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aPATH P COPY (SC) > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

role of haemostasis

A
  • Prevents bleeding
  • Prevents unnecessary coagulation allowing blood to flow
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2
Q

main principls of haemostasis

A

1) Make clot
2) Control clotting
3) Break it down

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3
Q

what are essential for haemostasis?

A
  • Movement of blood
    • Heart
    • Venous valves
    • Calf pump
  • Platelets
  • Coagulation factors
  • Anticoagulant factors
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4
Q

Haemostasis pathway

A
  1. Clot initiation
    • Platelet aggregation at site of damage
    • Activation of coagulation
  2. Clot formation
    • Activation of prothrombin to thrombin
    • Thrombin converts fibrinogen to fibrin
    • Fibrin polymers form
    • Retraction
  3. Fibrinolysis (during tissue repair)
    • Fibrin fragments
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5
Q

how are platelets produced

A

by megakaryocytes- bud from cytoplasm

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6
Q

normal platelet count

A

150-400 x10^9/l

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7
Q

lifespan of a platelet

A
  • Lifespan 7-10 days
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8
Q

what does a platelet look like

A
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9
Q

what happens to the vessel wall after famage

A

vasoconstriction and production of von willebrand factor

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10
Q

von willebrand factor

A
  • Involved in platelet adhesion to the vessel wall,
  • platelet aggregation
  • and also carries and protects Factor VIII
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11
Q

otulien the steps involvinf platelets

A

1) Platelet adhesion

2) Platelet activation

3) Platelet aggregation

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12
Q

1) Platelet adhesion

  • *
A
  • Damage to vessel wall
  • Exposure of underlying tissues
  • Platelets adhere to collagen via vWF/receptors
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13
Q

2) Platelet activation

A
  • Secrete ADP, thromboxane and other substances to become activated and activate other platelets
  • Involved in activation of clotting cascade
  • Provide some coagulation factors by secretion from internal stores
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14
Q

3) Platelet aggregation

A

Cross linking of platelets to form platelet plug

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15
Q

mediating factors of platelets role in haemostasis

A
  • Von Willebrand’s factors
  • Fibrinogen
  • Collagen
  • ADP
  • Thromboxane
  • Thrombin
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16
Q

the clotting cascade is an

A

amplficiation system

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17
Q

the clotting cascade activates preucrosor molecules to generate

A

IIa (thrombin)

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18
Q

Thrombin converts

A
  • Fibrinogen to fibrin
    • Enmeshes initial platelet plug to make a stable clot
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19
Q

how is the clotting cascade controlled

A
  • Natural anticoagulates that inhibits activation
  • Also clot destroying proteins
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20
Q

both the intrinsic and extrinsic pathwya lead to the activation of

A

Xa which actives prothrombin to thrombin (IIa)

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21
Q

The intrinsic pathway is activated through

A

exposed endothelial collagen

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22
Q

The extrinsic pathway is activated through

A

tissue factor released by endothelial cells after external damage.

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23
Q

Coagulation factors and natural anticoagulants are made in the

A

liver

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24
Q

coagulation factors

A
  • Fibrinogen
  • Prothrombin
  • Factors5,7,8,9,10,11,12,13, tissue factor
25
Q

natural anticoagulants

A
  • Protein C
  • Protein S
  • Antithrombin
  • Tissue factor pathway inhibitor
26
Q

how do we measure coagulation

A

Extrinsic/ PT (prothrombin time) test

  • VII

Intrinsic/ APTT (activated partial thromboplastin time) test

  • VIII, IX,XI, XII

V,X, prothrombin and fibrinogen can be done for both x

27
Q

Fibrinolysis

A
  1. Plasminogen is activated by tissue plasminogen activator to form plasmin (e.g. T-PA, alteplase)
  2. Plasmin breaks down the fibrin clot
  3. Forms D-dimers- broken down by proteases in the blood
28
Q

clinical relevance of haemostasis

A
  • Bleeding disorders
  • Arterial thrombotic disorders
  • Venous thrombotic disorders
  • Abnormal blood test results
  • Drug therapy for pro-antithrombotic purposes
29
Q

bleeding disorders can be due to

A

abnormalities in the vessel wall, platelts or coagulation factors

30
Q

bleeding disorders can be

A

congenital or acquired

31
Q

congenital bleeding disroders

A
  • Haemophilia A (factor 8)
  • Haemophilia B (Factor 9)
32
Q

acquired bleeding disorders

A
  • Liver disease
  • Vit K deficiency
  • Anticoagulants including warfarin (inhibit Vit K)
33
Q

vessel wall abnormalities

A
  • Easy bruising
  • Spontaneous bleeding from small vessels
  • Skin mainly
  • Can be mucous membranes
34
Q

congenital vessel wall abnormalities

A
  • Hereditary haemorrhagic telangiectasia (HHT)
  • Connective tissue disorders- Ehlers Danlos
35
Q

Hereditary haemorrhagic telangiectasia (HHT)

A
  • Autosomal dominant
  • Dilated microvascular swellings increase with time
  • GI haemorrhage can lead to iron deficiency anaemia
36
Q

acquired vessel wall abnormalities

A
  • Senile purpura
  • Steroids
  • Infection e.g. measles, meningococcal infections
  • Scurvy-Vit C def causing defective collagen production (cant be hydroxylated)
37
Q

Coagulation factor disorders

A

Clinical severity correlates with extent of deficiency

  • Muscle haematomas
  • Recurrent hemarthroses
  • Joint pain and deformity
  • Prolonged bleeding post dental extraction
  • Life threatening post op and post traumatic bleeding
  • Intracerebral haemorrhage
38
Q

haemophilia A is an

A

x-linked recessive disease which causes lack factor VII (8)

39
Q

severity of haemophilia A depends on

A

amount of VIII present

40
Q

when is haemophilia A diagnoseed

A

pre-natally or soon after birth if family history or usually in infancy if new spontaneous mutation

41
Q

where can bleeding occur with Haemophilia A

A
  • Bleeding into muscle and joints, and post-operatively
42
Q

treatment of haemophilia A

A

recombiannt factor VIII/ DDAVP

43
Q

which test will show an abnormality with haemophilia A

A

intrinsic/ APTT test

44
Q

haemophilia B has a

A

similar presentation to hameophilia A

45
Q

what causes haemophilia B

A

congenital reduction in factor IX

46
Q

Von Willebrand’s disease

A
  • Relatively common
  • Autosomal dominant, affects males and females
47
Q

role of VWF

A

carries factor VIII and mediates platelet adhesion to the endothelium

48
Q

von willebrand diseases causes abnormal

A
  • Causes abnormal platelet adhesion to the vessel wall
  • Reduced factor VIII amount/activity
    • Factor 8 can be low in addition to low VWF levels
49
Q

what causes VWD?

A

several genetic defects

50
Q

symptoms of coagulation factor disorders

A
  • Skin and mucous membrane bleeding
    • Epistaxis
    • Gum bleeding
    • Bruising
    • Prolonged bleeding after trauma
51
Q

Disseminated intravascular coagulopathy (DIC)

A
  • Type of microangiopathic haemolytic anaemia
  • Pathological activation of coagulation
  • Numerous microthrombi are formed in the circulation
  • Leads to consumption of clotting factors and platelets and a haemolytic anaemia
  • Clotting tests are affected- raised PT, raised APTT, low fibrinogen and raised D-dimers (fibrin degradation products)
52
Q

disseminated intravascular coagulopathy (DIC)

A
  • Type of microangiopathic haemolytic anaemia
  • Pathological activation of coagulation
  • Numerous microthrombi are formed in the circulation
  • Leads to consumption of clotting factors and platelets and a haemolytic anaemia
    *
53
Q

test results for DIC

A

Clotting tests are affected- raised PT, raised APTT, low fibrinogen and raised D-dimers (fibrin degradation products)

54
Q

triggers for DIC (always a trigger)

A
  • Malignancy
  • Massive tissue injury e.g. burns
  • Infection
  • Massive haemorrhage and transfusion
  • ABO transfusion reaction
  • Obstetric causes- placental abruption, pre-eclampsia, amniotic fluid embolism
55
Q

Thrombophilias

A
  • Acquired or congenital defects of haemostasis which cause increased risk of thrombosis
56
Q

congenital causes of thrombophilia

A
  • include deficiency in natural anticoagulants (protein C, protein S and antithrombin) and an abnormal factor V (factor V Leiden)
57
Q

acquired thrombophilia

A

Acquired causes include antiphosphopholipid syndrome

58
Q

thrombophilias are a relatively

A

rare conditions and many patients with them do not develop clots unless they have additional risk factors

aPATH P COPY (SC) (19 decks)

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