Diseases of haemostasis Flashcards

1
Q

What are the 4 normal stages of haemostasis?

A

Vasoconstriction
Primary haemostasis
Secondary haemostasis
Thrombus and antithrombin events

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2
Q

What is released to cause vasoconstriction and reduced blood loss during haemorrhage?

A

Endothelin

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3
Q

What happens if there is too much or too little haemostasis?

A

Too much = thrombosis

Too little = bleeding disorders

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4
Q

What happens during primary haemostasis?

A

Platelets adhere to exposed sub endothelial matrix
Adhesion of platelets causes activation and shape change
Platelets release secretory granules to form a haemostat plug

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5
Q

What happens during secondary haemostasis?

A

Endothelium exposure to tissue factor activates the coagulation cascade
Thrombin is activated and converts fibrinogen to fibrin

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6
Q

What happens during the antithrombotic evens of haemostasis (final stage)?

A

Fibrin and platelets form solid, permanent haemostatic plug

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7
Q

What are the normal components of haemostasis?

A

Endothelium
Platelets
Clotting pathway (coagulation cascade)
Fibrinoltic system

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8
Q

What produces the proteins in the coagulation cascade? What do they cause the release of?

A

Liver

Releases thrombin which converts fibrinogen to fibrin

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9
Q

What does the fibrinolytic system do?

A

Remove blood clot (thrombus)

Thrombin degrades fibrin

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10
Q

Give an example of an inherited coagulation deficiency

A

Haemophilia
Each clotting factor has different disorder associate with it
Haemophilia A and B are factors 8 and 9 deficiency

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11
Q

What causes thrombocytopenia? (can be acquired or inherited)

A

Immune system destroys platelets
Decreased platelet production
Removal of thrombocytes

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12
Q

Give examples of acquired coagulopathies

A

Poisoning with vitamin K antagonists
Hepatic disease
Disseminated intravascular coagulation

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13
Q

What is a thrombosis? What causes thrombosis?

A

Formation of solid mass (thrombus) on wall of blood vessel or heart
Excess clotting

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14
Q

What are mural thromboses and heart vegetations?

A

On heart wall = mural thrombus

On heart valves = heart vegetations

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15
Q

What 3 conditions predispose an individual to a thrombosis?

A

Endothelial injury
Hyper coagulability
Abnormal blood flow (turbulence or stasis)

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16
Q

How can endothelial injury cause predisposed to a thrombosis? What causes this?

A

Exposure of subendothelium causes platelet adherence

Bacteria, turbulent flow etc

17
Q

Hypercoagubaility can be classed as primary or secondary (depending on tissue damage). What disease is hypercoaguability seen in? Why?

A

Chronic renal disease

Loss of anti coagulant proteins

18
Q

What is an aneurysm?

A

Ballooning of weak spot in blood vessel wall

19
Q

What is a stenosis?

A

Narrowing of a vessel

Causes blood pools

20
Q

Turbulence can cause thrombosis. What may cause turbulent blood flow?

A

Endothelial damage

E.g. aneurysm, stenosis, dilated atria (don’t contract- blood pools and clots)

21
Q

How does blood stasis cause thrombosis?

A

Platelets in contact with endothelium
No dilution of activated clotting factors
No inflow of clotting factor inhibitors
Causes venous thrombus

22
Q

What are the 4 things a thrombus can lead to? (PEDO)

A

Propagation (becomes larger)
Embolisation (breaks off and spreads)
Dissolution (dissolves)
Organisation (formation of vascular channels within thrombus - recanalization)

23
Q

What is an infarct?

A

Area of ischaemic necrosis caused by blockage of blood vessel

24
Q

How can you tell thrombus from a post mortem clot?

A

Thrombus attached to vessel wall, postmortem clots not
Postmortem can be red or white
Histology - thrombi have course strands of fibrin, post mortem clots have fine strands of fibrin

25
Q

Infarction development depends on vascular supply, rate of occlusion development, O2 supply and more. Infarcts can be red or white. What does this mean?

A

Red infarct - haemorrhagic infarction, venous occlusion in loose tissue with dual circulation (lungs, liver, SI)
White infarct - arterial occlusion in solid organ (heart, spleen, kidney)

26
Q

What is disseminated intravascular coagulation (DIC)?

A

Thrombohaemorrhagic disorder

Occuring as a secondary complication a disease

27
Q

DIC can be acute, subacute or chronic. How is DIC caused?

A

Activation of clotting factors cause multiple small blood clots (multiple micro thrombi)
Develop throughout the bloodstream and blood small vessels

28
Q

What does DIC cause? What does this result in?

A

Hypoxia, infarction, haemorrhagic disorder
Causes swollen capillaries, hyalinisation, complete obstruction
Thrombosis and necrosis of arteries

29
Q

What problems cause DIC?

A
Severe systemic infections 
Septic shock 
Neoplastic disease
Extensive trauma 
Viral disease
30
Q

What viral disease are associated with dIC?

A

Blue tongue
Swine fever
Hepatitis in dogs

31
Q

What are the symptoms of acute DIC?

A
Petechia/purpura/ecchymoses 
Haemorrhagic diathesis (susceptibility to haemorrhage due to hypocoaguability)
32
Q

DIC can be immune complex mediated. Describe the pathogenesisis of this. What type of hypersensitivity reaction is this?

A

Immune complex deposition in vessel walls
Activates complement
Causes endothelial damage and coagulation cascade
Type III