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Semester 2-PP > Session 5-Haemostasis > Flashcards

Session 5-Haemostasis Flashcards

1
Q

Define haemostasis

A

Stoppage of bleeding or haemmorhage, either by normal vasoconstriction, abnormal obstruction or coagulation

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2
Q

What produces platelets in the bone marrow?

A

Megakaryocytes

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3
Q

What is the normal life span of platelets?

A

7-10 days

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4
Q

What are the principles of haemostasis? (3)

A

1) prevent bleeding
2) prevent unnecessary coagulation, allow blood to flow
3) make clot, control clotting and break it down

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5
Q

What is the normal platelet count?

A

150-400 x 10^9/L

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6
Q

When does platelet adhesion occur?

A

When there is damage to a vessel wall and underlying tissues are exposed

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7
Q

What do platelets adhere to and via which receptor do they do this?

A

Adhere to collagen via vWF (Von Willebrand factor) receptor

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8
Q

What activates platelets?

A

Secretion of ADP, thromboxane and other substances

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9
Q

How does platelet activation provide some coagulation factors?

A

By secretion from internal stores

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10
Q

What is platelet aggregation?

A

Cross linking of platelets to form platelet plug

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11
Q

What are some mediating factors of haemostasis?

A

1) Plt receptors - glycoprotein complexes
2) Von willebrands factor
3) fibrinogen
4) collagen
5) ADP
6) thromboxane/arachidonic acid
7) thrombin

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12
Q

What is the clotting cascade?

A

Amplification system activation of precursor proteins to generate thrombin

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13
Q

What does thrombin convert?

A

Soluble fibrinogen into insoluble fibrin

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14
Q

How is the clotting cascade controlled?

A

1) natural anticoagulants to inhibit activation

2) clot destroying proteins which are activated by clotting cascade

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15
Q

Give examples of coagulation factors

A

Fibrinogen
Prothrombin
Factors 5, 7, 8, 9, 10, 11, 13
Tissue factor

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16
Q

Give examples of natural anticoagulants

A

Protein C and S
Antithrombin
Tissue factor pathway inhibitor

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17
Q

What activates the extrinsic pathway?

A

Factor VII

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18
Q

What activates the intrinsic pathway?

A

Factors VIII, IX, XI, XII

19
Q

Describe the clot forming process (6)

A

1) tissue factor exposure
2) initiation produces small amount of thrombin
3) thrombin feeds back and activates other clotting factors
4) produces thrombin burst
5) thrombin cleaves fibrinogen to fibrin
6) clot forms

20
Q

What is the Von willebrand factor?

A

Involved in platelet adhesion to vessel wall, platelet aggregation and also carries and stabilises factor VIII

21
Q

How is the vessel wall important in haemostasis?

A

1) vasoconstriction (reduces haemorrhage)
2) production of vWF factor
3) exposure of collagen and tissue factor which initiates activation of clotting factors

22
Q

What is the purpose of fibrinolysis?

A

Breaks down thrombi to prevent them from remaining in place and growing

23
Q

Where is plasminogen produced?

A

Liver

24
Q

Which enzyme breaks down fibrin?

A

Plasmin

25
Q

What is the precursor of plasmin?

A

Plasminogen

26
Q

Give examples of congenital coagulation factor disorders

A 
Haemophilia A (factor 8 deficiency)
Haemophilia B (factor 9 deficiency)
27
Q

What is vitamin K needed for?

A

Metabolism of factors 2, 7, 9 and 10

28
Q

What complications can coagulation factor disorders cause?

A

1) muscle haematomas
2) recurrent haemarthroses (bleeding into joints)
3) joint pain and deformity
4) prolonged bleeding post dental extraction
5) life threatening post op bleeding
6) intracerebral haemorrhage

29
Q

True or false: haemophilia A is an X linked recessive condition

A

TRUE

30
Q

How is haemophilia A treated?

A

Recombinant factor VIII

31
Q

True or false: Von willebrand disease is autosomal dominant

A

TRUE

32
Q

What does Von willebrand’s disease lead to?

A

1) Abnormal platelet adhesion to vessel wall

2) Reduced factor VIII amount/activity

33
Q

What can vessel wall abnormalities lead to?

A

Easy bruising

Spontaneous bleeding from small vessels in skin and sometimes mucous membranes

34
Q

What can a low platelet count be due to?

A

1) Reduced production

2) Increased removal (non-immune destruction, immune destruction, splenic pooling)

35
Q

What causes the immune destruction of platelets?

A

Immune thrombocytopenic purpura- autoantibodies against glycoproteins

36
Q

How is immune thrombocytopenic purpura treated?

A

With immunosuppression

37
Q

What can lead to reduced production of platelets?

A

1) B12/folate deficiency
2) Infiltration of bone marrow by cancer cells or fibrosis
3) Drugs - chemo, antibiotics
4) Viruses - HIV, hepatitis

38
Q

True or false: patients with severe thrombocytopenia are always symptomatic

A

FALSE - generally not symptomatic until platelet count is less than 30

39
Q

What are the consequences of severe thrombocytopenia?

A

1) Easy bruising
2) Petechiae and purpura
3) Mucosal bleeding
4) Severe bleeding after trauma
5) Intracranial haemorrhage

40
Q

What is the difference between petechiae and purpura?

A 
Petechiae = small red spots of bleeding in skin
Purpura = rash of purple spots-internal bleeding of small vessels
41
Q

What is the main way in which platelet function disorders can be acquired?

A

Aspirin/NSAIDS/clopidogrel

42
Q

What is disseminated intravascular coagulopathy (DIC)?

A

Microthrombi form in circulation, leading to consumption of clotting factors and platelets and haemolytic anaemia

43
Q

What type of anaemia is disseminated intravascular coagulopathy?

A

Microangiopathic haemolytic anaemia

44
Q

What are the triggers of disseminated intravascular coagulopathy?

A

1) malignancy
2) massive tissue injury eg burns
3) infections (gram negative sepsis)
4) massive haemorrhage and transfusion
5) ABO transfusion reaction
6) obstetric causes

Semester 2-PP (13 decks)

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