Disorders of the circulation

Question 0

What is congestion?

Answer 0

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.

Question 1

What is hyperaemia?

Answer 1

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.

Question 2

What does chronic vascular congestion contribute to?

Answer 2

1) oedema
2) tissue hypoxia
3) Ischaemia
4) fibrosis

Question 3

What is haemorrhage and how can it occur?

Answer 3

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

Question 4

What are the four classifications of haemorrhage?

Answer 4

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

Question 5

What factors the significance of haemorrhage?

Answer 5

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.

Question 6

What is haemostasis?

Answer 6

The physiological process which arrests haemorrhage and involves a highly regulated interrelationship between blood vessels, vascular endothelium, platelets and coagulation factors.

Question 7

What steps are involved in primary haemostasis?

Answer 7

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.

Question 8

What are the steps involved in secondary haemostasis?

Answer 8

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.

Question 9

What is the fibrinolytic cascade?

Answer 9

Activated alongside the coagulation cascade. It prevents over production of fibrin.

Question 10

What are the steps involved in the fibrinolytic cascade?

Answer 10

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.

Question 11

What is fibrinolysis?

Answer 11

Small clots are remodelled or dispersed by fibrinolysis within 1-2 weeks but large clots undergo organisation and recanalisation.

Question 12

What two other systems are involved in haemostasis?

Answer 12

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.

Question 13

What are the two main categories of haemorrhagic disease?

Answer 13

1) increased vessel fragility- capillary damage by toxins, diabetes mellitus
2) inadequate haemostatic response- platelet dysfunction/deficiency or derangements of clotting factors

Question 14

How can thrombocytopaenia arise?

Answer 14

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.

Question 15

What is Von Willebrand’s disease?

Answer 15

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.

Question 16

How does vitamin K impact the ability of the blood to clot?

Answer 16

It activates factor II, VII, IX and X and can result from vitamin K anatagonism (rodenticides), vit K deficiency and liver disease.

Question 17

What do animals with inherited deficiencies of coagulation factors present with?

Answer 17

Focal/localised bleeding.

Question 18

What is a thrombus and what are the 5 causes of formation?

Answer 18

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

Question 19

What does a antemortem thrombus look like?

Answer 19

Granular, dull, friable, laminated, white (arterial), red/pink (veins), ovoid, attached to vessel wall or the chorda tendinae of the heart.

Question 20

What does a PM clot look like?

Answer 20

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.

Question 21

What is the first factor of Virchow’s triad?

Answer 21

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.

Question 22

What is the second factor of Virchow’s triad?

Answer 22

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.

Question 23

What is the third factor of Virchow’s Triad?

Answer 23

Hypercoagulability of blood. Altered activated haemostatic proteins (primary- genetic factor) or (secondary- DIC).

Question 24

What are the factors that make a thrombus significant?

Answer 24

Size, location and rate of formation. Small ones can be removed by thrombolysis. Rapid development is more significant and there is no time for collateral blood flow to occur and compensate for reduced perfusion.

Question 25

What happens to the area supplied by the thrombosed vessel and what are the two types of thrombus?

Answer 25

They will become hypoxic/infarcted. They can initially mural (attached to vessel wall) or they may block the lumen and become an occlusive thrombus.

Question 26

What is arterial thrombosis?

Answer 26

Can occur secondary to arteriosclerosis, vermoinous arteritis aneurysm in horses with Strongylus vulgaris infection ( root of cranial mesenteric, renal and aorta due to larval migration), iliac thrombosis (secondary to cardiomyopathy and arterial thrombosis).
Frequently occlusive.

Question 27

What is cardiac thrombosis?

Answer 27

Usually valvular but may be mural. Infection of the heart valves- valvular endocarditis

Question 28

What is venous thrombosis?

Answer 28

Secondary to repeated venepuncture or in dwelling jugular catheters- occlusive.

Question 29

What is capillary thrombosis?

Answer 29

Microthrombi which are only appreciated histologically and ma be associated with local acute inflammation or in DIC.

Question 30

What is dissolution?

Answer 30

The thrombus is removed by fibrinolysis, only in recent thrombi as the extensive fibrin deposition and cross linkage in older thrombi makes them more resistant.

Question 31

What is propagation and embolisation?

Answer 31

The thrombus extends caudally from its point of attachment. Blood flowing over the developing thrombus deposits platelets and fibrin on the head. The blood flow after the thrombus is slowed and more turbulent, RBCs and fibrin are deposited and a tail is created.
If the tail is exposed to free flowing blood (vessel branch) a white thrombus is created and the tail is prone to breaking off (embolism).

Question 32

What is organisation and recanalisation?

Answer 32

Neutrophils, macrophages, capillaries and fibroblasts invade the thrombus. It is converted into a vascularised CT mass attached to the vessel wall. Capillary channels anastomose and blood flow is re-established= recanalisation.

Question 33

What is the definition of an embolus?

Answer 33

Solid or gaseous mass carried by the bloodstream from its point of origin to a distant site within the circulation.

Question 34

What is embolism and what does it cause?

Answer 34

The embolus being carried through the bloodstream where it stops in a blood vessel with a smaller diameter than itself.
blockage of a major vessel (pulmonary trunk) will cause sudden death whereas blockage of a small vessel will lead to ischaemia and infarction of the supplied area. Or in areas will good collateral supply- organisation or fibrinolysis will occur.

Question 35

What are the characteristics of a thromboembolism?

Answer 35

fragments detach and spread throughout the circulation. e.g. bacterial endocarditis of heart valves= infected emboli= multifocal abscesses. Cardiac thromboemboli lodge in bifurcation of vessels e.g. aortic-iliac (saddle) thrombus in cats with dilated cardiomyopathy.
Omphalophlebitis- neonates, naval ill=infection of umbilical vv= infective embolus.

Question 36

What are the characteristics of gas embolism?

Answer 36

Air injected into the circulation will accumulate in the pulmonary trunk and cause a fatal airlock. Med size dog killed by 30ml air, horses are susceptible.

Question 37

What are the characteristics of a fat embolism?

Answer 37

Adipocytes from bone marrow released following fracture. Especially effects the CNS and pulm circ.

Question 38

What are the characteristics of tumour cell emboli?

Answer 38

Malignant neoplasms erode vessels or lymphatics forming friable thrombi- embolic fragments break off and circulate to other site (metastasis). Lodge in capillary beds in the lung, spleen, liver and kidney- produce secondary tumours.

Question 39

How can parasite be a type of emboli?

Answer 39

Heartworms (Dirofilaria immitis) may embolise into the pulmonary trunk after anthelminitc treatment. Embolism to the CNS is very significant.
(strongyles, filarial worms and fluke)

Question 40

What type of embolism can be caused by wounds?

Answer 40

foreign body embolism- fragments of skin/hair

Question 41

What are the 3 main causes of venous thrombosis?

Answer 41

1) Arteriospasm- aterial trauma, ergotism (ingestion of alkaloids)
2) compression of vessels- ligatures, tumours, torsion
3) thrmboembolism- vascular obstruction

Question 42

What factors dictate the consequences of ischaemia and infarction?

Answer 42

degree of occlusion, speed of occlusion, presence of collateral circulation and vulnerability of tissues to ischaemia.
In general- complete, sudden failure of blood supply results in ischaemic tissue necrosis (infarction).
Gradual and incomplete reduction of supply allows for accommodation by the tissue with atrophy/fibrosis due to tissue hypoxia.

Question 43

What is the definition of infarction?

Answer 43

Segmental or localised area of ischaemic necrosis due to occlusion of the blood supply due to thromboembolic occlusion of an artery.

Question 44

What does infarcation look like macroscopically?

Answer 44

the affected typically has a wedge-shaped appearance (occluded area at the apex of the wedge), the colour is red or pale, this depends on the degree of vascular engorgement and co-existing inflammation or infection- organs with a good blood supply will not show a wedge, they will be red and soft.

Question 45

What does infarction look like microscopically?

Answer 45

Coagulative necrosis occurs so the outline of the coagulated cells is preserved, there is increased eosinophilia of the affected area and loss of cellular detail due to denaturation of structural proteins and enzymes = necrosis.

Question 46

What are the two ways that necrotic tissue is replaced after an infarct?

Answer 46

Removed by phagocytosis.

1) regeneration- in capable tissues or if the stroma is maintained.
2) fibrosis which forms a scar.

Question 47

What is disseminated intravascular coagulation?

Answer 47

The activation of coagulation within the vascular system resulting in deposition of fibrin in the small vessels and consumption of coagulation factors and platelets.

Question 48

What happens in DIC?

Answer 48

Fibrin deposition within blood vessels leads to vascular obstruction and micro infarction. The fibrinolytic system is activated which removes some fibrin but also uses up clotting factors and forms fibrin degradation products (FDPs) which have anticoagulant properties. Causes hypercoagulability- infarct= severe bleeding tendency. Dogs and horses

Question 49

What are the causes of DIC and what is the best way to diagnose it?

Answer 49

Septicaemia, bacterial endotoxaemia, viral infection e.g. FIP.
Use the d-dimer (FDPs).