BI9.1-3 | Minerals, electrolytes, Water and Acid base balance — Summary & Reflection

REFLECT

A 32-year-old woman with type 1 diabetes presents with polyuria, polydipsia, and vomiting for 2 days. Blood gas: pH 7.20, pCO₂ 24 mmHg, HCO₃⁻ 9 mEq/L. Na⁺ 132, K⁺ 5.8, Cl⁻ 95.

(1) Calculate the anion gap. (2) What is the primary acid-base disorder? (3) What metabolites are causing the high anion gap? (4) The potassium is elevated now — but what will happen to the potassium when you treat with insulin and correct the acidosis? Why? (5) What is the Kussmaul's breathing the nurses noticed, and what is its physiological purpose?

KEY TAKEAWAYS

Iron:
- Haem iron (meat) better absorbed than non-haem iron (vegetables)
- Vitamin C enhances; phytates, tannins, oxalates inhibit non-haem absorption
- Hepcidin: master regulator — blocks ferroportin in ACD
- IDA: microcytic, hypochromic; low ferritin + TIBC elevated. Stage 3 = anaemia + microcytosis

Calcium/Phosphorus:
- PTH + Calcitriol + Calcitonin regulate Ca homeostasis
- Hypocalcaemia → tetany (Chvostek, Trousseau sign)
- Hypercalcaemia → "bones, stones, groans, psychic moans"

Trace Minerals:
- Copper: lysyl oxidase (collagen), caeruloplasmin. Wilson's (excess): KF rings, liver disease
- Zinc: 300+ enzymes. Deficiency: growth retardation, poor wound healing, ageusia

Electrolytes:
- Na⁺ = major ECF cation; K⁺ = major ICF cation
- Hyperkalaemia → fatal arrhythmias; most dangerous electrolyte emergency

Acid-Base:
- pH = 6.1 + log([HCO₃⁻] / 0.03×pCO₂). Normal: 7.35–7.45
- Metabolic acidosis (↓ HCO₃⁻): high AG (DKA, lactic acidosis) vs normal AG (diarrhoea, RTA)
- Respiratory acidosis (↑ pCO₂): COPD, respiratory failure
- Always check compensation: respiratory (minutes) vs renal (hours–days)