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PDA Block 2 > Anticoagulation > Flashcards

Anticoagulation Flashcards

1
Q

Hemostasis

A

process that prevents blood loss from damaged blood

vessels

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2
Q

3 parts of Hemostasis

A

Vasoconstriction
•  Adhesion and activation of platelets (platelet plug)
•  Formation of fibrin

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3
Q

Thrombosis

A

pathological formation of a ‘hemostatic’ plug

within the vasculature in the absence of bleeding

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4
Q

3 things that cause thrombosis

A

Injury to blood vessel wall ~ atherosclerosis, plaque rupture
•  Altered blood flow ~ veins of leg after sitting for long time
•  Abnormal coagulability of blood ~pregnancy, certain drugs, inheritable disease

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5
Q

Venous thrombosis

A

associated with red blood cells enmeshed in fibrin, often called red
thrombi

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6
Q

Where do most venous thrombi occur

A

in the superficial or deep veins of the leg

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7
Q

When is thrombosis the most dangerous

A

Deep vein Thrombosis (DVT) in the larger veins -at or above the knee is more serious because such thrombi more often embolize to the lungs and give rise to pulmonary infarction

-lower extremity DVTs are associated with hypercoaguable states

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8
Q

Arterial thrombosis

A
  • composed of platelets with little fibrin or red cells, giving the appearance of white thrombi
  • **usually occurs after the erosion or rupture of atheroscleoritc plaque
  • platelet-mediated thrombi can cause ischemic injuries in tissues with a terminal vascular be
  • **cardiac ischemia and stroke are the most severe cilnical manifestations of atherothrombosis
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9
Q

Describe the relationship between all of the major anti-coagulation drugs

A

they all have the same aim, anti-coagulation, but NOT THE SAME MECHANISM, to prevent complications of thrombosis

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10
Q

List the drugs responsible for inhibition of coagulation

anticoagulants

A
  • Heparin
  • Enoxaparin (LMWH)
  • Bivalirudin
  • Fondaparinux
  • Warfarin
  • Dabigatran
  • Rivaroxaban
  • Apixaban
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11
Q

Fibrinolytic agents/”clot-busters”

lysis of existing thrombus

A
  • Tissue plasminogen factor
  • Alteplase
  • Tenecteplase
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12
Q

Antiplatelet drugs

Inhibition of platelet aggregation

A
  •   Aspirin
  •   Abciximab/Eptifibatide
  •   Dipyridamole
  •   Clopidogrel/Ticlopidine
  •   Prasugrel/Ticagrelor
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13
Q

What is a side effect of ALL of these anticoagulant drugs

A

increased bleeding/ hemorrhage

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14
Q

Protamine sulfate

A

antagonist of heparin

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15
Q

Idarucizumab:

A

antagonist of dabigatran

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16
Q

Aminocaproic acid:

A

antagonist of thrombolytics

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17
Q

Coagulation cascade

A 
-series of transformations of proenzymes to activated enzymes
resulting in the formation of
thrombin (IIa) which converts
soluble fibrinogen to insoluble
fibrin
  • activation of Factor X to Xa
  • conversion of prothrombin (II) to thrombin (IIa)
  • thrombin-mediated transformation of fibrinogen to fibrin (the GLUE)
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18
Q

Synthesis of which factors is dependent on Vitamin K

A

II, IX, X, VII

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19
Q

heparin (unfractionated)

-physical properties

A
  • heterogenous mixture of sulfated polysaccharides
  • highly negatively charged
  • HIGH molecular weight
  • there is heterogeneity in composition in different commercial preps of heparin
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20
Q

Mechanism of action of heparin unfractionated

A
  • Antithrombin is a suicide substrate for a number of different activated coagulation factors, especially thrombin and Xa (also IXa, XIa, XIIa)
  • activated coagulation factor attacks a specific Arg-Ser peptide bond in the reactive site of AT
  • When thrombin is bound to antithrombin it becomes trapped and is inactivated
  • the way hearin works is it causes a 1000-fold increase in the reaction rate of antithrombin and thrombin inthe pressence of heparin
  • heparin serves as a catalytic template to which both AT and activated coagulation factor can bind.
  • Heparin induces a conformational change in AT making reactive site more accessible to proteases
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21
Q

Compare the ability of Unfractionated heparin vs low molecular weight heparin at catalyzing the inhibition of thrombin by AT

A

low molecular weight heparins poorly catalyze inhibition of thrombin by AT bc low molecular weight heparin isnt able to bind around antithrombin like unfractionated heparin does.

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22
Q

Name two common misconceptions about heparin, two things that heparin DOES NOT DO

A

Heparin DOES NOT-

  • affect the synthesis of clotting factors
  • does not lyse the existing clot
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23
Q

Name two things that heparin DOES DO

A

prevent further cloth formation

-prevent further extension of clot

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24
Q

How is heparin absorbed

A

it is not abrobed orally bc it is extremely large and negatively charged. it is given via IV infusion or subcutaneous injection
-Immediate onset of action if given IV

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25
Q

BRIEFLY explain the complicated kinetics of heparin

A

-Half-life dependent on dose

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26
Q

Is heparin safe to use during preganncy

A

YES it does not cross the placenta

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27
Q

How do you know heparin is working

A
  • by measuring the activated partial thromboplastin time (aPTT)
  • intrinsic and common pathway
  • Heparin is therapeutic when the aPTT is 1.5 to 2.5 times the normal mean

-this is done by collecting a blood sample with citrate to inactivate calcium and prevent clotting, then negatively charged phospholipids are added, and a particulate substance like aluminum sulfate and calcium

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28
Q

adverse reaction heparin

A

Bleeding/Hemorrhage
MAJOR ADVERSE REACTION

the bleeding is controlled with an antagonist, protamine sulfate

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29
Q

How do you treat increased bleeding that occurs as an adverse reaction from heparin

A

the antagonist protamine sulfate

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30
Q

Heparin-induced Thrombocytopenia

A
  • platelet counts decrease by 50% from normal values
  • occurs in a small number of patients (greater incidence in women)
  • can be life threatening and lead to amputation, limb ischemia, myocardial infarction, stroke
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31
Q

Mechanism for Heaparin Induced Thrombocytopenia

A

-IgG antibodies form against heparin-platelet factor 4
*Chemokine released during platelet activation/forms complex with proteoglycans like heparin
-Complex activates platelets by binding to FcγIIa receptors on the
platelet
-This causes platelet aggregation, release of PF4 and thrombin
generation; results in formation of clots and fall in platelet number

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32
Q

What do you do if someone has heparin induced thrombocytopenia

A

discontinue Heparinimmediately

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33
Q

Contraindication to the use of heparin

A

active bleeding

  • severe uncontrolled hypertension (bc of risk of hemorrhagic stroke)
  • recent surgery of eye, brain, spinal cord
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34
Q

Therapeutic clinical indications for heparin

A
  • Deep Vein Thrombosis or pulmonary embolism
  • initial treatment is heparin IV infusion
  • also low dose heparin may be used as prevention in surgical patients
  • INITIAL management of unstable angina or acute MI
  • drug of choice for anticoagulation during pregnancy bc it doesn’t cross the placenta so it is safe
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35
Q

Why is heparin not used for chronic anticoagulation use

A

it is difficult to give, it has to be given via IV so it just doesn’t really make sense to be used chronically

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36
Q

What is low molecular weight heparin called

A

Enoxaparin

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37
Q

properties of low molecular weight Heparin- Enoxaparin

A
  • it is fragments of standard MW heparins
  • administered subcutaneously
  • *has a longer half-life than heparin
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38
Q

Mechanism of action for Enoxaparin

A
  • this is low molecular weight heparin
  • Heparin normally binds to antithrombin and wraps around it and binds to thrombin to really increase their binding so AT can inactivate thrombin
  • Enoxaparin binds to just antithrombin (bc it is small and can’t wrap around) so it primarily works to inhibit the anti-thrombin Xa complex
  • Enoxaparin is a poor inactivator of thrombin bc it can’t wrap around to bind to thrombin
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39
Q

Difference in mechanism of action of unfractionate heparin and Enoxaparin

A

Enoxaprin binds to only AT and Xa

Heparin binds to AT and Xa AND 
AT andThrombin (bc it is big and can wrap around to bind to thrombin)
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40
Q

Pharmacokinetics of Enoxaparin

A
  • longer half-life than heparin: advantage in hospital setting
  • renal elimination: risk in patient with renal disease
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41
Q

Adverse effects of Enoxaparin

A
  • less risk of bleeding that unfractionated heparin

- lower risk (theoretically) of thrombocytopenia compared to heparin

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42
Q

Contraindications of Enoxaparin

A
  • similar to heparin ALSO renal impairment (bc Enoxaparin is excreted renally)
  • active bleeding, uncontrolled hypertension, recent surgery of the eye brain spinal cord
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43
Q

Therapeutic uses of Enoxaparin

A

-similar to unfractionated heparin

  • Acute DVT
  • Act and unstable angina and MI
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44
Q

other parenterally administered anticoagulations other than heparin and Enoxaparin

A
  • fondaparinux: selective Xa inhibitor, requires AT

- Bivalirudin: Direct Thrombin Inhibitors, does not require AT

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45
Q

Fondaparinux
-MOA
-Administration
Adverse effect

A
  • selective Factor Xa inhibitor
  • MOA: No effect on the AT-Thrombin complex, it only acts on the AT-Xa complex. BC just like Enoxaparin it isn’t big enough to wrap around and bind thrombin

-SQ administration: Important distinction to rivaroxaban –in
addition to different mechanism!
-hemorrhage

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46
Q

Bivalirudin

  • administration
  • MOA
  • excretion
  • adverse effect
  • contraindications
  • therapeutic use
A

DIRECT thrombin inhibitor

  • synthetic polypeptide, derived from leeches.
  • MOA: inactivate thrombin by blocking the substrate binding site in a 1:1 complex
  • doesn’t bind to/require antithrombin
  • IV administration
  • renal excretion
  • adverse side effect is hemorrhage
  • therapeutic use: alternative to heparin in patients who have had heparin-induced thrombocytoenia
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47
Q

Explain the advantages of a direct thrombin inhibitor

A

SO thrombin bund to fibrin (within a clot) within a thrombus remains enzymatically active (activates clotting factors) and is protected from inactivation b antithrombin (antithrombin cant bind to fibrin bound thrombin)

  • fibrin bound thrombin can locally activate platelets and trigger coagulation thereby causing thrombus growth
  • so drugs that are thrombin inhibitors are able to inactive thrombin even when it is bound to fibrin, but drugs (like heparin) that work via AT are not able to inhibit thrombin that is fibrin bound, bc AT can’t bind to fibrin bound thrombin
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48
Q

Protamine sulfate

A
  • Low MW, positively charged
  • chemical antagonist 1:1 binding with heparin results in an inactive complex
  • adverse effect: anaphylactic reaction
  • therapeutic use: heparin overdose with acute bleeding that cant be controlled by stopping heparin
  • reverse heaparin following cardiopulmonary bypass
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49
Q

What are the three oral anticoagulants

A
  • Warfarin
  • Dabigatran
  • Rivaroxaban
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50
Q

Warfarin physical properties

A
  • structural analog of vitamin K

- Vitamin K is in the diet in leafy greens, and is synthesized in the gut bacteria

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51
Q

How is warfarin administered

A
  • orally
  • it is administered in a racemic mixture os S-warfarin and R-Warfarin
  • S-warfarin is the more active form
52
Q

-

A

-prevents the γ-carboxylation of several
glutamate residues

-blockade results in incomplete coagulation
factor molecules that are biologically
inactive

-protein carboxylation reaction is coupled to
the oxidation of vitamin K. The vitamin
must then be reduced to reactivate it.

-S-Warfarin prevents reductive
metabolism of the inactive vitamin K
epoxide back to its active hydroquinone
form

-Competitive inhibition because Vit K
administration will displace warfarin

53
Q

How do you know warfarin is working?

A

prothrombin time (PT)

Normal INR between 0.8 and 1.2

54
Q

Why is the Therapeutic effect of warfarin not seen for several hours to days

A

-bc it inhibits the synthesis of clotting factors, and doesn’t effect the clotting factors that are already made. So it takes time for the effects to be seen
-Remember circulating factors (those already
synthesized) are not inhibited by warfarin
-End up with some already synthesized factors still around while no longer able to synthesize any more factors that can be
activated by the clotting cascade
-Depends on the half-life of the particular clotting
factor/varies with each

55
Q

absorption/metabolism/pharmacokinetics of warfarin

A

-oral administration
inactivated by liver microsomes (CYP)
-metabolized by CYP2C9 (S-warfarin)

56
Q

major adverse reaction to warfarin

A

hemorrhage

57
Q

contraindication to warfarin

A
  • similar to heparin but include:
  • CYP2C9 polymorphisms
  • genetic variations in VIt K epoxide reductase complex protein 1
  • pregnancy/teratogenic
  • Liver, kidney disease, vitamin K deficiency
58
Q

Reversal of warfarin

A
  • if INR is greater than 5 vitamin K is administered but there would be a time delay for effectiveness
  • Mechanism of delay? It take a while for new clottin g factors to be synthesized
59
Q

WHy is it important to monitor INR in patients taking Warfarin

A
  • Increased INR means increased risk for bleeding

- Decreased INR means increased risk of thrombosis

60
Q

How common are drug interactions with warfarin

A

very common CYP2C9

61
Q

Food interactions with warfarin

A

green vegetables has a lot of vitamin K and this decreases INR and causes the drug to not work as well leading to more risk of thrombosis (bc it is sort of competitive inhibition of VKORC1 with vit K so if you increase VIt K then the drug is less effective)
some food also increase INR and increase risk of bleeding

62
Q

Therapeutic clinical indications for warfarin

A

-Long-term treatment of venous thromboembolic disease.
-Prophylaxis against thromboembolism in atrial fibrillation.
-Prophylaxis against thromboembolism in patients with prosthetic
heart valves.
-Remember it takes time for warfarin to work so if you need immediate anticoagulation, will give heparin (or LMWH) followed by warfarin = bridging effect

63
Q

What is the bridging effect

A

Remember it takes time for warfarin to work so if you need immediate anticoagulation, will give heparin (or LMWH) followed by warfarin = bridging effect

64
Q

Dabigitran

A

pro-drug which is metabolized in vivo to an active entity dabigatran

65
Q

Dabigitran mechanism of action

A

-interacts with the active site of thrombin
-a potent, reversible,
competitive direct thrombin inhibitor
-inhibits both fibrin-bound
and free thrombin (rememeber if something works on the AT-thrombin complex then you can’t inactivate the thrombin when it is bound to a clot)

66
Q

Monitoring for Dabigitran

A

NONE (unlike warfarin)

67
Q

Dabigatran pharmacokinetics

A
  • oral administration, rapid onset (peak plasma levels by 2 hours)
  • short half-life
  • *it works immediately unlike warfarin
  • Not a substrate for a CYP450
  • excreted by the kidney and used therefore is carefully at doses appropriate for a patients renal function
68
Q

Dabigatran adverse effects

A
  • risk of bleeding
  • w/o antidote: reversal of dabigatran’s effects depends on excretion, with a plasma half-life of 14 hours
  • w antidote: Idarucizumab binds to dabigatran and neutralizes the anticoagulant effect within minutes
69
Q

Idarucizumab:

A

humanized monoclonal antibody fragment (Fab) that binds to dabigatran and neutralizes the anticoagulant effect within minutes

70
Q

Disease related concerns for dabigatran

A

renal impairment: concentrations may increase in any degree of renal impairment and increase the risk of bleeding

-Valvular heart disease: not recommended in patients with bioprosthetic heart valves
•  contraindicated in patients with mechanical prosthetic heart valves

71
Q

What is the only drug interaction with Dabigatran

A

P-glycoprotein limits oral absorption of drugs by transporting them back into the GI
-so P-glycoprotein could limit oral absorption

72
Q

Therapeutic use Dabigatran

A

-patients with nonvalvular atrial fibrillation at risk for
stroke or systemic embolism

-Not recommended for patients with coexisting prosthetic heart valve

73
Q

Rivaroxaban

A

direct factor Xa inhibitor

74
Q

Factor Xa

A

primary site of amplification of thrombin generation bc it is activated by both the intrinsic and extrinsic pathway

75
Q

Factor Xa inhibition

A
  • rivaroxaban
  • apixaban
  • inhibition decreases the amplified generation of thrombin without affecting existing thrombin levels
  • this remaining thrombin should be sufficient to ensure primary hemostasis, resulting in a favorable safety margin
  • so basically it decreases thrombin levels but keeps it at a safe enough level bc it just decreases amplification of thrombin not production
76
Q

Rivaroxaban- Mechanism of action

A
  • inhibits both free Factor Xa and Factor Xa in the prothrombinase complex
  • capable of gaining access to clotbound Factor Xa
  • the resulting inhibition of clot-bound Factor Xa prevents extension of the thrombus by blocking further generation of thrombin from within the clot
77
Q

Rivaroxaban Pharmacokinetics

  • administration
  • metabolism
  • elimination
A

-oral administration with rapid onset of action (peak by four hours)

  • metabolism 2 ways
    1. hepatic by CYP3A4/5 and CYP2J2
    2. CYP-independent mechanism
  • a dual mode of elimination
  • 2/3 of drug undergoes metabolic degradation in the liver
  • 1/3 of dose is eliminated as unchanges drug in the urine
  • It is a substrate for P-glycoprotein
78
Q

Major adverse effect of Rivaroxaban

A

bleeding

79
Q

Drug interactions for Rivaroxaban

A
  • CYP3A4 inhibitor/inducers

- P-glycoprotein inhibitors/inducers

80
Q

monitoring of Rivaroxaban

A

-In major clinical trials, monitoring of aPTT, PT/INR, or
anti-factor Xa levels did not occur.

-However, certain patient populations (eg, renal
insufficiency, hepatic impairment, low body weight,
extreme obesity) may require monitoring of the PT time

81
Q

Therapeutic use of Rivaroxaban

A

patients with nonvalvular atrial fibrilation at risk for stroke or systemic embolism, similar to dabigatran

82
Q

Apixaban

A

inhibits Xa

  • oral drug with reduced bioavailability
  • CYP P450 metabolism
  • Cleared by kidney (unmetabolized)
  • same concerns in patients as rivaroxaban
  • same clinical use as rivaroxaban
83
Q

NOAC

A

New Oral Anticoagulants

84
Q

What are the advantages to NOAC compared to warfarin

A
  • NOAC has faster onset and offset : reduces the need for “bridgin” in patients at high risk for thrombosis
  • absence of food interactions
  • few strong drug interactions
  • greater convenience for patients and physicians (less monitoring)
  • wide therapeutic window
  • fewer adverse side effects
  • lower risk of bleeding complications
85
Q

Disadvantages of NOAC compared to warfarin

A
  • Severe chronic kidney disease (don’t use or use lower dose)
  • More expensive
  • No specific antidote
  • *exception is new antidote for dabigitran
86
Q

List the thrombolytic agents

A
  •   Aminocaproic Acid
  •   Tissue Plasminogen Activator (t-PA)
  •   Alteplase
  •   Tenecteplase
87
Q

What is the triggering event in an MI

A

obstruction of coronary artery by thrombus (platelet origin)

88
Q

Reperfusion therapy

A

-thrombolytics (pharmacological reperfusion)

89
Q

T o dissolve clots plasminogen is converted to

A

plasmin (active version)

90
Q

Describe the cleavage of plasminogen (inactive precursor) to plasmin (active)

A
  • cleavage of single peptide bond
  • generation of a two chain disulfide linked molecule
  • Exposes the kringles
91
Q

Endogenous activator of plasminogen to plasmin

A

t-PA

92
Q

t-PA

A

Tissue Type plasminogen activator cleaves plasminogen to plasmin.

It is inhibited (a lot at the beginning of clot formation so that the brand new clot isn’t broken up)

inhibited by t-PA-I

93
Q

What happens to the free plasmin

A

FREE Plasmin inactivated by α2-antiplasmin

94
Q

Explain theconversion of plasminogen to plasmin

A
  • cleavage of Arg560 resulting in two-chained disulfide linked molecule
  • Exposes lysine-binding sites (kringles): bind fibrin
  • Cleavage initiated by plasminogen activators
  • Activity of t-PA controlled by endogenous inhibitors (PAI-1, PAI-2)
  • FREE Plasmin inactivated by α2-antiplasmin
95
Q

Alteplase

A
  • tissue Plasminogen activator (t-PA)
  • produced by recombinant DNA technology
  • activates bound plasminogen several hundred- fold more rapidly than free plasminogen
  • very short half-life/requires I infusion
96
Q

Tenecteplase

A
  • tissue-Plasminogen Activator (t-PA)
  • produced by recombinant DNA technology
  • longer half-life bc is resistant to the inhibitor
  • single bolus administration
  • resistant to inhibition of PAI-1
97
Q

What is the advantage of fibrin specificity

A

to limit systemic lysis/ increase bleeding risk

98
Q

Complications of thrombolytic therapy

A

Hemorrhage-systemic lytic state results from systemic formation of plasmin

but hemorrhage is just as common as with t-PA

-more bleeding combinations if combined with heparin and or aspirin

99
Q

therapeutic Indications for thrombolytic therapy

A
  • acute MI (STEMI)

- stroke ( only alteplase): within first 3 hours

100
Q

describe the contraindications of thrombolytic therapy

A

bleeding

some effects are absolute and some are relative

101
Q

Aminocaproic acid

A

a potent inhibitor of fibrinolysis

-lysine analog that binds to lysine binding sites on
plasminogen and plasmin thus blocking the binding
of plasmin to fibrin

102
Q

Low dose aspirin-Platelets

A 
-Irreversibly acetylates
cyclooxygenase-1 in
platelet
•  No COX-2 in platelet
-Blocks production of
thromboxane 
-Platelets lack nuclei so
permanant effect of  aspirin
103
Q

Low dose aspiring other cell types than platelets

A

Endothelial cells produce
prostacyclin (do have COX-1 and COX-2) but endothelial cells have a nucleus and can just synthesize more COX, so the effects don’t last as long, whereas platelets do not have a nucleus

104
Q

Adverse effects of aspirin

A
  • Bleeding

- GI-dose related

105
Q

Therapeutic uses of low dose aspirin

A

MI prophylaxis

stroke prophylaxis

106
Q

Dipyridamole

A

-Both a vasodilator and inhibitor of platelet aggregation
MOA:
*inhibition of phosphodiesterase
(probably both PDE3 and PDE5)
* this increases cAMP in platelet
*Inhibits platelet aggregation
-Therapeutic use: in combination with aspirin for prevention of MI or TIA

107
Q

Clopidogrel, Ticlopidine, Prasugrel, Ticagrelor

-MOA

A

-act through P2Y1
/P2Y12 receptors to inhibit ADP- induced platelet aggregation
-All are irreversible
EXCEPT ticagrelor

108
Q

Disadvantage of irreversible platelet inhibitor ?

A

If patient requires surgery (like coronary bypass
surgery) and is taking drug like clopidogrel (or
aspirin), waiting period is necessary to prevent
platelet function to return to normal.

109
Q

Clopidogrel, Ticlopidine, Prasugrel, Ticagrelor Pharmacokinetics

A

Prasugrel is a prodrug

Clopidogreal and Ticlopidine are prodrugs that are metabolized to active compound by CYP2C9

110
Q

Prasugrel

A
  • prodrug
  • increased potency because more efficient generation of active metabolite
  • More predictable effects on platelets than other P2Y antagonist drugs
111
Q

Clopidogrel, Ticlopidine, Prasugrel, Ticagrelor

adverse effects

A
  • Bleeding all drugs
  • Ticagrelor specific dyspnea
  • Ticlopidine neutropenia
112
Q

Clopidorgrel adverse reactions

A
  • 3-20% of poopulation have CYP2C19 polymorphism
  • poor metabolizers
  • Means that individuals don’t get as much active drug bc clopidrogrel is a prodrug and requires CYP2C19 to activate it
113
Q

What is another drug that is metabolized by 2C19

A

Omeprazole

114
Q

therapeutic Indications for antiplatelets drugs

A

-used in cases where there is increase risk of platelet aggregation that contributed to thrombus

115
Q

Clopidogrel therapeutic indications

A

STEMI (occlusive thrombus)

recent myocardial infarction

116
Q

Abciximab

A

-Fab fragmen
-Prevents binding of fibrinogen,
vW factor, and other adhesive molecules
-Steric hindrance a/o
conformational change
*blocks access of the molecules to
the receptor
-non-competitive

117
Q

Eptifibatide

A 
Contains a  KGD (Lys-Gly-Asp)
sequence motif  that binds
specifically to  GP IIb-IIIa
receptors on the platelet surface,
thereby blocking the binding of
fibrinogen activated platelets
-competitive reversible inhibitor
118
Q

Pharmacokinetics of Abciximab

A
  • IV administration
  • quick onset of action but delayed clearance
  • effective up to t7 days
119
Q

Pharmacokinetics of Eptifibatide

A
  • IV Administration
  • quick onset
  • quick offset 9platelet aggregation normal within 18 hours of stopping the drug
  • renal clearance
120
Q

Adverse effects of Eptifibatide and Abciximab

A

bleeding

121
Q

Clinical use Eptifibatide

A 
Patients undergoing
percutaneous coronary
intervention (PCI),
including angioplasty or
stent placement
122
Q

Clinical use Abciximab

A

Patients undergoing percutaneous coronary intervention (PCI) including angioplasty or stent placement

123
Q

Acute deep vein thrombosis (DVT) or pulmonary embolism (PE)

A

think heparin

124
Q

Chronic prevention of DVT or PE

A

think warfarin or NOAC

125
Q

Acute coronary syndrome

A

think thrombolytic

prevention: think aspriin

126
Q

stroke

A
  • think thrombolytic if within 3 hours

- prevention: think aspirin

127
Q

Atrial Fibrillation

A

-think warfarin or NOAC unless there is artificial value then think warfarin

PDA Block 2 (13 decks)

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