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Sustaining life > haemostasis > Flashcards

haemostasis Flashcards

1
Q

what are the principles of haemostasis

A

platelets - normal number and function
functional coagulation cascade
normal vascular endothelium

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2
Q

3 stages of generation of the haemostatic plug

A

platelet adhesion
platelet activation/secretion
platelet aggregation

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3
Q

what is converted during coagulation and by what

A

fibrinogen to fibrin by thrombin

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4
Q

what stabilises the platelet thrombus

A

polymerisation of fibrin

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5
Q

primary and secondary parts of hemostatic plug formation

A

primary - aggregation
secondary - coagulation

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6
Q

2 types of platelet defects

A

reduced number of platelets
abnormal platelet function

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7
Q

causes of abnormal platelet function

A

drugs such as aspirin and clopidogrel
renal failure

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8
Q

2 types of vessel wall defects?

A

abnormal vessel wall
abnormal interaction between platelets and vessel wall

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9
Q

causes of abnormal vessel wall - scurvy?

A

causes bruising and bleeding as inadequate vitamin C so cant produce collagen which is needed for epithelial layer

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10
Q

what type of haemorrhage occurs in scurvy

A

peri-follicular haemorrhage - bleed around hair follicle, follicle becomes corkscrew shaped due to lack of vitamin C

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11
Q

what does HHT stand for? what is abnormal?

A

hereditary haemorrhagic telangiectasia, abnormal vessel wall

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12
Q

HHT presentation

A

many capillaries on skin surface bleeding

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13
Q

drugs that inhibit platelet function examples

A

aspirin and COX inhibitors
reversible COX inhibitors (eg NSAIDS)

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14
Q

what is the name for bleeding into the skin that is non blanchable

A

purpura

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15
Q

what is ecchymosis

A

medical term for a bruise

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16
Q

name for discoloration of skin that doesn’t turn white when pressed

A

nonblanchable

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17
Q

what is IIa

A

thrombin

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18
Q

at which clotting factor does the intrinsic and extrinsic pathway merge

A

Xa (clotting factor 10)

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19
Q

commonest causes of congenital haemophilia

A

problems with factor 8 and factor 9 (cofactors)

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20
Q

coagulation cascade requirements?

A

right temperature, calcium present

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21
Q

why do hypothermic patients bleed

A

wrong temperature so clotting factors don’t optimally function

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22
Q

what do extrinsic and intrinsic factors do

A

convert X (inactive clotting factor 10) to Xa (active clotting factor 10)

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23
Q

what does Xa form? what does it need for this to occur?

A

prothrombinase.
requires Calcium, factor 5a, phospholipid surface membrane

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24
Q

what does prothrombinase do

A

converts II to IIa (thrombin)

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25
Q

which pathway is slow/fast?

A

extrinsic tenase - fast
intrinsic tenase - slow

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26
Q

what does intrinsic tenase do?

A

enables layers of thrombin to be generated and a fibrin clot to be consolidated, stops the first little clot by extrinsic tenase being washed away.

27
Q

what happens to clotting factors in haemophilia

A

not enough factor 8 or 9, or wrong proportions of 8 and 9, resulting in an unstable clot.

28
Q

do haemophiliacs bleed if you take their blood

A

no! their platelets work, their extrinsic pathway still works, but not their intrinsic - so they will bleed later on

29
Q

4 steps leading to coagulation

A

initiation
amplification
propagation
termination

30
Q

what inhibits TF-VIIa complex/fXa?

A

tissue factor pathway inhibitor (TFPI)

31
Q

what inhibits thrombin an fXa?

A

antithrombin

32
Q

what inhibits fVa and fVIIIa

A

protein C pathway

33
Q

what happens when a patient is vitamin C deficient

A

generates too much thrombin leading to skin necrosis

34
Q

laboratory measurements (coagulation screen)?

A

Prothrombin time (PT)
Activated Partial Thromboplastin Time (APTT)
Fibrinogen

35
Q

what is prothrombin time (PT) measured in and reflecting

A

reflects extrinsic and common pathway
measured in seconds

36
Q

what is the APTT measured in and reflecting

A

reflects intrinsic and common pathway
measured in seconds

37
Q

what is fibrinogen lab measurement measured in and reflecting

A

measured in grams/L
reflects functional activity of the fibrinogen protein

38
Q

haemophilia A defect and inheritance

A

VIII
X-linked recessive

39
Q

haemophilia B defect and inheritance

A

IX
X-linked recessive

40
Q

what are 30% of haemophilia A cases?

A

sporadic mutations - no family history

41
Q

haemophilia A clinical cases

A

traumatic bleed (mild)
spontaneous bleed (severe haemophilia)
chronic arthropathy (recurrent bleeding into joints)

42
Q

haemophilia management

A

ice, immobilisation, rest (joints)
replacement of missing protein
antifibrinolytic agents

43
Q

what is the name for bleeding into weight bearing joints

A

hemarthroses

44
Q

most common hereditary bleeding disorder

A

von Willebrand disease

45
Q

what type of bleeding occurs in von Willebrand disease

A

mucocutaneous bleeding - nose bleeds, mucosal bleeding, gum bleeding, rectal bleeding, menorrhagia (menstrual bleeding lasting more than 7 days)

46
Q

inheritance of Von Willebrand Disease

A

autosomal dominant

47
Q

Von Willebrand Disease management

A

antifibrinolytics (tranexamic acid)
DDAVP
contraceptive pill for menorrhagia

48
Q

acquired clotting disorders types?

A

underproduction of coagulation factors
anticoagulants
immune
consumption of coagulation factors

49
Q

acquired causes of underproduction of coagulation factors

A

liver failure
vitamin K deficiency

50
Q

anticoagulant drug example that cause coagulation disorders

A

warfarin

51
Q

immune causes of acquired coagulation disorders

A

acquired haemophilia and VW syndrome

52
Q

what occurs in relation to clotting factors in liver disease

A

reduced hepatic synthesis of clotting factors

53
Q

liver disease - complication of hypersplenism?

A

thrombocytopenia

54
Q

liver disease - what does cholestatic jaundice cause

A

reduced vitamin K absorption causing deficiencies of factors II, VII, IX, and X

55
Q

vitamin K dependant clotting factors?

A

II, VII, IX, X
(2, 7, 9, 10)

56
Q

monoclonal antibody which mimics factor 8?

A

emicizumab

57
Q

what does DIC stand for

A

disseminated intravascular coagulation

58
Q

what is DIC?

A

clotting pathways don’t work anymore. it is a syndrome. found in patients that are critically ill

59
Q

is DIC acquired or inherited?

A

acquired

60
Q

what occurs in DIC

A

thrombin explodes into action - too much generated or not enough regulation
deposition of fibrin in circulation
tissue ischaemia and multi-organ failure
severe bleeding

61
Q

what causes DIC (7)

A

sepsis, tumour, trauma, toxic, vascular, pancreatitis, obstetric (amniotic fluid in internal circulation)

62
Q

what can show in peripheral blood films for a patient with DIC

A

red cell fragments

63
Q

DIC coagulation parameters?

A

prolonged PT
prolonged APTT
low fibrinogen
raised D-dimers

64
Q

what are D-dimers

A

fibrinogen degradation products

Sustaining life (13 decks)

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