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J Haem > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

is platelet plug formation primary or secondary haemostasis

A

primary haemostasis

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2
Q

is fibrin clot formation primary or secondary haemostasis

A

secondary haemostasis

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3
Q

what injuries is platelet plug formation good for

A

small bleeds eg nose bleed, small cut

bc primary haemostasis

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4
Q

what injuries is fibrin clot formation good for

A

larger bleeds

bc secondary haemostasis and platelet plug formation isn’t sufficient

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5
Q

how long is platelet lifespan

A

7-10 days

so need to stop antiplatelet (eg aspirin) 1 week before surgery

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6
Q

first stage in platelet plug formation

A

endothelial damage

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7
Q

what is exposed after endothelial damage

A

collagen

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8
Q

what factor is released bc of endothelial damage

A

von Willebrand factor (vWF)

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9
Q

what does exposed collagen and von Willebrand factor attract to endothelial damage

A

platelets

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10
Q

once platelet adhesion at site of endothelial damage has occurred, what happens

A

platelet aggregation (more platelets come) = platelet plug formation

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11
Q

after platelet plug formation, what happens if insufficient to stop bleeding

A

fibrin clot formation

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12
Q

which clotting factors are attracted to platelet plugs to form a fibrin clot (8)

A 
tissue factor 
factor II (prothrombin) 
factor V 
factor VII 
factor VIII 
factor X 
factor IX

also fibrinogen

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13
Q

factor II

A

prothrombin

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14
Q

factor IIa (activated factor II)

A

thrombin (activated prothrombin)

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15
Q

which clotting factors initiate V/Xa (and hence initiate fibrin clot formation)

A

TF/VIIa

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16
Q

which clotting factors activate prothrombin (II) to thrombin (IIa)
via the production of which enzyme

A

V/Xa (most important ones, have central role)

via production of prothrombinase

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17
Q

what does activation of thrombin (IIa) from prothrombin (II) cause (2)

A

conversion of fibrinogen to fibrin (to make fibrin clots) activation of VIII/IXa (which goes on to amplify V/Xa etc)

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18
Q

what does activation of VIII/IXa by thrombin cause

A

amplification of V/Xa

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19
Q

which part of the fibrin clot formation system is classed as the ‘common’ pathway

A

from V/Xa onwards

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20
Q

which part of the fibrin clot formation system is classed as the ‘intrinsic’ pathway

A

VIII/IXa

XIIa converting XI to XIa combining with FVIII to convert IX to IXa

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21
Q

which part of the fibrin clot formation system is classed as the ‘extrinsic’ pathway

A

TF/VIIa

THINK: extrinsic bc TF comes from tissue damage (external factor)

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22
Q

by what process are fibrin clots normally broken down (normal part of haemostasis)

A

fibrinolysis

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23
Q

products of fibrinolysis

A

fibrin degradation productions (FDPs)

aka d-dimers

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24
Q

what substance is needed to break down fibrin clots to fibrin degradation products

A

plasmin

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25
Q

how is plasmin made from plasminogen

A

tissue plasminogen activator (tPA)

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26
Q

what are the 2 natural anti coagulant defences used to ensure normal haemostasis

A

anti-thrombin

protein C and protein S

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27
Q

how does antithrombin work as anti coagulants

A

switches off thrombin directly = anti coagulant

also switches off clotting factors = indirectly switches off thrombin

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28
Q

how does protein C and protein S work as anti coagulants

A

decrease factor V/Xa and VIII/Ixa =decreased thrombin production

ie switches off thrombin indirectly

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29
Q

presentation of failure of platelet plug formation (primary haemostasis problem)

A

easy bruising
nose bleeds
purpura of lower limbs - non blanching rash
menorrhagia

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30
Q

which type of haemostasis is lacking if failure of platelet plug formation

A

no primary haemostasis

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31
Q

how do steroids cause primary haemostasis

A

decrease collagen in vessel walls

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32
Q

what is the problem in Henoch-schonlein purpura

who gets it

A

antibodies to vessel walls = primary haemostasis problem hence present with purpura)

occurs in children

33
Q

which congenital MSK condition presents with primary haemostasis failure

why

A

marfans

bc collagen deformity = decreased platelet plug formation

34
Q

what are the 3 sources of problem that could cause primary haemostasis problems

A

vessel problem - eg marfans, steroids, Henoch schonlein purpura
platelet problem - reduced number
von Willebrand factor deficiency

35
Q

what can cause reduced number of platelets (= primary haemostasis problem) (7 in total, 3 categories)

A

reduced platelet production - bone marrow cancer, alcohol
increased platelet destruction - DIC, immune thrombocytopenic purpura (ITP), hypersplenism
reduced platelet function - antiplatelet drugs eg aspirin, renal failure

36
Q

haemostasis problem in alcoholics

A

probs primary and secondary

primary haemostasis failure - bc alcohol is toxic to bone marrow = decreased platelet production
secondary haemostasis failure - if liver failure = decreased clotting factor activation

37
Q

which autoimmune condition can cause increased platelet destruction = primary haemostasis problem

what is the problem

A

immune thrombocytopenic purpura (ITP)

antibody produced against platelets = increased destruction

38
Q

treatment of ITP causing primary haemostasis

A

immunosuppression prednisolone (bc autoimmune thing)

39
Q

why does hypersplenism cause primary haemostasis

A

platelets are removed by the spleen so hypersplenism = increased platelet removal from circulation

40
Q

most common inherited bleeding disorder

does it cause primary or secondary haemostasis problem

A

von Willebrand factor deficiency

causes primary haemostasis problem (no platelet plug formation)

41
Q

vWF deficiency inheritance pattern

A

autosomal dominant

42
Q

which pathway isn’t working (intrinsic or extrinsic) in vWF deficiency

hence which ‘time’ is prolonged

A

intrinsic pathway not working

need platelet plug formation to occur to allow VIII to bind

APTT prolonged

43
Q

presentation of failure of fibrin clot formation (secondary haemostasis problem)

A

delayed muscle bleeding

serious delayed post traumatic bleeding

44
Q

investigations for primary haemostasis problem

A

platelet count

if low = reduced production/increased destruction, need to do bone marrow aspiration to figure out which
if high = reduced function/vascular problem/vWF deficiency

45
Q

why do you want to do fundoscopy once primary haemostasis problem diagnosed

A

for retinal haemorrhages

46
Q

causes of failure of fibrin clot formation (5 causes, 2 categories)

A

single clotting factor deficiency - haemophilia A, haemophilia B
multiple clotting factor deficiency - DIC, liver failure, vit K deficiency

47
Q

do males/females get haemophilia

A

males (X linked)

48
Q

is haemophilia A or B more common

A

haemophilia A

49
Q

clotting factor VIII deficiency

A

haemophilia A

bc A is before B and VIII is before IX

50
Q

clotting factor IX deficiency

A

haemophilia B

bc B is after A so IX is after VIII

51
Q

Christmas disease

A

another name for haemophilia B

52
Q

in haemophilia, what happens if you have a small cut

A

will heal fine - bc still got platelet plug formation

53
Q

in haemophillia, no factor VIII/IX causes no factor …

which causes …

A

factor X = cant make fibrin

54
Q

presentation of haemophilia

at what age

A 
haemarthrosis - spontaneous and prolonged bleeding in joints (knee, ankle, elbow)
in toddlers (not babies bc not crawling)
55
Q

v painful bleeding into knee joint

A

haemarthrosis

occurs in haemophilia

56
Q

management of haemophilia A

A

IV factor VIII every 2-3 days, self administered

57
Q

management of haemophilia B

A

IV factor IX every 2-3 days, self administered

58
Q

APTT and PT in haemophilia

A 
APTT prolonged (abnormal extrinsic pathway VIII/IX) 
PT normal (normal intrinsic pathway TF/VII)
59
Q

how do you differentiate between haemophilia A and B if both prolonged APTT but normal PT (which investigation)

A

clotting factor assay

60
Q

3 causes of multiple clotting factor deficiency

A

vit K deficiency
DIC
liver failure eg alcoholics (may present with primary haemostasis problem too bc of toxic effect of alcohol on bone marrow = decreased platelet production)

61
Q

why does liver failure cause multiple clotting factor deficiency

A

clotting factors are made in the liver :(

62
Q

which vitamin is needed for activation of clotting factors (hence deficiency causes multiple clotting factor deficiency)

A

vitamin K

63
Q

causes of vitamin K deficiency

A

poor diet - is in leafy veg
malabsorption neg chrons
warfarin - is a vit K antagonist
newborn (none acquired in diet yet so need IM vit K)

64
Q

what does vit K deficiency in babies cause (if you don’t give IM vit K after birth)

A

haemorrhagic disease of the newborn

65
Q

which clotting factors does vit K activate

A

II, VII, IX, X

KNOW THIS!!

66
Q

causes of DIC

A

RTA
sepsis
obstetric emergencies
malignancy

lots of things - tbh any cause of bleeding

67
Q

what is there an increase of in DIC = causes the problem

A

excessive platelet plug formation
also
lots of TF release = overactivation of haemostasis = use up other clotting factors = none left

68
Q

presentation of DIC

A

‘bleeding from everywhere’ eg venflon holes, colostomy sites

bruising, purpura and generalized bleeding (bc primary and secondary haemostasis problem)

69
Q

PT and APTT in DIC

A

APTT prolonged

PT prolonged

70
Q

vit D deficiency PT and APTT

A

APTT prolonged

PT prolonged

71
Q

how do you differentiate between vit K deficiency and DIC as cause of prolonged APTT and PT

A

D-dimers increased in DIC

and presentation will differ !

72
Q

management of DIC

A 
treat underlying cause eg sepsis
platelets and FFP (asap) 
fibrinogen replacement 
cryoprecipitate 
RBC transfusion if bleeding
73
Q

what does a coagulation screen consist of

A

platelets
APTT
PT

74
Q

PT prolongation

where is the problem

A

extrinsic pathway (TF/VIIa) problem

THINK: extrinsic bc TF comes from tissue damage (external factor)

75
Q

APTT prolongation

where is the problem

A

intrinsic pathway (VIII/IXa) problem

THINK: Aptt = for All the many factors that contribute to VII/IXa (need XII, XI etc)

76
Q

PT prolongation differentials (2)

A

DIC

vit K deficiency

77
Q

APTT prolongation differentials (4)

A

DIC
vit K deficiency
haemophilia
vWF deficiency (primary haemostasis problem but no VIII)

78
Q

APTT prolonged
PT prolonged

what are the options (4)

A

DIC
it K deficiency
anticoags (warfarin)
liver problem

79
Q

increased d-dimers cause

A

fibrinolysis in DIC

d-dimers = fibrillin degradation products (FDPs)

J Haem (12 decks)

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