Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio > And more drugs > Flashcards

And more drugs Flashcards

Hyperlipidemia Anti-Arrhythmias Only a couple hyperlipidemia..

1
Q

MOA of statins

A

inhibits rate-limiting step of cholesterol synthesis, which:

  1. upregulates LDL receptors in liver
  2. reduces lipoprotein secretion in liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Statins reduce…

A

LDL (50%)
TG (~37%)

(and increase HDL ~15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Statins are predominately excreted through

A

feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

-mycin antibiotics, azoles, SSRI’s, CCB’s and grapefruit juice will have drug interactions with these statins:

A

Atorvastatin (lipitor) and Lovastatin

**via CYP3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cyclosporine and grapefruit juice are contraindicated with statins because they inhibit:

A

p-glycoprotein mediated intestinal absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

HMG CoA Reductase Inhibitors adverse effects: (7)

A 
mild GI distress
increased liver enzymes
sleep disturbance, memory loss
teratogenic 
myalgia without CPK rise
myositis with CPK rise
rhabdomyolysis with CPK rise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Statin which will have no effect on TG

A

lovastatins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do bile acid sequestrants interrupt recycling of cholesterol?

A

bile negatively charged bile acids in the gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Group of antilipemic drugs that are non-systemic

A

bile acid sequestrants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Group of antilipemic drugs that are safe for use in patients with liver disease

A

bile acid sequestrants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What side effects may limit use of bile acid sequestrants?

A

GI bloating
constipation
possible increase in TG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bile acid sequestrants prevent the absorption of what drugs?

A

digoxin
beta blockers
thyroxine
coumadin

(these should be taken an hour before or 3-4 hours after BAS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MOA of ezetimibe (zetia):

A

inhibits absorption of cholesterol in small intestine by 50%, which reduces delivery of cholesterol to liver

this results in upregulation of LDL receptors and increased clearance of LFL from plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ezetimibe (zetia) localizes to:

A

brush border of small intestinal epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Excretion of ezetimibe (zetia):

A

biliary (78%) and renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Effect of ezetimibe (zetia) on LDL, HDL, TG:

A

lowers LDL by ~18%
increased HDL by ~5%
lowers TG by ~11%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Drug interactions associated with ezetimibe (zetia):

A
  1. bile acid sequestrants (decrease absorption of ezetimibe by up to 80%)
  2. cyclosporine (3-4 fold increase in ezetimibe levels)
  3. fibrates (when combined, may increase biliary cholesterol excretion and increase risk of gallstones)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Most significant side effect associated with ezetimibe (zetia):

A

increased liver enzymes when co-administered with a statin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MOA of fibric acid derivatives

gemfibrozil and fenofibrate

A

serves as ligand for ligand-activated PPAR-alpha nuclear receptor, which then causes:

  1. supresses transcription of ApoCIII (which increases LPL)
  2. increased ApoA1 synthesis
  3. increases PL transfer protein activity
  4. increased FA oxidation (reduces TG synthesis)
  5. increased biliary cholesterol excretion via increased cholesterol 12a hydroxylase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q 
Effects of fibric acid derivatives on:
VLDL
TG
HDL
LDL
A

VLDL: reduced
TG: reduced by up to 50%
HDL: increased (~15%)
LDL: unchanged/-/+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Side effects of fibric acid derivatives:

A 
GERD, diarrhead
increased liver enzymes
gallstones
teratogenic/embryocidal in animals
    pregnancy category C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Side effect specific to fenofibrate (tricor):

A

reversible increase in creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Gemfibrozil reduces metabolism of what drugs?

A

statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Gemfibrozil is a good drug choice for patients with…

unlike fenofibrate

A

renal disease (extensively metabolized by liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MOA of niacin: (5)

A
  1. inhibits mobilization of FFA from adipocytes
  2. reduced hepatic TG synthesis
  3. reduces ApoB synthesis and secretion (VLDL)
  4. Enhanced ATP cassette-mediated transfer of cholesterol from macrophage to HDL
  5. Enhances LPL (promotes conversion of VLDL to LDL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q 
Niacin's effects on:
HDL
LDL
TG
Lp(a)
A

HDL: increased (via increased plasma ApoA1)
LDL: reduced
TG: reduced
Lp(a): reduced *unique feature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Side effects of niacin:

A
  1. flushing
  2. increased liver enzymes, hepatitis, failure
  3. GI irritation and activation of peptic ulcer disease
  4. hyperuricemia/gout
  5. retinal detachment
  6. cystoid macular edema
  7. myositis
  8. skin dryness, etc
  9. insulin resistance, hyperglycemia

*SMUGGLED
(skin flushed, myositis, uric acid, GI, glu, liver, eyes, dry skin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Effects of N3FA:

A 
low TG
antiplatelet
antiarrhythmic 
reduced BP
reduced CAD*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MOA of N3FA:

A

reduced hepatic TG synthesis by reducing SREBP

increased FA ox via PPAR-alpha activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Effects of N3FA on:
HDL
LDL
TG

A

HDL: none
LDL: none
TG: lowers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

N3FA is a formulation of ___ and ___

A

EPA

DHA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Class I antiarrhythmics

Examples?

A

Na channel blocker

lidocaine, procaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Class II antiarrhythmics

Examples?

A

beta blocker

propranolol, metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Class III antiarrhythmics

Examples?

A

K channel blocker

amiodarone, sotalol, ibutilide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Class IV antiarrhythmics

Examples?

A

Ca channel blocker

verapamil, diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Phase IV depol of the SA node is slowed by

A 
vagal activity (ACh)
digoxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Phase IV depol of the SA node is accelerated by

A 
sympathetic activity 
class II drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Phase 0 depol is slowed by

A 
Ca channel blockers
class IV drugs
39
Q

The cell is hyperpolarized by:

A

adenosine

40
Q

Class II drugs are used for:

A 
symptomatic PVC's
reducing arrhythmia's post-MI (*survival)
reducing enhanced automaticity
angina
HTN
41
Q

Class I drugs are used to treat:

how?

A

enhanced automaticity

blocking NA channels in the fast-conducting ventricular cells reduces membrane responsiveness
=slower recovery

42
Q

Class I drugs bind to Na channels in the _____ and ______ states

A

open and inactivated

43
Q

Class I drugs result in decreased rate of rise of phase ___ depol

A

0

44
Q

Procaineamide is a class ___; its dissociation rate is ___ sec and it slows conduction at ___ rates.

A

IA
>1 sec
slow

45
Q

Lidocaine is a class ___; its dissociation rate is ___ sec and it slows conduction at ___ rates.

A

IB
<1 (rapid!)
fast rates (and ischemia)

46
Q

Flecanide is a class ___; its dissociation rate is ___ sec and has a ______ effect on conduction

A

IC
>10 sec (very slow)
pronounced

47
Q

Side effects of procainamide:

A

drug induced lupus (more likely in slow metabolizers)

tosades de pointes (especially if drug accumulates, as in renal failure)

48
Q

Procainamide has little effect on:

A

SA and AV nodes

49
Q

EP effects of procainamide:

A
  1. prolongs AP duration
  2. suppresses ectopic PM activity in partially depol cells
  3. reduced conduction velocity
50
Q

Lidocaine preferentially binds to

A

Na channels in partially depolarized cells to suppress abnormal automaticity

51
Q

Lidocaine is effective for use in (atrial/ventricular) arrhythmias

A

ventricular

52
Q

How does lidocaines dissociation rate affect its regulation of HR?

A

because of its rapid dissociation, cells can recover between APs at a NORMAL HR; thus it blocks at high HR

53
Q

Lidocaine distributes into

A

fat tissue

54
Q

Side effects of lidocaine:

A

CNS, agitation, confusion, seizures

55
Q

Flecainide is contraindicated in patients with

A

structural heart disease

proarrhythmic in:

  • LV dysfunction
  • CHD
  • sustained VT
56
Q

Class III drugs will block phase ___, which prolongs the effective refractory period (or the __ on an EKG).

A

3

QT

57
Q

Prolonging effective refractory period in the slow conducting limb prevents:

A

re-entry

58
Q

Amiodarone blocks what channels?

A

K
Na
Ca
beta-adrenergic

59
Q

Amiodarone slows what portions of an EKG?

A

PR
QRS
QT
(also causes sinus bradycardia)

60
Q

IV amiodarone is used to treat:

A

life-threatening arrhythmias

used in cardiac resuscitation

61
Q

amiodarone is metabolized via

What does it interact with?

A

CYP3A4
digoxin
warfarin

62
Q

Side effects of amiodarone:

A 
pulmonary fibrosis
photosensitivity dermatitis 
corneal halos 
optic neuritis (possible blindness)
hypo/hyperthyroidism
muscle weakness
hepatitis
63
Q

Sotalol blocks what channels?

A

K

beta (in L isomer)

64
Q

Sotalol is excreted via

A

kidneys

65
Q

Sotalol is contraindicated in:

A 
prolonged QT
renal insufficiency 
Asthma/COPD
decompensated CHF
2nd/3rd AV block
sinus bradycardia
66
Q

Not so awesome sotalol side effect:

A

torsades de pointe

67
Q

Indicated for acute termination of a-fib or a-flutter

A

ibutilide

68
Q

“Pure” class II drug

A

ibutilide

69
Q

Major side effects of ibutilide

A

transient asystole

torsade de pointes (polymorph V-tach)

70
Q

Antiarrhythmics that block __ channels have torsade de pointes as a side effect

A

K

71
Q

Drugs that treat v-tach

A
  1. amiodarone
  2. lidocaine (IV)
  3. procaineamide
72
Q

Sotolol should not be given in the setting of:

A

acute MI

73
Q

Drugs that block conduction through the AV node are used to control:

A

rapid supraventricular arrhythmia

74
Q

Drugs that slow conduction through AV node:

A
  1. verapamil (class IV CCBs)
  2. propranolol (class II, beta-blockers)
  3. digoxin
75
Q

Drugs that will have NO effect on AV node:

A

procaineamide, lidocaine, ibutilide

76
Q

Effects of class IV drugs:

A

reduced SA node automaticity

reduced AV node conduction

77
Q

Adverse effects of class IV drugs:

A

SA/AV block
impaired myocardial contractility
hypotension

78
Q

Class IV are useful in what type of patients?

Contraindicated in?

A

can’t tolerate beta-blockers
normal LV function

CHF
LV dysfunction
Sinus bradycardia
AV block

79
Q

Effects of digoxin

A

increases vagal activity to reduce SA automaticity

inhibits Na/K/ATPase, which results in Ca overload

80
Q

Drug that terminates paroxysmal supraventricular tachycardia

A

adenosine

81
Q

Common adenosine side effects:

A

chest tightness
transient asystole
flushing
recurrent PSVT without additional trx

82
Q

What drug can be diagnostic for PSVT?

A

adenosine: if that fixes it = PSVT;

if not, try again

83
Q

Digoxin alone is contraindicated in patients with:

A

WPW

can induce vfib

84
Q

What drug class inactivates bradykinin?

A

ACEI

85
Q

Side effects of ACEI’s:

A 
Hypotension 
Azotemia (volume-reduced, reduced GFR) 
Cough (Bradykinin) 
Angioedema (Bradykinin)
Skin rash
Dysguesia (“metallic” taste) 
Hyperkalemia--may affect renal function
86
Q

ACEI or ARB’s: which is preferred in CHF?

A

ACEI

87
Q

How do beta blockers affect CHF patients?

A

short term not so great, but long term increases CO and decreases LVEDP

88
Q

What molecular effects do beta blockers have in CHF?

A
  1. Reverse desensitization
  2. Increase receptor number
  3. Restore fast signaling modes (contractility) over slow signaling modes (gene expression)
89
Q

Beta blockers approved for CHF

A

Metoprolol (Lopressor®, Toprol XL®)
Carvedilol (Coreg®)
Bisoprolol (Zebeta®)

***NOT nebivolol

90
Q

Digoxin will ___ contractility and ___CO

A

increase

increase

91
Q

ACEI and ARB prevent/reverse the mitogenic effects of AngII, which include:

A

hypertrophy of cardiac myocytes and vasc smooth musc

cardiac and vasc fibrosis

atherosclerosis

92
Q

What type of duiretic should you use with ACEI?

A

K sparing (like spironolactone)

93
Q

Do not give which 3 drugs with digoxin?

A

quinidine (decr elim)
amiodarone (decr elim)
verapamil (slowing of HR)

Cardio (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions