Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Step 1 - Pharm > cardiac pharm > Flashcards

cardiac pharm Flashcards

1
Q

drugs for essential hypertension

A

diuretics, ACEi, ARBs, CCBs

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

drugs for hypertension in CHF

A

diuretics, ACEi, ARBs, CCBs B-blockers (conpensated CHF only), K sparing diuretics

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

drugs for hypertension in DM

A

diuretics, ACEi, ARBs, CCBs, alpha blockers

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

reason for giving ACEi to DM pts

A

protective against diabetic nephropathy

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

-dine drugs

A

CCBs

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

CCB Mechanism

A

block voltage gated L-type Ca channels in cardiac and smooth muscles and reduce muscle contactability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

CCB NOT to be used in arrythmia

A

nifepidine

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

tox of CCBs

A

cardiac depression,AV block, peripherial edema, flushing dizzyness, constipation

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

hydralazine MOA

A

increase cGMP –> smooth muscle relaxation –> vasodilates arterioles –> reduces afterload

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

hydralazine use

A

severe hypertension, CHF.. Coadministered with B blocker to prevent reflex tachycardia

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

first line therapy for hypertension in pregnancy

A

hydralazine (with methyldopa)

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

treatment for malignant hypertension

A

nitroprusside, CCBs, labetalol, fenoldapam

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

tx of hydralazine

A

compensitory tachycardia, fluid retention, nausea, headache, angina, Lupus-like syndrome

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

Tox of nitroprusside

A

cyanide poisoning

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

MOA of nitroprusside

A

increase GMP by direct release of NO.

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

moa of fenoldapam

A

D1 receptor agonist, conorany, peripheral, renal and splachnic vasodilation

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

“monday disease”

A

development of tolerance during the week for isosorbide. loss of tolerance during the weekend. Start back up with tachycardia, dizzyness and headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

drugs NOT to be used in angina

A

pindolol and acebutolol

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

antilipid with the best effect on LDL

A

statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

MOA of statin

A

inhibit conversion of HMG-CoA to mevalonate

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

Side effects of statins

A

hepatotox, rhabdo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

antilipid with the best effect on HDL

A

niacin

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

MOA of niacin

A

inhibits lipolysis, reduces VLDL circulation

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

Side effects of niacin

A

flushing, hyperglycemia, hyperuricemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Bile acid resins examples
cholestyramine, colestipol, colsevelam
26
Bile acid resin effect
moderate lowering of LDL, slightly higher HDL and TGs
27
Bile acid MOA
prevent intestinal reaborption of bile acids - liver must use cholesterol to make more
28
Bile acid side effects
taste bad and screws with your gut. malaboprtion of fat soluable vitamins. cholesteral gallstones
29
ezetimibe effect
moderate lower LDL
30
ezetimibe MOA
prevent cholesteral reabsorption at SI brush border
31
ezetimibe side effects
rare increase in LFTs, diarrhea
32
fibrate effects
large reduction in TGs
33
fibrate MOA
upregulate LPL, clearing TGs
34
firate side effects
myositis, hepatotox, cholesterol gallstones
35
MOA of digoxin
direct inhibition of Na/K ATPase leading to direct inhibition of Na/Ca exchangers. increase in intracelluar Ca --> increase contractability. Also stimulates Vagus nerve to slow HR
36
use of digoxin
CHF, Afib (slow conduction at AV and depression of SA)
37
tox of digoxin
cholinergic (N/V, diarrha, blurry yellow vision) | increasedPR, lower QT, T wave inversion,a rrythmia - AV block
38
poor prognostic indicator in digoxin tox
hypokalemia
39
antidote for dig tox
normallize K+, lidocaine, anti-digoxin fab fragments, Mg2+
40
effect of Na+ channel blocker antiarrythmics (Class I)
slow or block conduction in abnormal pacemaker cels
41
causes increased tox in class 1 antiarrythmics
low K
42
class 1A antiarrythmics
Quinidine, Procainamide, disopyramide
43
class 1A antiarrythmics action
increase AP duration, increase refreactory period, increase QT
44
class 1A antiarrythmics use
A and V arrythmias. Ectopic supraventricular tachy and v tach
45
quinadine tox
cinchoism
46
procanamide tox
SLE-type syndrome
47
disopyramide
Heart failure, thrombocytopenia, torsades de pointes
48
class IB antiarrythmics effect
lower AP duration. affects aischemuc or depolarized purkinjie and ventriculartissue
49
class IB antiarrythmics use
acute ventricular arrythmias (especially post-MI) and digitalis induced arrythmias
50
class IB antiarrythmics
lidocaine, mexiletine, tocainide (phenytoin can be listed)
51
tox of class IB antiarrythmics
CNS stimulation/depression, CV depression
52
class IC antiarrythmics
flecainide, propafenone
53
class IC antiarrythmics effect
useful in ventricular tachycardias that progress to VF and in tractable SVT - used as last resort in refractory tachy
54
people NOT to use class IC antiarrythmics with
post-MI, structural heart disease
55
class IC antiarrythmics tox
proarrythmic, significantly prologs refreactory period in AV node
56
antiarrythmic beta blockers
metoprolol, proanolol, emolol, atenolol, timolol
57
antiarrythmic beta blockers MOA
decreases SA and AV nodal activity by deceraseing cAMP and lowering Ca currents
58
short acting antiarrythmic beta blocker
esmolol
59
use of antiarrythmic beta blockers
Vtach, SVT, slowing ventricular rate during afib and a flutter
60
tox of antiarrythmic beta blockers
impotence, worse asthma, bradycardia, CHF, sedation, may mask hypoglycemia
61
side effect of metoprolol
dyslipidemia (treat OD with glucogon)
62
can exacerbate vasospasm in prinzmetal's
propanolol
63
K+ channel blockers (Class III antiarythmics)
amidorone, ibutilide, dofeilite, soralol
64
effect of Class III antiarythmics
increase AP duration, used when other antiarrythmics fail, increase QT interval
65
tox of sotalol
torsades des pointes, excessive Beta blockade
66
tox of amidorine
pulmonary fibrosis, hepatotox, hypothyroidism (check PFTs, LFTs, TFTs) corneal and skin deposits, neuro effects,bradycardia, AV block
67
MOA of verapamil, diltiazem
CCB, lower conduction velocity, increase ERP and PR inverval, prevents nodal arrythmia
68
tox of verapamil, diltiazem
constipation, flushing, edema, sinus node depression
69
adenosine MOA
sends K out of cells - hyperpolarizes and lowering intracellular calcium,
70
adenosine is the DOC for
supraventricular tachy (VERY short acting)
71
T 1/2 for dig
40 hours
72
blocks effects of adenosine
theophylline and caffiene
73
Mg++ used for
torades des points and dig tox

Step 1 - Pharm (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions