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Haematology > Anticoagulant Drugs > Flashcards

Anticoagulant Drugs Flashcards

1
Q

what are the types of anticoagulant drugs

A

heparin and wafarin

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2
Q

why do you need to monitor heparin and warfarin

A

as have narrow theraputic windows

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3
Q

what drugs for arterial thrombosis

A

anti platelets

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4
Q

what drugs for venous thrombosis

A

anti coagulants

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5
Q

what are the indications for anticoagulant drugs

A

venous thrombosis

atrial fibrillation

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6
Q

why does AF cause venous thrombosis

A

as stasis of blood in LA causes clot to form on atrial wall - if this embolises it goes through carotids into brain

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7
Q

what do anticoagulant drugs target

A

the formation of fibrin clots

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8
Q

are platelets or coagulation cascade activated in venous thrombosis

A

coagulation cascade (clot is rich in fibrin)

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9
Q

how do you tell the type of clot causing a stroke

A

atheroma plaque rupture (platelet rich, need anti platelets)
AF (fibrin rich clot, need anticoagulants)

differentiated by ECG (presence of AF)

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10
Q

what does antithrombin do

A

switches of the action of thrombin (and thus its effect on factors 8 and 9 and fibrinogen)

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11
Q

what clotting factors do protein C and S turn off

A

5 and 8

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12
Q

what increases the activity of proteins C and S

A

thrombomodulin modulated thrombin

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13
Q

what drug affects proteins C and S

A

not usually targeted by drugs but can be affected by warfarin as dependent on Vit K for their synthesis

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14
Q

what are the naturally occurring anticoagulants

A

anti thrombin

proteins C and S

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15
Q

what is the action of heparin

A

potentiates the action of antithrobmin (joins to anti-thrombin and protein complex to help them stay together and act of thrombin or factor Xa)
(doesnt dissolve the blood clot (neutrophils do this) but stop it getting bigger and stabilises it to prevent embolisation

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16
Q

what are the forms of heparin

A

unfractionated (has to be given IV)

low molecular weight (IV or SC)

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17
Q

how long till herparin starts working

A

immediately effective

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18
Q

how is the dose of LWMH calculated

A

based on patient weight

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19
Q

does LWMH or unfractionated heparin need more monitoring

A

unfractionated heparin (why LMWH used more now)

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20
Q

when might unfractionated heparin be preferred

A

as effect only lasts 30 mins

can also be switched off or reversed so good if patient starts to bleed or needs operation

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21
Q

how long does the effect of LMWH last

A

12 hours

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22
Q

what does unfractionated heparin predominantly target

A

pro-thrombin (has small effect on CF Xa)

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23
Q

what does LMWH predominantly target

A

CF 10

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24
Q

how do you monitor heparin

A

APTT for unfractionated

anti Xa assay for LMWH (only needed in e.g. renal failure)

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25
Q

what test for monitoring warfarin

A

INR (ratio of PT)

26
Q

why is APTT used to monitor heparin

A

due to positive feedback thrombin usually has on factors 8 and 9 (intrinsic pathway)

27
Q

what are the potential complications of heparin use

A

bleeding
heparin induced thrombocytopenia
oesteoporosis with long tern use

28
Q

what is heparin induced thrombocytopenia

A

when antibodies form against heparin complex which causes platelets to aggregate (causes numbers to drop)
this creates risk of thrombosis

(if giving heparin and get sudden stop in platelets look for antibodies)

29
Q

how do you reverse heparin

A

stop heparin (usually enough as has short half life (30 mins)

in severe bleeding:
-protamine sulphate (reverses antithrombin effect- completely reversed unfractionated, partially reverses LMWH)

30
Q

what are courmarin anticoagulants

A

those that work to inhibit the synthesis of vitamin K:

  • warfarin
  • phenindione
  • acenocoumarin
  • phenprocoumon
31
Q

what generally are MWH and heparins used to treat

A

acute thrombosis situations

32
Q

what are coumarin anticoagulants used to treat (warfarin)

A

recurrent VTE (prophylaxis, long term- lifelong)

33
Q

what type of vitamine is Vit K

A

fat soluble (needs bile salts to be absorbed)

34
Q

where is vitamin K absorbed

A

upper intestine

35
Q

what is the role of vitamin K

A

final carboxylation of glutamic acid in clotting factors II, VII, IX and X (+ protein C and S)
this adds COOH group creating negative charge to CF allowing them to bind to calcium on phospholipids in platelets

36
Q

what factors are dependent on vitamin K

A

II (prothrombin), VII, IX and X

proteins C and S

37
Q

where is vit K synthesised

A

in the liver

38
Q

which Vit K CF has the shortest half life

A

7

39
Q

what should you always give with warfarin in an acute scenario

A

heparin (warfarin on its own can cause thrombosis)

40
Q

what is the mechanism of action of warfarin

A

antagonises vit K

41
Q

what are the different ways you would initiate warfarin

A

rapid- acute thrombosis, with heparin

slow- e.g. for AF in community, liver failure, malnourished, elderly etc

42
Q

when should warfarin be taken

A

at same time every day

43
Q

what influences warfarin metabolism

A

metabolised in the liver- cytochrome P450 levels

44
Q

how do you monitor warfarin therapy

A

INR (ratio of PT that corrects it for differences in reagents in the tests- allows for comparison between labs and standardises the PT)

(both PT and APTT will be affected but PT is much more sensitive)

45
Q

what is the major adverse event in warfarin therapy

A

haemorrhage

46
Q

what factors influence the bleeding risk on warfarin

A

intensity of anticoagulation
concomitant clinical disorders / medications (beware drug reactions- drugs that are metabolised by cytochrome P450)
quality of management

47
Q

what is the risk and benefit balance of warfarin therapy

A

risk- 1 in 200 with AF on warfarin have fatal ICH per year

reduced risk of stroke by 1 in 10

48
Q

what is the target INR ratio

A

2-3

49
Q

risk of what increases as the INR rises

A

risk of bleeding

50
Q

what are the types of bleeding complications when on anticoagulants

A

mild: skin bruising, epistaxis, haematuria
severe: GI, ICH, significant drop in Hb

51
Q

how do you reverse warfarin

A

for minor bruising/ bleeding with good INR= no action

high INR +/- minor bleedind/bruising= omit warfarin

non threatening bleeding, need to bring down INR= administer oral vit K (takes 6 hours)

ICH, major GI bleed, BP loss= administer clotting factors (concentrated of 2,7,8,9) (not given immediately as scarse resource

assess response (clinically and in lab- INR)

52
Q

how quickly does the administration of clotting factors work to reverse warfarin

A

immediately

53
Q

what do NOACs target

A

activated factor 10 (more specific)

some are direct thrombin inhibitors (dabigatran)

54
Q

do you need to monitor NOACs

A

no

55
Q

what is dabigatran

A

NOAC that is a thrombin inhibitor

56
Q

what are Xa inhibitors

A

NOACs
e.g. edoXABAN, rivaroXABAN, apiXABAN
target CF Xa (Xa-ban)

57
Q

are there less or more drug interactions and complication with NOACs

A

less

1 in 500 bleeding rate

58
Q

what is now first line for AF

A

NOAC

59
Q

what are NOACs used for

A

treatment of DVT/PE

AF stroke prophylaxis

60
Q

when is warfarin superior to NOACs

A

for artificial heart valves and at preventing arterial clots (APS)

61
Q

what should you give at same time as clotting factors in warfarin reversal

A

vit K

Haematology (27 decks)

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