

A primary increase in pCO2 (>45 mmHg) causing pH <7.35; caused by hypoventilation (COPD, respiratory depression, neuromuscular disease); compensated by renal HCO3- retention

The physiological response to a primary acid-base disorder that partially corrects pH: respiratory compensation (fast, minutes) adjusts pCO2; renal compensation (slow, hours-days) adjusts HCO3-

Accumulation of lactate (>4 mmol/L) causing high anion gap metabolic acidosis; Type A from tissue hypoxia (shock, arrest), Type B from metabolic causes (metformin, liver failure)