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Hematology > Pharmacologic Treatment of Clotting Disorders > Flashcards

Pharmacologic Treatment of Clotting Disorders Flashcards

1
Q

What are the anticoagulants that we are going to go over?

8

A 
Warfarin (Coumadin)
Dabigatran (Pradaxa)
Apixaban (Eliquis)
Rivaroxaban (Xarelto)
Heparin
Enoxaparin (Lovenox)
Dalteparin (Fragmin)
Fondaparinux (Arixtra)
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2
Q

What are the function of anticoagulants?

A

inhibit the action or formation of clotting factors.

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3
Q

What are the oral anticoagulants?

4

A

Warfarin (Coumadin, Jantoven)
Dabigatran (Pradaxa)
Apixaban (Eliquis)
Rivaroxaban (Xarelto)

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4
Q

What is the most widely used oral anticoagulant?

A

Warfarin

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5
Q

Describe the mechanism of action of warfarin?

2

A
  1. Inhibits the synthesis of vitamin K dependent coagulation factors II, VII, IX, X
  2. Also inhibit Protein C and Protein S (break up clots)
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6
Q

How long does it take for warfarin to achiveve the full therapeutic affect?

Why does it take this long for warfarin to take affect?

Which pathway does warfarin work on?

A

36-72

Because warfarin doesnt have an effect on existing clotting factors just the ones that are made from the liver after its been administered

extrinsic

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7
Q

What is the general use for warfarin?

A

prevent further clot formation (cant affect current ones-allows body to work out the clot itslef and prevents further clotting)

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8
Q

Indications for use fo warfarin?

7

A
  1. Venous and arterial thromboembolism
  2. Pulmonary embolism
  3. Stroke prevention in atrial fibrillation
  4. Thrombus prevention in cardiac valve replacement
  5. Stroke
  6. Transient ischemic attacks
  7. Prevention of clots
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9
Q

Describe the therapuetic range in pts taking warfarin

What is dosing of warfarin based on?

Whats a normal INR?

At what INR is warfarin creating therapeutic affects? And in what range do you want the INR for most indications?

A

very narrow therapeutic index

PT/INR

1

2
2-3

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10
Q

How soon should the INR be checked after each dose change?

A

2-3 days

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11
Q

What is a good place to start with the first dose of warfarin?

A

5mg nightly

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12
Q

What affects chronic dosing?

5

A 
diet
age
disease state
possible medication interactions
Pt's genetically determined rate of metabolism
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13
Q

Major interactions to know about with warfarin?

4

A

Statins
Most antibiotics
NSAIDs
Any drug cleared through the liver

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14
Q

What are nonmedication interactions that can affect the INR of warfarin?

A

Vitamin K containing foods (dark leafy greens, green tea)

Smoking/tobacco use decreases INR

Alcohol increases INR

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15
Q

How does warfarin affect vitamiin k?

A

Liver uses vitamin K to make clotting proteins. Warfarin reduces the livers ability to use vitamin k to produce normally functioning clotting factors.

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16
Q

So if you eat more vitamin K what will happen to the INR?

If you eat less vitamin k what will happen?

A

decrease in the INR

increase in the INR

Just keep it consistent

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17
Q

Adverse events for warfarin?

A
  1. BLEEDING

2. Skin and tissue necrosis leading to gangrene

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18
Q

When will skin/tissue necrosis develop with warfarin?

What is purple toe syndrome and when will it develop?

A

3-8 days after starting

Cholesterol emboli to the feet
may occur 3-8 weeks after starting

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19
Q

Why do these adverse events happen in warfarin/why do we have to give heparin?

A

Because it inactivates protein c and protein s which inhibit clotting factors themselves. Since these proteins have a shorter half life than thrombin their absense will be felt first = hypercoagulable state

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20
Q

Where are some places we could see thrombosis in the hypercoagulable state that is created by warfarin in the first few days if we dont give heparin?

A

fatty tissue
in the abdomen
even faster skin necrosis/gangrene in feet

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21
Q

If our patient on warfarin’s INR does become elevated how should we treat the patient?

No bleeding and INR5?
Life threatening bleeding?

A

hold warfarin

hold warfarin and give oral, IV or SQ vitamin K

Give vitamin K
Factor VII
FFP or prothrombin concentrate

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22
Q

How should we give warfarin reversal with vitamin k?

Whats the downside to vitamin k warfarin reversal?

A

IV usually affects 1-2 hours later

affects warfarin for up to a week after administration

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23
Q

What does patient education require with warfarin?

8

A 
indication, 
dosing, 
monitoring, 
side effects, 
drug interactions, 
diet, 
alcohol, 
birth defects
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24
Q

Why should you take your warfarin at night?

A
  1. This is done so that on those days when your blood test is checked, the dose can be adjusted that day, if needed
  2. take other meds with possible interactions in the morning?
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25
Q

How long should warfarin be held when anticipating a surgical or invasive procedure?

A

4-5 days

Make sure INR is less than 1.6

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26
Q

Name three newer oral anticoagulants?

A

Dabigatran (Pradaxa)
Rivaroxaban (Xarelto)
Apixaban (Eliquis)

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27
Q

What are the pros of the new anticoagulants?

3

A
  1. No need for routine lab monitoring
  2. Not affected by foods
  3. Not as many drug interactions
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28
Q

What are the cons of the new anticoagulants?

4

A
  1. No antidote
  2. No way to monitor anticoagulation
  3. Dose adjustments likely needed for renal patients
  4. Not for use in valvular heart disease
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29
Q

What does Dabigatron target in the clotting cascade?

Apixaban?

Rivaroxaban?

A

IIA

Xa

Xa

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30
Q

What are the brand names of Dabigatron, Apixaban and Rivaroxaban?

A

Pradaxa
Eliquis
Xarelto

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31
Q

In which of the newer anticoagulation meds do we need to monitor for renal damage?

A

Definitely dabigatron and probably rivaroxaban

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32
Q

Which of the newer antibiotics delays absorption of food?

A

Rivaroxaban

33
Q

What is the half life for Dabigatran (Pradaxa)?

Dosing schedule?

When do maximum anticoagulant effects occur?

When should we not use dabigatron?

A

Half life is 12-14 hours

twice daily

2-3 hrs

end stage renal disease

34
Q

What are the two kinds of heparin?

2 with subtypes

A 
Unfractionated heparin (UFH)
-heparin
Low molecular weight heparin (LMWH)
-Enoxaparin (Lovenox)
-Dalteparin (Fragmin)
-Fondaparinux (Arixtra)
35
Q

Heparin MOA?

2

A
  1. Heparin binds to antithrombin III causing its activation. Antithrombin III then inactivates thrombin and Xa. Also 9, 11, 12 and plasmin
  2. prevents the conversion of fibrinogen to fibrin
36
Q

Why is frequent monitoring needed in heparin?

A

narrow therapeutic index

37
Q

How do we administer Heparin?

How do we monitor heparin?

A

Bolus followed by IV drip

PTT

38
Q

Indications for heparin?

A 
DVT
PE
Atrial fibrillation
MI
Arterial or venous thrombosis
39
Q

Contraindications for heparin?

3

A

anaphylaxis and
recent major surgery or
ongoing bleeding

40
Q

Adverse affects of heparin?

4

A
  1. bleeding,
  2. hypersensitivity reactions,
  3. transaminitis,
  4. Heparin induced thrombocytopenia
41
Q

What is the antidote avilable for cases of severe bleeding or overdose in heparin?

How should we administer this?

A

Protamine sulfate

Slow IV infusion to prevent anaphylactic reaction

42
Q

What kind of heparin preparation is most likely to cause heparin induced thrombocytopenia?

A

UFH but can occur in both

43
Q

When is a patient said to have HIT?

What are the labs to check for diagnostic evaluation of HIT?

A

Noted when platelet count drops below 50% after initaition of therapy

Platelet factor 4 antibody
-Not specific by sensitive
Serotonin release assay***
-Specific and sensitive

44
Q

Describe the pathology of HIT?
3

When does this occur after initiation of therapy?

A
  1. Creates a pro-thrombotic state
  2. Antibodies bind: Platelet factor 4 antibodies bind to heparin and platelets
  3. Platelets are activated and destroyed
  4. Occurs 4-5 days after the initiation of therapy
45
Q

How should we treat HIT?
2

What should we not do?
2

A
  1. First course of action: STOP THE HEPARIN
  2. Next give an alternative anticoagulant therapy like direct thrombin inhibitor.
  3. No platelet transfusion
  4. Do not give warfarin until platelet count increases
46
Q

Kinds of direct thrombin inhibitors?

A

Bivalrudin (Angiomax), Lepirudin (Refludan), Argatroban

47
Q

What are the types of Low Molecular Weight Heparins (LMWH)?

3

A

Enoxaparin (Lovenox)
Dalteparin (Fragmin)
Fondaparinux (Arixtra)

48
Q

What are LMWH’s advantages compared to UFH?

4

A
  1. Can be given SQ once or twice daily without need for labs for daily monitoring
  2. Lower risk of HIT
  3. Home administration
  4. Safer than UFH for extended administration
49
Q

MOA for LMWH?

A

Inhibits Xa and excellerates AT
Indirect thrombin inhibitor
LMWH more storngly inhibits Xa than UFH

50
Q

How do we administer LMWH?

A

ongoing IV drip (short half life)

51
Q

How should we dose LMWH?

A

Once or twice daily administration

Time to effect is about 2 hours (SQ) with peak effect at 4 hrs

52
Q

How should we monitor LMWH?

2

A

PTT
Can monitor drug concentration with lab for anti-Xa activity in those who are obese, pregnant or with poor renal function

53
Q

What do antiplatelet drugs do?

A

inhibit platelet aggregation and prevent platelet plugs.

54
Q

What are the types of anti platelet therapy?

4

A
  1. aspirin
  2. P2Y12 antagonists
  3. Dipyridamole (aggrenox)
  4. GIIb/IIIa antagonists
55
Q

What are the kinds of P2Y12 antagonsits?

3

A

Clopoidogrel (Plavix), Prasugrel (Effient), Ticagrelor (Brilinta)

56
Q

What drug is used in combo with aspirin?

A

Dipyridamole (aggrenox)

57
Q

What are the types of GIIb/IIIa antagonists?

2

A

Abiciximab (Reopro), Eptifibatide (Integrelin)

58
Q

One thing we need to remember about ASAs?

A

Irreversible platelet inhibitor

59
Q

MOA for aspirin?

A

Prevents the formation of clots by inhibition of the platelet plug

60
Q

When are peak effects seen after administraion of aspirin?

A

Rapid absorption with peak effects in 1 hour

61
Q

Dosing recommendations for ASA:
Primary prevention of CVA/MI?
Secondary prevention of CVA/MI?
Acute coronary syndrome?

A
  1. 81 mg daily
  2. Depends on the other meds and how recent the event was (81-325mg daily)
  3. 325mg chewed X 1
62
Q

Aspirin is used to prevent! thromboembolism in a procoagulant state

A

Statement

63
Q

What should we monitor for in patients that are taking aspirin?

What may decrease the effects of aspirin that cause gastritis and GI bleeding?

What else can we do to increase the risk of GI bleeds?

A

GI BLEEDS!

H2 blockers and proton pump inhibitors

administer with food

64
Q

Side effects of ASA?

4

A

Bleeding
Tinnitus at higher doses
Resistance
Allergy

65
Q

When should we stop aspirin before surgery?

A

4 days prior to surgery

66
Q

What do we use Clopidogrel (Plavix) and the other P2Y12 antagonists to treat?
2

A
  1. Treatment and prevention of acute coronary syndrome

2. Treatment and prevention of thomboembolic events

67
Q

MOA for P2Y12 antagonists?

A

P2Y12 receptor is blocked and unable to activate GPIIb/IIIa complex therefore preventing platelet aggregation

68
Q

Can P2Y12 antagonists be reversed?

A

No

69
Q

Adverse affects of P2Y12 antagonists?
2

When should we stop it prior to surgery?

A
  1. Bleeding
  2. Multiple drug interactions with Plavix due to it’s action in the P450 system

Stop 7 days prior to surgery

70
Q

Indications for Dipyridamole?

In what form is it used most often?

A
  1. Secondary prevention in patients following stroke and TIA

2. Used often with aspirin in a single pill called Aggrenox

71
Q

MOA for Dipyridamole (aggrenox)?

How is it administered?

A
  1. it inhibits ADP and phosphodiasterase
    - This causes an accumulation of adenosine, c-AMP
    - These mediators cause vasodilation and inhibit platelet aggregation

pill form, twice daily

72
Q

MOA for GPIIb/IIIa antagonists: Abciximab (Reopro)

Eptifibatide (Integrelin)?

A

most powerful platelet inhibitor
decrease platelet bridge formation
-inhibit at G23A
-prevent binding of VWF

73
Q

Indications for GPIIb/IIIa antagonists?
2

How is it administered?

A
  1. Acute coronary syndrome
  2. Clot prevention during percutaneous coronary intervention

IV

74
Q

Side effects of GPIIb/IIIa antagonists?

3

A

Bleeding
Thrombocytopenia (reactive)
Allergy

75
Q

What are the fibrinolytic drugs?

3

A

tPA
Streptokinase
Urokinase

76
Q

What is MOA for fibrinolytic drugs?

Indications for thrombolytic drugs?
4

A

Breakdown existing clots:
Convert plasminogen to plasmin to facilitate breakdown of the fibrin strands

  1. MI if > 90 min to PCI
  2. Stroke within the first few hours
  3. Massive PE with unstable hemodynamics (not often)
  4. Limb threatening ischemia
77
Q

What are the side effects of thrombolytics?

A

massive life threatening bleeding.

78
Q

Absolute contraindications for thrombolytics?

7

A
  1. Previous intracranial bleeding at any time
  2. CVA within last 3 months
  3. Closed head or facial trauma within 3 months
  4. Suspected aortic dissection
  5. Active bleeding diathesis (disorder)
  6. Uncontrolled HTN SBP>180, DBP>100
  7. Known CV lesions (AV malformations)-abnormal and weak tangle of blood vessels
79
Q

Relative contraindications for thrombolytics?

8

A
  1. Current AC (already on warfarin for ex) use
  2. Invasive or surgical procedure in the last 2 weeks
  3. Prolonged (CPR) defined as more than 10 minutes
  4. Known bleeding diathesis
  5. Pregnancy
  6. Hemorrhagic or diabetic retinopathies
  7. Active peptic ulcer
  8. Controlled severe hypertension.

Hematology (18 decks)

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