Cology, Antiarrhythmics, Drugs 2

Front 1

class 3 are --- blockers

Back 1

K

Front 2

K blockers prolong/decrease ----

Back 2

prolong repolarization

Front 3

k blockers reduces K ---

Back 3

efflux

Front 4

K blockers prolong phase --- repolarization

Back 4

3

Front 5

k blockers prolong ---- ---

Back 5

refractory period

Front 6

k blockers prolong duration of --- ----

Back 6

action potential

Front 7

prolong phase 3 prevent movement of K ---

Back 7

out

Front 8

route of amiodarone

Back 8

oral

IV

Front 9

t1/2 of amiodarone

Back 9

40 days

Front 10

amiodarone has slow ---, slow -----

Back 10

onset

elimination

Front 11

due to long t1/2 and slow onset/elimination what might be required

Back 11

loading dose

Front 12

amiodarone used for recurrent ---- tach/fib that resistant to others

Back 12

vent tach/fib

Front 13

amiodarone maintains normal rate in ---- -----

Back 13

atrial fibrillation

Front 14

amiodarone replaces --- in MI in outpatient settings

Back 14

lidocaine

no longer the standard

Front 15

iv amiodarone terminate acute ---- ---- or ----

Back 15

v tach

v fib

Front 16

why does it take a while for amiodarone to reach tx dose

Back 16

due to wide distribution in tissues

Front 17

amiodarone is an analog of ----

Back 17

thyorid hormones

2 iodines

Front 18

why do se last so long

Back 18

cuz takes a long time to get out of body

Front 19

t/f

ok to maintain the mg's when switching from oral to iv

Back 19

f

iv, there might be an overdose

Front 20

why is amio used for alomost any type of arrhthymias

Back 20

due to multi actions

Front 21

amiodarone blocks -- channels

Back 21

K (prolong repolarization)

inactivated Na channels (class 1B activity)

Ca channels (class 4)

Front 22

amiodarone blocks --- and --- receptors

Back 22

alpha

beta

Front 23

amiodarone decreases ----

Back 23

automaticity

Front 24

amiodarone decreases ---- and prolongs --- intervals

Back 24

decreases conduction

prolongs PR, QRS, and QT interval. . . so it lenghten vent contraction and action potential

Front 25

amiodarone prolongs --- --- in all cardiac tissues

Back 25

refractory periods

Front 26

t/f

ok to take amiodarone w/ pregnancy

Back 26

f

due to iodine. . . pt should be on two methods of contraception and it should be switched if pt pregnant

Front 27

which will cause more hypotension w/ amiodarone

iv or oral

Back 27

iv

Front 28

t/f

amiodarone is dose and tx independent w/ pneumonitis, pulm fibrosis

Back 28

f

dependent

Front 29

amiodarone can cause ----- and --- w/ particular dose

Back 29

pneumonitis

pulm fibrosis

Front 30

amiodarone can cause neuro----- and neuro---

Back 30

neurotoxicity

neuropathy

also muscle weakness and ataxia

Front 31

skin color w/ amiodarone

Back 31

bue-gray skin color

Front 32

t/f

amiodarone can cause photosensitivity

Back 32

t

Front 33

what do you call the cloudy eyes due to amiodarone

Back 33

corneal deposits

occurs after 6 months

Front 34

if the pt had norm thyroid fx what will happen after taking amiodarone

Back 34

hypothyroidism

Front 35

if pt had hypothyroidism prior to amiodarone what will happen

Back 35

hyperthyroidism

watch for thyroid toxicosis

Front 36

hyperthyroidism prior to amiodarone

Back 36

then hypothyroidism

Front 37

black box warning of amiodarone

Back 37

bradycardia

av block

sick sinus syndrome

Front 38

amiodarone can interact w/

Back 38

dig

warfarin

flecanide

phenytoin

procainamide

Front 39

dronedarone approved for --- fib/flutter

Back 39

atria

Front 40

dronedarone approved for a fib/flutter w/ risk fators of age > ----, dm, ---tension, prior ---, lefter atrial diameter of >/= ---mm, LVEF

Back 40

70

hypertension

prior stroke

50

Front 41

remove iodine form amiodarone and you get

Back 41

dronedarone

Front 42

what's dronedrone metabolized by

Back 42

CYP3A4

Front 43

which has more pulm/thyroid problems? amiodarone or dronedarone

Back 43

dronedarone

Front 44

rate control you slow done --- thru the --- node

Back 44

conduction

AV

so rapid atrial rate won't get to ventricles

Front 45

rhythm control: you convert ---- to nsr

Back 45

arrhythmia

Front 46

since there's no I in dronadarone what's the t1/2

Back 46

24 days

Front 47

which has higher distribution dronaderone or amiodarone

Back 47

amiodarone

so dronedarone doesn't take 6 mo to get out of body

Front 48

what's dronedarone metabolized by

Back 48

CYP2D6

CYP3A4

Front 49

toxicity of dronedarone include:

Back 49

diarrhea

n/v

bradycardia

rashes

qt interval prolongation

hypokalemia

hypomagnesmia w/ K depleting diuretic

Front 50

toxicity of dronaderone

hypo-----/---------

--- cardia

--- interval prolongation

Back 50

hypomagnesemia

hypokalemia

bradycardia

QT interval prolongation

Front 51

dronedarone toxicity showed ---- abnormalities in animals

Back 51

fetal

Front 52

black box of dronedarone:

class --- or class -- - ---- w/ recent -----

Back 52

4

2-3

decompensation

Front 53

CI of dronedarone:

-- or --- heart block

---cardia

increased ---- interval

Back 53

2nd

3rd

bradycardia

QT

Front 54

CI of dronedarone

inhibitors of ----

Back 54

CYP3A4

Front 55

ibutilide:

---- opening of inward Na channel which counteracts opening of K channels

Back 55

prolongs

Front 56

ibutilide:

prolongs opening of inward ---- channel which counteracts opening of -- channels

Back 56

Na

K

Front 57

ibutilide prolongs --- and ----

Back 57

repolarization

action potential

Front 58

route of ibutilide

Back 58

IV

1 mg over 10 min

Front 59

ibutilide will convert --- or ----

Back 59

afib/flutter

Front 60

toxicity of ibutilide:

Back 60

torsades de points

heart block

Front 61

this med counteracts K going out and allows Na to go in

Back 61

ibutilide

Front 62

dofetilide is a potent pure -- channel blocker

Back 62

K

Front 63

dofetilide will convert ----

Back 63

a fib

Front 64

dofetilide is limited becasue

Back 64

adminstrator needs special training

Front 65

ae of dofetilide

Back 65

torsades de points

marked qt prolongation

mainly eliminated thru kidneys unchanged

Front 66

dofetilide mainly eliminated unchanged thru ---

Back 66

kidneys

Front 67

why is dofetilide difficult to work w/

Back 67

due to large impact on action potential

Front 68

which isomer of sotolol has bb activity

Back 68

L

Front 69

dofetilide is limited becasue

Back 69

adminstrator needs special training

Front 70

ae of dofetilide

Back 70

torsades de points

marked qt prolongation

mainly eliminated thru kidneys unchanged

Front 71

dofetilide mainly eliminated unchanged thru ---

Back 71

kidneys

Front 72

why is dofetilide difficult to work w/

Back 72

due to large impact on action potential

Front 73

which isomer of sotolol has bb activity

Back 73

L

Front 74

which isomer of sotolol inhibits K channels

Back 74

D-L

Front 75

sotolol inhibits K channels so it --- aciton potential

Back 75

lenghten

Front 76

sotolol decreases phase---

Back 76

phase 4 depolarization

Front 77

indication of sotolol:

--- flutter/fib and ----- -----

Back 77

atrial flutter/fib

ventricular tachyarrhythmia

Front 78

ventricular tacyarrhythmia by sotolold due to ----

Back 78

K channel effects

Front 79

sotolol will decrease ---- conduction

Back 79

AV node

so harder for impulse to get from atrium to ventricles

Front 80

toxicity of sotolol:

Back 80

torsades de points

bronchospasm

b blocking activity

Front 81

class 4 meds?

Back 81

Ca channel blockers

Front 82

class 4/ccb decreases -----

Back 82

automaticity

Front 83

class 4/ccb block ---type channel

Back 83

L type channel

Front 84

class 4/ccb slow ------- conduction

Back 84

AV node

Front 85

class 4/ccb has negative ---

Back 85

inotropic

Front 86

what part of heart dependent on Ca

Back 86

SA and AV node

Front 87

two ccb

Back 87

verapamil

diltiazem

Front 88

which channels do verapmil and diltiazem block

Back 88

both activated and inactivated

Front 89

verapamil and diltiazem most effective in most --- tissue

Back 89

active

(ischemia, increased action potential)

Front 90

verapamil and diltiazem will decrease ----- conduction and supress the --- node

Back 90

decrease AV conduction

suppress SA node

Front 91

clinical indication for vera and diltia

Back 91

PSVT

a fib

Front 92

t/f

vera and diltia stop afib

Back 92

f

blocks but doesn't stop

Front 93

toxicity of verapamil, diltiazem

--- tension

--- metabolism

avoid in --- arrhythmias

avoid in --- --- -----

avoid in depressed ---- function

Back 93

hypotension

hepatic

ventricular

sick sinus syndrome

cardiac

Front 94

t/f

verapamildiltiazem can cause edema

Back 94

t

Front 95

what's the cause of paroxysmal

Back 95

no specific cause

Front 96

psvt due to --- mechanism

Back 96

rentrant

Front 97

adenosine activates the --- channels in the ---

Back 97

K

atria

Front 98

adenosine blocks --- channels

Back 98

Ca

Front 99

adenosine --- cells and prevent the --- ----

Back 99

hyperpolarizes

action potential

Front 100

adenosine decreases conduction ----- and may stop the heart for -- to -- sec

Back 100

velocity

2-3

Front 101

adenosine decreases ----, prolongs the --- period

Back 101

automaticity

refractory

Front 102

t1/2 of adenosine

Back 102

10 sec

Front 103

clinical indict of adenosine

Back 103

PSVT

wolff-parkinson-white

Front 104

toxicity of adenosine:

--- in 20% of pts

---

-- in chest

Back 104

flushing

SOB

burning

Front 105

dig ---- inhibition

Back 105

Na/K ATPase

Front 106

dig slows -- conduction

Back 106

AV

Front 107

dig inhibit -- channels in --- node

Back 107

Ca

AV

Front 108

dig indirectly/directly increase ----- tone and decrease -----

Back 108

indirectly

parasympathetic

sympathetic

Front 109

dig can induce ---- block

Back 109

heart

Front 110

dig is -- dependent

Back 110

dose

Front 111

dig slow --- rate

Back 111

ventricular

Front 112

dig induces -----

Back 112

heart block

(afib/flutter)

Front 113

dig toxicity

GI

Back 113

n/v/d

anorexia

Front 114

dig cns toxicity

Back 114

confusion

delirium

ha

seizures

visual disturbances

Front 115

what do you avoid w/ dig

Back 115

ccb

bb

(due to additive effects)

Front 116

phenytoin is anti-----

Back 116

convulsant

Front 117

phenytoin blocks --- channels

Back 117

Na

Front 118

phenytoin used for ---- arrhytmias

--- and ----- induced arrhythmias

Back 118

ventricular

digitalis

tricyclic antidepressant induced

Front 119

toxicity of phenytoin:

cns:

Back 119

ataxia

nystagmus

gingival hyperplasia

bone marrow suppression

hypotension

Front 120

moricizine is a class --- --- channel acitivity

Back 120

class 1

Na channel activity

Front 121

moricizine has ---- metobolite

Back 121

active

Front 122

moricizine slows --- conduction and may increase --- ----

Back 122

AV

action potential

Front 123

moricizine ----- activity

Back 123

anticholinergic

Front 124

cast 2 study shows ---- show increased mortality in patients

Back 124

moricizine

Front 125

moricizine is used for

Back 125

life threatening vent arrhythmias

Front 126

toxicity of moricizine used for

Back 126

blurred vision

constipation

dizziness

euphoria

numbness

chf

Front 127

mg sulfate used for

Back 127

torsades de pointes

1-2 gms

Front 128

toxicity of mg sulfate

Back 128

bradycarida

flushing

ha

resp paralysis

Front 129

possible mg sulfate inhibits -- channels and prevents early -----

Back 129

Ca

depolarization

Front 130

t/f

mg sulfate effective even if mg levels are norm

Back 130

t