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Pharma: Cardiovascular System > Chapter 16: General Overview Drugs > Flashcards

Chapter 16: General Overview Drugs Flashcards

1
Q

What are the names of ACE inhibitors? (6)

A 
Captopril
Enalapril
Fosinopril
Lisinopril
Quinapril
Ramipril
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2
Q

What are the names of RAA receptor blockers? (4)

A

Candesartan
Losartan
Telmisartan
Valsartan

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3
Q

What are the names of B-adrenoreceptor blockers? (3)

A

Atenolol
Carvedilol
Metoprolol

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4
Q

What are names of diuretics? (4)

A

Bumetanide
Furosemide
Hydrochlorothiazide(HCTZ)
Metolazone

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5
Q

What are names of direct vasodilators? (4)

A

Hydralazine
Isosorbide dinitrate
Isosorbide mononitrate
Sodium nitroprusside

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6
Q

What are names of inotropic agents? (4)

A

Digoxin
Dobutamine
Inamrinone
Milrinone

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7
Q

What are names of aldosterone antagonists? (2)

A

Eplerenone

Spironolactone

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8
Q

What are the actions on the heart of ACE inhibitors?

ex: enapril

A
  • decrease vascular resistance, venous tone and blood pressure
  • reduce preload and afterload (increase CO)
  • improve symptoms in patients also taking thiazide/loop diruetics and/or digoxin
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9
Q

What are the indications of enapril use?

A
  • single agent therapy in patients with mild dyspnea on exertion who don’t show symptoms of edema
  • indicated in all patients presenting with left ventricular failure
  • ACE inhibitors may be used with diruetics, B-blockers, and aldosterone antagonists
  • initiate ACE inhibitors after MI
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10
Q

What are the pharmokinetics of ACE inhibitors?

A
  • oral administration, presence of food may decrease absorption
  • pro drugs except for captopril
  • renal elimination
  • ramipril and fosinopril require only once-daily dosing
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11
Q

What are the adverse effects of ACE inhibitors?

A
  • postural hypotension, renal insufficiency
  • hyperkalemia, angioedema
  • persistent dry cough
  • shouldn’t be used in pregnant women
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12
Q

What are the actions of angiotensin receptor blockers on the cardiovascular system?

A

-lower BP, used in HF as a substitute for ACE inhibitors in patients with severe cough or angioedema

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13
Q

What are the pharmokinetics of angiotensin receptor blockers?

A
  • orally active and require once daily dosing
  • losartan
  • eliminated in urine and feces
  • all are highly plasma protein bound except for candesartan which has a large volume of distribution
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14
Q

What are adverse effects of angiotensin receptor blockers?

A
  • similar to ACE inhibitors but do not produce cough

- contradindicated in pregnancy

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15
Q

What are the benefits of administering B blockers?

A
  • improved systolic function and reverse cardiac remodeling
  • decrease HR and inhibit release of renin
  • prevent direct deleterious effect of NE on cardiac muscle
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16
Q

What are the two B-blockers approved for use in HF?

A

-carvedilol and metoprolol

17
Q

What is the mechanism of carvedilol and metaprolol?

A
  • C: nonselective B-blocker and also blocks alpha- adrenoreceptors
  • M: B1-selective antagonist that reduces mortality
18
Q

When are B-blockers recommended?

A

-all patients with heart disease except those at high risk of acute HF but may not show any symptoms

19
Q

What is the mechanism of diuretics in HF?

A
  • relieve pulmonary congestion an peripheral edema
  • reduce symptoms of volume overload, orthopnea and paroxysmal nocturnal dyspnea
  • dec
20
Q

What is the mechanism of diuretics in HF?

A
  • relieve pulmonary congestion an peripheral edema
  • reduce symptoms of volume overload, orthopnea and paroxysmal nocturnal dyspnea
  • decrease venous return to the heart which decreases cardiac worklad and O2 demand
  • loop diruetics are the most commonly used diuretics
21
Q

What is the mechanism of direct vasodilators?

A
  • decrease in cardiac preload by increasing venous capacitance
  • arterial vasodilators reduce systemic arteriolar resistance and decrease afterload
  • nitrates are commonly used
  • if patient is intolerance of ACE inhibitors, combo of hydralazine and isosorbide dinitrate may be used (effective in black patients)
  • hydralazine decreases afterload and organic nitrate reduces preload
22
Q

What is the general mechanism of inotropic agents? ex: digitalis glycosides

A

-increase contractility of the heart and increase cardiac output by increasing cytoplasmic Ca2+ concentration that enhances contractility of the heart

23
Q

What is the specific mechanism of digitalis glycosides?

A
  • regulation of cytosolic Ca2+ concentration: decrease Na concentration gradient so that the Na*/Ca2+ exchanger cannot extrude Ca2+ from the myocyte in exchange for Na+ (the concentration gradient is a major determinant of the net movement of ions)
  • > there is also a Na+/K+ ATPase exchanger which restores the concentration gradient of Na+ so when digoxin is used to inhibit this Na+/K+ exchange the resting membrane potential is increased which makes the cardiac cell more excitable

-increased contracility of the cardiac muscle:

24
Q

What is the specific mechanism of digitalis glycosides?

A
  • regulation of cytosolic Ca2+ concentration: decrease Na concentration gradient so that the Na*/Ca2+ exchanger cannot extrude Ca2+ from the myocyte in exchange for Na+ (the concentration gradient is a major determinant of the net movement of ions)
  • > there is also a Na+/K+ ATPase exchanger which restores the concentration gradient of Na+ so when digoxin is used to inhibit this Na+/K+ exchange the resting membrane potential is increased which makes the cardiac cell more excitable
  • increased contracility of the cardiac muscle: increased myocardial contraction leads to a decrease in end diastolic volume, increases the ejection fraction
  • > the improved circulation results in a decrease of sympathetic stimulation which reduces peripheral resistance

digoxin slows down conduction through the AV node which accounts for its use in atrial fibrillation

25
Q

What are the indications of digoxin?

A
  • indicated in patients with severe left ventricular systolic dysfunction after inititation of ACE inhibitors and diuretic therapy
  • major indication: HF with atrial fibrillation
  • not indicated in patients with diastolic or right sided HF
26
Q

What is the general mechanism of inotropic agents? ex: digitalis glycosides, B-adrenergic agonists, phosphodiesterase inhibitors

A

-increase contractility of the heart and increase cardiac output by increasing cytoplasmic Ca2+ concentration that enhances contractility of the heart

27
Q

What are the pharmokinetics of digoxin?

A

digoxin: -very potent and eliminated in the kidneys
- large volume of distribution becuase it accumulates in muscle

digitoxin: much longer half life and metabolized by the liver before being excreted in the feces

28
Q

What are the adverse effects of digoxin?

A
  • hypokalemia
  • renal insufficiency
  • severe toxicity results in ventricular tacchycardia
  • GI: nausea anorexia
  • CNS: headache, fatigue, blurred vision
29
Q

What are factors predisposing to digoxin toxicity?

A
  • electrolyte disturbances: hypokalemia can percicpitate cardiac arrythmias , hypomagnesemia and hypercalcemia
  • drugs: quinidine, verapamil, and amiodarone can cause digoxin intoxication by displacing digoxin from tissue protein binding sites and by competing with digoxin for renal excretion
30
Q

What is the mechanism of B- adrenergic agonists?

ex: dobutamine

A
  • positive inotropic effect and vasodilation
  • dobutamine: increases intracellular cAMP which activates protein kinase which phosphorylates Ca2+ channels allowing Ca2+ to enter mycoardial cells
  • IV infusion most commonly used to treat acute HF in a hospital setting
31
Q

What is the mechanism of phosphodiesterase inhibitors?

A

Inamrinone and milirinone increase intracellular concentration of cAMP
-short term use IV

32
Q

What is the mechanism of aldosterone antagonists?

A
33
Q

What is the mechanism of aldosterone antagonists?

ex: spironolactone and eplerenone

A
  • patients with HF have elevated levels of aldosterone due to angiotensin II stimulation and reduced hepatic clearance of hormone
  • spironolactone: direct antagonist of aldosterone, reserved for most advance cases of HF; causes retention of K+ as a side effec
  • eplerenone: competitive antagonist of aldosterone at mineralocorticoid receptors; lower incidence of endocrine related side effects; reduces mortality in patients with left ventricular systolic dysfunction and HF after acute MI
34
Q

What are the steps of treatment in patients with HF?

A

Stage A: high risk with no symptoms

  • risk factor reduction, patient education, treat underlying cause (HT/diabetes/dyslipidemia)
  • ACE inhibitors and ARBs in some patients

Stage B: structural heart disease, no symptoms
-ACE inhibiots or ARB blockers in all patients, B-blockers in some patients

Stage C: structural heart disease, precious or current symptoms

  • ACE inhibitors and B-blockers in all patients
  • dietary sodium restriction, diuretics and digoxin

Pharma: Cardiovascular System (7 decks)

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