o Due to accumulation of unmeasured acids
o Causes:
Lactic acidosis (shock, hypoxia, metformin toxicity)
Ketoacidosis (diabetic, alcoholic, starvation)
Renal failure (↓ excretion of acids)
Toxins: methanol, ethylene glycol, salicylates
o Anion gap = [Na⁺] – ([Cl⁻] + [HCO₃⁻]); normal = 8–12 mmol/L
o Causes:
Diarrhoea: loss of HCO₃⁻
Renal Tubular Acidosis (RTA)
Ileal conduit, acetazolamide
o Causes:
Vomiting or nasogastric suction (H⁺ loss)
Diuretics (loop/thiazides)
Hyperaldosteronism (↑ H⁺ secretion)
o Due to hyperventilation:
Anxiety, hypoxia, sepsis, pregnancy
PaCO₂ ↓ → compensatory ↓ HCO₃⁻
o Impaired H⁺ secretion → ↑ urine pH (>5.5), hypokalaemia
o Nephrolithiasis common due to alkaline urine
o Causes: autoimmune (e.g. Sjögren’s, SLE), amphotericin B
o Impaired HCO₃⁻ reabsorption
o Urine pH initially >5.5, then <5.5 as HCO₃⁻ depletes
o Causes: Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors
o Hypoaldosteronism or aldosterone resistance
o ↓ Na⁺ reabsorption and ↓ K⁺/H⁺ excretion → hyperkalaemic acidosis
o Seen in diabetes, ACEi/ARBs, heparin
o Symptoms: weakness, cramps, arrhythmias (U waves)
o Causes:
GI losses: diarrhoea, vomiting
Renal losses: diuretics, hyperaldosteronism
Intracellular shift: insulin, β-agonists, alkalosis
o ECG: peaked T waves, widened QRS, sine wave pattern
o Causes:
CKD, ACEi/ARBs, spironolactone
Cell lysis: rhabdomyolysis, haemolysis, tumour lysis
Acidosis, Addison’s disease
o Emergency Rx: calcium gluconate, insulin + glucose, salbutamol, dialysis
o Symptoms: nausea, confusion, seizures if rapid onset
o Causes:
SIADH (euvolaemic)
Heart failure, cirrhosis, nephrotic syndrome (hypervolaemic)
Adrenal insufficiency, hypothyroidism
o Correct slowly to avoid central pontine myelinolysis (CPM)
o Usually due to water loss > Na⁺ loss
o Causes:
Dehydration, osmotic diuresis
Diabetes insipidus (DI)
o Treat with slow rehydration (risk of cerebral oedema)
o ↓ ADH secretion → dilute urine
o Causes: idiopathic, head trauma, pituitary surgery
o Responds to desmopressin
o Renal unresponsiveness to ADH
o Causes: lithium, hypercalcaemia, hypokalaemia
o No response to desmopressin
• Calcium
o Hypocalcaemia: tetany, seizures, prolonged QT
Causes: hypoparathyroidism, vitamin D deficiency, CKD
o Hypercalcaemia: "bones, stones, groans, psychiatric overtones"
Causes: hyperparathyroidism, malignancy, sarcoidosis
• Magnesium
o Hypomagnesaemia: ↑ neuromuscular excitability, associated with low K⁺ and Ca²⁺
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Author & Educational Disclaimer
Author:
Dr Phillip Cockrell BM FRCP DipClinEd
Dr Phillip Cockrell is a UK Consultant Physician in Internal Medicine, currently working at Queen Alexandra Hospital, Portsmouth University Hospitals NHS Trust. He has previously worked as a registrar across Intensive Care Medicine, Gastroenterology, Cardiology, Stroke Medicine, Acute Medicine, and Respiratory Medicine.
He has held senior leadership roles including Associate Clinical Director of the Acute Medical Unit, Clinical Director of Internal Medicine, and Chief of Medicine. Dr Cockrell has over 15 years’ experience in postgraduate medical education, having lectured extensively across the MRCP syllabus and contributed to MRCP revision teaching and course development.
Dr Cockrell holds a Bachelor of Medicine (BM), Fellowship of the Royal College of Physicians (FRCP), and a Diploma in Clinical Education (DipClinEd). His teaching approach is based on structured consolidation of complex medical topics to support efficient and effective revision for postgraduate examinations.
Purpose of this content:
The material on this page is intended solely for educational purposes to support revision for the MRCP (UK) Part 1 examination. It reflects examination-relevant principles of internal medicine and is designed to aid learning and pattern recognition.
Medical disclaimer:
This content is designed for postgraduate medical examination revision and does not constitute medical advice, diagnosis, or treatment guidance and must not be used as a substitute for professional clinical judgement, local guidelines, or specialist consultation. Clinical decisions should always be made in the context of individual patient circumstances and current national guidance.