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Year 2 CV > Exam 2 anticoagulants martin DSA and Lect > Flashcards

Exam 2 anticoagulants martin DSA and Lect Flashcards

1
Q

What are names of anticoagulant drugs

A

warfarin, heparin, LMWH, fondaprinuxm dabigatran, rivaroxaban, apixaban

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2
Q

what are the direct thrombin inhibitors

A

lepirudin, bivalirudin, argatroban

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3
Q

what are the antiplatelet drugs

A

aspirine, clopidogrel, prasugrel, cilostazol, dipyridamole, abciximab, eptifibatide, tirofiban

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4
Q

what are the thrombolytic drugs

A

rt-PA

ateplase, reteplase, tenecteplase, streptokinase

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5
Q

what are the differences between arterial thromboses and venous ones

A

arterial are white clots with many platelets

venous are red clots with lots of fibrin, due to stasis in venous circulation

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6
Q

what is the drug of choice for parenteral anticoagulant theraphy

A

heparin or unfractionated heparin

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7
Q

what is themechanism of heparin

A

binds to antithrombin III
then that complex will inactivate thrombin, Xa IXa XIa and XIIA
common and intrinsic pathways

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8
Q

What lab tests does haparin cause a prolonged time in

A

aPTT and the thrombin time

at high doses can prolong PT

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9
Q

How do we usually administer heparin

A

large IV bolus loading dose then continuous IV

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10
Q

When do we use SQ minidose of heparin

A

post surgery prophylaxis

now often use LMWH

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11
Q

Why is heparin not given IM

A

may cause huge hematoma

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12
Q

What do we use heparin for not on humans

A

to clear IV lines

heparin lock solution

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13
Q

what are the general pharmokinetics of heparin

A

immediate

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14
Q

where in the body is heparin metabolized

A

in liver or excreted unchanged

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15
Q

What are indications of heparin therapy

A 
prophylaxis of postoperative thrombosis
MI and unstable angina
extracorporal circulation
DIC
TIA
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16
Q

small doses of heparin are used for what

A

prevention thromboembolism

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17
Q

patient already has DVT to prevent propagation what woul dyou give

A

medium dose heparin

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18
Q

large doses of heparin are used when

A

inhibit established pulmonary embolus

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19
Q

what are signs of heparin toxicity

A

hemorrhage
hematoma at injection site
platelet aggregation, thrombocytopenia or HIT syndrome
acute HS, alopecia, osteoporosis and priapism

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20
Q

What is the initial Tx for heparin overdose

A

stop administration and infuse fresh frozen plasma to get protein levels up
or protamine sulfate if previous is not sufficient

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21
Q

how does protamine sulfate help with heparin toxicity

A

binds and inactivates heparin, must be given slowly IV

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22
Q

Describe HIT type I

A

transient reversible clumping of platelets
platelet count >100,000
usually occurs first few days of therapy
asymptomatic and recover ok

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23
Q

Describe HIT type II

A

delayed onset 5-14 days
severe thrombocytopenia
immune mediated reaction, heparin Ab complex causing platelet aggregation
peripheral thrombosis may lead to stroke, acute MI, skin necrosis
Amputation is necessary in up to 25% patients with type II HIT

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24
Q

how prevalent is type II HIT

A

3% of patients treated with heparin

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25
Q

what are contraindications of heparin

A 
any site of active or potential bleeding
severe HTN or known vascular aneurysm
recent hear, eye or spinal cord surgery
head trauma
lumbar punture or regional anesthetic block
TB, visceral carcinoma, GI ulcers
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26
Q

What do you test before starting heparin therapy

A

aPTT

goal is to be 1.5-2x the control

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27
Q

What are the names of the LMWH drugs

A

enoxaparin (lovenox), dalteparin, tinzaparin

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28
Q

What is the advantage of LMWH compared to regular heparin

A

smaller pieces
more specific to Xa activity, less anti-platelet activity
longer duration, simpler kinetics, clotting tests not usually required

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29
Q

what do we use LMWH for

A

SQ injection for prophylaxis of DVT associated with hip, knee, abdominal surgery

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30
Q

LMWH does not bind what factor as much as regular heparin does

A

thrombin

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31
Q

is aPTT monitoring or INR needed for LMWH

A

no

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32
Q

does heparin bind endothelial cells? LMWH?

A

heparin does, LMWH does not

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33
Q

which heparin has a longer elimnation half life

A

LMWH 2-5x longer

34
Q

what is the mechanism of warfarin

A

inhibits Vit K epoxide reductase so then secondarily inhibits thrombin, VII, IX, X Protein C and S

35
Q

what are the general pharmokinetics of warfarin

A 
delayed onset (~ 3days)
prolonged duration (25-60 hour t1/2)
rapid and complete absorption, 99% bound to albumin
delayed termination inliver and kidney metabolism
36
Q

how long does it take for warfarin to reach plateau therpeutically

A

~ 5 days becasue 5x half life

37
Q

what are the effects of warfarin

A

hemorrhage
anorexia, nausea, vomiting, diarrhea
skin necrosis

38
Q

what are the contraindications of warfarin

A 
pregnant patients-->congenital abnormalities
unreliable patient
any recent bleeding
recent eye brain or spinal cord surgery
severe HTN or known vascular aneurysm
39
Q

what are indications for warfarin

A

overlap with heparin therapy to avoid long delay in onset of action

  • DVT
  • PE
  • AFib
  • Rheumatic heart disease
  • Mechanical prosthetic heart valves
40
Q

how is warfarin administered

A

orally

41
Q

how do we determine the appropriate does of warfarin in patients

A

INR according to PT time

usual target is 2-3

42
Q

when do we usually start warfarin therapy

A

same time as heparin because takes 5 days to plateau

43
Q

Why is there such great variability with warfarin in patients

A

differences in absorption, elimination, liver function and drug-drug interactions
noncompliant and unreliable patients are not good candidates for warfarin therapy

44
Q

what drugs increase response to warfarin from unknown mech

A

acetaminophen, androgens, betablockers, corticosteroids, erythromycin, fluconazole, glucagon, isoniazid, sulfonamides, thioamides, thyroid hormones

45
Q

what drugs increase response to warfarin via inhibition of the anticoagulants hepatic metabolism

A 
cimetidine
lovastatin
metronidazole
omeprazole
quinidine
46
Q

what drugs increase warfarin because the displace it from plasma binding sites

A

chloral hydrate
loop diuretics
nalidixic acid

47
Q

what drugs increase warfarin activity from interference with Vit K

A

aminoglycosides, mineral oil, tetracyclines, Vit E

48
Q

what drugs increase anticoagulant effects of warfain because effect platelet function

A

cephalosporins, difunisal
NSAIDs
penicillins
salicylates

49
Q

what drug drug interaction mechanisms cause a decrease in warfarin activity

A

inductino of hepatic microsomal enzymes and increased metabolism
decrease absorption, increased synthesis of clotting factors
hemoconcentration clotting factors, by pass of site of action
or unknown

50
Q

what is dabigatran

A

a direct thrombin inhibitor

51
Q

describe general pharmokinetics of dabigatran and how is it taken

A

oral
peak 1 hour
half life 12-17 hours

52
Q

how does dabigatran work

A

rapid onset, no need for monitoring INR

binds thrombin and decreases thrombin stimulated platelet aggregation

53
Q

What has dabigatran been approved for by FDA

A

non valvular AF

54
Q

How do rivaroxaban and apixaban work

A

direct factor Xa inhibitors

55
Q

what are rivaroxaban and apixaban used for

A

oral anticoagulant for management of venous thromboembolism or stroke prevention in patients with non valvular AF

56
Q

Why are the newer drugs (antithrombolytics) better than warfarin

A

less sideeffects, less drug drug interactions

57
Q

What are direct thrombin inhibitors? and when are they used

A

no not require other proteins like antithrombin III for activity
approved for patients with HIT and during coronary angioplasty

58
Q

what are the names of direct thrombin inhibitors

A

hirudin, lepirudin, bivalirudin, argatroban

59
Q

antiplatelet drugs main target is what

A

thromboxane A2 TXA2

60
Q

How does aspirin work

A

at very low doses irreversibly inhibits COX 1 and 2

block TXA2 formation so 7-10 days for new platelets

61
Q

what occurs at higher doses of aspirin

A

inhibit enzyme in endothelial cells and prevent formation PGI2 which inhibits platelet secretion and stimulates vasodilation

62
Q

What are main uses for aspirin

A

MI
secondary prevention of MI and stroke
prevention of CV disease
reduction of thromboembolic complications in patient with artificial ehart valves, hemodialysis, coronary bypass grafts

63
Q

What is clopidogrel used for

A

prophylaxis of stroke, MI, peripheral artery disease and acute coronary syndrome

64
Q

how does clopidogrel work

A

irreversibly inhibits platelet adenosine diphosphate R and block activation of glycoprotein GPIIb/IIIa complex. Inhibits fibrinogen binding and platelet aggregation

65
Q

what is a not so good effect of clopidogrel

A

since irreversibly inhibits the ADP R, platelets exposed to clipodogrel are affected for remainder of lifespan

66
Q

a deficiency in GpIIb-IIIa is called what

A

Glanzmanns thrombasthenia

67
Q

a deficiecny in GpIb is called what

A

bernard soulier syndrome

68
Q

What is abciximab and how does it woek

A

a monoclonal Ab that prevents fibrinogen binding to glycorotein GP IIb-IIIa thus inhibiting platelet agregation

69
Q

when is abciximab sed

A

antithrombotic during angioplasty/PCI

70
Q

What is a common complaint after dipyridamole therapy

A

HA

71
Q

how does cilostazol work

A

inhibits PDEIII so increases cAMP
inhibits platelet aggregation
stimulates vasodilation
indicated for reduction of Sx of intermittent claudication

72
Q

What is cilostazole primarily used to Tx

A

intermittent claudication from peripheral arterial disease

contraindicated in patients with CHF

73
Q

What are the biggest problems with thrombolytics

A

bleeding

74
Q

what are the thrombolytic drugs

A

alteplase, reteplase, tencteplase and streptokinase

75
Q

What normally causes clots to dissolve

A

plasmin which was activated by tPA or urokinase

76
Q

describe how fibrinolysis is controlled

A

fast clearance tPA from inhibitor and also that tPA has higher affinity for firbinogen bound clots than free fibrinogen in circulation

77
Q

what are indications for thrombolytic therapy

A

AMI
PE
DVT
ischemic stroke (special circumstances only)

78
Q

how is tPA administered and what is adverse effect

A

IV bolus followed by IV infusion

serious hemorrhage

79
Q

what are the fibrinolytic drugs

A

reteplase and tenecteplase

80
Q

why is tenecteplase becoming the drug of choice for fibrinolytics

A

single bolus is given over 5-10 secnds
as effective as alteplase
easier to administer

81
Q

how does streptokinase work

A

nonenzymatic activator of plasminogen, extracted from hemolytic streptococci

82
Q

what is potential side effects of streptokinase

A

serious hemorrhage

Year 2 CV (31 decks)

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