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Vascular > Clotting, platelet-activation and their management > Flashcards

Clotting, platelet-activation and their management Flashcards

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1
Q

How does aspirin work?

A

Inhibits the COX enzyme which mediates vasoconstriction via TXA2 and mediates ADP release which causes GPIIb/IIIa expression leading to soft plug formation with fibrinogen
Inhibits thromboxane formation

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2
Q

How do P2Y12 antagonists work?

A

e.g. clopidogrel, prasugrel, ticagrelor

Attenuate the release of ADP preventing soft platelet plug formation

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3
Q

What is amplification/intrinsic clotting?

A

Thrombin initiates release of factors which further amplify clotting e.g. FV, FVIII, FIX and FX
Requires Ca ions and phospholipid

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4
Q

FXa:FVa complex does what?

A

Accelerates prothrombin to thrombin formation

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5
Q

What is the effect of thrombin?

A

Thrombin causes the conversion of fibrinogen on the surface of platelets to fibrin which provides a harder barrier that the soft plug

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6
Q

What is initiation?

A

The process of getting from tissue factor to thrombin

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7
Q

(initiation) TF + FVII -> FVIIa:TF goes to what?

A

FX -> FXa (:FVa)

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8
Q

(initiation) FXa causes what?

A

FII (prothrombin) -> FIIa (thrombin) this activates platelets

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9
Q

What stabilises the clot?

A

FXIIIa (fibrin stabilising factor)

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10
Q

Purpose of plasmin?

A

Breaks clot into soluble fragments

tPA bound to fibrin causes the conversion of plasminogen to plasmin which breaks down clot

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11
Q

Effect of Heparin?

A

Heparin activates antithrombin

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12
Q

LMWH:

A

Causes indirect inhibition of FXa

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13
Q

Warfarin:

A

Oral vitamin K antagonist

Inhibits vitamin K reductase in the liver, required for production of FII (prothrombin), FVII, FIX and FX

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14
Q

Fondaparinux:

A

Synthetic polysaccharide that acts like LMWH and inhibits FXa

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15
Q

Dabigatran and bivalirudin:

A

Direct thrombin (FIIa) inhibitors

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16
Q

Rivaroxaban:

A

Direct FXa inhibitor

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17
Q

Important factors in the history:

A 
Maternal grandparents
Cosanguinous marriage
Transfusion
Surgery
Childhood: epistaxis (nostril), umbilical stump bleeding
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18
Q

Platelet and/or vascular abnormality would be suggested by…

A

Skin (cutaneous) and mucous membrane bleeding e.g. petechiae, purport, epistaxis, gingival bleeding, menorrhagia or haematuria

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19
Q

Bleeding into deep tissues, joints and muscles suggests what?

A

A coagulation factor defect

different to cutaneous bleeding which suggests a platelet/vascular abnormality

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20
Q

What does prothrombin time (PT) measure?

A

Integrity of extrinsic system (initiation) as well as common factors (FVII, V, X, prothrombin (II) and fibrinogen)
11-15 seconds is normal
Prolonged can indicate a vitamin K deficiency

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21
Q

What does partial thromboplastin time (PTT) measure?

A

Integrity of intrinsic system and common factors
35 seconds is normal
Prolonged aPTT can indicate liver disease
Can be used to test the pharmacodynamics of heparin as heparin activates anti-thrombin III

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22
Q

What is INR?

A

International normalised ratio used to normalise PT, since this will be affected by the manufacturer’s TF
Normal = 0.8-1.2
Target for Warfarin = 2-3

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23
Q

What is thrombin time (TT)?

A

Thrombin time is the time for a clot to form in anti-coagulated blood after an excess if thrombin is added
Plasma with added thrombin vs normal plasma
It measures how efficiently the body can produce fibrin
12-14 seconds is normal
Batrotoxin added instead of thrombin with samples of people who take heparin

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24
Q

How can PT be used?

A

To test the pharmacodynamics of warfarin and to test FX inhibitors

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25
What does prolonged TT indicate?
Fibrinogen deficiency Fibrinogen dysfunction Pharmacodynamics of heparin Pharmacodynamics of direct thrombin inhibitors (dabigatran and bivalirudin)
26
What are D-dimers?
A fibrin degradation product Main use is to exclude thromboembolic disease Used in diagnosis of disseminated intravascular coagulation
27
PT factors:
Vitamin K dependent factors 2, 7, 9, 10
28
aPTT factors:
8, 9, 11, 12
29
Effect of heparin on coagulation:
Prevents activation factors 2, 9, 10, 11
30
Effect of warfarin on coagulation:
Affects synthesis of 2, 7, 9, 10
31
Effect of DIC on coagulation:
Factors 1, 2, 5, 8, 11
32
Effect of liver disease on coagulation:
Factors 1, 2, 5, 7, 9, 10, 11
33
Blood clotting test results of haemophilia:
PT: normal aPTT: increased Bleeding time: normal
34
Blood clotting test results of von Willebrand's disease:
PT: normal aPTT: increased Bleeding time: increased
35
Blood clotting test results of vitamin K deficiency:
PT: increased aPTT: increased Bleeding time: normal
36
Effect of jaundice?
Jaundice will impair synthesis of vitamin K dependent clotting factors, this will increase PT
37
What is bleeding time a measure of?
Platelet function
38
Can aPTT be affected by vitamin K deficiency?
Yes because factor 9 is vitamin K dependent, however to a lesser extent and this is more associated with severe liver disease
39
What do GPI's target?
GPIIb/IIIa
40
Main indications for anti-platelet drugs:
Primary prevention of atherothrombotic events in people who are at high risk Secondary prevention of atherothrombotic events in people with acute coronary syndrome, peripheral artery disease or angina Secondary prevention of CV events in those post-MI, stenting, stroke or TIA Prevention of atherothrombotic events in those undergoing PCI
41
Don't prescribe anti-platelets for...
Primary prevention of CV events unless very high risk of MI or stroke
42
Post-ACS management:
Dual anti-platelet therapy for a year Aspirin 300mg stat, 75mg od +Clopidogrel 300-600mg stat, 75mg od +Prasugrel 60mg stat, 10mg od +Ticagrelor 180mg stat, 90mg bd (post-STEMI or high risk NSTEMI) Ticagrelor can be given 60mg bd for further 2 years
43
What can be given for gastroprotection?
Ranitidine 300mg BD/PPI (history of reflux)
44
Side-effect of aspirin?
Can cause increase in leukotrienes triggering asthma attacks in asthmatics
45
How does aspirin have an anti-platelet effect?
Prevents thromboxane synthesis
46
Difference between clopidogrel and prasugrel and ticagrelor
Clopi and pras are prodrugs conjugated by CYP450 in the liver and are irreversible whereas ticagrelor is an active drug and is reversible Duration: clop = 3-10 days; pras = 5-10 days; tica = 2-5 days Bleeding risk: pras > tica > clopidogrel
47
Risks of prasugrel?
Increased bleeding risk in >75 y/o and <60kg so reduce maintenance dose from 10mg to 5mg And contra-indicated in CVA/TIA
48
Risks of ticagrelor?
Contraindicated in severe hepatic impairment and interacts with CYP3A inhibitors
49
Risks of clopidogrel?
CYP2C19 are poor metabolisers thus reduced anti-platelet effect Has interactions with omeprazole - avoid omeprazole/lanzoprazole if DAPT includes clopi
50
What must you have with dual anti-platelet therapy?
GI protection
51
Triple therapy:
Low does rivaroxaban 2.5mg bd (DOAC) given with DAPT improves CV outcomes but with increased bleed risk Indicated with MI but no AF
52
Aim with triple therapy?
Minimal dose possible for the shortest time
53
PCI: High risk bleed i.e. has bled >3 times?
4 weeks triple (clop, aspirin + VKA/DOAC) 12 months DAPT (clop, aspirin) Lifelong mono therapy (aspirin 75-100mg/day)
54
PCI: Low-intermediate risk bleed i.e. has bled 0-2 times?
6 months triple 12 months DAPT Lifelong mono
55
Medically managed/CABG?
12 months DAPT | Lifelong mono
56
Indications for VKAs (warfarin)? aka blood thinners
``` AF Heart valve replacements DVT PE Anti-phospholipid syndrome Rheumatic heart disease TIA ```
57
Features of VKAs/warfarin:
Slow onset of action (3-4 days) with initial pro-coat phase so require bridging with deltaparin (LMWH) Long duration of action (2-5 days)
58
DOACs:
Rivaroxaban Apixaban Dabigatran Edoxaban
59
When are DOACs prescribed over warfarin?
Non-valvular atrial fibrillation Prophylaxis of PE, DVT, systemic embolism and stroke VTE prophylaxis after hip or knee surgery Rivaroxaban (+ aspirin + clopi) can be used to reduce atheroembolic risk after ACS with raised cardiac biomarkers (rivaroxaban)
60
DOACs that are direct FXa inhibitors?
Rivaroxaban Apixaban Edoxaban
61
DOAC that is a direct thrombin (FIIa) inhibitor?
Dabigatran
62
Features of DOACs:
``` Short t(1/2) Quick onset - don't need bridge therapy Apix, riva (edox minimally) are metabolised in the liver Dabigatran can cause dyspepsia All have some degree of renal clearance ```
63
When should you dose reduce dabigatran from 150mg BD to 110mg BD?
Age > 80 On verapamil CrCl 30-50ml/min Bleed risk
64
When should you dose reduce apixaban from 5mg BD to 2.5mg BD?
2 of: age > 80, body weight < 60kg, Cr > 133umol/L | Or CrCl < 30ml/min
65
When should you dose reduce edoxaban from 60mg OD to 30mg OD?
CrCl < 50ml/min Body weight < 60kg Specific p-gp inhibitors
66
When should you dose reduce edoxaban from 20mg OD to 15mg OD?
CrCl < 50ml/min
67
Which DOAC for GI problems?
Apixoban
68
Which DOAC for pill burden?
VKA | Rivaroxaban
69
Which DOAC for high bleed risk?
Not rivaroxaban
70
Which DOAC for recurrent stroke/systemic embolic event/TIA despite good anti-coat control?
Dabigatran
71
Differences between warfarin and DOACs?
DOACs have fixed dose unlike warfarin which is variable (INR)
72
What is transexamic acid?
An Anti-fibrinolytic drug which stops plasmin from breaking down fibrin clots - used in profuse epistaxis that is unresponsive to pressure and nasal packing and menorrhagia Binds to plasminogen
73
What is von Willebrand's disease?
Hereditary cause of coagulopathies Autosomal dominant Increased bleeding time and nose bleeds
74
Features of haemophilia A:
Deficiency in factor VIII PT normal, aPTT increased, bleeding time normal TT normal Haemoarthroses, haemotomas
75
When is dipyridamole prescribed?
In combination with aspirin after stroke or TIA
76
Action of dipyridamole?
Phosphodiesterase inhibitor - reduces intracellular calcium levels Contraindicated with adenosine as prevents breakdown

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