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BRS Cardio & Respiratory > 1b// Haemostasis > Flashcards

1b// Haemostasis Flashcards

1
Q

what is the purpose of haemostasis?

A

prevention of blood loss from intact vessels
arrest bleeding from injured vessels
enable tissue repair

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2
Q

what is haemostasis?

A

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

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3
Q

describe the mechanisms of haemostasis

A

vessel constriction
formulation of unstable platelet plug
stabilisation of plug with fibrin
vessel repair and dissolution of clot

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4
Q

what is primary haemostasis?

A

unstable platelet plug

platelet adhesion, aggregation to limit blood loss and provides surface for coagulation

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5
Q

what is secondary haemostasis?

A

stabilisation of platelet plug (fibrin)

blood coagulation to stop blood flow

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6
Q

what is fibrinolysis in haemostasis?

A

final stage of haemostasis - vessel repair and dissolution of clot
restores vessel integrity

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7
Q

what is the importance of understanding haemostasis?

A 
diagnose/treat bleeding disorders
control bleeding in normal individuals
identify risk factors for fibrinolysis
treat thrombotic disorders
monitor treatment for bleeding/thrombotic disorders
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8
Q

how does platelet adhesion occur?

A

adheres to collagen in vessel wall
GlpIa receptor direct bonding
GlpIb receptor via Von Willebrand Factor

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9
Q

how does platelet aggregation occur?

A

platelets release ADP, fibrinogen and thromboxane A2 after they are activated
express GlpIIb/IIIa for adhesion of other platelets via fibrinogen and Ca2+

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10
Q

what conditions cause thrombocytopenia?

A 
bone marrow failure (leukaemia, b12 deficiency)
accelerated clearance (immune ITP, disseminated intravascular coagulation)
pooling and destruction in splenomegaly
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11
Q

what conditions cause impaired platelet function?

A

hereditary absence of glycoproteins or storage granules

latrogenic - aspirin, NSAIDs, clopidogrel

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12
Q

what is immune thrombocytopenic purpura? ITP

A

antiplatelet autoantibodies bind to sensitised platelets
macrophages then bind to the platelets and destroy them (spleen)
this causes low platelet count

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13
Q

what are some hereditary platelet defects?

A

Glanzmanns thrombasthenia - absence of GlpIIb/IIIa
bernard soulier syndrome - absence of GlpIb
storage pool disease - absence of dense or alpha granules

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14
Q

what is aspirins MOA?

A

binds irreversibly to cyclooxygenase
inhibits thromboxane A2 synthesis
therefore prevents platelet aggregation
effects last around 7 days

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15
Q

what is clopidogrels MOA?

A

irreversibly blocks ADP receptor (P2Y12) on platelet cell membrane
therefore platelets cannot be activated to cause aggregation

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16
Q

what are the functions of von willebrand factor?

A

binding to collagen and capturing platelets

stabilising factor VIII

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17
Q

what is von willebrand disease?

A

hereditary autosomal dominant disease causing failure of primary haemostasis
deficiency of VWF (type 1&3)
VWF with abnormal function (type 2)

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18
Q

what are some causes of vessel wall disorders?

A 
hereditary haemorrhagic telangiectasia
ehlers danlos syndome
steroid therapy
ageing
vasculitis
scurvy
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19
Q

how does typical primary haemostasis bleeding present?

A 
immediate
prolonged bleeding from cuts
prolonged nose bleeds, gum bleeding
menorrhagia
ecchymosis - easy and spontaneous bruises
prolonged bleeds after trauma/surgery
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20
Q

what specific symptom occurs for thrombocytopenia?

A

petechiae - bleeding under skin

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21
Q

what disorders cause purpura as a symptom?

A

platelet or vascular disorders (thrombocytopenia pupura)

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22
Q

what tests are used in diagnosis of primary haemostasis disorders?

A 
platelet count and morphology 
PFA100 (platelet function analysis - bleeding time)
assays of VWF
clinical observation
PT and aPTT
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23
Q

what tests are usually normal in primary haemostasis disorders?

A

PT and aPTT

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24
Q

how do you treat failure of production/function platelet disorders?

A

replace missing platelets/factor e.g VWF prophylactically or therapeutically
stop aspirin/nsaids

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25
Q

how do you treat immune destruction of platelets?

A

immunosuppression

splenectomy for ITP

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26
Q

how do you treat increased consumption of platelets?

A

treat underlying cause

replacement

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27
Q

how can desmopressin be used to treat primary haemostatic abnormalities?

A

causes 2-5 fold increase of VWF and factor VIII

releases endogenous stores therefore only used in mild disorders

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28
Q

how is tranexamic acid used?

A

traumatic bleeds, strokes

antifibrinolytic

29
Q

when are fibrin glues/sprays used?

A

during surgeries

30
Q

what is the overall role/end goal of coagulation in haemostasis?

A

generate thrombin IIa to convert fibrinogen to fibrin

31
Q

what are the acquired causes of factor deficiencies?

A

liver disease

anticoagulant drugs - warfarin, DOACs

32
Q

what are the hereditary causes of factor deficiency?

A

haemophilia A/B (VIII/IX)

33
Q

what are the causes of dilution coagulopathy?

A

blood transfusions

34
Q

what are the causes for increased consumption coagulopathy?

A

disseminated intravascular coagulation DIC

immune autoantibodies

35
Q

what is haemarthrosis?

A

spontaneous joint bleeding
causes long term chronic muscle wasting
prophylaxis from around 9mths age

36
Q

what does a deficiency of factor II cause?

A

incompatibility with life - prothrombin is necessary

37
Q

what does a deficiency of factor XI cause?

A

bleeds after trauma no spontaneous bleeding

38
Q

what does a deficiency of factor XII cause?

A

no bleeding

39
Q

what factors aren’t produced in the liver?

A

VWF (endothelium), factor V (platelets)

40
Q

what is disseminated intravascular coagulation?

A

generalised activation of coagulation - tissue factor
consumes and depletes coagulation factors
platelets consumed - thrombocytopenia
fibrinolysis depletes fibrinogen causing raised D-dimer and red cell fragmentation
deposition of fibrin in vessels causes organ failure
risk of sepsis, cancer, obstetric disorders

41
Q

different types of factor replacement therapy

A

Fresh Frozen Plasma
Cryoprecipitate
Factor Concentrates
Recombinate forms of FVIII and FIX

42
Q

FFP

A

contains all Coagulation factors

43
Q

cryoprecipitate

A

Fibrinogen, Factor VIII (8), XIII and VWF

44
Q

factor concentrates

A

Concentrates available for all factors except factor V.

Prothrombin complex concentrates (PCCs) Factors II, VII, IX, X

45
Q

whn are recombinant forms of FVIII and FIX used?

A

‘On Demand’ to treat bleeds

Prophylaxis to prevent bleeds

46
Q

disorders of thrombosis present with

A

pulmonary embolism

deep vein thrombosis

47
Q

pulmonary embolism symptoms

A 
Tachycardia
Hypoxia
Shortness of breath
Chest pain
Haemoptysis
Sudden death
48
Q

features of DVT

A 
Painful leg
Swelling
Red
Warm
May embolise to lungs
Post thrombotic syndrome
49
Q

What is thrombosis

A

inappropriate intravascular coagulation
Venous (or arterial)
Obstructs flow
May embolise to lungs

50
Q

What is Virchow’s triad

A 
Three contibutory factors to thrombosis
Blood (dominant in venous)
Vessel wall (dominant in arterial)
Blood flow (both)
51
Q

what is indicative of thrombosis

A

Thrombosis at young age
‘spontaneous thrombosis’
Multiple thromboses
Thrombosis whilst anti-coagulated

52
Q

anticoagulant proteins

A

antithrombin
protein C
protein S

53
Q

risk factors of venous thrombosis

A

age]
genetic
environmental

54
Q

prevention of thrombosis

A

prophylactic anticoagulant therapy

55
Q

acquired causes of coagulopathy

A

liver failure
anticoagulant drugs
dilution
increased consumption -DIC

56
Q

blood test sign of DIC

A

raised D-dimer

red cell fragmentation

57
Q

clinical features of coagulation disorders

A 
superficial cuts dont bleed
bruising common, nosebleeds rare
spontaneous bleeds are deep - joints etc
bleeding after trauma may be late and prolonged
bleeding frewuently restarts
58
Q

differences between platelet/vascular and coagulation disorders

A

platelet - superficial bleeds, immediate bleeds

coagulation - deep bleeds, prolonged but delayed

59
Q

tests for coagulation disorders

A

clotting screen - APTT, PT, FBC
coagulation factor assays
tests for inhibitors

60
Q

what does APTT measure

A

intrinsic pathway

61
Q

what does PT measure

A

extrinsic factor VII via tissue factor pathway

62
Q

prolonged APTT indicates

A 
haemophilia A/B
factor XI deficiency 
or XII (no bleeds)
63
Q

prolonged PT indicates

A

factor VII deficiency

64
Q

prolonged APTT and PT

A 
liver disease
anticoagulant drugs
DIC
dilution
factor X, II, V (common pathway) deficiencies
65
Q

treatments for failure of production

A

replaces as necessary

stop drugs e.g nsaids, aspirin

66
Q

treatments for immune destruction

A

immunosuppresion - prednisolone

splenectomy - ITP

67
Q

treatments for increased ocnsumption

A

treat cause

replace as necessary

68
Q

how to reduce recurrence of thrombosis

A

lower procoagulants - DOACs, warfarin

increase anticoags - heparin

BRS Cardio & Respiratory (28 decks)

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