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

Screenshot 2023-03-23 at 10.47.29 am

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

Screenshot 2023-03-23 at 11.31.02 am

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