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haemostasis Flashcards

1
Q

what is haemostasis

A

cellular and biochemical process that enables both specific and regulated cessation of bleeding in response to vascular insult

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2
Q

what do we need haemostasis for

A
  • prevention of blood loss from intact vessels
  • arrest bleeding from injured vessels
  • enable tissue repair
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3
Q

what is the first role of haemostasis in response to injury to endothelial cell lining

A

vessel constriction -
vascular smooth muscle cells contract locally
limits blood flow to injured vessel

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4
Q

what is primary haemostasis

A

formation of unstable platelet plug -
platelet adhesion
platelet aggregation
limits blood loss and provides surface for coagulation

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5
Q

what is secondary haemostasis

A

stabilisation of plug with fibrin
BLOOD COAGULATION
stops blood loss

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6
Q

what is last step - fibrinolysis

A

vessel repair and dissolution of clot
cell migration/proliferation and fibrinolysis
restores vessel integrity

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7
Q

why is it important to understand haemostatic mechanisms

A
  • diagnose and treat bleeding disorders
  • control bleeding in those without disorders
  • identify risk factors for thrombosis
  • treat thrombotic disorders
  • monitor drugs used
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8
Q

what is the equilibrium in normal haemostasis

A

fibrinolytic factors and anticoagulant factors balance coagulant factors and platelets

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9
Q

what can cause a reduction in coagulation factors/plts

A 
lack of specific factor - 
failure of production: 
-congenital and acquired
-increased consumption/clearance
OR
defective function of specific factor - 
- genetic
- acquired - drugs,synthetic defect,inhibition
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10
Q

what happens during platelet adhesion

A

damaged endothelial cells causes collagen to be exposed on surface
platelets can bid directly to collagen via glp1a or indirectly via glp1b to vwf

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11
Q

what does binding of platelets to collagen cause

A

release of adp and thromboxane

platelets are activated

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12
Q

what happens during platelet activation

A

glp2b/3a receptor on platelets is activated

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13
Q

what do we call low number of platelets

A

thrombocytopenia

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14
Q

what causes thrombocytopenia

A
  • bone marrow failure e.g leukaemia,b12 deficiency
  • accelerated clearance e.g immune(itp),disseminated intravascular coagulation (dic)
  • pooling and destruction in enlarged spleen (splenomegaly)
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15
Q

what happens in immune thrombocytopenic purpura

itp

A

antiplatelet antibodies bind to sensitised platelet

these are then cleared by macrophages of the reticulo-endothelial system in spleen

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16
Q

what causes impaired function of platelets

A
  • hereditary absence of glycoproteins /storage granules (rare)
  • acquired due to drugs: aspirin,NSAIDs,clopidogrel (common)
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17
Q

what are some examples of hereditary platelet defects

A

Glanzmanns thrombasthenia
Bernard Soulier syndrome
storage pool disease

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18
Q

what are antiplatelet drugs commonly used for

A

prevention and treatment of cardiovascular and cerebrovascular disease

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19
Q

most common antiplatelet drugs

A

aspirin

clopidogrel

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20
Q

what is action of aspirin

A

irreversibly blocks cox enzyme results in reduced platelet aggregation

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21
Q

how many days does action of aspirin last for

A

7 days

platelets at time of aspirin ingestion are replaced by new platelets

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22
Q

what is action of clopidogrel

A

works by irreversibly blocking adp receptor p2y12, found on platelet cell membrane

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23
Q

what causes von willebrand disease

A

autosomal hereditary disease of quantity +/function (common)

acquired due to antibody (rare)

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24
Q

role of vwf

A

binding to collagen and capturing platelets

stabilising factor 8

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25
Q

what is type 1/3 vwd

A

deficiency in vwf

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26
Q

what is type 2 vwd

A

vwf with abnormal function

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27
Q

how can vessel wall cause disorder of primary heamostasis

A

inherited (rare)
hereditary haemorrhagic telangiectasia Ehlers Danlos syndrome and other connective tissue disorders
aquired (common): steroid therapy, age(senile purpura,), scurvy vit c def

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28
Q

how can steroids affect vessel walls in primary haemostasis

A

long term use can cause atrophy of collagen fibres that support vessels

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29
Q

how can scurvy( vit c def) affect vessel walls

A

defective collagen synthesis leading to weakening of capillary walls

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30
Q

summary of disorders of primary haemostasis

A

platelets: thrombocytopenia, drugs
VWD
vessel wall - hereditary vasc disorders, steroids,age,scurvy,vasculitis

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31
Q

what are some clinical features of disorders of primary haemostasis

A 
immediate bleeding
prolonged bleeding from cuts
prolonged nose bleeding
gum bleeding
menorrhagia
eccymosis - easy bruising
prolonged bleeding after trauma/surgery
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32
Q

what is a sign of thrombocytopenia

A

petechiae -
small spots caused by bleeding under skin
<3mm

33
Q

what is purpura

A

red/purple discoloured skin
- dont blanch when pressure applied
3-10 mm

34
Q

how big does bleeding spot need to be for eccymosis

A

> 10 mm/cm?

35
Q

how to test for disorders of primary haemostasis

A 
platelet count/ morphology
bleeding time - pfa100 now
assays of vwf
clinical observation
coagulation screens pt and aptt is normal except severe vwd where f8 is low
36
Q

normal range of platelet count

A

150 -400 x10^9/l

37
Q

how to treat failure of production/function in abnormal haemostasis

A

replace missing factors/platelets e.g vwf containing concentrates
prophylactic
therapeutic
stop drugs e.g nsaids/aspirin

38
Q

how to treat immune destruction in abnormal haemostasis

A

immunosuppression e.g prednisolone

splenectomy for itp

39
Q

how can we treat increased consumption in abnormal haemostasis

A

treat cause

replace whats necessary

40
Q

what are some additional treatments for abnormal haemostasis

A

desmopressin ddavp causes 2-5 fold of vwf
tranexamic acid - antifibrinolytic
fibrin glue/spray
other approaches e.g ocp for menorrhagia

41
Q

what is the role of coagulation

A

generate thrombin (f2a) which converts fibrinogen to fibrin

42
Q

what does the deficiency of any coagulation factor cause

A

failure of thrombin generation and hence fibrin formation

43
Q

what causes deficiency of coagulation factor production

A

hereditary - f8/9 def : haemophilia a/b,
prothrombin def
f11,12 def
acquired - liver disease, anticoagulant drugs

44
Q

what causes dilution in disorders of coagulation

A

acquired - blood transfusion

45
Q

what causes increased consumption in disorders of coagulation

A 
acquired - disseminated intravascular coagulation
immune autoantibodies (rare)
46
Q

what are the hereditary coagulation disorders

A

haemophilia a- f8 def
haemophilia b - f9 def
= sex linked
other are very rare - autosomal recessive

47
Q

what was the hallmark of haemophilia

A

haemathrosis - bleeding in joint

long term can get muscle wasting

48
Q

what does liver failure cause

A

reduction in coagulation factors as that where they are formed

49
Q

what can disseminated intravascular coagulation be caused by

A

sepsis
cancer
obstetric disorders e.g pre eclampsia
associated with major tissue damage

50
Q

what does unregulated coagulation in dic result in

A

widespread consumption and depletion of coag factors
thrombocytopenia
activation of fibrinolysis - raised d dimer
deposition of fibrin in vessels causing organ failure

51
Q

what are the clinical features of coagulation factors

A

superficial cuts dont bleed
bruising is common, nosebleeds are rare
spontaneous bleeding is deep - into muscles and joints
bleeding after trauma is delayed and prolonged
bleeding frequently restarts after stopping

52
Q

tests for coagulation disorders

A

screening test - clotting screen
pt,aptt,fbc
coagulation factors assays
test for inhibitors

53
Q

what can be given for factor replacement therapy

A

ffp
cyroprecipitate
factor concentrates
recombinant forms of f8 and f9

54
Q

what is found in ffp

A

contains all coagulation factors

55
Q

what is in cyroprecipitate

A

rich in fibrinogen, f8,vwf,f13

56
Q

what is found in factor concentrates

A

concentrates available for all factors except f5

prothrombin complex concentrates f2,7,9,10

57
Q

novel treatments for haemophilia

A

gene therapy
bispecific antibodies - mimics procoagulant function of f8
rna silencing

58
Q

what are some other factors that can increase bleeding

A

increase in fibrinolytic factors
increase in anticoagulant proteins
rare but induced by tpa or heparin

59
Q

how does a pulmonary embolism present

A 
tachycardia
hypoxia
shortness of reath
chest pain
haemoptysis
sudden death
60
Q

how does deep vein thrombosis present dvt

A 
painful leg
swelling
red
warm
may embolise to lung
post thrombotic syndrome
61
Q

what is thrombosis

A

intravascular inappropriate coagulation
venous/arterial
obstructs flow
may embolise to lungs

62
Q

what is virchows triad

A

3 contributory factors to thrombosis
blood - dominant in venous thrombosis
vessel wall - dominant in arterial thrombosis
blood flow - bith

63
Q

what is thrombophilia

A

increased risk of venous thrombosis

64
Q

how can thrombophilia present

A

thrombosis at young age
spontaneous
multiple thromboses
thrombosis while anticoagulated

65
Q

what can cause venous thrombosis

A

reduction in anticoagulant factors - antithrombin, protein c, protein s
or increase in coagulant factors/ myeloproliferative disorders e.g increase in plts

66
Q

when can reduced flow increase risk of thrombosis

A

pregnancy

long haul flight

67
Q

how to prevent venous thrombosis

A

assess and prevent risks

prophylactic anticoagulant therapy

68
Q

how to reduce risk of recurrence/extension of thrombosis

A

lower procoagulant factors e.g warfarin,DOACs

increase anticoagulant activity e.g heparin

69
Q

what are some indications for anticoagulant treatment

A

venous thrombosis
atrial fibrillation
mechanical prosthetic heart valves
preventative too e.g following surgery, during hosp admission, pregnancy

70
Q

what is heparin

A

naturally occurring glycosaminoglycans
produced by mast cells
porcine products used in uk

71
Q

what is the action of unfractionated heparin

A

enhancement of antithrombin -

inactivation of thrombin - hep binds at and thrombin

72
Q

action of lmwh

A

shorter polysaccharide chain

activity is predominantly against f10a

73
Q

what is warfarin

A

vit k antagonist
f2,7,9,10, protein c and s are dependent on vitK
effective in vte and mi

74
Q

why does warfarin require monitoring

A

has diff effects on diff individuals

many dietary, physiological and drug interaction

75
Q

what are some effects of warfarin

A

bleeding
skin necrosis
purple toe syndrome
embryopathy - chondrodydplasia punctata

76
Q

how to monitor warfarin

A

inr - international normalised ratio

standardised measure reflecting correction for diff thromboplastins

77
Q

what can cause resistance to warfarin

A

lack of patient compliance - diet high in vit k

increased metabolism cytp450

78
Q

examples of doacs

A

f10a inhibitors - rivaroxaban
apixaban
edoxaban
f2a inhibitor - dabigratan

79
Q

compare doacs to warfarin

A 
rapid 
fixed dosing
no food effect
few drug interactions as apposed to many in warfarin
no monitoring required
some renal dependance, none in warfarin

brs2 (65 decks)

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