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Cardiovascular 2 > Thromboembolic Disorder Drugs - Konorev > Flashcards

Thromboembolic Disorder Drugs - Konorev Flashcards

1
Q

White thrombus

  • Seen where?
  • Seen when?
A

Platelet-endothelium aggregation, little fibrin

  • High pressure arteries
  • Ischemia via coronary occlusion (MI or unstable angina)
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2
Q

Red thrombus

  • Seen where?
  • Seen when?
A

Fibrin-rich with trapped RBCs in fibrin tails

  • Low pressure veins, and in heart
  • Embolic stroke, pain and severe swelling
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3
Q

Anticoagulant drugs - function

Used when?

A

Regulate clotting factors

  • Used to prevent red thrombi (veins, heart)
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4
Q

Anti-platelet drugs - function

Used when?

A

Inhibit platelet aggregation

  • Used to prevent white thrombi (arteries)
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5
Q

Thrombolytics - function

Used when?

A

Destroy clots

  • Used to re-establish flow once clots have formed
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6
Q

2 types of anticoagulants

A
  • Parenteral

- Oral

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7
Q

2 types of parenteral anticoagulants

A
  • Indirect thrombin/factor Xa inhibitors

- Direct thrombin inhibitors

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8
Q

3 classes of indirect thrombin/Xa inhibitors (w/ members)

A 
Unfractionated heparins
   - Heparin sodium
Low molecular weight heparins
   - ...-aparin (x3)
Synthetic pentasaccharide
   - Fondaparinux
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9
Q

Indirect thrombin/Xa inhibitors - mechanism of action

A

Increase ANTITHROMBIN 3 activity by binding to it and TOGETHER binding/inactivating factor Xa (at least)

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10
Q

Contrast the 3 indirect thrombin/Xa inhibitors

A

HMW (unfractionated) Heparin - binds/inhibits BOTH

LMW Heparin - binds/inhibits factor Xa mostly

Fondaparinux - inhibits Xa only

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11
Q

Using HMW vs. LMW Heparin

A

LMW - less frequent injections, more predictable dosing

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12
Q

Uses for Heparin

A

Red thrombi prevention

  • Protect against embolic stroke/pulmonary emboli
  • DVT, atrial arrhythmias
  • Emboli prevention during surgery/hospital
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13
Q

Monitoring Heparin use

A
  • aPTT should be longer (50-75 sec vs. 30-50 sec)

- Anti-Xa assay

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14
Q

Adverse effects of Heparin

A
  • Bleeding

- Thrombocytopenia, thrombosis (platelet/immune complex)

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15
Q

Contraindications to Heparin use

A
  • Severe HTN
  • Active TB
  • GI ulcers
  • Recent surgery
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16
Q

A patient on heparin begins developing multiple thrombi. How to treat?

A

Stop heparin, give DTI

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17
Q

How to stop heparin action?

A

Protamine sulfate

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18
Q

Fondaparinux - function

Indications?

A

Bind/stimulate antithrombin 3 –> inactivate factor Xa

  • Prevent DVT
  • Treat DVT (w/ warfarin)
  • Treat pulmonary embolism
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19
Q

How is Fondaparinux unlike Heparin? (3)

A
  • Does not inhibit thrombin
  • Does not induce HIT
  • NOT reversed by protamine sulfate
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20
Q

Direct thrombin inhibitors (parenteral) - MoA

A

Directly inhibit auto-protease activity of thrombin

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21
Q

2 types of direct thrombin inhibitors (and drugs)

A 
Bivalent (bind active site AND substrate site)
   - Lepirudin
   - Bivalirudin
Bind active/catalytic site ONLY
   - Argatroban
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22
Q

Contrast function of 3 direct thrombin inhibitor drugs

A

Lepirudin - irreversible inhibitor
Bivalirudin - reversible inhibitor + platelet inhibitor
Argatroban - short-acting/IV

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23
Q

Clinical uses for direct thrombin inhibitors

A
  • HIT

- Coronary angioplasty (reversible inhibitors)

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24
Q

Adverse effect of direct thrombin inhibitors

A
  • Bleeding
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25
Q

Adverse effect of long-term LEPIRUDIN (irreversible inhibitor)

A

Anaphylactic reaction (allergic)

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26
Q

2 types of oral anticoagulants

A
  • Coumarin (Warfarin)

- Novel oral anticoagulants (NOAC)

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27
Q

Warfarin - MoA (2)

A
  • Inhibit vitamin K reactivation via vitatmin K epoxide reductase
  • Inhibit carboxylation/activation of factors via GGCX
28
Q

Which factors are inhibited by warfarin?

A

Prothrombin, 7, 9, 10

29
Q

Warfarin pharmacokinetics

A

Oral, 100% bioavailability, delayed onset, long half life,
99% BOUND TO ALBUMIN

R-isomer - CYP3A4 metabolism
S-isomer - CYP2C9 metabolism

30
Q

Major thing to know about Warfarin

A

Significant individual variability in dose based on disease state, genetics, etc.

31
Q

Clinical uses of warfarin

A
  • Prevent thrombosis or thromboembolism
  • A. fib.
  • Prosthetic heart valves
32
Q

Adverse effects of warfarin

A
  • TERATOGENIC (NOT in PREGNANCY)
  • Skin necrosis, organ infarction
  • Osteoporosis
  • Bleeding
33
Q

How to dose Warfarin?

A
  • Based on PT (prothrombin time)
  • VKORC1 haplotype
  • CYP2C9
34
Q

VKORC1 haplotypes

A 
High dose (resistant) - more in african americans
Low dose - more in asians
35
Q

Diseases to be cautious of when giving warfarin

A
  • Liver disease (where clotting factors are made)

- Thyroid status

36
Q

Benefits of warfarin

A
  • Oral, long duration, renal function not important

- CAN REVERSE IT

37
Q

How to reverse Warfarin? (2)

A
  • Administer vitamin K (12-24 hours)

- FFP or prothrombin complex concentrate (rapid)

38
Q

Drawbacks of warfarin

A
  • High dosing variability, hard to maintain concentration
  • Bleeding complications
  • Requires INR monitoring
39
Q

NOAC factor Xa inhibitors - suffix

A

-xaban (x3)

40
Q

Clinical use of NOAC factor Xa inhibitors

A
  • Prevent/treat thromboembolism

- Prevent stroke w/ A. fib.

41
Q

Advantages of NOAC factor Xa inhibitors

A
  • Oral
  • Fixed doses, no monitoring
  • Seems equal to Warfarin
  • RAPID ONSET compared to Warfarin
42
Q

Drawbacks of NOAC factor Xa inhibitors

A
  • No antidotes

- Dose adjustment in renal disease (renal excretion)

43
Q

Dabigatran

- Clinical use

A

NOAC direct thrombin inhibitor

- Reduce risk of stroke and embolism w/ A. fib

44
Q

Advantages to Dabigatran (compared to Warfarin)

A
  • Predictable pharma and bioavailability
  • Fixed dosing and action
  • Rapid onset and offset
45
Q

Disadvantage to Dabigatran

A
  • 80% renal excretion (not good for renal patients)
46
Q

4 classes of anti-platelet drugs

A
  • TxA2 synthesis inhibitors
  • ADP receptor blockers
  • Platelet glycoprotein receptor blockers
  • Phosphodiesterase inhibitors
47
Q

TxA2 synthesis inhibitor

MoA?
Use?
Adverse effects?

A

Aspirin

  • COX inhibition
  • Prevent M.I. and other vascular events
  • Peptic ulcer, GI bleeding
48
Q

ADP receptor blockers - names (4)

A
  • Clopidogrel
  • Prasugrel
  • Ticlopidine
  • Ticagrelor
49
Q

ADP receptor blockers - MoA

A
  • Inhibit receptor –> ACTIVATES A.C. –> increased cAMP
50
Q

Phosphodiesterase inhibitors - MoA

A
  • Inhibition of cAMP degradation

- Increased platelet cAMP

51
Q

Phosphodiesterase inhibitors - names (2)

A
  • Dipyridamole

- Cilostazol

52
Q

Clinical uses of ADP receptor blockers

A
  • Prevent arterial thrombosis in stroke
  • Prevent thrombosis w/ ACS and recent MI, stroke, peripheral vascular disease
  • Patients undergoing PCI and stenting
53
Q

Clinical uses of Dipyridamole (PDE inhibitor) (2)

A
  • In combo w/ aspirin to prevent cerebrovascular ischemia

- In combo w/ warfarin to prevent thromboembolic w/ prosthetic valves

54
Q

Clinical use of Cilostazol (PDE inhibitor)

A

Intermittent claudication

55
Q

Adverse effects of Ticlopidine (ADP receptor blocker)

A
  • TTP, GI stuff, leukopenia
56
Q

A patient is on Ticlopidine, but has blotching on his skin. What to give instead?

A

Another ADP receptor blocker (Clopidogrel, Prasugrel, Ticagrelor)

57
Q

Function of platelet glycoprotein (GP) receptor antagonists

A

Prevent binding of fibrinogen to platelets for aggregation

58
Q

Clinical use of platelet glycoprotein (GP) receptor antagonists

A
  • Prevent thrombosis in unstable angina
  • Coronary angioplasty
  • W/ other anti-platelet agents
59
Q

Adverse effects of platelet glycoprotein (GP) receptor antagonists

A
  • Hypotension, myalgia, thrombocytopenia
60
Q

Platelet glycoprotein receptor antagonists - drugs

A
  • Abciximab (Anti-2b/3a monoclonal Ab)
  • Tirofiban (2b/3a antagonist)
  • Eptifibatide (2b/3a antagonist)
61
Q

3 types of thrombolytic (fibrinolytic) drugs

A
  • tPA - cleaves plasminogen
  • Urokinase - cleaves plasminogen
  • Streptokinase - converts plasminogen to plasmin
    • Purified from bacteria
62
Q

tPA drugs - suffix

A

-plase (x3)

63
Q

Clinical uses of fibrinolytic drugs

A
  • Embolic/thrombotic stroke
  • M.I.
  • Pulmonary embolism
  • DVT
  • Ascending thrombophlebitis
64
Q

When should fibrinolytic drugs be used?

A

WITHIN 3 HOURS

65
Q

Adverse effects of fibrinolytic drugs

A
  • Bleeding from the fibrinogenolysis

- Allergic reactions (streptokinase)

Cardiovascular 2 (20 decks)

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