Normal Haemostasis

Endothelium
Antithrombotic
- Anti-platelets (PGI2,NO)
- Anticoagulant (ATIII, Heparin-like molecules)
- Fibrinolytic (t-PA)
Prothrombotic
- Platelet Effects (Collagen, vWF)
- Procoagulant effects (Tissue Factor)
- Antifibrolytic Effects (Plasminogen inacitivators)
Platelets
Alpha granules: fibrinogen, factors V & VIII, platelet factor 4
(heparin binding chemokine), PDGF
Delta granules: ADP, Ca2+, adrenaline/epinephrine
Role in haemostasis: adhesion -> activation/secretion ->
aggregation
Coagulation Cascade
Procoagulation
Extrinsic Tissue factor, VII
Intrinsic XII, XI, IX, VIII
Common X, V, II, fibrinogen
Anticoagulation
- antithrombins
- protein c & S
- Tissue factor plasminogen activator
- Plasmin, fibrin split products
Thrombosis
Virchows Triangle
Endothelial injury
Alterations in Normal Blood Flow
Hypercoagulability
Clinical Consequences
Arterial
Cool
Pulseless
Pale
Painful
Venous
Embolism
Pulmonary
- Breathlessness
Systemic

Fat & Marrow

Air: Decompression Sickness
Amniotic
Infarction
Mechanism: thrombus, embolus, compression, vasospasm
Morphology
- Red infarcts
- White infarcts
Histological Pattern
- Coagulative
- Liquefactive
Outcomes:
Nature of vascular supply, rate of occlusion, tissue vulnerability,
oxygen content
If an organ has dual blood supply there tends to be haemorrhagic
infarction
General Principles: Vascular Response to injury
Endothelial activation
Definition: intact endothelial cells responding to various
pathophysiologic stimuli by adjusting their functions or expressing
newly acquired properties
Causes: Immune/infections, haemodynamic stress, metabolic
Endothelial dysfunction
Disorders
Petechia
Heparin induced thrombocytopenia
Shock
Classifications
- Pathogenic (cardiogenic, hypovoaemic, septic)
- Clinical (Low output, vasodilation)
Mechanism
- Septic
- Anaphylactic (BPT: Immune-mediated disorders)
Stages
Other random notes
Bradykinin Potentiates pain, vasodilates, broken down by ACE
S4 stiff myocardium (atria has to contract