Disorders of the circulation Flashcards
(50 cards)
What is congestion?
Due to reduced outflow of blood from a tissue (passive) e.g. heart failure. In congested areas capillary rupture will lead to microscopic haemorrhages and haemosiderin laden macrophages.
What is hyperaemia?
It occurs when arteriolar dilation increases blood flow to the tissue, it is an active process that leads to tissue erythema e.g. reddening at the sites of inflammation.
What does chronic vascular congestion contribute to?
1) oedema
2) tissue hypoxia
3) Ischaemia
4) fibrosis
What is haemorrhage and how can it occur?
The escape of blood from blood vessels due to vascular damage which may lead to the loss of RBCs from the body.
e.g. surface wound or extravasated RBCs accumulating internally.
Haematoma- massive accumulation of blood within a tissue
Haemothorax- accumulation of blood within the thorax
What are the four classifications of haemorrhage?
1) petechiae- 1-2mm, thrombocytopaenia or inc local vasc pressure
2) Purpura- >3mm, vasculitis and above.
3) Ecchymoses- 1-3cm, bruise
4) Rhectic/suffusive- large contiguous areas of tissue
What factors the significance of haemorrhage?
The volume, rate and location of blood loss. Rapid loss of 20% or slow loss of this vol will be tolerated but 30-40% will mean hypovolaemic shock. A small haemorrhage in the brain is serious compared to one in the skin and recurrent loss from the skin may lead to an iron deficiency whereas if it was internal the RBCs would be retained.
What is haemostasis?
The physiological process which arrests haemorrhage and involves a highly regulated interrelationship between blood vessels, vascular endothelium, platelets and coagulation factors.
What steps are involved in primary haemostasis?
1) Vascular injury causes arteriolar vasoconstriction = platelet activation due to the thrombogenic subendothelial ECM being exposed.
2) Shunts develop to redistribute the blood flow past the area
3) Sludging effects occur do to increased blood viscosity and RBC packing- plasma lost through leaky vessels.
4) increased pressure of fluid in surrounding tissues results in pressure on the vessel walls.
5) Activated platelets change to flat discs and release the secretory granules which recruit more platelets and form a haemostatic plug.
What are the steps involved in secondary haemostasis?
1) Tissue factor is exposed at the point of vascular injury.
2) It acts alongside factor VII to initiate the coagulation cascade which results in the formation of thrombin.
3) Thrombin turns fibrinogen into fibrin which forms a meshwork that attracts more platelets to consolidate the primary plug.
4) Polymerisation forms a plug which stops further haemorrhage.
What is the fibrinolytic cascade?
Activated alongside the coagulation cascade. It prevents over production of fibrin.
What are the steps involved in the fibrinolytic cascade?
1) Plasminogen is converted to plasmin by factor XII-dependant pathway or via plasminogen activators.
2) Plasmin breaks down fibrin into fibrin degradation products.
3) The FDP d-dimer is most useful diagnostically
4) free plasmin is inactivated by a2-plasmin inhibitor.
What is fibrinolysis?
Small clots are remodelled or dispersed by fibrinolysis within 1-2 weeks but large clots undergo organisation and recanalisation.
What two other systems are involved in haemostasis?
1) Kinin system- associated within inflammation. e.g. bradykinin= vasodilator= inc. vasc perm
2) Complement system- classic and alternative pathways, bacterial enzyme// ag-ab complexes.
What are the two main categories of haemorrhagic disease?
1) increased vessel fragility- capillary damage by toxins, diabetes mellitus
2) inadequate haemostatic response- platelet dysfunction/deficiency or derangements of clotting factors
How can thrombocytopaenia arise?
Decreased production e.g. bone marrow disease secondary to megakaryocyte destruction (FeLv) or radiation. Increased destruction/utilisation of platelets e.g. primary immune-mediated disease, neoplasia, DIC or septicaemia.
What is Von Willebrand’s disease?
Due to deficiency of plasma von willebrand factor which is produced by endothelial cells. It acts as an adhesion molecule and is key for primary haemostasis- common in dobermans. There are three types with 3 being the most severe.
How does vitamin K impact the ability of the blood to clot?
It activates factor II, VII, IX and X and can result from vitamin K anatagonism (rodenticides), vit K deficiency and liver disease.
What do animals with inherited deficiencies of coagulation factors present with?
Focal/localised bleeding.
What is a thrombus and what are the 5 causes of formation?
Layered mass containing RBCs, granular leucocytes and platelets held together by fibrin. It is formed by thrombosis.
1) spread of inflammatory lesions
2) spread of malignant neoplasms
3) pressure from local space-occupying lesions
4) venepuncture
5) cardiac thrombosis involving the valves or endocardium
What does a antemortem thrombus look like?
Granular, dull, friable, laminated, white (arterial), red/pink (veins), ovoid, attached to vessel wall or the chorda tendinae of the heart.
What does a PM clot look like?
smooth, shiny, gelatinous, homogenous, uniformly dark red or plasma and RBCs separate= ‘chicken fat’, conforms to vessel shape, not adherent to vessel wall by may be trapped in chorda tendinae.
What is the first factor of Virchow’s triad?
Damage to endothelium- physical disruption or anything that alters pro/anti-thrombotic effects of the endothelium, release of ADP, exposure of BM collagen e.g. viruses, bacteria, toxins or DIC.
What is the second factor of Virchow’s triad?
Stasis and irregular/turbulent flow. Normally blood flow is laminar with plasma peripherally and cells centrally. Disruption of this can lead to stagnation hypoxia and stasis which encourages platelet deposition. Also due to slow flow excess coagulation factors are not washed away. e.g. shock, compression of vessel.
What is the third factor of Virchow’s Triad?
Hypercoagulability of blood. Altered activated haemostatic proteins (primary- genetic factor) or (secondary- DIC).
