haemostasis Flashcards

1
Q

what is haemostasis?

A

the arrest of bleeding and maintenance of vascular patency

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2
Q

what are the 4 stages?

A

platelet plug formation (primary)
fibrin clot formation (secondary)
fibrinolysis
anticoagulant defences

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3
Q

what is primary haemostasis?

A

platelet plug formation
damage to endothelium = collagen + VWF -> platelet adhesion at site of injury
secretion of various chemicals -> platelet aggregation at site of injury

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4
Q

what is secondary haemostasis?

A

formation of fibrin clot
platelets are negatively charged
platelets release calcium when activated (positive charge)
blood clotting factors (negatively charged) are attracted to sit on phospholipid surface sue to positive calcium

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5
Q

what is fibrinolysis?

A

fibrin clot broken down by plasmin

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6
Q

what are the anticoagulant defences?

A

anti-thrombin, protein C and protein S

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7
Q

what factors are involved in the intrinsic pathway?

A

8, 9, 11, 12

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8
Q

what does the intrinsic pathway increase?

A

activated partial thromboplastin time (APTT)

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9
Q

what clotting factors are involved in extrinsic pathway?

A

7 (activated)

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10
Q

what increases in the extrinsic pathway?

A

partial thrombin time (PTT)

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11
Q

what factors are involved in the common pathway?

A

5, 10, 2, 1

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12
Q

what is increased in the common pathway?

A

APTT and PTT

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13
Q

what factors are affected by heparin?

A

2, 9, 10, 11

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14
Q

what clotting factors are affected by warfarin?

A

2, 7, 9, 10 (1972)

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15
Q

what clotting factors are affected in DIC?

A

1, 2, 5, 8, 11

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16
Q

what factors are affected in liver disease?

A

1, 2, 5, 7, 9, 10, 11

17
Q

what factor is affected in von willebrands?

A

8

18
Q

what does VWF increase?

A

APTT

19
Q

what is increased in haemophilia?

A

APTT

20
Q

what is increases in von willebrands?

A

APTT and bleeding time

21
Q

what is increased in vitamin K deficiency?

A

APTT and PTT

22
Q

what type of drug is heparin?

A

anticoagulant

23
Q

what is unfractionated heparin MOA?

A

antithrombin agonist leading to inhibition of factor 2a and 10a

24
Q

when in UFH used over LMWH and why?

A

in patients with higher risk of bleeding or renal impairment
due to shorter half-life

25
Q

what are some examples of low molecular weight heparin?

A

dalteparin, enoxaparin

26
Q

what is LMWH MOA?

A

targets factor 10a and inhibits it -> stops formation of thrombin and prevents conversion of fibrinogen to fibrin = stops clotting process

27
Q

what is warfarin MOA?

A

vitamin K antagonist - inhibits synthesis of vitamin K dependent clotting factors (1972) as well as protein C and protein S

28
Q

what type of medication is warfarin?

A

anticoagulant

29
Q

when is warfarin indicated?

A

mechanical heart valves
a fib
recurrent VTE or not suitable for DOAC

30
Q

what needs monitored in patients on warfarin?

A

INR - international normalised ratio

31
Q

what is target INR for patients with conditions such as VTE, AF and MI?

A

2.5

32
Q

what is warfarin metabolised by?

A

CYP450 enzymes

33
Q

what is an example of a CYP450 inducer and what does it do?

A

carbamazepine, primidone
reduce efficacy of warfarin

34
Q

what is an example of a CYP450 inhibitor and what does it do?

A

macrolides and metronidazole
increase INR levels

35
Q

what drugs does warfarin interact with and what is the risk?

A

NSAIDS and SSRIs
inc risk of bleeding

36
Q

how does a patient with a primary haemostatic disorder usually present?

A

menorrhagia, easy bruising, mucosal blood loss (epistaxis - nosebleeds), retinal haemorrhages

37
Q

what are the causes of primary haemostatic disorders?

A

vascular - elderly, CTD, vit C deficiency, vasculitis
thrombocytopenia
- dec production = marrow failure
- inc production = DIC, autoimmune ITP, liver failure
VWF deficiency

38
Q

what are secondary haemostatic disorders due to?

A

clotting factor deficiencies

39
Q
A