Pathophysiology
This domain tests the mechanisms by which disease disrupts normal function: cell injury, inflammation, fluid shifts, thrombosis, shock and neoplasia. Questions often present a scenario and ask for the underlying mechanism rather than a diagnosis.
Core rules and concepts
- Cell injury: reversible injury causes swelling; irreversible injury causes necrosis. Apoptosis is programmed cell death and does not trigger inflammation.
- Inflammation: vasodilation and increased capillary permeability produce redness, heat, swelling, pain and loss of function. Neutrophils arrive first, followed by macrophages.
- Starling forces: oedema results from increased hydrostatic pressure, reduced oncotic pressure, increased permeability or lymphatic obstruction.
- Virchow’s triad: stasis, endothelial injury and hypercoagulability predispose to thrombosis.
- Shock: hypovolaemic, cardiogenic, distributive (septic, anaphylactic, neurogenic) and obstructive. All cause inadequate tissue perfusion and rising lactate.
- Neoplasia: malignant tumours invade and metastasise via lymphatics or blood; grading describes differentiation, staging describes spread.
Worked example
A patient with pneumonia develops fever, hypotension and confusion. Early septic shock is distributive: vasodilation lowers systemic vascular resistance, so the skin may be warm and flushed while blood pressure falls. This contrasts with cardiogenic shock, where the skin is cold and clammy and the lungs fill with fluid. The rising lactate confirms hypoperfusion, and fluids plus antibiotics are urgent.
Traps that cost marks
- Assuming all shock presents with cold, clammy skin.
- Confusing oncotic and hydrostatic causes of oedema.
- Calling apoptosis inflammatory.
- Mixing grading with staging.