ALL Pharm cards for Final Review

1421 terms by jclare 

Create a new folder

Advertisement Upgrade to remove ads

what is the cause of heart failure?

heart is unable to pump blood in sufficient amounts from the ventricles to meet the body's metabolic needs

Drugs commonly used for heart failure?

ACE inhibitors (vasodilators)
Angiotensin receptor blockers
diuretics
spironolactone
beta blockers
cardiac glycosides
phosphodiasterase inhibitors
b-type natriuretic peptides

what does inotropic mean?

force or energy of muscular contractions

definition of chronotropic

rate of the heartbeat

definition of dromotropic

the conduction of electrical impulses

How do ACE inhibitors help wtih decreased cardiac output?

vasodilator- get more blood out

decrease the after load, increase cardiac output

how do ARBs help with heart failure?

same as ACE inhibitors
decrease afterload, increase cardiac output

how do diuretics treat heart failre?

decrease volume around heart

what effect do beta blockers have on contractility of the heart? Why is this good for heart failure?

-decrease contractility
-beta blockers are cardioprotective against catecholamines

Spironolactone is what kind of diuretic?

potassium sparing diuretic

what effect does aldosterone have on the heart?

remodeling

why is spironolactone good for heart failure?

decreases chance of remodeling from occuring

what are the 2 major side effects of spironolactone?

hyperkalemia and gynecomastia

what is another name for Cardiac Glycosides?

Digoxin, digitalis

Is digoxin used to prolong life?

No, improves quality of life

what effect does digoxin have on the heart?

-increase in force of myocardial contraction without an increase in oxygen consumption
-reduced heart rate
-decreases automaticity at SA node, decreases AV nodal conduction

In other words digoxin does what?

-increased stroke volume and cardiac output
-pseudodiuretic- improved renal perfusion

digoxin adverse effects

colored vision (green, yellow, purple), seeing halos
nausea, vomiting, anorexia
dysrhythmias, bradycardia

therapeutic range for digoxin?

very narrow, 1-2ng/ml

what increases risk of toxicity in digoxin?

hypokalemia

what should be monitored prior digoxin dose?

potassium levels, heart rate (hold dose: <60, >120 bpm)

What food should be avoided with digoxin?

high fiber foods

what effect do phosphodiesterase inhibitors have on heart?

vasodilation=decrease after load, increase cardiac output
positive inotropic response= increase heart rate

common inodilators?

"rinone"
-inamrinone (Inocor)
-milrinone (Primacor)

When should phosphodiesterase inhibitors be used?

When patient has not responded to treatment of digoxin, diuretics, and/or vasodilators

How long should phosphodiesterase inhibitors be used?

short term

Adverse effects of Phosphodiesterase inhibitors

-thrombocytopenia
-elevated liver enzymes
-dysrhythmias

B-type natriuretic peptide (BNP)

nesiritide (Natrecor)

What effect does nesiritide (Natrecor) have on heart?

vasodilation=decreased after load, increased cardiac output

When should b-type natriuretic peptides be used?

Last resort

How is nesiritide (Natrecor) administered?

IV, in IC unit

What causes angina?

when the supply of oxygen int he blood is insufficient to meet the demands of hte heart, the heart muscle "aches"

what are the main objectives in treating angina?

1.increase blood flow to heart muscle
2. decrease myocardial oxygen demand

Main drug classes to treat angina

-nitrates
-beta blockers
-calcium channel blockers

routes of administration for nitrates?

sublingual, buccal, oral, chewable tablets, iv, ointments, transdermal patches, translingual sprays

nitrates MOA

-cause relaxation of smooth muscles of blood vessels leading to vasodilation
-potent dilating effect especially on coronary arteries

Result of nitrates

increase oxygen to myocardial tissues

nitrates can also help what symptom?

alleviate coronary artery spasms

Do rapid acting forms of nitrates treat or prevent angina? What about long-acting forms?

-rapid acting-treat acute anginal attacks (sublingual tablets, intravenous infusion)
-long acting- prevent episodes

adverse effects of nitrates

-headache
-tachycardia, postural hypotension
-tolerance

When does tolerance of nitrates occur?

patients taking around the clock or with long acting forms

how to prevent tolerance

allow regular nitrate free period

transdermal patch-remove at bedtime for 8 hrs, apply new patch in morning

when do you take prn nitrates?

first hint of anginal pain

what is the proper technique for sublingual NTG for anginal pain?

Take 1 SL tab, wait 5 min, if no relief call 911

how many SL tabs can patient take?

up to 3

is burning sensation with SL tabs normal?

yes, indicates drug is still potent

when should NTG be replenished?

potency is lost in 3 months after bottle has been opened

Which drug should nitrate patients avoid?

"afil" drugs
sildenafil (viagra)
cause additive hypotension effect, potentially dangerous

Beta Blockers MOA

Beta receptors on heart blocked

Effect of Beta Blockers

DECREASE: HR, myocardial contractility, myocardial oxygen demand

How are beta blockers cardioprotective?

block harmful effects of caetcholamines, improving survival afterr MI

adverse effects of BB?

bradycardia, hypotension, altered glucose and lipid metabolism, wheezing and dyspnea

common beta blockers?

atenolol (Tenormin)
metoprolol (Lopressor)
nadolol (Corgard)-nonselective
propranolol (Inderal)- nonselective

what should be monitored on beta blockers?

pulse rate daily- lower than 60 bpm needs to be reported

what may happen if drugs discontinued abruptly?

risk of rebound hypertensive crisis

are beta blockers used for immediate relief or long term prevention of anginas?

long term prevention

Calcium Channel Blockers MOA

cause coronary artery vasodilation

effects of CCBs

decrease myocardial contractility: decreased myocardial oxygen demand

adverse effects of CCBs

acceptable s.e
hypotension, palpitations, tachycardia, bradycardia, CONSTIPATION, nausea

Name three classes of CCBs

Benzothiazepines-diltiazem (Cardiazem, Dilacor)
Phenylalkamine- verapamil (Calan, Isoptin)
Dihydropyridines- "dipines"

how can patients help decrease risk of constipation?

adequate fluids and eat high fiber foods

should patients be warned about postural hypotension?

yes, need to change positions slowly

what should be avoided or cautioned of using when on antianginal drugs?

alcohol consumption, hot baths, hot tubs, whirlpools, saunas
may cause vasodilation, hypotension, and possibility of fainting

4 stages of hypertension

normal <120/<80
prehyper 120-139/80-89
stage 1 140-159/90-99
stage 2 >160/>100

first line drug therapy without other "compelling" indicators

Thiazide diuretics

Compelling indicators

post-MI, high cardiovascular risk, heart failure, diabetes mellitus, chronic kidney disease, previous stroke

Drugs more effective in white patients

beta blockers and ACE inhibitors

Drugs more effective in african americans

CCBs and diuretics

Drugs to tx hypertension

diuretics
adrenergic agents
ACE inhibitors
Angiotensin II Receptor Blockers
Calcium Channel Blockers
Vasodilators
Direct Renin Inhibitors

Diuretics do what?

decrease fluid volume
decrease: preload, cardiac output, total peripheral resistance, workload of heart, BP

Most common diuretic used for BP?

Thiazide

How do alpha 1 antagonists lower BP?

vasodilate

"osin"

How do alpha 2 agonists lower BP?

inhibit norepinephrine, dilate blood vessels

Common alpha 2 agonists?

clonidine (Catapress)
methyldopa (Aldomet)

How do Beta Blockers decrease BP?

reduce heart rate through beta1 blockade
cause reduced secretion of renin

What does antiotensin do?

potent vasoconstrictor

what does ACE do?

converts angiotensin I to angiotensin II

What does angiotensin II do?

potent vasoconstricor
causes aldosterone secretion from adrenals

ACE inhibitors do what?

block ACE
"pril"

ACE inhibitors are beneficial to who?

diabetics
slows progression of renal disease in hypertensive diabetics with renal diseases

Adverse effects of ACE inhibitors

dry unproductive cough
hyperkalemia
angioedema-rare but potentially fatal

What do you need to check before administering ACE inhibitor?

BP
K level
Pregnant or not

Angiotensin II Receptor Blockers (ARBs)
MOA?

allow angiotensin I to be converted to angiotensin II but BLOCK receptors that receive angiotensin II
Block vasoconstriction and release of aldosterone

Common ARB side effect

URI and HA
does NOT cause cough or significant hyperkalemia

ARB suffix?

sartan

CCB MOA?

cause smooth muscle relaxation by blocking the binding of calcium to the receptors, preventing muscle contraction
Decreased BP

indications for CCB?

angina, hypertension, dysrhythmias

CCB adverse effects

hypotension, palpations, tachycardia
CONSTIPATION

Benzothiazepines

diltiazem (Cardizem, Dilacor)
hypertension, angina, dysrhythmia

Phenylalkamines

verapamil (Calan, Isoptin)
hypertension, angina, dysrhythmia

Dihydropridines

"dipine"
hypertension and angina
amlodipine (Norvasc)

nimodipine (Nimotop)

used for vasospasms following subarachnoid hemorrhage

Direct-Acting vasodilators MOA?

directly relax smooth muscle walls of blood vessels

lowerr peripheral resistance and BP
HR increased

Common vasodilators

diazoxide (Hyperstat)
hydralazine (Apresoline)
minoxidil (Loniten)
sodium nitroprusside (Nipride)-used for hypertensive crisis

Direct Renin Inhibitors MOA?

inhibit renin and blocks conversion of angiotensinogen to angiotensin I
ultimately decreases level of angiotensin II

What must be corrected before direct renin inhibitors can be started?

correct hypovolemia and monitor fluid volume closely

Should antihypertensive drugs be stopped abruptly?

NO- may cause rebound hypertensive crisis, may lead to stroke

What must you monitor during therapy?

BP

Is medication only thing patient can do to treat hypertension?

No- watch diet, stress level, weight and alcohol intake

Can patients experience postural hypotension with antihypertensives?

yes-change positions slowly

What should men be aware of that may cause compliance issues?

impotence

What should patients avoid or use with caution when on drug therapy?

hot tubs, hot weather, prolonged sitting or standing, alcohol ingestion.

may lead to fainting and injury

What are pharmacodynamics

What the drug does to the body

What are pharmacokinetics

What the body does to the drug

Absorbtion

movement from the site of administration into the bloodstream

What factors influence absorbtion?

1. route of administration
2. rate of dissolution
3. surface area
4. blood flow to area
5. lipid solubility
6. first pass effect

Distribution

When the drug reaches the target site from bloodstream

Metabolism

breakdown of dug by liver

excretion

elimination of drug from body

Bioavailability

quantifies drug absorption

What does it mean if drug is highly protein bound?

There is less "free" drug to be distributed to tissue which will increase the duration of action

What will happen if a patient takes 2 drugs that are both highly protein bound?

The 2 drugs will compete for binding sites on the protein. One will win and the other will have more "free" drug in the bloodstream which will shorten its expected duration of action and increase the chance of toxicity

Why is hyopalbumenia dangerous for patients taking highly protein bound drugs?

The risk of toxicity will be increased because the lack of available protein will result in more "free" drug in circulation than expected.

What are the 6 rights of drug administration?

1. Right Patient
2. Right Drug
3. Right Dose
4. Right Route
5. Right Time
6. Right Documentation

Mneumonic: Patients Do Drugs Round The Day

In laymans terms what does the PSNS do?

Rest & Digest

What are the 2 divisions of the ANS

1. Parasympathetic
2. Sympathetic

What is the primary neurotransmitter for the PSNS?

Acetyl Choline (ACh)

What are the indicated uses of cholinergic agonists?

1. urinary Retention
2. myasthenia gravis
3. alzheimers disease
4. xerostomia
5. glaucoma

What are the contraidications for cholinergic agonists?

1. drug allergy
2. bowel obstruction
3. bradycardia
4. hypotension
5. COPD
6. peptic ulcers

What are the signs and symptoms of cholinergic crisis?

1. hypotension
2. shock
3. salivation

how do you treat cholinergic crisis?

with an anticholinergic

What does SLUDGE stand for?

S=Salivation
L=Lacrimation
U=Urinary incontenence
D=Diarrhea
G=GI Motility & Secretions
E=Emisis

Used to describe the actions of cholinergic agonists

What happens when cholinergic receptors are activated?

1. Miosis
2. decreased heart rate & contractility
3. bronchial contriction & increased secretions
4. increased GI motility & secretions
5. emptying of bladder and bowel
6. vasodilation
7. sex organ = erect

How do direct acting cholinergic agonists work?

They bind to cholinergc receptors and activate them

How do indirect acting cholinergic agonists work?

They inhibit the action of cholinesterase

What are the types of cholinergic receptors?

1. muscarinic
2. nicotinic

In laymans terms what does the SNS do?

Fight or Flight

What is the primary neurotransmitter of the SNS

norepinephrine

What are the principal actions of the SNS?

1. mydriasis
2. increased heart rate & contractility
3. bronchdilation
4. decrease GI motility & secretions
5. urinary retention
6. constipation
7. vasoconstriction

What is a saying to describe the actions of the SNS?

Can't See, Can't Pee, Can't Spit, Can't ****

What are the receptors of the SNS

1. alpha 1 & 2
2. beta 1 & 2
3. dopamine

What are the effects of alpha 1 activation?

1. vasoconstriction
2. increased BP
3. mydriasis
4. urinary retention

What are the effects of alpha 2 activation?

1. inhibition of norepinephrine
2. vasodilation
3. decreased BP

What are the effects of beta 1 activation?

1. increased heart rate
2. increased contractility (positive inotropic effect)
3. increased renin secretion

What are the effects of beta 2 activation?

1. bronchodilation
2. uterine relaxation

What are the effects of dopaminergic receptor activation?

improved renal perfusion r/t dilation of renal blood vessels

What is the prototype cholinergic direct acting muscarinic agonist?

bethanechol (Urecholine)

What is the MOA for bethanechol (Urecholine)?

relaxes the bladder sphincter

What is bethanechol (Urecholine) used for?

urinary retention, commonly given post-op and/or post partum

What are the S/E of bethanechol (Urecholine)?

* S/E rare by PO, more common by SC *
1. hypotension
2. bradycardia
3. diarrhea

What is the indirect-acting cholinergic agonist prototype:

pyridostigmine (Mestinon)

What is the MOA for pyridostigmine (Mestinon)?

1. inhibits cholinesterase
2. increases force of muscular contractions

What is the primary indication for pyridostigmine (Mestinon)?

myasthenia gravis

What is/are the S/E of pyridostigmine (Mestinon)?

* S/E Rare but Serious *
cholinergic crisis

What are the contraindications of pyridostigmine (Mestinon)?

1. GI obstruction
2. Urinary Obstruction

What is the anticholinergic prototype?

Atropine

What is the MOA of Atropine?

Competes with ACh for binding and inhibits nerve tranmission at those receptors

What are the effects of Atropine?

1. Decreases in salivary, bronchial, GI, and seat gland secretions
2. mydriasis
3. increased HR
4 bronchodilation
5. decreased bladder tone
6. decreased GI Motility

What is Atropine used for?

1. CPR
2. perioperative to decrease GI secretions and motility