Vascular Disturbances
Coagulation disorders
Platelet abnormalities
Haemorrhage Within Tissue
Haemophilia A
Petechiae: 1-2mm (Pin point)
Purpura: >3mm (Extensive)
Ecchymoses: >1-2cm (Bruising)
Haematoma
Extravascular collection of blood
Haemostatic Process
Consequences of endothelial injury
Secondary
Primary
vWF release (from endothelial cells & platelets)
Initiation of thrombin
Amplification of thrombin
Propagation of thrombin
Fibrin formation
Fibrinolysis
Abnormalities of blood flow
Reduced blood flow
Physiological responses
Reduced tissue perfusion
Ischaemia
Generalised
Localised
Hypovolemia, poor cardiac output/low mean arterial pressure
Obstruction to blood flow by intralumenal vascular obstruction
Consequences of haemorrhages
Rapid loss of up to 20% of blood volume
Rapid loss of more than 20 - 30% of blood volume
Increased blood flow
To dehydration (reduction of ECF)
Three stages
Baroreceptors
Renin (Kidney)
High osmolarity
Hyperaemia
Active - pathological or physiological
Hyperaemia: Increased blood within the vessels of a region (not haemorrhage)
Passive - pathological
Congestion
Darker or blue and engorged with blood
Skeletal muscles during exercise
Region is warm, red, oxygenated
Increased arterial blood supply
Reduced venous drainage
Regulation of mean arterial pressure
Short Term
Long term - requires volume regulation
SA Node
Myocardial cells
Arterioles
Veins
Sympathetic activity increases heart rated --> increased CO
Parasympathetic activity decreases heart rate --> decreased CO
Sympathetic activity increases ventricular contractility --> increased SV --> increased CO
Sympathetic activity causes venoconstriction
Sympathetic activity causes vasoconstriction --> increased TPR
Water follows sodium distribution osmotically
Sodium is regulated primarily by renal excretion
Total body sodium is key determinant of ECF volume
Injured endothelial cells release tPA that convert plasminogen --> plasmin
Binding of plasminogen to clot amplifies its conversion to plasmin
Binding of both plasminogen & plasmin to fibrin serves to localise fibrinolysis to the clot
Haemophilia B
Functional or quantitative deficiency of FVIII
Functional or quantitative deficiency of FIX
Decreased production of coagulation factors
Increased consumption of coagulation factors
Severe liver disease
Vit K deficiency
DIC (Disseminated Intravascular Coagulation)
Systemic
Consumptive
Not restricted to site of injury
Platelets & coagulation factors
Abnormal number
Thrombocytopenia
Decreased production
Increased utilisation
Thrombocytosis
Abnormal function
Acquired defects
Hereditary defects
Intrinsic
Extrinsic
Vascular spasm
Exposure of sub-endothelial matrix proteins (collagen, fibronectin)
Abnormalities of haemostasis associated with adhesion & aggregation defects
Von Willebrand Disease (vWD)
Type 1
Type 2
Type 3
Equal decrease in all sizes of multimers = quantitative change
Decreased in only large multimers = qualitative change
No detectable vW factor
Glanzmann Thromboasthenia: Intrinsic platelet disorder in which the fibrinogen receptor (GPIIb/IIIa) is absent or reduced on the surface of platelets
Type I
Type 2
Variant
Less than 5% of receptor is detectable on platelet surfaces
10 - 20% of the receptor is present on platelet surfaces
Receptor is present but dysfunctional
Hypovolemia
Carotid & aortic bodies stimulates vasomoter centres + adrenaline release
Oncotic pressure replaces lost fluid
Regeneration (increased erythropoiesis) + increased protein synthesis
Blood supply to vital organs is maintained
Hypovolemic shock & death