pharm exam 2

beta blockers: MOA

reduce CO by blocking beta 1 receptors on the heart, suppress reflex tachycardia in vasodilation, block renin release from kidneys, long term use reduces vascular resistance

mixed alpha 1 and beta 1/2: promote vasodilation

beta blockers: indications

hypertension, angina (decrease workload), dysrhythmias (suppress AV node conduction), MI (reduce pain and infarct size), HF, hyperthyroidism (block heart sensitivity to norepinephrine), migraine prophylaxis, stage fright (decrease tachycardia), pheochromocytoma

beta blockers: adverse effects

beta 1: bradycardia, reduced CO, precipitation of HF, AV heart block, rebound cardiac excitation on rapid withdrawal

beta 2: bronchoconstriction (do not use with asthma patients), hypoglycemia in diabetes/inhibition of glycogenolysis

both: CNS if lipid soluble (propanolol, metoprolol) - depression, insomnia, nightmares, hallucinations

all can affect neonates

signs of HF: SOB, night coughs, extremity edema

beta blockers: naming conventions

-olol: specific to beta

-ilol/-alol: mixed alpha/beta

generic name starting with A-O: B1 selective

generic name starting with P-Z: non-selective

alpha 1 blockers: MOA

block alpha 1 receptors in periphery leading to vasodilation

arterial dilation > decreased BP

venous dialtion > decreased return to heart and decreased CO

alpha 1 blockers: indications

hypertension, reversal of alpha 1 agonist toxicity, benign prostatic hypertrophy, pheochromocytoma, raynaud’s disease

alpha 1 blockers: adverse effects

orthostatic hypotension: move slowly from sitting to standing, take at bedtime

reflex tachycardia

nasal congestion

male sexual dysfunction

alpha 1 blockers: naming convention

-osin

centrally acting alpha 2 agonists: MOA

act in CNS on presynaptic neurons to decrease norepinephrine release

leads to decreased CO, vasodilation

centrally acting alpha 2 agonists: adverse effects

drowsiness

xerostomia (dry mouth) - chew gum, fluids

rebound hypertension with withdrawal - 2-4 days

alpha 2 agonists: names

clonidine, methyldopa

clonidine

alpha 2 agonist

HTN, severe pain, ADHD

not used in pregnancy

abuse potential

patch on upper arm

methyldopa

alpha 2 agonist

prodrug - requires conversion in the brain

does not effect HR or CO

choice in pregnancy

adverse effects: hemolytic anemia, hepatotoxicity

-osin

alpha 1 blocker

-olol/-ilol/-alol

beta blocker

direct acting vasodilators

hydralazine, minoxidil, nitroprusside

hydralazine

MOA: select dilation of arterioles on vascular smooth muscles, no effect on veins > decreased peripheral resistance

indications: HTN with beta blocker to reduce reflex tachycardia, hypertensive crisis, HF

adverse effects: reflex tachycardia, increased blood volume, systemic lupus erythematosus like syndrome (joint and muscle pain, fever, must d/c hydralazine)

minoxidil

MOA: selective dilation of arterioles through direct action on vascular smooth muscles

indications: severe HTN

adverse effects: reflex tachycardia, sodium and water retention, pericardial effusion, excessive hair growth

nitroprusside

MOA: venous and arteriolar dilation

indications: drug of choice for hypertensive emergencies

adverse effects: minimal tachycardia, sodium and water retention, cyanide poisoning, thiocyanate toxicity if used over 3 days (disorientation, psychotic behavior, delirium)

IV infusion

immediate return of previous BP when stopped without another medication

diuretics: types

MOA: block sodium and chloride reabsorption in the nephron to excrete sodium and water

loop, thiazide, potassium sparing, osmotic

loop diuretics: MOA

act in the lick ascending loop of henle (15-20%, most effect on Na reabsorption)

loop diuretics: indications

pulmonary edema in CHF

edema

HTN not controlled by other agents

IV in critical situations

good for patients with severe renal impairment

loop diuretics: adverse effects

ototoxicity (ear damage at high IV doses)

loop diuretics: drugs

furosemide, bumetanide, torsemide, ethacrynic acid

thiazide type diuretics: MOA

act in the distal convoluted tubule (ineffective in severe renal impairment)

thiadize type diuretics: indications

HTN, edema, diabetes insipidus, protection against postmenopausal osteoporosis

thiazide type diuretics: adverse effects

hyperglycemia

hyperuricemia

Mg deficiency

thiazide diuretics: drugs

chlorothiazide

hydrochlorothiazide

thiazide like diuretics: drugs

chlorthalidone

indapamide

metolazone

potassium sparing diuretics: MOA

act in the late distal convoluted tubule and collecting duct

used to counteract potassium loss from loop and thiazide diuretics

potassium sparing diuretics: drugs

spironolactone

triamterene

amiloride

spironolactone

potassium sparing diuretic

MOA: aldosterone antagonist, prevents synthesis of proteins used for Na/K transport (takes 48 hours to work)

indications: HTN, edema, HF

adverse effects: gynecomastia, menstrual irregularities

reduced mortality for patients with HF

triamterene

MOA: direct Na/K exchange inhibitor

indications: HTN, edema

amiloride

MOA: direct Na/K exchange inhibitor

indications: HTN, edema

mannitol

diuretic

MOA: not reabsorbed so it creates high osmotic pressure preventing water from being reabsorbed

indications: reduction of intracranial pressure

diuretics: adverse effects

excessive loss of sodium, chloride, water > dry mouth, thirst, oliguria, weight loss

hypotension > dizziness, light headedness, fainting

hypokalemia (except with potassium sparing) > muscle weakness, cramping, thirst, confusion > eat potatoes and bananas

INTERACTS WITH DIGOXIN > DIGOXIN TOXICITY

RAAS inhibitors: types

ACEi, ARBs, aliskiren, eplerenone

RAAS inhibitors: counseling

monitor BP for 2 hours after first dose, lie down if hypotensive

dry, nonproductive cough

avoid potassium supplements

angioedema - seek immediate medical attention, do not take that class

minimize NSAID use

ACEis: MOA

angiotensin converting enzyme inhibitors

stops angiotensin I > angiotensin II

stops bradykinin > inactive product

ACEis: indications

HTN, HF, MI, nephropathy, primary prevention in patients with high CV risk, diabetic retinopathy

ACEis: adverse effects

first dose hypotension (start low, temporarily stop diuretics)

cough

hyperkalemia

renal failure in renal artery stenosis

fetal injury

angioedema

increased lithium levels

ACEis: naming convention

-pril

-pril

ACE inhibitor

ARBs: MOA

block angiotensin II receptors

ARBs: indications

HTN, HF, nephropathy, MI, stroke prevention, primary prevention, diabetic retinopathy

ARBs: naming convention

-sartan

-sartan

ARB

aliskiren

MOA: direct renin inhibitor

indications: only HTN

adverse effects: angioedema, cough, diarrhea, hyperkalemia, fetal injury and death

eplerenone

MOA: selective aldosterone receptor blocker

indications: HTN, HF

adverse effects: hyperkalemia

calcium channel blockers: types

dihydropyridines, nondihydropyridines

calcium channel blockers: counseling points

monitor BP

note slow HR, SOB, weight gain

edema - ankle and feet swelling

dihydropyradines

calcium channel blocker

MOA: act primarily on vascular smooth muscle > peripheral arteriole vasodilation, increased coronary perfusion; binds and blocks Ca channels directly

indications: angina pectoris (with beta blocker), HTN

adverse effects: flushing, dizziness, headaches, peripheral edema, gingival hyperplasia, reflex tachycardia

more effect on vasodilation, less effect on heart function

nondihydropyradines

calcium channel blockers

MOA: vasodilation to reduce arterial pressure and increased coronary perfusion

indications: angina, HTN, dysrhythmias

adverse effects: CONSTIPATION, excessive cardiac suppression, significant CYP3A4 drug interactions

less effect on vasodilation, more effect on heart function

dihydropyridines: naming convention

-dipine

nondihydropyridines: drugs

verapamil

diltiazem

-dipine

dihydropyradine (CCB)

verapamil

nondihydropyridine (CCB)

diltiazem

nondihydropyradine (CCB)

HTN and pregnancy

chronic HTN: RAAS contraindicated, use methyldopa or labetalol

preeclampsia: use labetalol, magnesium sulfate (antiseizure prophylaxis)

drugs for angina

stable: nitrates, beta blockers, calcium channel blockers, ranolazine

variant: nitrates, calcium channel blockers

organic nitrates: MOA

dilates veins to decrease preload in stable angina

relaxes coronary vasospasm to increase oxygen supply in variant angina

converted to active form of nitric oxide in presence of sulfhydryl groups

organic nitrates: adverse effects

headache, orthostatic hypotension, reflex tachycardia

interacts with PDE5 inhibitors (sildenafil/viagra) from excessive vasodilation

organic nitrates: indications

stable and unstable angina, HF

SL doses for rapid action and lower doses

rapid onset for ongoing angina effect

tolerance develops in a single day - >8 hours drug free overnight

organic nitrates: drugs

nitroglycerin

isosorbide mononitrate

isosorbide dinitrate

beta blockers for angina

exertional angina, reduces risk of death

reduces HR by blocking beta 1 receptors - increase diastole time, increase time blood flows through vessels

suppresses reflex tachycardia when vessels are dilated

goal: 50-60 BPM resting, <100 BPM exertional

start low, increase slowly, do not stop abruptly - may worsen angina attack

calcium channel blockers for angina

arteriolar dilation leads to reduced afterload and relaxed vasospasm

primary drugs: verapamil, diltiazem, nifedipine

reflex tachycardia

ranolazine: MOA

reduces sodium and calcium in myocardial cells > allows efficient energy use

limited efficacy

ranolazine: adverse effects

limited efficacy

risk of dysrhythmias

QT prolongation - do not use with other QT prolongation meds

elevates BP especially in severe renal impairment

constipation, dizziness, nausea, headache

interacts with CYP3A4 inducers and inhibitors - can only be used with amlodipine as a CCB

nitroglycerin: counseling

SL: under tongue until fully dissolved

call 911 or go to ED if pain is not relieved in 5 minutes

can take 2 more doses 5 minutes apart

storage: dry, room temperature, original container

avoid alcohol

do not abruptly stop long term therapy

HF drugs

OP - first line: diuretics, RAAS inhibitors, beta blockers

OP - second line: digoxin, isosorbide dinitrate/hydralazine

IP: dopamine, dobutamine, milrionone, nitroglycerin, nesiritide

diuretics for HF

for symptom reduction in volume overload

decreases venous and arterial pressure, edema, cardiac dilation

thiazide, loop, potassium sparing

ACEi/ARBs for HF

improve functional status and prolongs life

ACEi: first line, impacts cardiac remodeling by elevating bradykinin

venous and arteriolar dilation, suppression of aldosterone release

start slowly, titrate up

sacubitril + valsartan

sacubitril: neprilysin inhibitor

valsartan: ARB

increases natiuretic peptides, promotes vasodilation, promotes sodium and water loss

aldosterone antagonists for HF

most commonly used: spironolactone

used when benefit over ACEi is needed

aldosterone antagonists for HF: MOA

decrease myocardial remodeling

decrease risk of dysrhythmias

blocks sympathetic NS activation

beta blockers for HF

ONLY carvedilol, bisoprolol, extended release metoprolol succinate

prevents heart from excessive sympathetic stimulation

start low, go slow

digoxin: MOA

increases myocardial contractility: inhibits Na/K/ATPase pump > increased calcium > increased cardiac contractility > increased CO

increased CO = decreased renin release, decreased sympathetic tone, increased urine production

does not fix underlying problem of cardiac remodeling

therapeutic range: 0.5-0.8 ng/mL

oral or IV

digoxin: adverse effects

low potassium > digoxin toxicity

high potassium > digoxin ineffective

alters electrical properties of the heart = dysrhythmias > withdraw from digoxin and diuretics, use antidysrhythmic drugs

anorexia, nausea, vomiting - acts on chemoreceptor trigger zone

fatigue

visual disturbances

low HR

DIGIFAB for overdose

digoxin: contraindications

AV block

ventricular dysrhythmia

severe heart disease

digoxin: drug interactions

drugs affecting potassium: diuretics, ACEis, ARBs

quinidine

beta blockers and non-DHP CCBs

drugs changing dixogin absorption or bioavailability

digoxin: counseling

take exactly as prescribed, do not double dose

limit salt and excessive fluids

1 alcoholic drink/day

mild exercise

monitor pulse

monitor digoxin toxicity

sympathomimetic inotropes: MOA

activation of B1 receptors to increase heart contractility > increased CO and kidney perfusion > elimination of water and sodium > decreased heart workload

sympathomimetic inotropes: adverse effects

tachycardia

cardiac dysrhythmias

possible anginal pain

monitor HR, BP, ECG, urine output continuously and adjust dose as needed

sympathomimetic inotropes: drugs

dobutamine or dopamine IV infusions - give through dedicated line

phosphodiesterase inhibitor inotropes: MOA

inhibits PDE3 > prevents cAMP breakdown > increases cardiac contractility

continuous HR, BP, ECG monitoring

phosphodiesterase inhibitor inotropes: adverse effects

ventricular dysrhythmias, hypokalemia, hypotension

phosphodiesterase inhibitor inotropes: drugs

milrinone IV - use dedicated IV line

drugs to avoid in HF

antidysrhythmic agents

CCBs

NSAIDs - can also increase toxicity of HF medications

antidysrhythmic class IA

sodium channel blockers

delays repolarization

widens QRS, prolongs QT

quinidine, procainamide, disopryamide

antidysrhythmic class IB

sodium channel blockers

accelerate repolarization

no change to ECG

lidocaine, phenytoin, mexiletine

antidysrhythmic class IC

pronounced prodysrhythmic action

widens QRS, prolongs PR

flecainide, propafenone

antidysrhythmic class II

beta blockers

reduce Ca entry and depresses phase 4 repolarization

prolongs PR, bradycardia

propanolol, esmolol, acetbutolol

antidysrhythmic class III

potassium channel blockers

delay fast potential repolarization

prolongs QT and PR, some widen QRS, some bradycardia

amiodarone, dronedarone, sotalol, dofetilide, ibutilide

antidysrhythmic class IV

calcium channel blockers

inhibit Ca entry, depresses phase 4 repolarization

prolongs PR, bradycardia

verapamil, diltiazem

antidysrhythmic other drugs

adenosine - prolongs PR

digoxin - prolongs PR, depresses ST

class IA sodium channel blockers: MOA

moderate sodium channel blockage

decrease conduction velocity in atria, ventricles, his-purkinje system

delays ventricular depolarization and repolarization

oral, IV, IM

class I sodium channel blockers: drugs

procainamide, quinidine

procainamide: MOA

Na channel blocker

antidysrhythmic short term treatment

evenly spaced around the clock

procainamide: adverse effects

systemic lupud erhythematous (SLE) like syndrome

blood dyscrasias: signs of infection, bruising, bleeding

quinidine: indications

Na channel blocker

long term antidysrhythmic

supraventricular and ventricular dysrhythmias

antimalarial, antipyretic