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organ systems > cardio pharm > Flashcards

cardio pharm Flashcards

1
Q

diabetic nephropathy

A

ACE inhibitors and ARBS are protective

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2
Q

calcium channel blockers

A

block voltage dependant L-type calcium channels of cardiac and smooth muscle –> reduce muscle contractility

Vascular smooth muscle: amolidipine = nifedioine > diltiazem> verapamil

Heart: verapamil> diltiazem > amlodipine = nifedipine

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3
Q

dihydropyridines (amlodipine and nifedipine) are used for?

A

HTN, angina (including prinzmetal), raynaud

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4
Q

non-dihydropyridines (diltiazem, verapamil) are used for?

A

HTN, angina, atrial fibb/flutter

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5
Q

Nimodipine a calcium channel blocker is used for?

A

subarachnoid hemorrhage (prevents cerebral vasospasm)

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6
Q

Calcium channel blockers side effects

A

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

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7
Q

Class IV antiarryhthmics - Ca2+ channel blockers:

Verapamil and diltiazem

A

-slow the rise of the action potential on nodal cells (Ica phase 0)
-prolongue the repolarization at the AV node
… decrease in conduction velocity, increase in ERP and an increase in PR interval

used:
prevention of nodal arrhthmias (SVT), rate control in a fibb

side effects: constipation, flushing, edema, CHF, AV block, sinus node depression

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8
Q

Hydralazine

A

increases cGMP–smooth muscle relaxation. Vasodilates arterioles> veins; decreases after load

use: HTN, CHF, first line with pregnancy with methyldopa, frequently coadministered with a beta blocker to prevent reflex tachycardia
tox: compensatory tach (contraindicated in angina/CAD), fluid retension, nausea, headache, angina can cause lupus like syndrome

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9
Q

hypertensive emergency

A

nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam

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10
Q

nitroprusside

A

short active increases cGMP –> NO–> vasodilation, can cause cyanide toxicity as it release CN

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11
Q

Fenoldopam

A

Dopamine D1 receptor agonist - coronary, peripheral, renal, splanchnic vasodilation –> decrease BP and increase naturesis

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12
Q

Nitrogylcerin, isosorbide dinitrate

A

-vasodilate increase NO via cGMP increase
dilate veins» arteries decrease preload
use: angina, acute soronary syndrome and pulmonary edema

toxicity: reflex tach (treat with a beta blocker), hypotension, flushing, headahce

Monday disease in industrial exposure:
development of tolerance for the vasodilating action during the work week, loss of tolerance over the weeknd. on monday exposure–> tach, dizzy, headache

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13
Q

Mg

A

effective in torsades de pointes and digoxin toxicity

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14
Q

Cadiac gycoside: digoxin

A

75% bioavailabilty
20-40% protein bound
t1/2 = 40 hours
urinary excreted

mech: inhibits na/k/atpase leads to less Na out of cell and a build up of Na in the cell, so less Na wants to enter the cell to kick out the Ca in the Na/Ca exchanger

increase in the intracellular Ca –> positive inotropy.
It also stimulates the vagus nerve –> decrease the HR

treat: CHF, increase contractility; a fibb (decreases conduction at the AV node and depression of the SA node)

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15
Q

digoxin antidote

A

slowly normalize K, cardiac pacer, anti digoxin Fab fragments, Mg

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16
Q

Digoxin toxicity

A

cholinergic (stimulates vagus) - nausea, vomiting, diarrhea, blurry yellow vision
ECG- increase PR, decreases QT, ST scooping, T-wave inversion, arrhythmia, AV block

Can lead to hyperkalemia
factors predisposing to toxicity:
renal failure, hypokalemia (permits digoxin to bind at the K+ binding site on ?Na/k/atpase since less competition), verapamil and miodarone, quinidine (decreases digoxin clearance; diplaces digoxin from tissue binding sites)

17
Q 
HMG CoA reductase inhibitors:
lovastatin
pravastatin
simvastatin
atorvastatin
rosuvastatin
A

decrease LDL
Increase HDL
Decrease TG’s
-inhibit hmgcoa conversion to mevalonate a cholesterol precurser

side effects: hepatotoxicity (increase LFTS)
rhabdomyolysis, espeically when used with vibrates and niacin

18
Q

Niacin (vitamin B3)

A

decrease LDL
Increase HDL
Decrease TG

Inhibit lipolysis in adipose tissue (decrease VLDL to IDL and LDL); reduces hepatic VLDL synthesis

side effects:
red flushed face, which is decreased with aspirin
cause:
hypergycemia, may see acanthosis nigricans
hyperuricemia (exacerbate gout)

19
Q

Bile acid resins :

cholestyramine, colestipol, colesevelam

A

decrease LDL
Slightly increase HDL
Slightly increase TG

Prevent intestinal reabsorption of bile acids; so the liver must use cholesterol to make more!

side effects: patients hate it tastes bad, GI discomfort, decreased absorption of fat soluble vitamins, you can also get cholesterol gallstones

20
Q

Cholesterol absorption blockers:

Ezetimibe

A

decrease LDL
Prevent cholesterol absorption at small intestine brush border

side effects: rare increase in LFTS
diarrhea

21
Q

Fibrates (gemfibrozil,clofibrate, bezafibrate, fenofibrate)

A

decrease LDL a bit
increase HDL a bit
Super decrease TG

Upregulate lipoprotein lipase, this will increase TG clearance. Activate PPAR-a to induce HDL synthesis

side effects: myositis (expeically with concurrent statins)
hepatotoxicity (increased LFTS)
cholesterol gallstones (esp with concurrent bile resins)

22
Q

Name the Antiarrhthmic Na channel blockers

Class 1A

A

Quinidine, Procainamide, Disopyriamide

The Queen Proclaims Disco pyramid partayyyy

23
Q

Name the Antiarrhthmic Na channel blockers

Class 1B

A

Lidocaine, Mexiletine

24
Q

Name the Antiarrhthmic Na channel blockers

Class 1C

A

Flecainide, Propafenone

25
Q

Name the Antiarrhthmic Beta blockers

Class II

A

Metoprolol, propanolol, esmolol, atenolol, timolol, carvediol

26
Q

Name the Antiarrhthmic K+ channel blockers

Class III

A

Amiodarone, Ibutilide, Dofetilide, Sotalol

27
Q

amiodarone toxicity

A 
pulmonary fibrosis
hepatotoxicity
hypothyroidism/hyper
40% iodine by wt
corneal deposits
skin deposits (blue grey) resulting in photo dermatitis
neurologic effects
constipation
bradycardia, heart block, CHF

it has Class i , ii,iii and iv effects!

remember check PFT, LFT and TFT

28
Q

Antiarrhthmic Na channel blockers
Class 1A:
Quinidine, Procainamide, Disopyriamide

A
  • decreases the slope of phase 0
  • increased action potential
  • increased the ERP
  • Increase the QT interval (ventricle contraction)

clinical use: atiral and ventricular ayyhythmias, espeically re-entrant and ectopic SVT and VT

toxicity:
Cinchonism (headahce, tinnitus with quinidine)
reversible SLE syndrom with procainamide
heartfailure with disopyrimide
-thrombocytopenia
-torsades de points due to increased QT interval

29
Q

Antiarrhthmic Na channel blockers

Class 1B: Lidocaine, Mexiletine, phenytoin

A
  • decrease action potential duration, steeper slope of phase 3
  • preferentially affect ischemic or depolarized purkinge and ventricular tissue.

use:
acute ventricle arrhthmia escially post MI, gigitalis induces arrhythmias

tox:
CNS stimulation/depression, cardiovascular depression

30
Q

Antiarrhthmic Na channel blockers
Class 1C
Flecainide, Propafenone

A
  • prolongs refractory period at AV node
  • minimal affect on AP duration, slope at phase 3 is the same

use:
SVT, including AF, onyl as a last reost in VT

tox:
proarrhthmic, especially post-MI (contraindicated). Contraindicated in structural and ischemic heart disease

31
Q

Antiarrhthmic Beta blockers
Class II
Metoprolol, propanolol, esmolol, atenolol, timolol, carvediol

A
  • decrease SA and AV nodal activity
  • decrease cAMP and thus PKA and thus less SR release of Ca
  • decrease Ca inward currents
  • decrease the slope of phase 4 depolarization in abnormal pacemaker cells
  • AV node is particularily sesistive, increase the PR interval

note esmolol is very short acting

32
Q

Antiarrhthmic K+ channel blockers
Class III:
Amiodarone, Ibutilide, Dofetilide, Sotalol

A
  • increase action potential
  • increase ERP
  • prolong repolariation slope of phase 3 decreases
  • increase QT interval

use:
a fibb, atrial flutter, v tach (amiodarone and sotolol)

note sotolol- cause torsades de pointes and excessive B blockade

ibutilide-torsades de points

33
Q

Antiarrhthmic Na channel blockers

Class 1A general:

A 
slow or block conduction especially in depolarized cells. they decrease the slope of phase 0 (depolarization) and increase the threshold for firing in abnormal pacemaker cells.
they are state dependent, selectively depress tissue that is frequently depolarized 
hyperkalemia cause increased toxicity for all class I drugs
34
Q

Antiarrhthmic Beta blockers

Class II toxicity

A
  • impotence, exacerbation of COPD and asthma
  • bradycardia, AV block, CHF
  • sedation, sleep alterations
  • may mask the signs of hypoglycemia
  • metoprolol can cause dislipidemia
  • propanolol can exacerbate vasospasm in prinzmetal angina
  • contrain in cocaine users

Treat overdose with glucagon

organ systems (25 decks)

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