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3 IIH > 2.1 Haemostasis > Flashcards

2.1 Haemostasis Flashcards

1
Q

What is the role of platelets in venous thrombosis?

What is the clinical significance of this?

A

minimal, coagulation is way more important

venous thrombosis is therefore treated with anti-coagulants, and not anti-platelets

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2
Q

What is primary haemostasis?

A

formation of platelets aggregates, very fast (5 mins)

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3
Q

What is secondary haemostasis?

A

formation of a stable fibrin clot (within 10 mins)

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4
Q

What prototypic disorder is associated with primary and secondary haemostasis?

A

primary - TTP

secondary - haemophilia

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5
Q

What is the lifespan of a platelet?

A

10 days

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6
Q

What are platelets regulated by? how does this feeback?

A

TPO, produced in the liver

platelets destroy it

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7
Q

How do platelets form from erythromegakaryocytic cells?

A

endomitosis

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8
Q

What is the intermediate in between magakaryocytes and platelets?

A

proplatelets

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9
Q

Name 4 structural things about the platelet

A

no nucleus
open canalicular system
dense tubular system
lots of cytoskeleton

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10
Q

Name 3 dense granules and their function

A

ADP/ATP - platelet activation

5-HT (serotonin) -vasoconstrictino

Polyphosphate - contact activation

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11
Q

What do platelets form when activated?

A

thromboxane

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12
Q

What 3 things do platelets secrete?

A

dense granules
de novo synthesis products (thromboxane)
alpha - granules

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13
Q

What 3 things do endothelial cells release keeping platelets quiescent?

A

CD39
NO
eicosanoids

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14
Q

What are the 3 main stages in primary haemostasis?

A

adhesion
activation
aggregration

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15
Q

What happens when collagen is exposed to the blood?

A

is is bound to by the platelet, either via vWF - GPib, or directly to integrin a1/b2 receptor on the platelet

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16
Q

Where does vWF come from?

A

endothelial cells

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17
Q

What happens to vWF as it binds to collagen and GPIb?

A

it unfolds as the platelet rolls, revealing more platelet binding sites

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18
Q

What is vWF regulated by?

A

a protease

ADAMts13

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19
Q

What does binding to collagen stimulate in the platelets?

A

intracellular calcium release, and hence dense granule and alpha-granule release

thrombin regeneration on cell surface

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20
Q

What do the dense granules do?

A

activate receptors on this receptors and others

a positive amplificaiton loop

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21
Q

What is the target for aspirin?

A

COX-1

stopping this will ultimately stop the formation of thromboxane

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22
Q

Which of aspirin or non-steroidal anti-coagulants are reversible?

A

non-steroidal anti coagulants

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23
Q

In general, what do alpha-granules promote?

A

haemostasis and healing

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24
Q

What does ADP bind to?

A

P2Y1
P2Y12

both are necessary for aggregation

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25
Q

What types of drugs target PSY12?

A

clopidogrel

superclopidogrels

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26
Q

What stimulates integrin a2/b3 activaton?

A

activated platelet secretions

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27
Q

What can integrin a2/b3 bind to?

A

Fibrinogen
vWF
Fibronectin

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28
Q

Name 3 drugs that target the binding of integrin a2/b3

A

abciximab
eptifibatide
tirofiban

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29
Q

What are the 2 transformations that platelets undergo?

A

lamelipodia

pseudopodia

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30
Q

What are the 3 areas of a clot?

A

outer shell
inner core
procoagulant membranes

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31
Q

what does scramblase do?

A

rotates the phospholipids so that the negative charges are on the outside

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32
Q

What is the effect of scramblase?

A

vitamin K dependent coagulation factors can form prothrombinase factors - thrombin

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33
Q

What does thrombin need to activate fibrinogen?

A

serine protease

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34
Q

What does Xa need to activate prothrombin?

A

prothrombinase complex (cofactor V, PL ‘-‘, Calcium)

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35
Q

What does IXa need to activate X?

A

tenase complex

cofactor VIII, PL’-‘, calcium

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36
Q

What is used to activate X in the extrinsic pathway?

A

TF: VIIa

37
Q

What 3 sections did Hoffman divide the clotting cascade into?

A

Initiation
Priming
Propagation (amplification loop)

38
Q

what 3 things prevent intravascular clot formation?

A

unobstructed, non-turbulent blood flow
intact vascular endotheilum
circulating anticoagulant proteins (antithrombin, protein C/S)

39
Q

What does thrombomodulin do?

A

binds to thrombin, the changed thrombins conformation to activate protein C

40
Q

Where is thrombomodulin?

A

on the cell wall of blood endothelium

41
Q

What does activated protein C do?

A

binds to protein S, the whole complex then inactivates Factor V and VIII, halting clot formation

42
Q

What does Tissue Factor Pathway Inhibitor do?

A

prevents factor x from being activated

43
Q

What does antithrombin do?

A

in the presence of heparans or heparins, it inihbis enzymes in clotting cascade (10a, 9a, 12a, 7a)

44
Q

What is fibrinolysis?

A

the breakdown of fibrin

45
Q

When is fibrinolysis switched on?

A

at the same time that the clot is forming, regulating clot formation

46
Q

How does fibrinolysis work?

A

thrombin activates endothelium to release tissue plasminogen activator (tPA)

this is incorporated into the Fibrin clot, plasminogen can be activated, forming plasmin

plasmin breaks down the fibrin, releasing fibrinogen degradation products (including D-dimers)

47
Q

Name 5 hereditary disorders causing venous thrombosis

A 
factor V Leiden mutation
prothrombin gene mutation
antithrombin deficiency
protein C deficiency
protein S deficiency
48
Q

What happens in Factor V Leiden mutations?

A

activated protein C can’t break down factor 5, so it remains active

49
Q

Name one acquired disorder causing venous thrombosis

A

lupus anticoagulant

50
Q

What would you consider a normal platelet count?

A

150-400 x10^9/L

51
Q

Where is the platelet transfusion threshold?

A

10 x 10^9/L

52
Q

What is significant for platelet counts in those with thrombocytoponea?

A

some counters are inaccurate around the threshold

53
Q

Is thrombocytopenia inherited or acquired?

A

both

54
Q

How might thrombocytopenia be acquired?

A

drug induced

55
Q

In what 3 ways can platelets have congenital disorders?

A

disorder of adhesion
disorder of aggregation
disorder of granules

56
Q

How would you test the different clotting pathways?

A

intrinsic - aPTT (25-39s)

extrinsic - PT (12s)

57
Q

What is aPTT?

A

activated partial thromboplastin time

evaluates coagulation factors XII, XI, IX, VIII, X, V, II I

58
Q

What is PT?

A

Prothrombin time

evaluates coagulation factors VII, X V, II and I

59
Q

What might cause isolated prolongation of PT?

A

FVII deficiency

60
Q

What might cause FVII deficency?

A

hereditary deficiency
mild liver disease
mild vitamin K deficiency

61
Q

What might you do with isolated prolongation of APTT?

A

mixing test, APTT on 50:50 patient/normal plasma

62
Q

How would you interpret a mixing test?

A

correction to normal, clotting factor deficiency

failure to correct (there must be an inhibitor present!)
Lupus anticoagulant, FVIII ab

63
Q

What might cause prolongation of both PT and APTT?

A

single factor deficiency in common pathway

multiple factor deficiencies

64
Q

What might cause multiple factor deficiencies?

A 
liver disease
vit k deficiency
warfarinisation
DIC
dilutionsl coagulopathy
65
Q

what is the use of PT and APTT?

A

finding the fault int he system
monitoring response to replacement of clotting factors
monitoring effect of anticoagulants

66
Q

What clotting factors may be reduced in a prolonged aPTT?

A

VIII
IX
XI
XII

67
Q

What clotting factors may be reduced in a prolonged PT?

A

VII

68
Q

What clotting factors may be reduced in prolonged PT and aPTT?

A

II
V
X
fibrinogen

69
Q

Name 3 hereditary defects of the haemostatic system causing a bleeding tendency

A

clotting factor deficiencies
von willebrand’s disease
platelet disorders

70
Q

what are haemophilia A and B deficiencies in?

A

FVIII - haemophilia A

FIX - haemophilia B

71
Q

How are haemophilia inherited?

A

sex-linked recessive

72
Q

how might haemophilia effect APTT and PT?

A

aptt prolonged

PT normal

73
Q

How might an autosomal recessive disease cause prolonged PT/APTT?

A

factor II, VII, X, XI, fibrinogen deficiencies

cause bleeding

74
Q

What happens in factor XIII deficiency?

A

autosomal recessive
PT/APTT normal
clot solubility abnormal
excessive bleeding

75
Q

Name 3 autosomal recessive coagulation factor deficiencies which don’t cause bleeding, and why?

A

Factor XII deficiency
prekallikrenin
HMWK deficiencies

they are near the top of the process

76
Q

How is von willebrand’s disease inherited?

A

autosomal dominant (although type 3 is recesive)

77
Q

What does vWF carry?

What is the clinical significance of this?

A

it carries factor VIII, stabilising it

therefore people with von willebrand’s disease have low factor 8 levels too

78
Q

How would von willebrand’s disease present?

A

mucocutaneous bleeding pattern

79
Q

What are the classifications of vWD?

A

type 1 - partial quanitative deficiency (molecule same size, just fewer)
Type 2 - qualitative deficiency (smaller, same number)
type 3 - total quantitative deficiency (none!)

80
Q

What does catastrophic thrombosis cause?

A

vessel stenosis

81
Q

How do Abciximab, Eptifibatide, and Tirofiban work?

A

inhibit fibrinogen platelet binding

82
Q

How do aspirin and Trifusal work?

A

inhibit COX-1

83
Q

How to Clopidogrel, Prasugrel, and Ticagrelor work?

A

inhibi ADP receptors

84
Q

Name 4 classes of antiplatelet drugs

A

COX-1 inhibitors
ADP receptor antagonist
GpIIb/IIa antagonists
PAR-1 antagonists

85
Q

When might we use monotherapy?

A

secondary prevention of MI/stroke

86
Q

When might we use combination therapy?

A

ACS patients undergoing percutaneous coronary interventions and AF

87
Q

What is one problem associated with antiplatelet drugs?

A

higher risk of bleeding

88
Q

Name the 4 inhibitors of coagulation

A

Tissue Factor Pathway Inhibitor (TFPI)
Antithrombin
Protein C
Protein S

3 IIH (23 decks)

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