The flashcards below were created by user
on FreezingBlue Flashcards.
Name all the classes of anti-hypertensives
- 1. Diuretics
- 2. B-antagonists (blockers)
- 3. alpha1 antagonists
- 4. alpha 2 agonists (centrally acting)
- 5. Mixed alpha/beta antagonists
- 6. ACE Inhibitors
- 7. ARBs
- 8. Direct Renin Inhibitors
- 9. Ca+ Ch blockers
- 10. Vasodilators
What is the site of action of Thiazide diuretics?
Distal tubule (where concentration of drug is higher than concentration in the blood)
What is the MOA of Thiazide Diuretics? What do they promote?
MOA: competitive antagonism of Na/Cl- cotransporter in DISTAL TUBULE- which inhibits Na/H2O reabsorption
- -decrease intravascular volume
- -direct vasodilatory effect
What are 4 common AE's of Thiazides?
- Hypokalemia (decreased reabsorption of K+
When should Thiazides NOT be used?
- 1. In renal failure or if CrCl is <30 ml/min
- 2. In pts with Gout
Name the prototypical Thiazide Diuretic?
Name 3 Potassium-Sparing Diuretics?
- Maxide (combo: HCTZ/TMT)
Where is the site of action of K+ Sparing Diuretics?
Renal collecting duct
What is the MOA of K+ Sparing Diuretics? (2)
- 1. Na+ channel blockade in collecting duct
- 2. Increased reabsorption of K+
Are K+ sparing diuretics commonly used as monotherapy?
No. They are usually used in combo with HCTZ's.
What is common AE of K+ Sparing Diuretics?
Name 2 aldosterone antagonists used in heart failure?
Name 3 Loop Diuretics?
- Lasix (furosemide)
What is the MOA of Loop diuretics?
MOA: inhibit Na+, K+, Cl- cotransporters in the Loop of Henle
What 5 AE's can occur with Loop Diuretics?
- Dose related ototoxicity
- "Sulfa" allergy
What are the MOA's of aldosterone antagonists? (2)
- 1. competitive antagonism at the aldosterone receptor
- 2. Inhibition of mineralcorticoid receptors
What AE can aldosterone receptor antagonists cause?
How do B-Blockers work? (6 functions)
- 1. antagonism of catecholamines at B-receptor, which prevents activation of alpha 1 receptor
- 2. Decrease cardiac output via decrease of HR and contractility
- 3. Cause initial compensatory increase in PVR
- 4. Long-term decrease in PVR by inhibition of B-receptors in the kidneys which decrease renin
- 5. Produce resting bradycardia
- 6. Reduce exercise-induced tachycardia
What are common AE's of B-Blockers? (7)
- Acute asthma, wheezing
- Symptomatic bradycardia
- Sexual dysfunction
- Lipid increases
How should B-Blockers be stopped if necessary?
Avoid abrupt stopping of B-Blockers!
What are MOA's of non-selective B-Blockers?
- 1. antagonize catecholamines at B1 and B2 receptors
- 2. inhibit sympathetically induced renin secretion
What are CI of non-selective B-Blockers?
- 1. asthma
- 2. drug interactions with other CYP2D6, 2C19 drugs
Name a non-selective B-Blocker?
What are selective B-Blockers? What suffix do they end with?
- Selective for B1 (end in "olol") have less CNS AE's
- Metoprolol (Lopressor, Toprol XL, atenolol, bisoprolol, esmolol
Name some partial B-Blockers? (suffix ending)
- Acebutolol, carteolol, penbutololm pindolol
What is MOA of Partial B-Blockers?
- ISA (intrinsic sympathomimetic activity
- - less decrease in HR and CO
- -agonism when sympathetic tone is low (less resting bradycardia)
- -antagonism when sympathetic toneis high (still blocks exercise-induced tachycardia)
Name some mixed alpha1/Beta 1, 2 Blockers?
Labetolol and Carvedilol
When is Labetolol (Normodyne, Trandate) used?
- 1. Orall with 3:1 B to alpha antagonism
- 2. IV to treat hypertensive crisis
When is Carvedilol (Coreg) used?
- Primarily in heart failure.
- Non-selective B-blockade and an alpha blockade??
What is the MOA of Apha-1 Blockers?
Inhibit peripheral vasomotor tone, reducing vasoconstriction and decreasing SVR and therefore BP
Prazosin, Terazosin, Doxazosin
What is a precaution with Alpha-1 blockers/antagonists? How are they dosed to prevent this?
- "First dose effects" -postural hypotension
- Dose at HS then titrate up slowly
Which Alpha-1 antagonists are used for BPH?
Terazosin, Doxazosin, Tamsulosin
What is MOA of centrally acting Agents?
- 1. agonize alpha 2 receptors in brain
- 2. reduce sympathetic outflow from vasopressor centers in the brain
What are 7 common AE's with Centrally acting agents?
- impaired concentration
- lactation in men
Which Central agent is used in pregnancy and why?
- Methyldopa (Aldomet)
- Renal blood flow is maintained- so good for renal insufficiency
What are cautions for use of Clonidine?
- 1. avoid abrupt cessation which can lead to rebound hypertension
- 2. PO or transdermal available
- 3. 50/50 hepatic metabolism and renal excretion
Name some ACE inhibitors. What is the common suffix?
Lisinopril, captopril, ramipril, enalapril, fosinopril, quinapril, benzapril
What is the site of action and MOA of ACE Inhibitors?
- ACE receptor in endothelium
- MOA: block conversion of angiotensin 1 to angiotensin II; block inactivation of bradykinin
Name some of the Pro-Drug ACEI?
Ramipril, enalapril, benzepril, fosinopril
Name a population particularly suited for ACEI
Diabetics with proteinuria
Name common AE's of ACEI?
Hyperkalemia, angioedema, cough (due to bradykinin) (NSAIDS may impair effects by blocking bradykinin-mediated vasodilation)
What are CI for ACEI?
- Renal artery stenosis
Name some ARBs? Common suffix?
Losartan, valsartan, candesartan, irbesartan, telmisartan, eprosartan
What is the site of action of ARB's?
Ang II receptor
What is the MOA of ARB's? What makes them different from ACEI's
- competitive binding of Ang II receptor results in decreased peripheral vasoconstriction;
- no effect on ACE or bradykinin- thus no SE of cough or angioedema
What are possible AE's of ARBs? CI's?
- AE: hyperkalemia
- CI: pregnancy
Name a Direct Renin Inhibitor?
- Aliskiren (Tekturna)
- SOA: Renin binding pocket
- MOA: prevents conversion of Angiotensinogen to Ang I by Renin
- CI: pregnancy
What are the 4 general MOAs of Anti-arrhythmics?
- 1. Alter maximum diastolic potential in pacemaker cells and/or the resting membrane potential in ventricular cells
- 2. Alter rate of phase 4 depolarization
- 3. Alter threshold potential
- 4. Alter the action potential duration
Name the Class of Antiarrhythmics which affect Na+ Channels (subclasses)
- Ia: Na and K+:
- Ib: Na
- Ic: Na
Which Class of Antiarrhythmics affect Beta-1 receptors?
Class II.: Beta Blockers
What Channel do Class III Antiarrhythmics affect?
Which Channel does Class IV Antiarrhythmics affect?
Class IV: Ca+: Ca+ Ch blockers
Class Ia Antiarrhythmics block ___ and ____ Channels which have 3 effects on EKG.
- Ia block Na+ and K+
- 1. Prolong repolarization
- 2. Prolong QT interval → torsades de pointes (TdP)
- 3. Decreases conduction velocity
What AE's occur with Class Ia?
What degree of affect do the following Class Ia drugs exhibit these AE's?
(quinidine, procainamide, disopyramide)
- Anti-cholinergic effects due to K+ blockade
- (can't pee, can't spit, can't see)
Name 3 specific facts about quinidine (Class Ia)
- AE: diarrhea, nausea, headache, dizziness
- Met: CYP450
- DI: increases Digoxin levels
Name 3 specific facts about procainamide (Class Ia)
- 1. AE: lupus-like syndrome, thrombocytopenia, neutropenia, anemia
- 2. Requires renal and hepatic adjustments
- 3. Active metabolite is NAPA
Which of the 3 Class Ia agents is a Negative Inotrope with anti-cholinergic AE's? Which condition should it be avoided in?
- Do not use in Heart Failure
Class Ib Antiarrhythmics block____channels.
Examples are ______ and ________
Na+ (binds to both open and inactivated Na+ channels.
Lidocaine and mexilitine
How do Class Ib agents work?
What condition are they used for?
What condition are they ineffective for?
Which enzyme are they metabolized by?
- 1. Shorten repolarization and QT interval
- 2. Used for ventricular arrythmias
- 3. Not effective for supraventricular arrythmias
- 4. Metabolized by CYP450
What are the AE's possible for Class Ib agents?
Neurological: paresthesias, agitation, slurred speech, somnolence, confusion, psychosis and seizure
Class II Anti-arrhythmics are also known as __________
What is MOA of Class II agents? (4)
- 1. Block sympathetic stimulation of B-1 receptors
- 2. Slow SA node firing and conduction through AV node
- 3. Prolong repolarization
- 4. Decrease the rate of repolarization
AE's for Class II drugs?
Excessive negative inotropic effects, heart block, bradycardia, bronchospasms and insomnia. (Off-target effects of B2 blockade)
Of the Class I (a, b,c) antiarrythmics, which is the most potent Na+ channel blocker?
What are the effects on cardiac function?
- Class Ic
- Depressive effects on cardiac function
- Pro-arrythmic effects
What are AE's of Class Ic drugs?
Sinus-node dysfunction, marked decrease in conduction velocity, conduction block, blurred vision, dizziness
Name 3 Class Ic drugs
Flecainide, propafenone, moricizine, encainide
Class III antiarrhythmics block ____ channels which ________ repolarization.
Ibutilide, dofetilide, sotalol, amiodarone, dronedarone
________ is a Class III drug which also blocks ______ receptors.
___________ is a Class III drug which also blocks ___ and _____ and ______ receptors.
This drug also has a ______ half-life (20-50 days)
- Ca+ and N+ and Beta
_________ is a Class III drug which is similar to amiodarone but it is _______ and therefore has a shorter half-life and has_______ AE's.
- less lipophilic
Class III drugs: Ibutilide and Dofetilide are used for _____________. Which one requires registration by providers and patients if Rx
AE: they can cause ___________
CI: K+ and Mg++ must be monitored
- Atrial flutter/fibrillation and chemical cardioversion.
- Torsades de Pointe
Amiodarone is used to treat _______ and _______.
It has many potential AE's such as (9)
- ventricular and atrial arrhythmias.
- 1. Decrease AV/SA node fx: bradycardia
- 2. Pneumonitis, pulmonary fibrosis
- 3. Hyperthyroidism or hypothyroidism
- 4. Elevated LFT's
- 5. Optic neuritis, corneal microdeposits
- 6. PEripheral neuropathy
- 7. Skin discoloration, photosensitivity
- 8. GI upset
- 9. CYP450 drug interactions
____________ has a more favorable SE profile than Amiodarone. But it may cause __________ and should be used with caution in systolic HF.
Class IV drugs block ____channels. They ____ firing at the ____node and cause slowed conduction velocity through the ____ node. They have ___inotropic effect. They are used for treatment of ____________
- Ca++ into cardiac muscle cells.
- slow, SA, AV
- PSVTs and rate control for afib/aflutter.
Class IV drugs are NOT used for_______.
Examples of the 2 non-dihydropyridines are:
- ventricular arrythmias.
- Verapamil and diltizem
AE's for Class IV drugs are:
- Excessive AV block
- Heart failure
- Constipation, dizziness (Verapamil)
Class IV Ca+ Ch blockers can be divided into __________ and _________.
Dihydropyridines and Nondihydropyridines
The dihydropyridines are selective for _____________. AE's associated with these drugs are____________.
Names of drugs: Amlodipne, felodipine, nifedipine, nicardipine, nimodipine.
- 1. Smooth muscle over cardiac muscle (skeletal muscle is unaffected since contraction is not dependent on extracellular Ca+.
- 2. Reflex tachycardia, peripheral edema, flushing, HA, dizziness
How do vasodilators work? 3 MOA
- 1. NO formation
- 2. K+ channel openers
- 3. D1 stimulation
_______ is a vasodilator which stimulates endogenous ____ to be produced which dilates arterioles only (no venous dilation). IT is rapidly metabolized by _________ and AE's include______________
- SLE-like syndrome with higher doses
________ is a vasodilator which gives off NO itself and causes arterial AND venous dilation. ROA is __________. IT is used in __________. AE's include ____________.
- IV only
- Hypertensive crisis
- Cyanide toxicity
Fenoldopam is a vasodilator which is a _____ receptor agonist. IT decreases PVR and increases renal blood flow. AE's: SLE-like syndrome with high doses.
________ is a K+ channel opener with AE of hypertrichosis when used topically.
ACLS protocol (ABCD)
2 pulseless shockable rhythms responsive to defibrillation
2 non-shockable states unresponsive to defibrillation
- Pulseless electrical activity (PEA)
5 Meds for tx of VT or VF
What is epinephrine's MOA for VT/VF?
Stimulates alpha, B1, B2 to increase cardiac output and BP. Benefits of Epi outweigh the risks in pulseless arrest.
Direct vasoconstrictor, ADH. No inotropic effects.
Acronym for tx of Stable Angina (ABCDEO)
- A: ASA, anti-anginals
- B: B-Blockers, BP
- C: cholesterol, cigarettes
- D: diet, DM
- E: exercise, education
- O: obesity