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haemostasis Flashcards

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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
what is type 1/3 vwd
deficiency in vwf
26
what is type 2 vwd
vwf with abnormal function
27
how can vessel wall cause disorder of primary heamostasis
inherited (rare) hereditary haemorrhagic telangiectasia Ehlers Danlos syndrome and other connective tissue disorders aquired (common): steroid therapy, age(senile purpura,), scurvy vit c def
28
how can steroids affect vessel walls in primary haemostasis
long term use can cause atrophy of collagen fibres that support vessels
29
how can scurvy( vit c def) affect vessel walls
defective collagen synthesis leading to weakening of capillary walls
30
summary of disorders of primary haemostasis
platelets: thrombocytopenia, drugs VWD vessel wall - hereditary vasc disorders, steroids,age,scurvy,vasculitis
31
what are some clinical features of disorders of primary haemostasis
``` immediate bleeding prolonged bleeding from cuts prolonged nose bleeding gum bleeding menorrhagia eccymosis - easy bruising prolonged bleeding after trauma/surgery ```
32
what is a sign of thrombocytopenia
petechiae - small spots caused by bleeding under skin <3mm
33
what is purpura
red/purple discoloured skin - dont blanch when pressure applied 3-10 mm
34
how big does bleeding spot need to be for eccymosis
>10 mm/cm?
35
how to test for disorders of primary haemostasis
``` 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
normal range of platelet count
150 -400 x10^9/l
37
how to treat failure of production/function in abnormal haemostasis
replace missing factors/platelets e.g vwf containing concentrates prophylactic therapeutic stop drugs e.g nsaids/aspirin
38
how to treat immune destruction in abnormal haemostasis
immunosuppression e.g prednisolone | splenectomy for itp
39
how can we treat increased consumption in abnormal haemostasis
treat cause | replace whats necessary
40
what are some additional treatments for abnormal haemostasis
desmopressin ddavp causes 2-5 fold of vwf tranexamic acid - antifibrinolytic fibrin glue/spray other approaches e.g ocp for menorrhagia
41
what is the role of coagulation
generate thrombin (f2a) which converts fibrinogen to fibrin
42
what does the deficiency of any coagulation factor cause
failure of thrombin generation and hence fibrin formation
43
what causes deficiency of coagulation factor production
hereditary - f8/9 def : haemophilia a/b, prothrombin def f11,12 def acquired - liver disease, anticoagulant drugs
44
what causes dilution in disorders of coagulation
acquired - blood transfusion
45
what causes increased consumption in disorders of coagulation
``` acquired - disseminated intravascular coagulation immune autoantibodies (rare) ```
46
what are the hereditary coagulation disorders
haemophilia a- f8 def haemophilia b - f9 def = sex linked other are very rare - autosomal recessive
47
what was the hallmark of haemophilia
haemathrosis - bleeding in joint | long term can get muscle wasting
48
what does liver failure cause
reduction in coagulation factors as that where they are formed
49
what can disseminated intravascular coagulation be caused by
sepsis cancer obstetric disorders e.g pre eclampsia associated with major tissue damage
50
what does unregulated coagulation in dic result in
widespread consumption and depletion of coag factors thrombocytopenia activation of fibrinolysis - raised d dimer deposition of fibrin in vessels causing organ failure
51
what are the clinical features of coagulation factors
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
tests for coagulation disorders
screening test - clotting screen pt,aptt,fbc coagulation factors assays test for inhibitors
53
what can be given for factor replacement therapy
ffp cyroprecipitate factor concentrates recombinant forms of f8 and f9
54
what is found in ffp
contains all coagulation factors
55
what is in cyroprecipitate
rich in fibrinogen, f8,vwf,f13
56
what is found in factor concentrates
concentrates available for all factors except f5 | prothrombin complex concentrates f2,7,9,10
57
novel treatments for haemophilia
gene therapy bispecific antibodies - mimics procoagulant function of f8 rna silencing
58
what are some other factors that can increase bleeding
increase in fibrinolytic factors increase in anticoagulant proteins rare but induced by tpa or heparin
59
how does a pulmonary embolism present
``` tachycardia hypoxia shortness of reath chest pain haemoptysis sudden death ```
60
how does deep vein thrombosis present dvt
``` painful leg swelling red warm may embolise to lung post thrombotic syndrome ```
61
what is thrombosis
intravascular inappropriate coagulation venous/arterial obstructs flow may embolise to lungs
62
what is virchows triad
3 contributory factors to thrombosis blood - dominant in venous thrombosis vessel wall - dominant in arterial thrombosis blood flow - bith
63
what is thrombophilia
increased risk of venous thrombosis
64
how can thrombophilia present
thrombosis at young age spontaneous multiple thromboses thrombosis while anticoagulated
65
what can cause venous thrombosis
reduction in anticoagulant factors - antithrombin, protein c, protein s or increase in coagulant factors/ myeloproliferative disorders e.g increase in plts
66
when can reduced flow increase risk of thrombosis
pregnancy | long haul flight
67
how to prevent venous thrombosis
assess and prevent risks | prophylactic anticoagulant therapy
68
how to reduce risk of recurrence/extension of thrombosis
lower procoagulant factors e.g warfarin,DOACs | increase anticoagulant activity e.g heparin
69
what are some indications for anticoagulant treatment
venous thrombosis atrial fibrillation mechanical prosthetic heart valves preventative too e.g following surgery, during hosp admission, pregnancy
70
what is heparin
naturally occurring glycosaminoglycans produced by mast cells porcine products used in uk
71
what is the action of unfractionated heparin
enhancement of antithrombin - | inactivation of thrombin - hep binds at and thrombin
72
action of lmwh
shorter polysaccharide chain | activity is predominantly against f10a
73
what is warfarin
vit k antagonist f2,7,9,10, protein c and s are dependent on vitK effective in vte and mi
74
why does warfarin require monitoring
has diff effects on diff individuals | many dietary, physiological and drug interaction
75
what are some effects of warfarin
bleeding skin necrosis purple toe syndrome embryopathy - chondrodydplasia punctata
76
how to monitor warfarin
inr - international normalised ratio | standardised measure reflecting correction for diff thromboplastins
77
what can cause resistance to warfarin
lack of patient compliance - diet high in vit k | increased metabolism cytp450
78
examples of doacs
f10a inhibitors - rivaroxaban apixaban edoxaban f2a inhibitor - dabigratan
79
compare doacs to warfarin
``` rapid fixed dosing no food effect few drug interactions as apposed to many in warfarin no monitoring required some renal dependance, none in warfarin ```

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