• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/90

Click to flip

90 Cards in this Set

  • Front
  • Back
1. What are the centrally acting drugs?
a. Clonidine
b. Guanabenz
c. Guanfanine
d. Methyldopa
1. Which drugs are Ace Inhibitors
a. Captopril
b. Analapril
c. Lisinopril
d. Benazepril
e. Fosinopril
f. Quinapril
g. Ramipril
h. Enalapril (IV only)
1. Which drugs are Angeotensin receptor antagonist
a. Losartan
b. Valsartan
c. Condesartan
1. Which drugs are Direct rennin inhibitor
a. Aliskiren
1. Which drugs are Dihydropyridine Ca+ channel blockers
a. Amlodpine
b. Felodopine
c. Isradipine
d. Nicardipine
e. Nifedipine
1. Which drugs are Non- dihydropyridine Ca+ channel blockers
a. Dilitazem
b. Verapamil
c. Bepridil
1. Which drugs are in the “other vasodilators” category?
a. Hydralazine
b. Minoxidil
c. Nitroprusside
d. Fenoldopam
1. Whet effect does alpha blockers have on total cholesterol
a. Decrease it
1. Common drug interactions for Alpha blockers
a. Hypotensive effects is increased by BB and diuretics
1. What effects do BB have on total cholesterol?
a. No change or slight increase
1. Common drug interactions fo BB
a. Cardiac depression increased by diltizem and verapamil
b. Hypotensive effect increased by NSAID’s
1. MOA of clonidine
a. Centrally acting drug
1. What physiological effects do the centrally acting drugs have on the body?
a. Decrease peripheral vascular resistance
b. Decrease LVH
1. Adverse effects of clonidine
a. Dry mouth
b. Fatigue
c. Rebound HTN
d. Sedation
1. Drug interactions of clonidine
a. Hypotensive effect decreased by tricyclic antidepressants
a. Sedative effect increased by CNS Depressants
1. MOA of Guanabenz
a. Centrally acting drugs
1. Adverse effects of Guanabenz
a. Dry mouth
b. Fatigue
c. Rebound HTN
d. Sedation
1. Drug interactions of Guanabenz
a. Hypotensive effect decreased by tricyclic antidepressants
a. Sedative effect increased by CNS Depressants
1. MOA of Guanfanine
a. Centrally acting drugs
1. Adverse effects of Guanfanine
a. Same as clonidine but milder
• Dry mouth
• Fatigue
• Rebound HTN
• Sedation
1. Drug interactions of Guanfanine
a. Hypotensive effect decreased by tricyclic antidepressants
a. Sedative effect increased by CNS Depressants
1. MOA of Methyldopa
a. Centrally acting drugs
1. Adverse effects of methyldopa
a. Autoimmune hemolytic anemia
b. Hepatitis
c. Lupus like syndrome
d. Other adverse effects are the same as clonidine
• Dry mouth
• Fatigue
• Rebound HTN
• Sedation
1. Drug interactions of methyldopa
a. Hypotensive effect increased by levodopa
b. Other interactions are the same as clonidine
1. Methyldopa is the DOC for…
a. DOC during pregnancy for central acting antihypertensive (safest one for short term use during pregnancy)
1. What uis the 1st choice drug of the angeotensin inhibitors?
a. ACE inhibitors
1. Physiological effects of ACE inhibitors
a. Decrease peripheral resistance
b. No change or increase Cardiac output
c. **no change in blood volume
d. Decrease in LVH
e. Increase serum K+
f. No change in total cholesterol
1. If he asks for the active metabolite for an ace inhibitor…how can you ID it?
a. The active metabolite has the name of the parent drug at the beginning…ends in prilet
• Benzapril = Benzeprilat
1. DOA for the ace inhibitors?
a. DOA for all the ACE inhibitors = 24 hours
b. except captopril which is 6-12 hours
1. there are 2 ACE inhibitors that when taken with food they are absorbed less
a. Captopril
b. Quinapril
1. Common adverse effects of ACE inhibitors
a. Acute renal failure in pts with bilateral renal stenosis
b. Cough
c. Hyperkalemia
d. Loss of taste
e. Neutropenia
f. Rash
g. ACE inhibitors are contraindicated during the 2nd and 3rd trimester of pregnancy. Avoid if possible during 1st trimester
1. Common drug interactions of ACE inhibitors
a. Increases serum levels of lithium
b. Hyperkalemic effects increased by potassium sparring diuretics and potassium supplements
c. Hopotensive effects decreased by NSAID’s
1. Which ACE inhibitors can be used for CHF?
a. Captopril, Enalapril, and lisinopril
• ACE inhibitors in CHF cause a Decrease in activation of cardiac angiotensin receptors
• Which causes a decrease in cardiac remodeling and wall thinning 
• Which causes an increase in ventricular performance
• Which causes a decrease in morbidity and mortality
• Studies show that ACE inhibitors decreased the risk of CHF by 37% in post myocardial infarction pts with LV dysfunction
1. Physiological effects of Angeotensin receptor antagonist (ARB)
a. Decrease peripheral resistance
b. No change or increase in Cardiac output
c. No change or increase in blood volume
d. Decrease in LVH
e. Increase in serum K+
f. No change in total cholesterol
1. DOA for the Angeotensin receptor antagonist (ARB)
a. 24 hours
1. There are 2 ARB’s which when taken with food they are absorbed less
a. Losartin
b. Valsartan
1. Common adverse effects of ARB’s
a. Avoid during pregnancy
b. Hyperkalemia
1. Common drug interactions of ARB’s
a. Serum levels of drug increased by cimetidine and decreased by phenobarbitol
1. How are ARB’s useful in CHF?
a. Decrease preload and afterload
1. MOA of Aliskiren
a. Direct rennin inhibitor
1. Is Aliskiren affected by diet?
a. Absorption is reduced by high fat foods
1. DOA of Aliskiren
a. 24 hours
1. Common adverse effects of Aliskiren
a. Hyperkalemia
b. Avoid during pregnancy
c. Little data for renal impairment
1. Common drug interactions of Aliskiren
a. Alkisiren reduces serum levels of furosimide,
b. Cyclosporine increases serum levels of aliskiren
c. Contraindicated with verapamil, cyclosporine, and quinidine
1. MOA of Amlodpine
a. Dihydropyridine Ca+ channel blockers
1. Cardiac effects of the Dihydropyridine Ca+ channel blockers
a. *** Mostly vascular effects (less cardiac effects than the non-dihydropyrdine drugs)
b. Increase in coronary blood flow (good for tx of angina)
c. Decreases peripheral vascular resistance (mostly arterial effect)
d. No change or increase in Cardiac output
e. No change or increase in plasma rennin activity
f. Decrease LVH
g. No effects on
• SA node
• Cardiac capacity
• AV node
• Blood volume
h. Nicardipine and Nifedipine have the least cardiac effects of the CCB
1. Adverse effects of Dihydropyridine Ca+ channel blockers
a. Dizziness
b. Edema
c. Gingival hyperplasia
d. Headache
e. Tachycardia (reflex tachycardia)
1. Common drug interactions of Dihydropyridine Ca+ channel blockers
a. Serum levels of drug increased by
• azole antifungal agents,
• cimetidine,
• and grape fruit juice
1. Elimination half life of Amlodpine
a. 40 hours
1. Clinical use of Amlodpine
a. Amlodipine is a long acting dihydropiridine CCB that is suitable for the control of BP and prevention of angina symptoms
• Studies have shown that amlodipine reduces hospitalization and the need for revascularization in angina pts
• Combining amliodipine with a diuretic will enable the pt to achieve normal BP in a shorter amount of time using a lower dose of each drug
1. MOA of Felodopine
a. Dihydropyridine Ca+ channel blockers
1. Elimination half life of Felodopine
a. 14 hours
1. MOA of Isradipine
a. Dihydropyridine Ca+ channel blockers
1. MOA of Nicardipine
a. Dihydropyridine Ca+ channel blockers
1. Elimination half life of Nicardipine
a. 3 hours
1. MOA of nifedipine
a. Dihydropyridine Ca+ channel blockers
1. MOA of Dilitazem
a. Non- dihydropyridine Ca+ channel blockers
1. Cardiac effects of Non- dihydropyridine Ca+ channel blockers
a. Increase in coronary blood flow (good for angina)
b. Decrease SA node automaticity
c. Decrease cardiac contractility
d. Decrease AV node conduction velocity
e. Decreases peripheral vascular resistance (mostly arterial effect)
f. No change or increase in Cardiac output
g. Strong cardiac effects
h. No change or increase in plasma rennin activity
i. Decrease LVH
j. No change in Blood volume
1. Common adverse effects of the Non- dihydropyridine Ca+ channel blockers
a. AV Block
b. Bradycardia
c. Constipation
d. Dizziness
e. Edema
f. Gingival hyperplasia
g. Headache
h. Heart failure
1. Common drug interactions of the Non- dihydropyridine Ca+ channel blockers
a. Increased serum levels of carbamazepine, digoxin, and theophyline
b. Decrease serum levels of lithium
1. Clinical uses of Dilitazem
a. Used as a antiarrhythmic drug
1. How is Dilitazem used as an antiarrhythmic drug?
a. Used to treat reentrant supraventricular tachycardia and protect the ventricles in atrial flutter and fibrillations
b. Of the 2 CCB used for antiarrhythmics verapamil is preferred during pregnancy
c. Specific electrophysiologic properties for Class IV drugs
• Decrease automaticity of the AV node
• Decrease conduction velocity in the AV node
• Increase refractory period in the AV node
------Thereby terminating the AV node reentry that is responsible for the supraventricular tachycardia
• Decrease HR
• Increase PR interval
------By slowing the AV node conduction velocity
• No change in QRS or QT
• Slow phase 4 depolarization markedly prolonging the PP interval
1. onset of action of Dilitazem
a. 2 hours
1. DOA of Dilitazem
a. 8 hours
1. Elimination half life of Dilitazem
a. 5 hours
1. MOA of verapamil
a. Non- dihydropyridine Ca+ channel blockers
1. Clinical uses of Verapamil
a. Used as an antiarrhythmic
1. How is verapamil used as an antiarrhythmic drug?
a. Used to treat reentrant supraventricular tachycardia and protect the ventricles in atrial flutter and fibrillations
b. Of the 2 CCB used for antiarrhythmics verapamil is preferred during pregnancy
c. Specific electrophysiologic properties for Class IV drugs
• Decrease automaticity of the AV node
• Decrease conduction velocity in the AV node
• Increase refractory period in the AV node
------Thereby terminating the AV node reentry that is responsible for the supraventricular tachycardia
• Decrease HR
• Increase PR interval
------By slowing the AV node conduction velocity
• No change in QRS or QT
• Slow phase 4 depolarization markedly prolonging the PP interval
1. Onset of action of verapamil
a. 2 hours
1. DOA of verapamil
a. 9 hours
1. Elimination half life for verapamil
a. 5 hours
1. MOA of Bepridil
a. Non- dihydropyridine Ca+ channel blockers
1. Elimination half life of Bepridil
a. 25 hours
1. MOA of Hydralazine
a. Falls under the”other vasodilator” class
1. Physiological effects of Hydralazine
a. Decrease peripheral vascular resistance
b. increase cardiac output
c. increase blood volume
d. increase plasma rennin activity
e. Increase LVH
1. Adverse effects of Hydralazine
a. Angina
b. Dizziness
c. Fluid retention
d. Headache
e. Lupuslike syndrome
f. Tachycardia
1. Drug interactions of Hydralazine
a. Hypotensive effects decreased by NSAID’s
1. Clinical uses of Hydralazine
a. Can be used to tx heart failure
b. **Cardiac effects
• Reflex tachycardia
• Decrease afterload
1. MOA of Minoxidil
a. Falls under the ”other vasodilator” class
1. Physiological effects of Minoxidil
a. Decrease peripheral vascular resistance
b. Increase Cardiac output
c. Increase blood volume
d. Increase plasma rennin activity
e. Increase LVH
1. Adverse effects of Minoxidil
a. Angina
b. Dizziness
c. Fluid retention
d. Headache
e. Hypertrichosis
f. Pericardial effusion
g. Tachycardia
1. drug interactions of minoxidil
a. Hypotensive effects decreased by NSAID’s
1. Clinical uses of Minoxidil
a. Used for severe HTN in hypertensive emergencies only
1. MOA of Nitroprusside
a. Falls under the ”other vasodilator” class
b. ROA = IV only
1. Physiological effects of Nitroprusside
a. Decrease peripheral vascular resistance
b. Increase Cardiac output
c. Increase blood volume
d. Increase plasma rennin activity
e. **No change in LVH
1. Common adverse effects of Nitroprusside
a. Dizziness
b. Headache
c. Increased intracranial pressure
d. Methemaglobinemia
e. Thiocyanate / cyanide toxicity
1. Clinical uses of Nitroprusside
a. Used for severe HTN and hypertensive emergencies only
1. MOA of Fenoldopam
a. Other vasodilators
b. ROA = IV only
1. Physiological effects of Fenoldopam
a. Decrease peripheral vascular resistance
b. Increase Cardiac output
c. **No change in blood volume
d. Increase plasma rennin activity
e. **No change in LVH
f. **Decreases serum K+
1. Common adverse effects of Fenoldopam
a. Headache
b. Nausea