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Haematology Week 2 > Drugs used in Haemostasis > Flashcards

Drugs used in Haemostasis Flashcards

(51 cards)

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1
Q

What are some of the chemicals which are secreted from the platelets to initiate platelet aggregation?

A

ADP and thromboxane A2

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2
Q

How does aspirin work?

A

Inhibits the cyclo-oxygenase enzyme which is necessary to produce thromboxane A2

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3
Q

What are the main side effects of aspirin?

A

Bleeding and blockage of production of prostaglandins (which can cause bronchospasm and ulceration)

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4
Q

What is the mechanism of clopidogrel and prasugrel?

A

ADP receptor antagonists

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5
Q

What is the mechanism of dipyridamole?

A

Phosphodiesterase inhibitor which reduces production of cAMP - a second messenger in platelet activation

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6
Q

What type of drug is abciximab?

A

GP IIb/IIIa inhibitor

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7
Q

How do GP IIb/IIIa inhibitors work?

A

They inhibit aggregation as platelets adhere to each other via GPIIbIIIa and fibrinogen

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8
Q

Anti-platelet drugs tend to affect platelet function for how long?

A

Their 7-10 day lifespan

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9
Q

If someone is having an elective operation, when should anti-platelets be stopped?

A

7 days before

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10
Q

If there is serious bleeding in someone on anti-platelets, how can their action be reversed?

A

Platelet transfusion

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11
Q

What are the main indications for anticoagulant drugs?

A

Venous thrombosis and atrial fibrillation

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12
Q

How long should anti-coagulant drugs be used for following a) a one off venous thrombosis? b) multiple venous thrombosis?

A

a) 6 months b) lifelong

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13
Q

How does AF form a thrombus? What happens when this thrombus forms?

A

Due to stasis in the left atrium / it embolises and travels to the brain, causing a stroke

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14
Q

If someone has AF, they should be anticoagulated for how long?

A

Lifelong

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15
Q

What part of haemostasis do anticoagulants target?

A

Fibrin clot

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16
Q

How are the ways that anticoagulants can target the fibrin clot?

A

Inhibit a specific part of the haemostatic mechanism / promote one of the natural anticoagulants

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17
Q

How long does it take for heparin to act?

A

Immediately

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18
Q

How is heparin given?

A

IV or SC

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19
Q

The dose of heparin is based on what?

A

Weight

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20
Q

In general, heparin works how?

A

By potentiating anti-thrombin

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21
Q

Unfractionated heparin mainly affects what interaction?

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A

Anti-thrombin/thrombin

22
Q

LMWH mainly affects what interaction?

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A

Anti-thrombin/activated factor 10

23
Q

When is unfractioned heparin used?

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A

Rarely, useful if the patient has a thrombus but is also at risk of bleeding (e.g. pregnancy, coinciding GI ulcer)

24
Q

What investigation is used to monitor unfractioned heparin use?

25
What investigation is used to monitor LMWH? Why is this monitoring not used regularly?
Anti-Xa assay / it has a fairly predictable response
26
What are the main complications of heparin?
Bleeding, heparin induced thrombocytopenia (autoimmune) and long-term osteoporosis
27
Why is it not ideal to use heparin as a long term treatment?
Can cause osteoporosis and injections are unpleasant
28
How are the effects of heparin usually reversed?
By stopping heparin (it has a short half life)
29
In severe bleeding, what can be used to reverse the effects of heparin? What effect does this have on a) unfractioned heparin? b) LMWH?
Protamine sulphate / a) complete reversal b) partial reversal
30
Phenindione is what type of medication? It should be used when?
Vitamin K antagonist / should be used when patients are resistant to warfarin
31
How to coumarin anticoagulants work?
By inhibiting vitamin K and hence blocking clotting factors II, VII, IX and X
32
Which type of anticoagulant is better to give to people who require treatment lifelong? Why?
Coumarin anticoagulants as they don't require injection
33
When should the dose of warfarin be taken?
At the same time every day
34
How is warfarin therapy monitored? This is based on what?
INR / PT
35
What is the main adverse effect of warfarin? What are some factors which may increase the risk of this?
Haemorrhage / comorbidities, intensity of anticoagulation, drug interactions
36
What are some examples of mild bleeding complications which may be seen in patients on warfarin?
Skin bruising, epistaxis and haematuria
37
What are some examples of severe bleeding complications which may be seen in patients on warfarin?
GI and intracerebral bleeds, any bleeds causing a significant drop in Hb
38
What are the main ways of reversing the effects of warfarin?
Stop the drug, oral vitamin K, clotting factors via factor concentrate
39
How long does it take for oral vitamin K to counteract the effects of warfarin?
6 hours
40
If you need something to counteract the effects of warfarin immediately, what can you use? What is important to know about this however?
Factor concentrate / only works for a short period of time
41
What happens to level of warfarin and risk of bleeding if a person consumes other drugs which are metabolised by the cytochrome P450 system (including alcohol)
Decreases the effect of warfarin and increases the risk of bleeding
42
What is important to be aware of when starting patients on warfarin?
Protein S and C are also dependent on warfarin, so initially this can cause their levels to fall which actually makes the person prothrombotic
43
When patients are initially started on warfarin, they should be covered by what?
LMWH
44
What effect will warfarin have on the APTT?
Eventually it will prolong it due to decreased factor IX, but it will take much longer to do this than heparin would
45
Dabigatran is a NOAC which works how?
Direct inhibition of thrombin
46
How are oral direct thrombin inhibitors excreted? What is the disadvantage of this?
Renally, if there is renal failure, this can accumulate and lead to bleeding
47
Rivaroxaban, apixaban and edoxaban are NOACs which work how?
Direct factor Xa inhibitors
48
Which type of NOAC is used more commonly and why?
Oral Xa inhibitors as they are excreted by the hepatobiliary system
49
What are the advantages to NOACs?
Oral, no monitoring required, less drug interactions
50
What is the main disadvantage of NOACs? Why is this not too much of a big deal?
No specific antidote / they are less likely to cause bleeding in the first place
51
When should NOACs be used?
Prophylaxis in elective orthopaedic surgery, stroke prevention in AF, treatment of DVT/PE

Haematology Week 2 (4 decks)

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