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167 Cards in this Set

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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