Fluid And Haemodynamic Disorders
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Direct answer
Fluid and haemodynamic disorders arise from disturbed flow and fluid balance: oedema from Starling force imbalance or lymphatic obstruction, congestion from impaired venous drainage, thrombosis from Virchow's triad, embolism from travelling material, infarction from vessel occlusion and shock from inadequate perfusion. Hallmark morphology includes heart failure cells, nutmeg liver, lines of Zahn and wedge-shaped infarcts. FMGE concentrates on mechanisms, classic gross appearances and embolism and infarction types.
What you must remember
- Oedema mechanisms: raised hydrostatic pressure (heart failure, DVT), low oncotic pressure (nephrotic syndrome, cirrhosis, malnutrition), lymphatic obstruction (filariasis, post-mastectomy) and sodium retention.
- Chronic passive congestion: haemosiderin-laden heart failure cells and brown induration of lung, nutmeg liver in right heart failure, congestive splenomegaly in portal hypertension.
- Virchow triad: endothelial injury, abnormal flow, hypercoagulability; arterial thrombi are pale and platelet-rich with lines of Zahn, venous thrombi red and stasis-related, while post-mortem clots are gelatinous without lines of Zahn.
- Embolism types: thromboembolism from calf veins to lungs, fat embolism after long bone fractures, nitrogen bubbles in decompression sickness, amniotic fluid embolism with fetal squames and DIC in labour.
- Infarcts: pale in solid end-arterial organs (heart, kidney, spleen); red in dual-supplied or loose organs (lung, intestine) and with venous occlusion; brain infarcts are liquefactive.
- Shock: hypovolaemic, cardiogenic and distributive (septic, anaphylactic, neurogenic); septic shock starts warm and vasodilated through nitric oxide and TNF, then turns cold; complications include DIC, ARDS and acute tubular necrosis.
- Stages: compensated, progressive and irreversible, with early tachycardia and vasoconstriction.
Common confusion
Red versus white infarct: solid end-arterial organs bleed little, giving pale wedges, while dual circulation, loose tissue or congestion allows blood into necrotic tissue, making it haemorrhagic. Thrombus versus post-mortem clot is the second trap — attachment, granularity and lines of Zahn mark a true thrombus; chicken-fat layering marks a clot after death.
Exam-focused takeaway
FMGE frames scenario stems: a post-partum collapse (amniotic fluid embolism), a diver with joint pains (decompression sickness), a fractured femur with dyspnoea and petechiae (fat embolism). Virchow triad, organ-specific infarct colour and warm-to-cold septic shock progression recur every session, so pair each buzzword with its diagnosis.
Frequently asked questions
Why does nephrotic syndrome cause oedema?
Urinary albumin loss lowers plasma oncotic pressure, while renal sodium retention adds water. The result is generalised oedema or anasarca.
What are heart failure cells?
Alveolar macrophages loaded with haemosiderin from congested capillaries in chronic left heart failure, giving brown induration of the lung.
What do lines of Zahn indicate?
Alternating pale platelet-fibrin and dark red cell layers proving a thrombus formed ante-mortem in flowing blood. Post-mortem clots lack them.
Which infarct is haemorrhagic?
Pulmonary infarction, because bronchial collateral flow leaks into necrotic lung; intestinal and torsion infarcts are also red.
How do warm and cold septic shock differ?
Early vasodilatation from nitric oxide gives warm flushed limbs; progression to vasoconstriction and myocardial depression gives cold clammy extremities.
How does fat embolism present?
Dyspnoea, hypoxaemia, restlessness and a chest-conjunctival petechial rash one to three days after long bone fracture, from capillary obstruction by fat and toxic free fatty acids.