Diseases of haemostasis

Question 1

What are the 4 normal stages of haemostasis?

Answer 1

Vasoconstriction
Primary haemostasis
Secondary haemostasis
Thrombus and antithrombin events

Question 2

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

Answer 2

Endothelin

Question 3

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

Answer 3

Too much = thrombosis

Too little = bleeding disorders

Question 4

What happens during primary haemostasis?

Answer 4

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

Question 5

What happens during secondary haemostasis?

Answer 5

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

Question 6

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

Answer 6

Fibrin and platelets form solid, permanent haemostatic plug

Question 7

What are the normal components of haemostasis?

Answer 7

Endothelium
Platelets
Clotting pathway (coagulation cascade)
Fibrinoltic system

Question 8

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

Answer 8

Liver

Releases thrombin which converts fibrinogen to fibrin

Question 9

What does the fibrinolytic system do?

Answer 9

Remove blood clot (thrombus)

Thrombin degrades fibrin

Question 10

Give an example of an inherited coagulation deficiency

Answer 10

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

Question 11

What causes thrombocytopenia? (can be acquired or inherited)

Answer 11

Immune system destroys platelets
Decreased platelet production
Removal of thrombocytes

Question 12

Give examples of acquired coagulopathies

Answer 12

Poisoning with vitamin K antagonists
Hepatic disease
Disseminated intravascular coagulation

Question 13

What is a thrombosis? What causes thrombosis?

Answer 13

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

Question 14

What are mural thromboses and heart vegetations?

Answer 14

On heart wall = mural thrombus

On heart valves = heart vegetations

Question 15

What 3 conditions predispose an individual to a thrombosis?

Answer 15

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

Question 16

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

Answer 16

Exposure of subendothelium causes platelet adherence

Bacteria, turbulent flow etc

Question 17

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

Answer 17

Chronic renal disease

Loss of anti coagulant proteins

Question 18

What is an aneurysm?

Answer 18

Ballooning of weak spot in blood vessel wall

Question 19

What is a stenosis?

Answer 19

Narrowing of a vessel

Causes blood pools

Question 20

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

Answer 20

Endothelial damage

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

Question 21

How does blood stasis cause thrombosis?

Answer 21

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

Question 22

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

Answer 22

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

Question 23

What is an infarct?

Answer 23

Area of ischaemic necrosis caused by blockage of blood vessel

Question 24

How can you tell thrombus from a post mortem clot?

Answer 24

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

Question 25

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

Answer 25

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)

Question 26

What is disseminated intravascular coagulation (DIC)?

Answer 26

Thrombohaemorrhagic disorder | Occuring as a secondary complication a disease

Question 27

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

Answer 27

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

Question 28

What does DIC cause? What does this result in?

Answer 28

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

Question 29

What problems cause DIC?

Answer 29

``` Severe systemic infections Septic shock Neoplastic disease Extensive trauma Viral disease ```

Question 30

What viral disease are associated with dIC?

Answer 30

Blue tongue Swine fever Hepatitis in dogs

Question 31

What are the symptoms of acute DIC?

Answer 31

``` Petechia/purpura/ecchymoses Haemorrhagic diathesis (susceptibility to haemorrhage due to hypocoaguability) ```

Question 32

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

Answer 32

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