Brainscape's Knowledge GenomeTM

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


See full index

STEP 1 STUFF > Cardiology Pharm - First Aid > Flashcards

Cardiology Pharm - First Aid Flashcards

1
Q

Hypertension in pregnancy

A

hydralazine, labetalol, methyldopa, nifedipine

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

Calcium channel blockers, mechanism

A

block voltage dependent L-type calcium channels of cardiac smooth muscle, decreasing muscle contractility.

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

calcium channel blockers working on vascular smooth muscle

A

amlodipine, nifedipine (class called dihydropyridines)

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

calcium channel blockers acting on heart

A

diltiazem, verapamil (non-dihydropyridines)

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

specific clinical uses nimodipine

A

subarachnoid hemorrhage

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

dihydropiridines

A

hypertension, angina (including prinzmetal), raynauds

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

Hydralazine mechanism of action

A

increases cGMP leading to smooth muscle relaxation. vasodilates arterioles > venules. reduces afterload.

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

Hydralazine clinical uses

A

severe hypertension, particularly acute. safe to use in pregnancy.

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

Hydralazine adverse effects

A

compensatory tachycardia (treat with beta blocker), fluid retention, headache

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

Treatment of hypertensive emergency

A

nitroprusside - increases cGMP via direct release of NO. can causes cyanide toxicity

fenoldopam - dopamine D1 receptor agonist. coronary, peripheral, renal, splanchnic vasodilation. decrease BP, increases naturiesis.

nitrates - vasodilate by increasing NO in vascular smooth muscle. increase cyclic GMP leading to smooth muscle relaxation in veins&raquo_space; arteries. decrease in preload.
–> adverse effects, reflex tachycardia, treat with beta blocker.

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

HMG-CoA reductase inhibitors mechanism of action

lovastatin, pravastatin

A

decrease LDL, increase HDL, decrease triglycerides. They inhibit the conversion of HMG COA to mevalonate a cholesterol precursor.

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

HMG-CoA reductase inhibitors adverse effects

A

hepatotoxicity (increase LFTs), myopathy (especially when used with fibrates or niacin)

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

bile acid resins mechanism of action

cholestyramine, colestipol, colesevelam

A

decrease LDL, slightly increase HDL, slightly increase triglycerides. prevent intestinal reabsorption of bile acids. liver must use cholesterol to make more bile acids.

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

bile acid resins adverse effects

A

GI upset. decreased absorption of other drugs and fat soluble vitamins

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

Ezetimibe mechanism of action

A

decrease cholesterol reabsorption. prevent cholesterol absorption at the brush border.

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

Ezetimibe adverse effects

A

rare increas in LFTs, diarrhea

17
Q

Fibrates mechanism of action

gemfibrozil, bezafibrate, fenofibrate

A

DECREASE triglycerides. increase HDL. slight decrease in LDL. upregulate LPL to TG clearance. activates PPAR-alpha to induce HDL synthesis.

18
Q

Fibrates adverse effects

A

myopathy (increased risk with statin), cholesterol gall stones

19
Q

Niacin (Vitamin B3) mechanism of action

A

decrease LDL, increase HDL, decrease triglycerides. Inhibits lipolysis (hormone sensitive lipase) in adipose tissue, reduces hepatic VLDL synthesis.

20
Q

Niacin (Vitamin B3) adverse effects

A

red, flushed face, which can be improved with NSAIDs or long term use,
hyperglycemia
hyperuricemia

21
Q

image page 300 for lipid lowering agents

A

first aid page 300

22
Q

Digoxin mechanism of action

A

direct inhibition of Na/K ATPase –> indirect inhibition of Na/Ca exchanger. Increase Ca –> positive inotropy. Stimulates vagus nerve, decrease HR

23
Q

Digoxin adverse effects

A

cholinergic - nausea, vomiting, afib, blurry yellow vision, arrhythmias, AV block,
–> can lead to hyperkalemia, poor prognosis.
factors predisposing to toxicity: renal failure leading to decreased excretion, hypokalemia

24
Q

Antiarrhythmics - class I mechanism of action

A

sodium channel blockers. they slow or block conduction especially in depolarized cells. they decrease slope of phase 0.

25
Q

Class IA drugs

A

Quinidine, procainamide, disopyramide

26
Q

Class IA mechanism of action

A

Increase AP duration, increase effective refractory period in ventricular action potential, increase QT interval.

27
Q

Class IB drugs

A

lidocaine, mexiletine

28
Q

Class IB mechanism of action

A

decrease AP duration, preferentially affect ischemic or depolarized purkinje and ventricular tissue.

29
Q

Class IC drugs

A

flecainide, propafenone

30
Q

Class IC mechanism of action

A

significantly prolongs effective refractory period in AV and accessory bypass tracts. No effect on ERP in purkinje and ventricular tissue. Minimal effect on action potential duration.

31
Q

Antiarrhythmics - class II beta blocker - mechanism of action

A

decrease SA and AV nodal activity by decreasing cyclic AMP, decreasing Ca currents.

32
Q

Antiarrhythmics - class II beta blocker - clinical use

A

SVT, ventricular rate control for afib, atrial flutter

33
Q

Antiarrhythmics - class II beta blocker - adverse effects

A

impotence, exacerbation of COPD and asthma, cardiovascular effects (Av block, bradycardia, heart failure), CNS effects (sedation, sleep alterations), unopposed alpha antagonism if given with pheo or cocaine toxicity,

Tx of beta blocker overdose with saline, atropine, glucagon.

34
Q

Antiarrhythmics - class III potassium channel blockers - mechanism of action

A

amiodarone, ibutiide, dofetilide, sotalol

–> increase AP duration, increased effective refractory period, increased QT interval.

35
Q

Antiarrhythmics - class III potassium channel blockers - clinical use

A

afib, a flutter, ventricular tachycardia

36
Q

Antiarrhythmics - class III potassium channel blockers - amiodarone adverse effects

A

pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, acts as hapten leading to corneal deposits.

–> check PFTs, LFTs, TFTs.

37
Q

Antiarrhythmics - class IV calcium channel blockers - mechanism of action

A

verapamil, diltiazem

–> decrease conduction velocity, increase effective refractory period, increase PR interval.

38
Q

Antiarrhythmics - class IV calcium channel blockers - clinical use

A

prevention of nodal arrhythmias (SVT), rate control for afib.

39
Q

Antiarrhythmics - class IV calcium channel blockers - adverse effects

A

constipation, flushing, edema

STEP 1 STUFF (15 decks)

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