Exam 2 anticoagulants martin DSA and Lect Flashcards Preview

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Flashcards in Exam 2 anticoagulants martin DSA and Lect Deck (82):
1

What are names of anticoagulant drugs

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

2

what are the direct thrombin inhibitors

lepirudin, bivalirudin, argatroban

3

what are the antiplatelet drugs

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

4

what are the thrombolytic drugs

rt-PA
ateplase, reteplase, tenecteplase, streptokinase

5

what are the differences between arterial thromboses and venous ones

arterial are white clots with many platelets
venous are red clots with lots of fibrin, due to stasis in venous circulation

6

what is the drug of choice for parenteral anticoagulant theraphy

heparin or unfractionated heparin

7

what is themechanism of heparin

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

8

What lab tests does haparin cause a prolonged time in

aPTT and the thrombin time
at high doses can prolong PT

9

How do we usually administer heparin

large IV bolus loading dose then continuous IV

10

When do we use SQ minidose of heparin

post surgery prophylaxis
now often use LMWH

11

Why is heparin not given IM

may cause huge hematoma

12

What do we use heparin for not on humans

to clear IV lines
heparin lock solution

13

what are the general pharmokinetics of heparin

immediate

14

where in the body is heparin metabolized

in liver or excreted unchanged

15

What are indications of heparin therapy

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

16

small doses of heparin are used for what

prevention thromboembolism

17

patient already has DVT to prevent propagation what woul dyou give

medium dose heparin

18

large doses of heparin are used when

inhibit established pulmonary embolus

19

what are signs of heparin toxicity

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

20

What is the initial Tx for heparin overdose

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

21

how does protamine sulfate help with heparin toxicity

binds and inactivates heparin, must be given slowly IV

22

Describe HIT type I

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

23

Describe HIT type II

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

24

how prevalent is type II HIT

3% of patients treated with heparin

25

what are contraindications of heparin

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

26

What do you test before starting heparin therapy

aPTT
goal is to be 1.5-2x the control

27

What are the names of the LMWH drugs

enoxaparin (lovenox), dalteparin, tinzaparin

28

What is the advantage of LMWH compared to regular heparin

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

29

what do we use LMWH for

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

30

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

thrombin

31

is aPTT monitoring or INR needed for LMWH

no

32

does heparin bind endothelial cells? LMWH?

heparin does, LMWH does not

33

which heparin has a longer elimnation half life

LMWH 2-5x longer

34

what is the mechanism of warfarin

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

35

what are the general pharmokinetics of warfarin

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

how long does it take for warfarin to reach plateau therpeutically

~ 5 days becasue 5x half life

37

what are the effects of warfarin

hemorrhage
anorexia, nausea, vomiting, diarrhea
skin necrosis

38

what are the contraindications of warfarin

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

39

what are indications for warfarin

overlap with heparin therapy to avoid long delay in onset of action
-DVT
-PE
-AFib
-Rheumatic heart disease
-Mechanical prosthetic heart valves

40

how is warfarin administered

orally

41

how do we determine the appropriate does of warfarin in patients

INR according to PT time
usual target is 2-3

42

when do we usually start warfarin therapy

same time as heparin because takes 5 days to plateau

43

Why is there such great variability with warfarin in patients

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

44

what drugs increase response to warfarin from unknown mech

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

45

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

cimetidine
lovastatin
metronidazole
omeprazole
quinidine

46

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

chloral hydrate
loop diuretics
nalidixic acid

47

what drugs increase warfarin activity from interference with Vit K

aminoglycosides, mineral oil, tetracyclines, Vit E

48

what drugs increase anticoagulant effects of warfain because effect platelet function

cephalosporins, difunisal
NSAIDs
penicillins
salicylates

49

what drug drug interaction mechanisms cause a decrease in warfarin activity

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

what is dabigatran

a direct thrombin inhibitor

51

describe general pharmokinetics of dabigatran and how is it taken

oral
peak 1 hour
half life 12-17 hours

52

how does dabigatran work

rapid onset, no need for monitoring INR
binds thrombin and decreases thrombin stimulated platelet aggregation

53

What has dabigatran been approved for by FDA

non valvular AF

54

How do rivaroxaban and apixaban work

direct factor Xa inhibitors

55

what are rivaroxaban and apixaban used for

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

56

Why are the newer drugs (antithrombolytics) better than warfarin

less sideeffects, less drug drug interactions

57

What are direct thrombin inhibitors? and when are they used

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

58

what are the names of direct thrombin inhibitors

hirudin, lepirudin, bivalirudin, argatroban

59

antiplatelet drugs main target is what

thromboxane A2 TXA2

60

How does aspirin work

at very low doses irreversibly inhibits COX 1 and 2
block TXA2 formation so 7-10 days for new platelets

61

what occurs at higher doses of aspirin

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

62

What are main uses for aspirin

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

What is clopidogrel used for

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

64

how does clopidogrel work

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

65

what is a not so good effect of clopidogrel

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

66

a deficiency in GpIIb-IIIa is called what

Glanzmanns thrombasthenia

67

a deficiecny in GpIb is called what

bernard soulier syndrome

68

What is abciximab and how does it woek

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

69

when is abciximab sed

antithrombotic during angioplasty/PCI

70

What is a common complaint after dipyridamole therapy

HA

71

how does cilostazol work

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

72

What is cilostazole primarily used to Tx

intermittent claudication from peripheral arterial disease
contraindicated in patients with CHF

73

What are the biggest problems with thrombolytics

bleeding

74

what are the thrombolytic drugs

alteplase, reteplase, tencteplase and streptokinase

75

What normally causes clots to dissolve

plasmin which was activated by tPA or urokinase

76

describe how fibrinolysis is controlled

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

77

what are indications for thrombolytic therapy

AMI
PE
DVT
ischemic stroke (special circumstances only)

78

how is tPA administered and what is adverse effect

IV bolus followed by IV infusion
serious hemorrhage

79

what are the fibrinolytic drugs

reteplase and tenecteplase

80

why is tenecteplase becoming the drug of choice for fibrinolytics

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

81

how does streptokinase work

nonenzymatic activator of plasminogen, extracted from hemolytic streptococci

82

what is potential side effects of streptokinase

serious hemorrhage