Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
167 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
What is the suffix for all Angiotensin Receptor Blocking Agents (ARB)?
|
-sartan
|
|
|
|
What is the suffix for all Dihydropyridine (DHP) Calcium Channel Blockers (CCB)?
|
-dipine
|
|
|
|
What are the 8 classes of anti-hypertensives?
|
Diuretics, Beta-blockers, ACE Inhibitors, Angiotensin Receptor Blockers, Calcium Channel Blockers, Alpha-1 antagonists, Alpha-2 agonists, and direct vasodilators
|
|
|
|
What is the suffix for all Alpha-1 antagonists?
|
-zosin
|
|
|
|
What is the equation for BP?
|
BP= cardiac output (CO) x peripheral vascular resistance (PVR)
or BP = CO x PVR |
|
|
|
What can cause an increase in CO but not PVR?
|
increased fluid volume
|
|
|
|
What can cause an increase in PVR and CO?
|
excess stimulation of the RAAS and SNS overactivity
|
|
|
|
What are the 4 types of diuretics?
|
Carbonic Anhydrase Inhibitors, Loop diuretics, Thiazide diuretics, and K+ Sparing Diuretics
|
|
|
|
What are the characteristics of Carbonic Anhydrase Inhibitors?
|
MOA: promotes the excretion of Na+, H20, & HCO3- by inhibiting carbonic anhydrase
PK: Short-half life & absorbed from GI tract Agents: acetazolamide Indications: high-altitude sickness & glaucoma Misc: Limited usefulness as a diuretic |
|
|
|
All diuretics reduce:
|
PVR, CO, and blood volume
|
|
|
|
What are the properties of diuretics?
|
Diuretics are drugs that increase urine production
Carbonic anhydrase inhibitors –Weak diuretics Loop diuretics –Increase sodium, potassium, calcium, and magnesium excretion –Mainly used to decrease volume (water) in states of edema Thiazide diuretics –Increase sodium, potassium, and magnesium –Mainly used to treat high blood pressure (hypertension) and to decrease volume (water) in states of edema Potassium-sparing diuretics –Inhibit potassium excretion –Mainly used to prevent significant losses of potassium |
|
|
|
What are the agents for Potassium-Sparing Diuretics?
|
triamterene (PO)
spironolatone (PO) |
|
|
|
What are the AEs of Potassium-Sparing Diuretics?
|
Decreased BP, GI problems, & increased K+ levels
|
|
|
|
What is the MoA for Beta-blockers?
|
–Decrease heart rate (chrontropic) and cardiac output (inotropic); blocks Beta-1 receptors in heart
-SNS inhibition –Inhibit the release of renin from the kidneys - |
|
|
|
Which Beta-blockers are available in IV form?
|
Esmolol (only)
Labetalol Propranolol |
|
|
|
What are the 4 differences between the beta-blockers?
|
1) Beta-selectivity (B-2 is respiratory)
2) Alpha-1 blockade 3) ISA (intrinsic sympathomimetic activity); pts with bradycardia may experience tachycardia **4) Lipid Solubility 4A) lipophilic = more 1st pass hepatic metabolism 4B) hydrophilic = renal elimination |
|
|
|
Which 3 beta-blockers have beta-selectivity?
|
atenolol
esmolol metoprolo |
|
|
|
Which 2 beta blockers have alpha blockade activity?
|
carvedilol
labetalol |
|
|
|
Which beta-blocker has the shortest half-life?
|
esmolol (10 mins)
|
|
|
|
Which beta blockers have high lipid solubility?
|
carvedilol
propanolol |
Carve a Pumpkin
|
|
|
Which beta blockers have low lipid solubility?
|
esmolol
atenolol |
|
|
|
What are the AEs of beta blockers?
|
-Bronchospasm due to B-2 blockade
- bradycardia - weight gain - (-) psych effects (highly lipid soluble more likely to cause these as they more readily cross blood-brain barrier - hypotension |
|
|
|
What are the four factors Beta-Blockers reduce?
|
PVR, CO, plasma renin activit, and left ventricular hypertrophy
|
|
|
|
What is the MoA for Angiotensin-Converting Enzyme Inhibitors (ACEI)?
|
Inhibit RAAS by preventing conversion of angiotensin I to angiotensin II, resulting in lower PVR
- Inhibit degradation of bradykinin and increase synthesis of vasodilating prostaglandins |
|
|
|
What is the only ACE Inhibitor whose route is IV only and whose name doesn't end in -pril?
|
Enalaprilat
|
|
|
|
Are ACE Inhibitors fast acting or slow acting?
|
Fast
|
|
|
|
Which ACE Inhibitor has the shortest half-life?
|
captopril (2.2 hrs)
|
|
|
|
What is the only ACE Inhibitor that undergoes hepatic metabolism?
|
captopril
|
Liver Captain
|
|
|
Which ACE Inhibitor has the lowest bioavailability?
|
lisnopril (25 %)
|
Lying Belgians Lied
|
|
|
What is monitored in Pts on ACE Inhibitors?
|
CrCl
|
|
|
|
What are the AEs of ACE Inhibitors?
|
- Increased K+
- Acute Renal Failure - angioedemea - cough due to accumulation of bradykinin |
|
|
|
What drugs interact with ACE Inhibitors?
|
K+ supplements and K+ sparing diuretics
|
|
|
|
What special population consideration is there for ACE Inhibitors and why?
|
African-Americans due to low renin activity resulting in hgiher amts of angioedema and cough
|
|
|
|
Why are Angiotensin Receptor Blocking Agents (ARB)used?
|
When ACE Inhibitors can't be used due to cough
|
|
|
|
What is the MoA for Angiotensin Receptor Blocking Agents (ARB)?
|
Selectively block the vasoconstrictive effects of
angiotensin II by blocking binding of angiotensin II to its receptor |
|
|
|
What is the only route of administration for Angiotensin Receptor Blocking Agents (ARB)?
|
PO
|
|
|
|
What effects do ACEIs and ARBs have on PVR, CO, blood volume, plasma renin activity, and left ventricular hypertrophy?
|
Decreases PVR, neutral for CO, neutral for BV, increases PRA, decreases LVH
|
|
|
|
What is the MoA for Calcium Channel Blockers (CCB)?
|
Decreases PVR by block Ca++ entry into smooth muscle
|
|
|
|
Which DHP Calcium Channel Blockers (CCB) is available IV?
|
nicardipine
|
|
|
|
What is the primary DHP Calcium Channel Blockers (CCB)?
|
amlodipine
|
pine tree
|
|
|
What are the non-DHP Calcium Channel Blockers (CCB) and what is different about their PK?
|
verapamil (PO, IV)
diltiazem (PO, IV) |
Vera Insinuates Dilbert Is Vain
|
|
|
What are the AEs of DHP Calcium Channel Blockers (CCB)?
|
-reflex tachycardia
-headache and flushing -peripheral edema |
|
|
|
What are the AEs of non-DHP Calcium Channel Blockers (CCB)?
|
bradycardia
cardiac arrest |
|
|
|
Which lowers HR more, verapamil or diltiazem?
|
verapamil
|
|
|
|
Which causes a greater reduction in BP: DHP or non-DHP Calcium Channel Blockers (CCB)?
|
DHP
|
|
|
|
What are the only two factors Calcium Channel Blockers (CCB) reduce?
|
PVR and left ventricular hypertrophy
|
|
|
|
What is the MoA of both Alpha-1 antagonists and Alpha-2 agonists?
|
Decrease sympathetic stimulation to cause
vasodilation and thus reduce blood pressure |
|
|
|
When should the use of Alpha-1 antagonists be restricted?
|
In Pts with cardiovascular disease
|
|
|
|
What are the AEs of Alpha-1 antagonists?
|
1st dose: hypotension
Chronic dosing: Na+ and H20 accumulation |
|
|
|
What are the 2 Alpha-2 agonists and what forms are they available in?
|
clonidine: PO & transdermal
methyldopa: PO |
|
|
|
What AEs are general to Alpha-2 agonists?
|
Sedation and headache
|
Shipping and Handling
|
|
|
What Alpha-2 agonist AEs are specific to methyldopa?
|
depression
auto-immune disorder (hepatitis) |
|
|
|
What advantage do Alpha-2 agonists have as anti-HTN meds?
|
They're Pregnancy Category B
|
|
|
|
What class of anti-HTN drugs are considered 3rd or 4th line?
|
Direct Vasodilators
|
|
|
|
What are the two Direct Vasodilators agents?
|
hydralazine
sodium nitroprusside |
|
|
|
What are the AEs of hydralazine?
|
tachycardia
fluid retention hepatitis |
Fast hands Retain Holdings
|
|
|
What are the AEs of sodium nitroprusside?
|
hypotension, cyanide toxicity, dizziness, weakness, flushing
|
|
|
|
T/F: A1 antagonists, A2 agonists, and Direct Vasodilators all raise PVR.
|
False
|
|
|
|
Direct Vasodilators have what effect on blood volume?
|
They increase it.
|
|
|
|
What is coronary ischemia?
|
lack of O2 saturation to the heart
|
|
|
|
What are the drugs used for angina?
|
Nitrite and Nitrates
CCB B-blockers |
|
|
|
What is the MoA for Nitrates?
|
Convert to nitrate oxide leading to vasodilation
|
|
|
|
What route of administration of nitrates is used in unstable angina?
|
IV
|
|
|
|
What route of administration of nitrates is used in acute angina?
|
SL
|
|
|
|
What routes of administration are used for angina prophylaxis?
|
topical, transdermal, and oral
|
|
|
|
What is the difference between the oral nitrates isosorbide dinitrate/mononitrate
|
The mono- salt is long acting and the di- salt is short acting.
|
|
|
|
Can nitrates be used as monotherapy?
|
NO
|
|
|
|
What is the MoA behind nitrate tolerance?
|
Depletion of sulfhydryl groups required to activate cyclic GMP (responsible for
vasodilation) |
Gimp
|
|
|
What should nitrates be used with?
|
calcium antagonist or B-blocker
|
|
|
|
What are the AEs of nitrates?
|
hypotension
headache |
|
|
|
What drug class do nitrates have significant interactions with?
|
Phosphodiesterase-5 inhibitors (Viagra); causes shock
|
|
|
|
When are CCBs used for angina?
|
When a pt has a CI for a beta-blocker
|
|
|
|
Beta-blockers with ISA should never be used in pts with:
|
coronary artery disease
|
|
|
|
What is the sinoatrial (SA) node's function?
|
natural pacemaker
|
Picante
|
|
|
What is the atrioventricular (AV) node's function?
|
To relay impulse from SA after atrial contraction down through Perknje system, causing stimulation of ventricular muscle fibers
|
|
|
|
What's the difference in the kinds of channels between the SA & AV nodes and the atrial and ventricular muscle?
|
SA & AV nodes are predominantly calcium channels (slow
conduction channels Muscle is predominantly sodium channels (fast conduction channels) |
|
|
|
What action do Class I antiarrhythmic drugs have?
|
Block sodium channels
|
|
|
|
What effect do Class Ia drugs have on the cardiac conduction system?
|
Slow phase 0 depolarization (Na+ influx)
|
|
|
|
What effect do Class Ib drugs have on the cardiac conduction system?
|
Shortens phase 3 repolarization (slow inward movement of Ca++)
|
|
|
|
What effect do Class Ic antiarrhytmic drugs have on the cardiac conduction system?
|
Slows phase 0 depolarization (Na+ influx)
|
|
|
|
What effect do Class II antiarrhytmic drugs have on the cardiac conduction system?
|
Suppresses phase 4 depolarization
|
|
|
|
What effect do Class III antiarrhytmic drugs have on the cardiac conduction system?
|
Prolongs phase 3 repolarization (rapid efflux of K+)
|
|
|
|
What effect do Class IV antiarrhytmic drugs have on the cardiac conduction system?
|
Shortens action potential
|
|
|
|
What are the Class Ia antiarrhytmic drugs?
|
Quinidine
Procainamide Disopyramide |
|
|
|
What additional effect does the Class Ia antiarrhytmic drug Quinidine have?
|
Blocks K+ channels
|
|
|
|
What are the Class Ib antiarrhytmic drugs?
|
**Lidocaine**
Mexiletine Tocainide Phenytoin |
|
|
|
What are the Class Ic antiarrhytmic drugs?
|
Flecainide
Propafenone |
Flecks of Property
|
|
|
What additional effect does the Class Ic antiarrhytmic drug propafenone have?
|
Beta-blockade effect
|
|
|
|
Class Ib antiarrhytmic drug lidocaine is indicated for:
|
Ventricular arrhythmias due to ischemic heart disease
|
|
|
|
What are the PKs of Class Ib antiarrhytmic drug lidocaine?
|
IV only; heavily metabolized by the liver
|
|
|
|
What is the therapeutic plasma concentration of Class Ib antiarrhytmic drug lidocaine?
|
1.5-5 micrograms/ml
|
|
|
|
What are the adverse effects of Class Ib antiarrhytmic drug lidocaine?
|
Convulsions
Arrhythmia bradycardia CV collapse edema hypotension |
|
|
|
What significant drug interactions does Class Ib antiarrhytmic drug lidocaine have?
|
Substrate of CYP 2D6 & 3A4
Inhibits CYP 1A2, 2D6, & 3A4 |
|
|
|
What is the MoA for Class II Antiarrhythmic Drugs?
|
Block cardiac beta receptors, suppressing phase 4 depolarization, decreasing HR
|
|
|
|
What are the therapeutic uses for Class II Antiarrhythmic Drugs?
|
HR control for supraventricular arrhytmias; prevention of arrhythmias post-cardiothoracic surgery and post-MI
|
|
|
|
How do all Class III Antiarrhythmic Drugs work?
|
Block K+ channels, prolonging phase 3 repolarization
|
|
|
|
What additional effects does Class III Antiarrhythmic Drug solatol have?
|
non-selective beta-blocking effect which means it affects phase 3 and phase 4 conduction
|
|
|
|
What are the PK of Class III Antiarrhythmic Drug solatol?
|
PO only; renal elimination
|
|
|
|
What are the AEs of Class III Antiarrhythmic Drug solatol?
|
- Bradycardia, hypotension, heart failure exacerbation
-fatigue -bronchospasm (since not selective beta-blocker) |
|
|
|
What is the therapeutic use of Class III Antiarrhythmic Drug solatol?
|
refractory atrial and ventricular arrhytmias
|
|
|
|
What is the therapeutic use of Class III Antiarrhythmic Drug ibutilide?
|
acute termination of new onset atrial arrhytmias
|
|
|
|
What are the PK of Class III Antiarrhythmic Drug ibutilide?
|
IV only; extensive 1st pass hepatic metabolism
|
|
|
|
What are the AEs of Class III Antiarrhythmic Drug ibutilide?
|
cardiac arrest
|
|
|
|
What are the drug interactions for Class III Antiarrhythmic Drug ibutilide?
|
Should not be taken with other Class III antiarrhytmic agents (solatol & amiodarone
|
|
|
|
What sets Class III Antiarrhythmic Drug amiodarone apart from other Class III Antiarrhythmic Drugs?
|
Drug of choice for pts with heart failure and has an extremely long half life (40-60 days)
|
|
|
|
What are the PK of Class III Antiarrhythmic Drug amiodarone?
|
PO & IV; erratic absorption when given PO; highly lipophilic; hepatically metabolized
|
|
|
|
What are the AEs of Class III Antiarrhythmic Drug amiodarone?
|
-tremor and visual changes
-corneal microdeposits -hypothyroid (inhibits conversion of T4 to T3) or hyperthyroidism (contains 5 I per molecule) -cardiac arrest and hypotension -pulmonary fibrosis -hepatic failure and hepatitis -skin photosensitivity |
|
|
|
What drug interactions do Class III Antiarrhythmic Drug amiodarone have?
|
Substrate of CYP 3A4
Inhibits 2C9, 2D6, & 3A4 |
|
|
|
What drug interaction does Class III Antiarrhythmic Drug dofetilide have?
|
Substrate of CYP 3A4
|
Simple
|
|
|
What PKs does Class III Antiarrhythmic Drug dofetilide have?
|
PO only; renal excretion; minimal hepat. metabolism
|
|
|
|
What AEs does Class III Antiarrhythmic Drug dofetilide have?
|
cardiac arrest
headache dizziness nausea insomnia |
|
|
|
What therapeutic use does Class III Antiarrhythmic Drug dofetilide have?
|
treatment of atrial arrhythmias
|
|
|
|
What actions do Class IV Antiarrhythmic Drugs have?
|
Blocks Ca++ channel
Shortens Action Potential Slows HR |
|
|
|
What are the MoA of digoxin?
|
–Na+K+ATPas inhibitor---enhance Ca++
entry into the cell---increases contractility (positive inotropic effect) –Slows heart rate (chronotropic effect) –Decreases central sympathetic outflow |
Nancy Kicked Alan Inside to Elicit Cock Entry into her Cervix and Increased his Cum; Sympathy is not therapeutic
|
|
|
What are the therapeutic uses of digoxin?
|
–Atrial arrhythmias
–Chronic heart failure |
|
|
|
What are some PK properties of digoxin?
|
-Renally eliminated--not dialyzable
-Long half life -IV, tablet, capsule, & elixir -Large volume of distribution |
|
|
|
What determines whether or not a loading dose will be used with digoxin?
|
Whether or not it's used to slow heart rate(chronotropic)
|
|
|
|
How is dosing of digoxin modulated?
|
Based on renal function
|
|
|
|
What are the AEs of digoxin?
|
GI distress, emesis
headache, "halos" cardiac arrhytmias |
|
|
|
How do you adjust the dose of digoxin if taking with amiodarone, quinidine, or verapamil?
|
Cut the normal dose in half of digoxin
|
|
|
|
What is digoxin a substrate of?
|
CYP 3A4
|
|
|
|
What is adenosine?
|
Endogenous adenine nucleoside occurring naturally in
all body cells |
|
|
|
What is adenosine used for?
|
atrial arrhytmias (to slow HR)
|
|
|
|
What are the PKs of adenosine?
|
-EXTREMELY short half life (0.6-10 secs)
-rapidly removed by plasma and vascular endothelial wall |
|
|
|
What are the AEs of adenosine?
|
bradycardia
**cardiac arrest** (flatline upon administration) flushing bronchospasm headache |
|
|
|
Question
|
Answer
|
|
|
|
What happens after renin is released?
|
"It stimulates AI
|
|
|
|
How do the sulfonylureas work?
|
Block ATP-DEPENDENT K+ CHANNEL -> membrane depolarization -> CA2+ influx -> insulin release
|
|
|
|
How does tolbutamide work?
|
Block ATP-DEPENDENT K+ CHANNEL -> membrane depolarization -> CA2+ influx -> insulin release
|
|
|
|
How does glyburide work?
|
Block ATP-DEPENDENT K+ CHANNEL -> membrane depolarization -> CA2+ influx -> insulin release
|
|
|
|
Diuretics
|
reduce volume overload
|
|
|
|
Beta blockers
|
block adrenergic receptors in the heart (reduces h/r and workload)
|
|
|
|
Neuron - Affrent/ Efferent
|
Transmit impulses toward brain/spinal cord | transmits away from the brain and spinal cord
|
|
|
|
ACE Inhibitors
|
"dilates blood vessels
|
|
|
|
Vasodilators
|
"relaxes arterials
|
|
|
|
Alpha2 agonists
|
reduces sympathetic outflow from the brain
|
|
|
|
Alpha 1 blockers
|
vasoldilation
|
|
|
|
What are the different classifications of diuretics?
|
"1. Thiazide Diuretics
|
|
|
|
4. Osmotic Diuretics"
|
|
|
|
|
"Thiazide Diuretics - MOA
|
Uses
|
|
|
|
MOA: Blocks reabsorption of Na and Cl in the distal convoluted tubule. (won't reabsorb water
|
blood volume decreases)
|
|
|
|
S/E: Lyte/H2O imbalance
|
increases uric acid (which causes gout)
|
|
|
|
Loop Diuretics - MOA
|
"Most effective & strongest; produces the greatest amount of diuresis.
|
|
|
|
MOA: Acts in the loop of Henle to block reabsorption of Na & Cl (where the most usually gets absorbed). Doesn't require good renal blood flow."
|
|
|
|
|
"Loop Diuretics - Uses
|
S/E
|
|
|
|
S/E: Lyte and H2O imbalance.(loss of H2O and K)
|
ototoxicity
|
|
|
|
NI: Assess for FVD
|
lyte disturb.; IV does start to work within 5 min. and last up to 2 hrs. Oral dose takes 30-60 min. and lasts up to 8hrs."
|
|
|
|
Potassium Sparing Diuretics
|
"The degree of diuresis is small. It's used as an adjunct to loop or thiazide diuretics. Balances the potassium.
|
|
|
|
S/E: Can cause hyperkalemia
|
arrythmias.
|
|
|
|
NI: Monitor for hyperkalemia."
|
|
|
|
|
ACE Inhibitors
|
"MOA: prevents the conversion of angiotensin I to angiotension II by blocking ACE. End result is vasodilation and decreased reabsorption of Na and H2O.
|
|
|
|
Uses: HTN
|
CHF - reduces blood volume
|
|
|
|
S/E: hypotension
|
first does effect - signif. drop in b/p
|
|
|
|
NI: Start w/ low dose
|
monitor b/p
|
|
|
|
Angiotensin II receptor antagonist
|
"MOA: blocks the receptors of AII
|
|
|
|
S/E: Hypertension
|
headache
|
|
|
|
NI: Instruct patient about multiple drug interactions."
|
|
|
|
|
Beta blockers
|
"They are selective
|
|
|
|
Uses: HTN (first line drug)
|
decreases preload & afterload
|
|
|
|
S/E: Hypotension
|
bradycardia (less than 60). High doses can cause bronchoconstriction & hypoglycemia.
|
|
|
|
NI: Safety
|
monitor h/r
|
|
|
|
Beta 2 Stimulation
|
"Lung: Bronchial dilation
|
|
|
|
Beta 1 stimulation
|
"Cardiac: increase heart rate
|
|
|
|
S/E: tachycardia
|
arrythmias
|
|
|
|
alpha 2 stimulation
|
"Regulates transmitter release. Decreases NE. Blocks sympathetic stimulation.
|
|
|
|
S/E: Hypotension
|
headache
|
|
|
|
alpha 1 stimulation
|
"vasoconstriction: increase b/p
|
|
