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Pharmacology Term 6 > 6.2- Anti-coagulants > Flashcards

6.2- Anti-coagulants Flashcards

1
Q

What can disorders of haemostats be divided into?

A

Arterial Thrombo-embolic events

Venous Thrombo-embolic events

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2
Q

Name 2 types of arterial thromboembolic events?

A

Stroke ( CVA)

MI

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3
Q

Name 2 types of venous thromboembolic events?

A

DVT

PE

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4
Q

Name the components of Virchow’s Triad

A

Hypercoagulability
Endothelial damage
Vascular stasis

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5
Q

What does Warfarin do?

A

inhibits production of Vitamin K dependent clotting factors ie factor II ( Prothrombin), VII, IX and X

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6
Q

Briefly describe warfarin

A

long half life
slow onset and offset of action
anticoagulant effect is potentially reversible
only ORAL anti-coagulant which can be measured therefore safe

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7
Q

Describe the PK of warfarin

A

good GI absorption therefore give orally/ PO
slow onset of action so give Heparin as a cover
Slow OFFSET; half life is 48 hrs but varies–> so you need to stop it 5 days before surgery

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8
Q

Describe a consequence of Warfarin’s hepatic metabolism

A

CYP450 system

  • CAUTION w alcoholics/ liver disease bc their INR fluctuates
  • caution w drugs that affect P450 system bc they can affect the metabolism of Warfarin ( induce/ inhibit)
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9
Q

Is Warfarin given in pregnancy?

A

NO bc it crosses the placenta
in first trimester it is TERATOGENIC

in third trimester, there is a risk of bleeding at delivery

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10
Q

Why would you be at risk of clotting in pregnancy?

A

Immobility
Oestrogen is dominant during pregnancy –> increases all the pro-coagulant factors and reduces the anti-coagulant factors therefore you are at HIGH risk of clots

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11
Q

How do you monitor Warfarin?

A

Prothrombin Time
using citrated plasma and light blue tube
PT is standardised into INR, which allows a STANDARD VALUE between labs
but PT varies ( INR will be the same

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12
Q

Which drugs POTENTIATE Warfarin ie increase its affect and HOW

A

1) INHIBIT hepatic metabolism; AMIODARONE, QUINOLONE, CIMETIDINE, ingesting alcohol

2) REDUCE VIT K from GUT BACTERIA
Cephalosporin antibiotics

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13
Q

How do drugs INHIBIT warfarin

give 2 examples

A

INDUCE hepatic enzymes thereby increasing metabolism of Warfarin; therefore DECREASING INR ie HIGHER risk of clot
e.g. Rifampicin
Anti-epileptics EXCEPT Na Valproate

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14
Q

Which conditions does Warfarin treat to raise INR range to 2-3?

A

DVT/PE
AF
Dilated cardiomyopathy

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15
Q

Which conditions does Warfarin need to raise INR event higher in, to 3-4?

A

Mechanical prosthetic valves; need an even higher INR than 2-3, bc HIGH risk of thrombotic event

Thrombosis associated w ANTI-Phospholipid syndrome

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16
Q

What is ANTI-PHOSPHOLIPID SYNDROME?

A

autoimmune, acquired
type of thrombophilia, INCREASED risk of clotting
young patients<45 yrs presenting w stroke/ MI

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17
Q

What are women w anti-phospholipid syndrome at risk of?

How is this treated?

A

RECURRENT MISCARRIAGE

treat with aspirin and heparin

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18
Q

Name 8 LIMITATIONS of Warfarin Therapy

A

1) Unpredictable response; bc of its high protein binding and lots of ADR’s
2) Narrow therapeutic window; INR range 2-3
3) Requires ROUTINE coagulation monitoring
4) SLOW onset and offset of action
5) Requires FREQUENT DOSE ADJUSTMENTS
6) Drug-drug interactions
7) Drug-food interactions
8) Warfarin resistance

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19
Q

What is the trouble with warfarin’s narrow therapeutic range?

A

INR 2-3
If a patient’s INR is sub-therapeutic

If INR<2, their stroke risk is HIGH bc increased clotting

If INR>3 ie too high, THEN there is a risk of an intracranial bleed

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20
Q

Name 2 adverse effects of Warfarin

A

TERATOGENIC ( in 1st trimester and at 3RD trimester there is a high risk of bleeds)

BLEEDING/BRUISING; epistaxis, intracranial, GI loss

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21
Q

How do you reverse warfarin therapy?

A

stop warfarin
PARENTERAL VITAMIN K( Slow)
FRESH FROZEN PLASMA(Fast)

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22
Q

What do you consider during warfarin reversal?

A

Bleeding, INR, Indication

Mechanical valve ; ask consult

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23
Q

Name agents for Warfarin reversal?

A

IV Vitamin K; pro-coagulant effects for 6 weeks

Prothrombin Complex Concentrate (PCC)

Fresh Frozen Plasma

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24
Q

Which is better for Warfarin reversal, FFP or PCC

A

PROTHROMBIN COMPLEX CONCENTRATE ( completely reverses Warfarin , unlike FFP)

25
Q

Why is PCC preferred to FFP?

A

FFP is given in a large volume, so if you give an elderly patient a large volume of FFP, they could get a volume overload–> therefore RISK of heart failure

Whereas in PCC, it is given in a SMALL VOLUME, so no risk of heart failure

26
Q

How does Heparin’s route of admin differ from Warfarin’s?

A

1) Heparin is given via SUBCUTANEOUS INJECTION ( if low molecular weight) whereas Warfarin is given orally
2) If in un-fractionated form, it is given IV or SC

27
Q

What is Heparin?

A

glycosaminoglycan; glucose backbone

Produced by MAST CELLS

28
Q

Give the general action of Heparin

A
  • binds to Anti-Thrombin III; ATIII via a unique pentasaccharide sequence
  • leads to activation fo ATIII and inactivation of Factor Xa, IIa( prothrombin), IXa
29
Q

How does UFH become LMWH

A

UFH can be fractionated to produce molecules with LMWH

LMWH has more PREDICTABLE PHARMACODYNAMICS

30
Q

How does Heparin work on the clotting cascade?

A

Heparin stimulates ATIII, which then inactivates Thrombin and factor IIa therefore no clotting

Warfarin inhibits the production of Prothrombin from Factor X–> therefore no Thrombin produced-> no clot

31
Q

Describe the structure of UFH

A

long length heparin chains
usually given by continuous IV infusion

Occasionally given via SC for prophylaxis in patients w renal failure who are unsuitable for LMWH

long enough length to inhibit activation of PROTHROMBIN ( IIa) and factor XA

32
Q

How can UFH be monitored

A

via APTT but cannot measure LMWH by this

done every 2-3 hours to check the effect and level of unfractionated heparin in blood of patient

33
Q

What is LMWH

A

smaller chains

given SUBCUTANEOUSLY

34
Q

Describe the PK of LMWH

A

PREDICTABLE
high bioavailability
long half life–> cleared by kidneys

THEREFORE given at a fixed once daily dose, monitoring is not usually required

35
Q

What are the 3 instances for which you DO have to monitor LMWH?

A

Monitored by Anti Xa level not APTT if monitoring required

1) Pregnancy
2) MODERATE renal failure
3) Patients with very high or low body weight

36
Q

Describe the mechanism of LMWH

A

to catalyse the inhibition of IIa by AT-III, heparin needs to bind SIMULTANEOUSLY to IIa and AT III

LMWH is not large enough for this therefore it can only inhibit Factors Xa but NOT IIa

37
Q

Why can’t LMWH be measured with APTT, unlike UFH?

A

un-fractionated heparin can bind to both thrombin and factor Xa
WHEREAS
LMWH can only bind to factor Xa NOT thrombin ie IIa

THIS IS WHY you cannot check LMWH with APTT bc the APTT blood test depends on this point of thrombin activation

38
Q

Describe the route of administration of heparin

A

MUST be given parenterally as poor GI absorption
RAPID onset and offset of action
UFH: IV
LMWH: SC

39
Q

Which anti-coagulant do you give before surgery?

A

HEPARIN
i.e. it has a much smaller half life than Warfarin therefore once you stop a patient on Warfarin when they come in for surgery (5 days before), you replace it with Heparin
because you can stop the Heparin on the morning of the procedure and still provide the patient with an anti-co-agulatory effect all the way up to the procedure AND

Reducing the risk of them clotting in the TIME BETWEEN the surgical procedure and stopping the Warfarin

QUICK OFFSET TIME of Heparin allows its cessation if bleeding

40
Q

How is heparin is used for prevention of VTE?

A

Used prophylactically in hospital bc all admitted patients are at HIGH risk of clotting, therefore all in-patients should be on anti-coagulant

in patients
Post-op patients
Immobility

41
Q

What instances is heparin given in?

A

Administered prior to warfarin; quick onset to cover patient whilst warfarin loading is achieved
LMWH is often used

in PREGNANCY, it can be used in place of Warfarin

42
Q

What are the side effects of heparin?

A

Bruising/ bleeding

Osteoporosis; for long term use, UFH is preferred> to LMWH

Thrombocytopenia ( HIT)

43
Q

What is HIT?

A

Heparin Induced Thrombocytopenia

autoimmune phenomenon ( 4-14 days Rx)
tend to present w thrombosis not bleeding
diagnosed by Lab assay and clinical probability

44
Q

What action do you take if a patient has HIT?

A

STOP HEPARIN

Treat with Fondaparinux ( synthetic form of Heparin) or Lepirudin

45
Q

How is heparin therapy reversed?

A

Stop Heparin

If on UFH and actively bleeding–> give PROTAMINE
Monitor APTT if unfractionated

46
Q

What is Protamine and what is it used for?

A

Protamine sulphate

dissociates heparin from AT-III ( anti-thrombin III)

47
Q

Are anti-platelet drugs used for arterial or venous drugs?

A

Arterial clots

48
Q

Differentiate between arterial and venous clots

A

Arterial clots are more related to Virchow’s triad—> related to ATHEROSCLEROSIS ie vessel wall integrity
WHEREAS
venous clots are more related to the STASIS of blood

Therefore drugs treating arterial clots aim to have a greater effect on PLATELETS

and venous clot drugs focus on ANTI-COAGULATION specifically

49
Q

Name 4 anti-platelet drugs used to treat arterial clots

A

ASPIRIN; COX inhibition affecting Plt activation

DIPYRIDAMOLE; phosphodiesterase inhibition

CLOPIDOGREL; inhibits ADP dependent Platelet aggregation

GLYCOPROTEIN IIb/ IIIa inhibitors ( inhibits platelet crosslinking and activation

50
Q

What are thrombolytics used for?

A

to lyse already formed clots
STEMI
Massive PE w haemodynamic compromise
Stroke; AS LONG AS haemorrhage is EXCLUDED by CT scan

51
Q

How do thrombolytics work?

A
  • promote fibrinolysis by converting inactive plasminogen to active plasmin
  • Plasmin DEGRADES fibrin clot
52
Q

How can a massive PE cause haemodynamic compromise?

A

a SADDDLE EMBOLUS–» thromboembolus at the bifurcation of the pulmonary artery —> causing acute haemodynamic compromise

53
Q

Why are thrombolytics given in ADDITION to Warfarin and Heparin?

A

Warfarin and Heparin do not actually break down clots, they just prevent them from enlarging ie prevent clot propagation
But they are still relying on the body’s inherent fibrinolytic system to break them down

BUT there are certain situations where there is not enough time to wait for the fibrinolytic system to breakdown the clot THEREFORE you administer thrombolytics

54
Q

What is an instance of when you HAVE to give a thrombolytic? ( and not wait for fibrinolytic system to take action)

A

1) MI; collateral damage occurs during the period of time when there is a major obstruction to the vessel
IF you don’t thrombolyse a patient with STEMI, the will have a NON-FUNCTIONING LEFT VENTRICLE—> will go into cardiac failure–> will die

2) STROKE; window to reduce clot or neurological symptoms will occur
3) MASSIVE PE–> patient will die of hypoxia

55
Q

Name the 2 types of thrombolytics

A

Recombinant tissue plasminogen activator e.g. rt-PA

Streptokinase

56
Q

What are NOAC’s?

A

Novel Oral Anticoagulants

Direct thrombin Inhibitor- DABIGATRAN

Direct factor Xa inhibitors- APIXABAN

57
Q

Name 5 advantages of NOACs over Warfarin

A
  • rapid onset/offset of action
  • few drugs interactions
  • predictable pharmacokinetics
  • wide therapeutic window
  • eliminated the need for regular coagulation monitoring and allowed fixed dosing in adults
58
Q

Give 4 indications for the use of NOAC’s?

A

AF
Treatment of PE/DVT
Prevention of recurrent PE/DVT
Prevention of DVT/PE post hip/knee surgery

Pharmacology Term 6 (10 decks)

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