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Step1: Pharm from 1st AID > Cardio > Flashcards

Cardio Flashcards

1
Q

Drugs used for essential HTN

A

Diuretics
ACEI
ARBs
Ca-chan blockers

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2
Q

Drugs used for CHF

A

Diuretics
ACEI/ARBs
Beta-blockers (only in compensated CHF)
K+ -sparing diuretics

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3
Q

Diabetes mellitus

A 
ACEI (protective against diabetic nephropathy)
ARBs
Ca-chan blockers
Diuretics
Beta-blockers
Alpha-blockers
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4
Q

Calcium Channel Blockers

A

Nifedipine, Verapamil, Diltiazem, Amlodipine

Mechanism of Action –>
Block voltage-dependent L-type calcium channels of cardiac and smooth m. to reduce m. contractility

Use -->
HTN
Angina
Arrhythmias (not nifedipine)
Prinzmetal's angina 
Raynaud's 
Toxicity -->
Cardiac depression
AV block
Peripheral edema
Flushing/dizziness/constipation
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5
Q

Hydralazine

A

Mechanism of action:
increase cGMP —> smooth m. relaxation
vasodilates arterioles > veins
afterload reduction

Use:
Severe HTN
CHF
usually given with B-blocker to prevent reflex tachy

Toxicity:
Compensatory tachy
Fluid retention
Nausea
HA
Angina
Lupus-like syndrome
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6
Q

Drugs used to Tx malignant HTN

A

Nitroprusside & Fenoldopam

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7
Q

NItroprusside

A

Mechanism of action:
Short acting
Increases cGMP through direct release of NO

Toxicity:
Can cause cyanide toxicity (releases cyanide)

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8
Q

Fenoldopam

A

Mechanism of action:

  • Dopamine D1 receptor agonist—> coronary, peripheral, renal and splanchnic vasodilation
  • Decrease BP
  • Increase natriuresis
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9
Q

Nitroglycerin

Isosorbide dinitrate

A

Mechanism of action:

  • Vasodilation by release of NO in smooth m. –> increase in cGMP & smooth m. relaxation
  • Dilate veins&raquo_space; arteris
  • Decreases preload

Use:

  • Angina
  • PE

Toxicity:

  • Reflex tachy
  • HypTN
  • Flushing
  • HA
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10
Q

Statins

A

major effect is lowering LDL

Mechanism of action:
-Inhib’s HMG-CoA —> Mevalonate, a chol precursor
(enzyme is HMG-CoA reductase)

Toxicity:

  • Hepatotoxicity ( high LFTs)
  • Rhabdo
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11
Q

Niacin (vit B3)

A

major effect is increasing HDL

MOA:

  • Inhib’s lipolysis in adipose tissue
  • Reduces hepatic VLDL secretion into circulation

Tox:

  • Red, flushed face (reduced by aspirin or long term use)
  • Hyperglycemia (acanthosis nigricans)
  • Hyperuricemia (exacerbates gout)
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12
Q

Cholestyramine
Colestipol
Colesevelam

A

major effect is decreasing LDL

MOA:

  • Prevent intestinal reabsorption of bile acids
  • Liver must use cholesterol to make more

Tox:

  • Pt’s hate it, tastes bad, causes GI issues
  • Decreases absorption of fat sol vit’s
  • Cholesterol gallstones
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13
Q

Ezetimibe

A

major role is decreasing LDL

MOA:
-Prevent chop reabsorption at small int brush border

Tox:

  • Rare increases in LFTs
  • Diarrhea
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14
Q 
**Fibrates**
Gemfibrozil
Clofibrate
Bezafibrate
Fenofibrate
A

major role is decreasing Triglycerides

MOA:
-Upreg LPL —> increase TG clearance

Tox:

  • Myositis
  • Hepatotoxicity (high LFTs)
  • Cholesterol gallstones
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15
Q

Digoxin (Cardiac glycoside)

A

MOA:

  • Direct inhib of Na+/K+ ATPase —–> inhib of Na+/Ca2+ exchanger/antiport
  • High [Ca2+]i —-> positive inotropy
  • Stimulates vagus nerve —-> lowers HR

Use:

  • CHF (increase contractility)
  • Afib (decrease conduction @ AV node and depression of SA node)

Tox:

  • Cholinergic effects (N/V/D, blurry yellow vision)
  • ECG–> ↑PR, ↓QT, ST scooping, T-wave inversion, arrhythmia, AV block
  • Hyperkalemia (bad times!)
  • Quinidine (↓ digoxin clearance; displaces digoxin from tissue-binding sites)
  • Must be adjusted for older ppl with decrease renal Cl

Antidotes:

  • Lidocaine
  • Anti-digoxin Fab fragments
  • Mg2+
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16
Q

Antiarrhythmics- Na+ channel blockers (Class 1A)

Quinidine
Prcainamide
Disopryramide

“Double Quarter Pounder”

“The Queen Proclaims Diso’s pryramid.”

A

MOA:
- ↑ AP duration, ↑ effective refractory period (ERP), ↑ QT int.

Use:
-Both atrial and venricular arrhythmias, especially re-entrant and ectropic SVT and VT

Tox:

  • Cinchonism (HA, tinnitus w/ quinidine)
  • Reversible SLE-like syndrome (procainamide)
  • HF (disopyramide)
  • Thrombocytopenia, torsades de pointes due to ↑ QT int.
17
Q

Antiarrhythmics- Na+ channel blockers (Class 1B)

Lidocaine
Mexiletine

“Lettuce Mayo”

A

MOA:
- ↓ AP duration. Preferentially affect ischemic or depolarized purkinje and ventricular tissue. Phenytoin can also fall into the 1B category.

Use:

  • Acute ventricular arrhythmias (especially post MI)
  • Digitalis induced arrhythmias
  • 1B is Best for post-MI

Tox:
-CNS stim/depression, cario depression

18
Q

Antiarrhythmics- Na+ channel blockers (Class 1C)

Flecainide
Propafenone

“Fries, Please”

A

MOA:

  • Significantly prolongs refractory period in AV node.
  • Minimal effect on AP duration

Use:

  • SVTs, including atrial fibrillation
  • Only as a last resort in refractory VT

Tox:

  • Proarrhythmic, especially post-MI (contraindicated)
  • 1C is Contraindicated in structural and ischemic heart disease
19
Q

Antiarrhythmics- β-blockers (Class 2)

Metoprolol
Propranolol
Esmolol
Atenolol
Timolol
Carvedilol
A

MOA:

  • ↓ SA & AV nodal activity by ↓ cAMP
  • ↓ Ca2+ currents
  • Suppress abnormal pacemakers by ↓ slope of phase 4
  • AV node particularly sensitive (↑PR int)
  • Esmolol very short acting

Use:

  • SVT
  • slowing ventricular rate during Afib and Aflutter

Tox:

  • Impotnece
  • Exacerbation of COPD and asthma
  • CNS/Cardio effects
  • May mask sign of hypoglycemia
  • Metroprolol—> dyslipidemia
  • Propranolol can exacerbate vasospasm in Prinzmetal angina
  • C/I in cocain users (risk of unopposed α-adrenergic R activity)
  • Tx OD w/ glucagon
20
Q

Antiarrhythmics- K+ channel blockers (Class 3)

Amiodarone
Ibutilide
Dofetilide
Sotalol

“AIDS”

A

MOA:

  • ↑ AP duration
  • ↑ ERP
  • Used when other antiarrhythmics fail
  • ↑QT interval

Use:

  • Afib, Aflutter
  • Vtach (amiodarone, sotalol)

Tox:
Sotalol –> torsades de pointes (TDP), excessive β blockade
Ibutilide –> TDP
Remember to check PFTs, LFTs, and TFTs when using amiodarone

21
Q

Antiarrhythmics- Ca2+ channel blockers (Class 4)

Verapamil
Diltiazem

A

MOA:

  • ↓Conduction velocity
  • ↑ ERP (effective refractory period)
  • ↑ PR interval

Use:

  • Prevention of nodal arrhythmias (e.g., SVT)
  • Rate control in Afib

Tox:

  • Constipation
  • Flushing
  • Edema
  • CV effects (CHF, AV block, sinus node depression)
22
Q

Adenosine

A

MOA:
-↑ K+ out of cells (hyperpolarizing the cell and ↓Intracellular Ca2+)

Use:

  • Dx’ing/abolishing SVT
  • Very short acting

Tox:

  • Flushing, HypoTN, chest pain
  • Effects blocked by theophylline and caffeine
23
Q

Magnesium (Mg2+)

A

Effective in torsades de pointes and digoxin tox

Step1: Pharm from 1st AID (12 decks)

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