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Vascular Disturbances, Hyperaemia: Increased blood within the vessels of a…
Vascular Disturbances
Coagulation disorders
Haemophilia A
Functional or quantitative deficiency of FVIII
Haemophilia B
Functional or quantitative deficiency of FIX
Decreased production of coagulation factors
Severe liver disease
Vit K deficiency
Increased consumption of coagulation factors
DIC (Disseminated Intravascular Coagulation)
Systemic
Not restricted to site of injury
Consumptive
Platelets & coagulation factors
Haemorrhage
Within Tissue
Petechiae: 1-2mm (Pin point)
Purpura: >3mm (Extensive)
Ecchymoses: >1-2cm (Bruising)
Haematoma
Extravascular collection of blood
Abnormalities of blood flow
Reduced blood flow
Reduced tissue perfusion
Ischaemia
Generalised
Hypovolemia, poor cardiac output/low mean arterial pressure
Localised
Obstruction to blood flow by intralumenal vascular obstruction
Physiological responses
Consequences of haemorrhages
Rapid loss of up to 20% of blood volume
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
Rapid loss of more than 20 - 30% of blood volume
Hypovolemic shock & death
To dehydration (reduction of ECF)
Three stages
Baroreceptors
Renin (Kidney)
High osmolarity
Increased blood flow
Hyperaemia
Active
- pathological or physiological
Skeletal muscles during exercise
Region is warm, red, oxygenated
Increased arterial blood supply
Passive
- pathological
Congestion
Darker or blue and engorged with blood
Reduced venous drainage
Platelet abnormalities
Abnormal number
Thrombocytopenia
Decreased production
Increased utilisation
Thrombocytosis
Abnormal function
Acquired defects
Hereditary defects
Intrinsic
Extrinsic
Haemostatic Process
Consequences of endothelial injury
Primary
vWF release (from endothelial cells & platelets)
Vascular spasm
Exposure of sub-endothelial matrix proteins (collagen, fibronectin)
Secondary
Initiation of thrombin
Amplification of thrombin
Propagation of thrombin
Fibrin formation
Fibrinolysis
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
Regulation of mean arterial pressure
Short Term
SA Node
Sympathetic activity increases heart rated --> increased CO
Parasympathetic activity decreases heart rate --> decreased CO
Myocardial cells
Sympathetic activity increases ventricular contractility --> increased SV --> increased CO
Arterioles
Sympathetic activity causes vasoconstriction --> increased TPR
Veins
Sympathetic activity causes venoconstriction
Long term
- requires volume regulation
Water follows sodium distribution osmotically
Sodium is regulated primarily by renal excretion
Total body sodium is key determinant of ECF volume
Abnormalities of haemostasis associated with adhesion & aggregation defects
Von Willebrand Disease (vWD)
Type 1
Equal decrease in all sizes of multimers = quantitative change
Type 2
Decreased in only large multimers = qualitative change
Type 3
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
Less than 5% of receptor is detectable on platelet surfaces
Type 2
10 - 20% of the receptor is present on platelet surfaces
Variant
Receptor is present but dysfunctional
Hyperaemia:
Increased blood within the vessels of a region (not haemorrhage)
