Brainscape's Knowledge GenomeTM

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


See full index

Step 1 Flash Cards > Cardio Drugs > Flashcards

Cardio Drugs Flashcards

1
Q

Calcium Channel Blockers - names

A

amlodipine, nimodipine, nifedipine (dihydropyridine), diltiazem, verapamil (non-dihydropyridine)

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

CCB mechanism of action

A

block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reducing muscle contractility

  • vascular smooth muscle – amlodipine = nifedipine > dilt > verapamil
  • heart – verapamil > dilt > amlodipine = nifedipine
  • verapamil likes the ventricle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CCB clinical use

A

dihydropyridine (except nimodipine): HTN, angina, Raynaud
non-dyhydropyridine: HTN, angina, afib/flutter
Nimodipine: SAH (prevents cerebral vasospasm)

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

CCB toxicity

A

cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia and constipation

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

hydralazine mechanism

A

increases cGMP –> smooth muscle relaxation. vasodilates arterioles > veins; afterload reduction

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

hydralazine clinical use

A

severe HTN, CHF. first line therapy for HTN in preggos, with methyldopa. frequently co-administered with a beta blocker to prevent reflex tachycardia

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

hydralazine toxicity

A 
compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina.
**Lupus like syndrome (due to liver acetylation of the drug)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Drugs to treat hypertensive emergency

A

nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam
- Neil likes Neil’s fun clonipine

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

nitroprusside

A

short acting, increases cGMP via direct release of NO. can cause cyanide toxicity (releases cyanide)

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

fenoldopam

A

dopamin D1 receptor agonist - coronary, peripheral, renal and sphlanchnic vasodilation. Decreases B and natriuresis

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

nitroglycerin, isosorbide mononitrate mechanism

A

vasodilate by increasing NO in smooth muscle –> increases cGMP and smooth muscle reladation. dilates veins&raquo_space; arteries, decreases preload

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

clinical use of nitro/isosorbide mononitrate

A

angina, ACS, pulmonary edema

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

toxicity of nitro/isosorbide mononitrate

A 
reflex tachycardia (treat with beta blockers), hypotension, flushing, headache
"Monday disease" - lack of use over the weekend causes lack of tolerance, more side effects on reexposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

niacin effects on LDL, HDL and TG

A

significantly decreases LDL, significantly increases HDL, decreases TG
**best for increasing HDL

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

bile acid resins effects on LDL, HDL and TG

A

significantly decrease LDL, slightly increases HDL and TG

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

HMG CoA reductase inhibitors effects on LDL, HDL and TG

A

significantly decreases LDL, increases HDL and decreases TG

** best for decreasing LDL

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

cholesterol absorption blockers effects on LDL, HDL and TG

A

significantly decreases LDL, no effect on HDL/TG

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

fibrates effects on LDL, HDL and TG

A

significantly decreases TG, decreases LDL and increases HDL

** best at decreasing TG

19
Q

niacin mechanism of action and SE

A
  • inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis
  • SE: flushing (dec by aspirin, long term use), hyperglycemia, hyperuricemia
20
Q

HMG CoA reductase mechanism of action and SE

A

inhibits conversion of HMG CoA –> mevalonate, a cholesterol precursor

  • increase LDL receptor density
  • hepatotoxic, rhabdo
21
Q

bile acid resins mechanism of action and SE

A
  • prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more
  • tastes bad, GI discomfort, decreased absorption of fat-soluble vitamins, cholesterol gallstones
22
Q

cholesterol blockers mechanism/SE

A
  • blocks absorption at the small intestine brush border

- rare inc in LFTs, diarrhea, hepatotox when given with statins

23
Q

fibrates mech of action/SE

A
  • upregulate lipoprotein lipase, increase TG clearance
  • activates PPARalpha to induce HDL synthesis
  • suppresses 7alpha hydroxylase
  • myositis, hepatotoxicity, cholesterol gallstones (esp with bile acid resins)
24
Q

Digoxin pharmacokinetics

A
  • 75% bioavailability
  • 20-40% protein bound
  • t 1/2 = 40 hours
  • urinary excretion
25
Q

digoxin mechanism and clinical use

A
  • direct inhibition of Na/K ATPase leads to indirect inhibition of the Na/Ca exchanger/antiport
  • more Ca means positive intropy
  • stimulates vagus nerve –> decreased HR
  • used in CHF, afib
26
Q

dig toxicity

A
  • cholinergic - n/v/d, blurry yellow vision
  • ECG - increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block
  • can lead to hyperK
  • precipitators of tox: renal failure, hypoK, verapamil, amiodarone, quinidine
  • antidote: normalize K, cardiac pacer, anti-dig Fab fragments, Mg
27
Q

Class 1 antiarrythmics - Na blockers

A

slow or block conduction, decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells. Hyperkalemia causes increased toxicity for all class I drugs

28
Q

Class 1A antiarrhythmics (names)

A

Quinidine, Procainamide, Disopyramide

- “Quarter PounDer”

29
Q

Class 1A mechanism/clinical use

A

increase AP duration, increase effective refractory period, increase QT
- used for both atrial and ventricular arrhythmias, esp re-entrant and ectopic SVT and VT

30
Q

Class 1A toxicity

A

cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades

31
Q

Class 1B meds

A

lidocaine, mexiletine, also phenytoin?

“Lettuce and mayo”

32
Q

Class 1B mechanism/use

A
  • decreased AP duration, preferentially affect ischemic or depolarized purkinje/ventricle tissue
  • acute ventricular arrhythmias (esp post MI)
33
Q

Class 1B tox

A

CNS stimulation/depression, CV depression

34
Q

Class 1C meds

A

flecainide, propafenone

“Can i have Fries Please?”

35
Q

Class 1C mech/use

A
  • significantly prolongs refractory period in AV node
  • minimal effect on AP duration
  • used in SVTs, including afib. only as a last resort in refractory VT
36
Q

Class 1C toxicity

A

proarrhythmic, esp post-MI (contraindicated)

- fries are contraindicated post-MI

37
Q

Class 2: beta blockers (names) and mechanism and use

A

metoprolol, propranolol, esmolol (short-acting), atenolol, timolol, carvedilol

  • decrease SA and AV node activity by decreaseing cAMP and Ca currents. supress abnormal pacemakers by decreasing the slope of phase 4
  • AV node particularly sensitive - inc PR
  • used in SVT, afib and aflut
38
Q

beta blocker toxicity

A

impotence, exacerbation of COPD and asthma, bradycardia, AV block, CHF, sedation, sleep alterations

  • may mask the signs of hypoglycemia
  • metop can cause dyslipidemia
  • prop can exacerbate vasospasm of P. angina
  • contraindicated in cocaine users
  • treat overdoses with glucagon
39
Q

Class III antiarrhythmics - K channel blockers mech and use

A

amiodarone, ibutilide, dofetilide, sotalol (AIDS)

  • increase AP duration, inc ERP, used when other antiarrhythmics fail. increase QT!
  • used in afib, aflut, Vtach (amiodarone, sotalol)
40
Q

K channel blockers tox

A
  • sotalol - torsades, excessive B blockade
  • ibutilide - torsades
  • amiodarone - LOW risk torsades, pulm fibrosis, hepatotoxic, thyroid up or down, corneal deposits, photodermatitis, neuro, constipation, CHF, bradycardia, heart block
41
Q

Class IV antiarrhythmics - Ca channel blockers

A

verapamil, diltiazem (non-dihydropyridine)

  • decrease conduction velocity, increased ERP, inc PR
  • prevent nodal arrhythmias (SVT), rate control of afib
42
Q

Ca channel blocker tox

A

constipation, flushing, edema, AV nodal block, CHF

43
Q

adenosine

A

increases K out of cells, hyperpolarizes cell and decreases ICa

  • drug of choice for diagnosing/abolishing SVT
  • lasts 15 sec
  • SE: flushing, hypotension, chest pain
  • effects blocked by thephylline and caffeine
44
Q

Mg2+

A

effective in torsades and dig tox

Step 1 Flash Cards (36 decks)

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