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BRS YEAR 2 > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

stages of haemostasis

A

local vessel constriction → formation of unstable platelet plug (primary haemostasis) → stabilisation of plug with fibrin (secondary haemostasis) → vessel repair and clot dissolution (fibrinolysis)

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2
Q

what does primary haemostasis involve

A

platelet adhesion and platelet migration
Adhesion via Gp1a to endothelial cell or VWF and Gp1b
aggregation via release of ADP and thromboxane
fibrinogen and GpIIb/GpIIIa links platelts

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3
Q

low platelet count

A

thrombocytopenia may be caused by

bone marrow failure → leukemia, B12 deficiency

accelerated clearance → ITP, disseminated intravascular coagulation

pooling and destruction in large spleen

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4
Q

immune thrombocytopenia

A

antiplatelet autoantibodies bind → sensitised platelet detected and removed by macrophages of reticuloendothelial system in spleen

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5
Q

what is glanzmann’s thrombasthenia?

A

hereditary defect in GpIIb/IIIa production

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6
Q

what is bernard soulier syndrome?

A

hereditary defect in GpIb production

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7
Q

what is storage pool disease?

A

hereditary issue with storage granules inside platelets

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8
Q

how can platelet defects be acquired?

A

drugs e.g. aspirin vs COX (no thromboxane A2) thus platelet aggregation decreases, clopidogrel vs ADP receptor P2Y12 on platelets

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9
Q

VWF functions in homeostasis?

A

bind to collagen and collect platelets

stabilise factor VIII

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10
Q

what is von willebrand disease?

A

usually hereditary decrease in amount or function of VWF

can rarely be acquired due to antibodies

  • subtypes of hereditary variation?1, 3 → deficiency of VWF2 → VWF with abnormal function
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11
Q

examples of inherited disorders in vessel wall leading to haemostasis issue?

A

hereditary haemorrhagic telangiectasia

ehlers-danlos syndrome

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12
Q

acquired causes of vessel wall

A

steroid therapy, aging ‘senile purpura’, vasculitis, vit C deficiency (scurvy)

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13
Q

typical bleeding characteristics in primary haemostasis disorders?

A

immediate, prolonged bleeding from cuts/after trauma or surgery

nosebleeds 20+ mins, prolonged gum bleeding, menorrhagia

easy or spontaneous bruising

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14
Q

difference between petechiae and purpura?

A

purpura bigger (3-10mm) vs 3mm, don’t blanche when pressure is applied

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15
Q

tests for primary haemostasis disorders?

A

VWF assay, bleeding time, platelet count and morphology

coagulation screen (PT, APTT) normal

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16
Q

treatment for failure of production/function of platelets

A

replace missing factor or platelets by VWF concentrates
prophylatic
therapeutic

stop drugs e.g. NSAIDs or aspirin

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17
Q

treatment for immune destruction of platelts

A

immunosuppressants eg prednisolone

ITP → splenectomy

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18
Q

treatment for increased consumtipn of platelets

A

treat cause, replace as necessary

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19
Q

additional haemostatic treatments for primary haemostasis

A

desmopressin → mild disorders, releases endogenous stores

tranexamic acid (antifibrinolytic)

fibrin glue/sprays

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20
Q

what is the role of coagulation

A

secondary haemostasis → generate thrombin (IIa) to convert fibrinogen to insoluble fibrin

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21
Q

hereditary coagulation disorders → examples?

A

haemophilia A (factor VIII deficiency), haemophilia B (factor IX deficiency)

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22
Q

hallmark of haemophilia

A

haemarthrosis (bleeding into joint cavity)

chronic leads indirectly to muscle wasting

sex linked
must not give intravascular injections

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23
Q

how similar are different coagulation factor deficiencies?

A

potentially v different →

VIII and IX serious but survivable, II fatal, XI bleed after trauma but not spontaneous, XII no bleeding at all

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24
Q

how are coagulation disorders acquired?

A

liver failure, some anticoagulant drugs, haemophilia A/B

dilution in blood due to transfusion(lots of rbc given no plasma)

increased consumption e.g. disseminated intravascular coagulation (acquired),immune autoantibodies (rare)

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25
Q

what is disseminated intravascular coagulation?

A

generalised activation of coagulation by tissue factor

associated with major tissue damage, inflammation, sepsis

consumes and depletes platelets, coagulation factors

activates fibrinolysis thus depleting fibrinogen which will show raised D dimer
fibrin depostion in vessels causes organ failure

26
Q

clinical features of coagulation disorders?

A

superficial cuts don’t bleed (taken care of by platelets)

bruising common nosebleeds rare

spontaneous bleeding = deep e.g. into muscles, joints

bleeding after trauma may be delayed, prolonged

bleeding often restarts after stopping

27
Q

tests for coagulation factor disorders?

A

PT, APTT, FBC for platelets

coagulation factor assays

test for inhibitors

28
Q

what do PT and APTT each measure?

A

PT = extrinsic pathway

APTT = intrinsic pathway

extrinsic: TF, factor VII

intrinsic: XII, XI, IX, VIII

common: X, V, II, fibrinogen → fibrin

29
Q

normal times for PT and APTT

A

PT → 9.6 - 11.6

APTT → 26 - 32

30
Q

how are missing coagulation factors replaced?

A
  • plasmaall coagulation factors
  • cryoprecipitateesp fibrinogen, VIII, XIII, VWF
  • factor concentratesavailable for all except V
  • recombinantsVIII and IX, on demand or prophylactically

can give desmopressin,tranexamic acid ,firbin glue

31
Q

novel treatments for haemophilia?

A

gene therapy for haem A and B

bispecific antibodies mimicking factor VIII procoagulant function by binding to factor IXa and X.Emicizumab

RNA silencing targeting antithrombin for haem a and b

32
Q

how do disorders of thrombosis present

A

pulmonary embolism
DVT

33
Q

pulomonary embolism

A

tachycardia, hypoxia, shortness of breath, chest pain, haemoptysis,sudden death

34
Q

deep vein thrombosis presentation?

A

painful leg, red, swollen, warm

thrombus can embolise to lungs
post thrombotic syndrome (valve damage causing long standing pain)

35
Q

thrombosis

A

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

36
Q

virchows triad

A

three contributory factors to thrombosis:

blood, vessel wall, blood flow

37
Q

which kinds of thrombosis is each prominent in?

A

blood dominant in venous, vessel wall dominant in arterial, blood flow contributes to both

38
Q

what is thrombophilia? presentation?

A

increased risk of venous thrombosis

thrombosis at young age, spontaneous, multiple,thrombosis whilst anticoagulated

39
Q

prominent anticoagulant proteins?

A

antithrombin, protein C, protein S

40
Q

how does thrombsosi arise

A

excess coagulant factors/platelets (increased due to activated protein c resistance or myeloproliferative disorders)
decrease in anticoaglant proteins

41
Q

protein c and s

A

inactivate factor Va and VIIIa

42
Q

what aspect of blood flow can increase thrombosis risk?

A

reduced flow increases riss eg pregnancy,surgery,long haul flight

43
Q

venous thrombosis prevention methods?

A

prophylactic anticoagulation therapy

lower procoagulant factors eg warfarin/doacs

increased anticoagulant activity eg heparin

44
Q

SARS-Cov-2 relevance?

A

contributes to many procoagulative pathways → microthrombus, venous thrombus, arterial thrombus formation

45
Q

indications for anticoagulation treatment?

A

venous thrombosis (inital treatment to minimise clot extension,LT to reduce risk of recurrence)

atrial fibrillation (reduce risk of embolic stroke)

mechanical prosthetic heart valve

prophylactic → post-op, during hospital stay, pregnancy as a preventative

46
Q

heparin

A

naturally occuring glycosaminoglycans
prodcued by mast cells
porcine products used in uk

47
Q

different forms of heparin

A

unfractionated (long chains) → IV administration,short half life

low molecular weight → subcutaneous administration

48
Q

what does unfractionated heparin do?

A

enhances antithrombin
inactivates thrombin by binding to antithrombin and thrombin
inactvates factor Xa by binding to antithrombin
inactivates IXa,XIa,XIIa

49
Q

what does LMWH do?

A

enhances antithrombin → inactivates factor Xa (not long enough to wrap around antithrombin and thrombin)

50
Q

differences in effect on APTT?

A

LMWH increases clotting time by less than fractionated
normally dont monitor in LMWH

51
Q

what kind of drug is warfarin?

A

blocks recycling of vitamin K
reduces production of functional clotting factors

slowly induces anticoagulative state

52
Q

what factors does warfarin inactivate

A

II,VII,IX,X
protein c and s

53
Q

how do we reverse affects of warfarin

A

slowly by vit k administration which takes several hours to wrok
or rapidly by infusion of coagulation factors
Prothrombin complex concentrate contains II,VII,IX,X
fresh frozen plasma

54
Q

warfarin side effects

A

bleeding, skin necrosis, purple toe syndrome, embryopathy-chondrodysplasia punctata

55
Q

what is used for warfarin monitoring?

A

international normalised ratio
measures correction for different hromboplastin used

56
Q

target and normal values?

A

normal = 1, target usually 2-3
higher INR sows higher risk of all bleeding

57
Q

what can cause resistance to warfarin?

A

vit K dietary intake, increased cytochrome P450 metabolism of warfarin, reduced binding,lack of patient compliance

58
Q

what do direct oral anticoagulants do?

A

directly target a clotting factor to inhibit
work agasint factor Xa inhibitor or IIa

59
Q

compare to warfarin DOACs

A

faster acting, not affected by diet, fixed dose

fewer interactions, no monitoring required

some renal dependence

reversible by specific antidotes

60
Q

when should DOACs be avoided?

A

for mechanical prosthetic heart valves

as medical prothrombo-prophylaxis (e.g. during hospital admission)

in pregnancy

61
Q

choice of anticoagulant

A

venous thrombosis:
initital give DOAC/LMWH followed by DOAC/warfarin
long term give DOAC/warfarin

atrial fibrillation:
DOAC/warfarin

Mechanical prosthetic valve
warfarin

preventative:
after surgery give LMWH/DOAC
pregnacny LMWH

BRS YEAR 2 (43 decks)

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