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2nd year > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

what are the treatment options for thromboembolic disease?

A

antiplatelets
anticoagulants
thrombolytics/fibrinolytics
mechanical options

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2
Q

what do antiplatelets do?

A

prevent clots

arterial use

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3
Q

what do anticoagulants do?

A

prevent clots

arterial and venous use

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4
Q

what do thrombolytics/fibrinolytics do?

A

destroy clots

arterial and venous use

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5
Q

mechanical options for thromboembolic disease

A

PCI

stents and angioplasty

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6
Q

common antiplatelets

A 
aspirin
clopidogrel
dipyridamole
prasugrel
ticagrelor 
abciximab
tirofiban
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7
Q

common anticoagulants

A 
warfarin
heparins
apixaban
rivaroxaban
dabigatran
danaparoid
fondaparinux 
argatroban
epoprostenol
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8
Q

common thrombolytics and fibrinolytics

A

tissue plasminogen activator
streptokinase
urokinase

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9
Q

what is VTE?

A

PE and DVT

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10
Q

ACS

A

acute coronary syndrome

MI

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11
Q

haemostasis

A

balance between haemorrhage and thrombosis

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12
Q

virchow’s triad

A

causes of thrombus formation:

  • blood stasis
  • hypercoagulability
  • endothelial injury
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13
Q

what is thrombophilia?

A

pro-thrombotic state

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14
Q

what determines thrombosis treatment?

A

where the thrombus is

capillaries, veins or arteries

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15
Q

what are the stages of haemostasis?

A

formation of platelet plug
propagation of clotting
termination of clotting
fibrinolysis and clot removal

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16
Q

formation of platelet plug

A

platelet adhesion, aggregation, activation and secretion

activation of thrombin

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17
Q

propagation of clotting

A

intrinsic and extrinsic pathway activation
clotting cascade
amplification of cascade
recruitment of platelets

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18
Q

termination of clotting

A

limitation of clot formation
muting clotting cascade
restoring anti-thrombotic state

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19
Q

fibrinolysis and clot removal

A

activation of plasmin
lysis of cross-linked fibrin
production of D-dimer and FDPs

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20
Q

end of clotting cascade/ common pathway

A

factor X to Xa
Xa causes Va to convert
prothrombin to thrombin
Thrombin causes fibrinogen to fibrin and XIII to XIIIa which converts fibrin to cross linked fibrin

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21
Q

what triggers the coagulation cascade?

A

intrinsic pathway = response to sepsis, toxins and hyperlipidaemia
extrinsic pathway = tissue factor caused by injury

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22
Q

lining of blood vessels

A

antithrombotic

deeper down in the vessel wall is more thrombotic

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23
Q

fibrinolysis

A

plasminogen is converted to plasmin by tissue plasminogen activator
plasmin breaks down cross linked fibrin into fibrinogen degradation products (FDPs) and D-dimer

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24
Q

what are the antithrombotic factors?

A

activated protein C
protein S
anti-thrombin

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25
Q

what do anti-thrombotic factors do?

A

block coagulation cascade

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26
Q

How do protein S and C work?

A

protein S activates protein C

Protein C inhibits factor Va to prevent prothrombin conversion to thrombin

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27
Q

how does anti-thrombin work?

A

directly inhibits thrombin

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28
Q

tombstone ST elevation

A 
indicates full thickness 
acute 
large MI 
needs immediate treatment - stent 
thrombolytic given to open coronaries
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29
Q

best treatment for STEMI MI

A

PCI

more effective than drugs

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30
Q

MI

A

atheroma causes ischaemia and thrombotic occlusion causes the infarction

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31
Q

when to use anti-platelets vs anticoagulants

A

have similar effects

can be used in same setting but anti-platelets are used more in arterial disease

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32
Q

why are anti-platelets used in arterial disease over anti-coagulants?

A

in arterial disease platelet plug is already occluding the artery and is a more important factor in the occlusion
platelet rich clots form in arteries
in veins more fibrin than platelets cause occlusion

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33
Q

how to treat ischaemic stroke?

A

antiplatelet

anticoagulation if in AF

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34
Q

what antiplatelets are used in treating ischaemic stroke?

A

aspirin
clopidogrel
dipyridamole

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35
Q

AF

A

risk of clot formation in left atrial appendage and other parts of heart
clots are clotting factor and fibrin rich
can cause bowel ischaemia or stroke

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36
Q

AF treatment

A

need treatment with anticoagulation

don’t use aspirin

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37
Q

who needs AF treatment?

A

younger people with no other comorbidities = bleeding risk from treatment is greater than risk of thrombus so no anticoagulation indicated
older people and those with comorbidities = risk of thrombus exceeds bleeding risk so treatment required

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38
Q

what comorbidities indicate AF treatment?

A

hypertension
high cholesterol
etc.

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39
Q

assessment for AF stroke risk

A

CHA2DS2-VASc score

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40
Q

CHA2DS2-VASc scoring system

A
  • 0 points = no anticoagulation needed
  • 1 = needs anticoagulation but may opt out in some circumstances
  • > 1 = ANTICOAGULATION!! (unless good reason not to)
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41
Q

what are the classes of anticoagulants?

A

DOACs
warfarin
heparins
fondaparinux

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42
Q

e.g. of heparin

A

dalteparin

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43
Q

DOACs

A

direct oral anticoagulants

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44
Q

what are the indications for anticoagulants?

A

treatment of thromboembolism
prevention of thromboembolism
high risk thrombophilias

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45
Q

treatment of thromboembolism

A 
arterial = warfarin and DOACs 
venous = heparins, DOACs and warfarin
46
Q

prevention of thromboembolism

A

in stroke and AF = warfarin and DOACs

VTE prophylaxis = low does LMWH

47
Q

treatment for high risk thrombophilias

A

seek specialist advice

48
Q

advantages of DOACs?

A

fewer interactions with other drugs
no INR monitoring required
simpler for patients and doctors

49
Q

disadvantages of DOACs?

A

no easy way to reverse them - but there is for warfarin

less long-term data on efficacy and safety

50
Q

use of DOACs

A

relatively new

most people are now started on these and not warfarin

51
Q

examples of DOACs

A

apixaban
rivaroxaban
edoxaban
dabigatran

52
Q

how do DOACs work?

A

rivaroxaban and apixaban directly inhibit factor Xa and prevent activation of thrombin from prothrombin
dabigatran directly inhibits thrombin so fibrin cannot be formed

53
Q

rivaroxaban

A
  • caution in renal disease
  • no monitoring required
  • used for VTE prevention
  • used for AF
  • cannot be used in people with mechanical heart valve
  • apixaban is increasingly common in place of this
54
Q

Dabigatran

A
  • renally excreted – avoid in severe CKD
  • careful in acute kidney injury
  • no monitoring required
  • coagulation tests can demonstrate activity but poorly relate to actual degree of action
  • dyspepsia and hepatobiliary disease = common side effect
55
Q

Interactions with dabigatran

A

drugs that are inhibitors or inducers of P-glycoprotein affect dabigatran levels

56
Q

parenteral anticoagulants

A

= anticoagulants that cannot be given orally

57
Q

examples of parenteral anticoagulants

A

LMWH
unfractionated heparin
fondaparinux

58
Q

LMWH administration

A

subcutaneous injection

59
Q

use of fondaparinux

A

ACS/ MI

60
Q

how does heparin work?

A

alone antithrombin is relatively weak at inhibiting thrombin but heparin binds and induces a conformational change that increases the binding of thrombin and Xa and increases activity of anti-thrombin and further inhibits thrombin

61
Q

LMWH

A

affects Xa inhibition more than thrombin

62
Q

fondaparinux mechanism of action

A

similar to heparin mechanism of action

63
Q

how is heparin administered?

A

LMWH = subcutaneous injection of dalteparin

unfractionated heparin = less commonly used, given by IV injection (can be reversed quickly and titrated up and down)

64
Q

who is LMWH given to?

A

large number of immobile patients
pregnant women
post-op patients

65
Q

side effects of heparin

A
  • bleeding
  • thrombocytopenia – long-term use (need to monitor platelets)
  • hypokalaemia
  • osteoporosis in long-term use
  • can accumulate in renal failure – needs dose reduction depending of eGFR
66
Q

fondaparinux

A
  • similar mode of action to heparin
  • given by subcutaneous injection
  • causes less thrombocytopenia
  • replaced LMWHs for treatment of acute coronary syndromes (MIs)
67
Q

warfarin

A
  • common
  • prescription complications are common
  • complicated
68
Q

disadvantages of warfarin

A
  • no one dose
  • variable doses between individuals and difficult to predict
  • lots of interactions with drugs and foods
  • dangerous – teratogenic in pregnancy
  • non-fatal effects
  • initial high-dose therapy is pro-thrombotic
69
Q

normal vitamin K activation of clotting factors

A

clotting factors = serine protease
Carboxylase requires reduced vitamin K (abundant for activation)
During the process vitamin K is oxidised and no longer able to be used
NADH and vitamin K reductase can then reduce vitamin K again to be recycled and used for activating clotting factors again

70
Q

warfarin mechanism of action

A
  • blocks vitamin K reductase
  • once all vitamin K is oxidised
  • no more reduced vitamin K is present to activate clotting factors
  • new vitamin K needed to activate serine protease/clotting factors
  • warfarin keeps vitamin K oxidised
71
Q

diet and warfarin

A

dietary intake of vitamin K can affect warfarin because warfarin inhibits carboxylation of vitamin K dependent coagulation factors

72
Q

INR

A

international normalised ratio

73
Q

what is INR?

A

measure of prothrombin time

74
Q

use of INR

A

measures anticoagulant effect of warfarin and its effect on the clotting cascade

75
Q

how to calculate INR?

A

prothrombin time of patient/prothrombin calibrated normal

76
Q

benefit of INR

A

eliminates assay variation between places

77
Q

INR of 2

A

prothrombin time is twice that of a normal control using that assay

78
Q

what is the target INR for people on warfarin?

A

2-3

79
Q

how to prescribe warfarin?

A 
dedicated chart 
own policies 
risk assessment - balance of risk factors for bleeding and indication for use 
baseline monitoring 
advice on interactions
80
Q

warfarin and drug interactions

A

enzyme inducers increase warfarin metabolism and reduce INR and its effect
enzyme inhibitors decrease metabolism of warfarin and so increase INR and bleeding risk

81
Q

what else can affect warfarin?

A

other anticoagulants

protein binding

82
Q

high risk drugs for warfarin interactions

A 
anticonvulsants 
antibiotics 
analgesics - NSAIDs 
anticoagulants 
antidepressants 
anti-platelets
83
Q

what common drugs enhance the effect of warfarin?

A 
anabolic steroids 
antidepressants 
antidiabetics
allopurinol
amiodarone
antibiotics 
aspirin 
NSAIDs 
phenytoin 
statins
84
Q

what other substances enhance the effect of warfarin?

A

cranberry juice
grapefruit juice
smoking cessation
alcohol

85
Q

what common drugs reduce the effect of warfarin?

A 
azathioprine
carbamazepine 
rifampicin
oral contraceptive pills 
st john's wort
86
Q

what other substances reduce the effect of warfarin?

A

chronic alcohol use
broccoli
green leafed vegetables

87
Q

Initial parenteral treatment

A

when instant anticoagulation is required

88
Q

initial oral treatment

A

when slower anticoagulation is needed

89
Q

how to reverse warfarin?

A 
depends on urgency and severity 
vitamin K oral or IV 
IV = 5mg 
varied doses 
omit the warfarin dose 
FFP 
prothrombin complex concentrates
90
Q

FFP

A

frozen fresh plasma
instant effect
variable effect
new clotting factors

91
Q

dried prothrombin complex concentrates

A

instant effect
e.g. octaplex
pooled clotting factors from other patients
given with vitamin K

92
Q

warfarin reversal with vitamin K

A

slow

93
Q

reversal of DOACs

A

support measures/resuscitation
normal INR excludes significant dabigatran effect but doesn’t exclude therapeutic concentrations of the other DOACs
need to wash out DOACs
if severe = dried prothrombin complex

94
Q

wash out for DOACs

A

12 hours for dabigatran and apixaban

24 hours for rivaroxaban

95
Q

new antidote for dabigatran

A

idarucixumab

expensive

96
Q

reversal of heparin

A

depends on severity and urgency
omit dose of LMWH or stop the infusion of unfractionated heparin
protamine sulphate

97
Q

what are thrombolytics?

A

clot busters

98
Q

uses of thrombolytics

A 
acute ischaemic stroke
PE with cardiovascular collapse 
massive DVT
upper limb DVT
other rare uses
99
Q

how do thrombolytics work?

A

activates plasmin
breaks down clot
TPA - tissue plasminogen activator

100
Q

consent for thrombolysis

A

get verbal consent for administration
risks can be severe
make sure risks are explained

101
Q

what are the risks of thrombolytics?

A 
intra-cerebral haemorrhage
other haemorrhages 
all clots in the body are broken down 
haemorrhagic strokes
massive GI bleed
102
Q

Criteria for TP in ischaemic acute stroke

A

<4.5 hours since clear onset
>18 years old
diagnosis of ischaemic CVE

103
Q

most common PE ECG finding

A

sinus tachycardia

104
Q

when to consider thrombophilia?

A

when atypical thrombosis is present or there is recurrent unprovoked disease

105
Q

antiplatelets

A

irreversible COX inhibitors
P2Y12 receptor antagonists/ ADP receptor inhibitors
glycoprotein inhibitors

106
Q

aspirin

A

inhibition of thromboxane synthesis in platelets

inhibits platelet aggregation

107
Q

P2Y12 receptor antagonists examples

A

clopidogrel
prasugrel
ticagrelor
ticlopidine

108
Q

how do P2Y12 receptor antagonists

A

inhibits P2Y12 receptor on platelets
inhibits platelet aggregation
no activation of Gp IIb/IIIa receptors

109
Q

glycoprotein inhibitors examples

A

abciximab
eptifibatide
tirofiban

110
Q

how do glycoprotein inhibitors work?

A

bind and block glycoprotein IIb/IIIa receptors on platelet surface
prevents platelets binding to fibrinogen
inhibits platelet aggregation and thrombus formation

2nd year (48 decks)

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