Pharm exam 1 Flashcards
what are the 3 levels of prescriptive authority?
- full- no physician oversight
- reduced- need oversight to prescribe
- restricted- need oversight to prescribe, diagnose, and treat
3 phases of drug testing before approval
phase 1- test healthy subjects
phase 2- pt. with targeted disease/disorder
phase 3- controlled and uncontrolled clinical trials for safety/efficacy
legend drugs
drugs that have been approved by the FDA that are required by federal or state law to be dispensed only on PRESCRIPTION by a licensed provider
bioavailability
% of drug that’s absorbed and available to reach the target tissues; not all of the administered dosage may be dissolved, absorbed, or survive liver passage.
types of immune mediated ADRs
type 1- hypersensitivity reaction, IgE mediated (angioedema with anaphylaxis)
type 2- antibody dependent cytotoxicity (heparin induced thrombocytopenia)
type 3- immune complex hypersensitivity (arthrus reaction, vasculitis)
type 4- cell mediated or delayed hypersensitivity (drug rash, eosinophilia)
most common herbal preparations for:
anxiety
insomnia
depression
anxiety- kava, mugwort, wormwood, pill-bearing spurge, passionflower
insomnia- melatonin, chamomile, mugwort, valerian,
depression- St Johns wort
most common herbal preparations for:
confusion/forgetfulness
constipation
indigestion
confusion/forgetfulness- ginko, ginseng, chaparral
constipation- cascara, senna, castor bean
indigestion- caraway, licorice, papaya enzyme
most common herbal preparations for:
arthritis
muscle/ligament pain
headache/migraine
arthritis- glucosamine and chondroitin
muscle/ligament pain- wintergreen oil and liniments
headache-migraine- feverfew
factors that influence metabolism of a drug
age, liver disease, pregnancy, genetics, time of day, environment, diet, alcohol, drug interactions
two types of chemical reactions in the liver that prep and tag molecules for excretion
phase 1- involves oxidation, hydrolysis, or reduction to increase water solubility of drug molecules
phase 2- conjugation or union of drug molecules with water soluble substances
prodrug
administered inactive (or significantly less active) and becomes active when metabolized
pharmacodynamics
the effects of drugs on the body; drug receptor interaction and activity, dose response relationship, and drug potency/efficacy
dose response curve
the higher the concentration of a drug at its site of action the more the drug will bind at the site of action and the greater the response will be
potency
how much drug is needed (dose or concentration) to produce biological response
efficacy
the ability of a drug to produce a max effect at any dosage
pharmacokinetics
absorption, distribution, metabolism, and excretion of drugs; movement of drugs throughout the body
peak blood levels
rapid absorption leads to higher peak blood levels and greater risk of toxicity
absorption
movement of drug from site of administration into the blood
distribution
movement of absorbed drug in bodily fluids throughout the body to target tissues
free drug
drugs not bound to protein in circulation (active drugs)
drugs in bound states?
unbound states?
- bound- travel
- unbound- cross membranes. more drug eliminated if unbound
what are the only drugs that cross the blood brain barrier?
lipid soluble
metabolism(biotransformation)
chemical change of a drug structure to:
- enhance excretion
- inactivate the drug
- increase therapeutic action
- activate a prodrug
- increase/decrease toxicity
rational drug selection WHO 6 step model
- define pt. problem
- specify therapeutic objective
- collaborate with pt.
- pick treatment
- educate pt.
- monitor effectiveness (passive-teach, active-follow ups)
Medicare Part D
- started in 2004
- covers 75% after $250 deductible met
- patient pay 25% for RX between $250 and $2,250
“donut hole” of medicare part D
- patient pay 100% between $2,250-$5,100
- covered 100% after $5,100
half life of a drug
how long it takes or half of the dose to be metabolized and eliminated from the bloodstream
first pass metabolism
the concentration of a drug is greatly reduced before it reaches systemic circulation
low plasma proteins (low albumin) has what effect on drug binding?
there will be more free drug in circulation, since there is less for the drug to bind to. this puts the patient at a greater risk for toxicity
inhibitors?
inducers?
- inhibitors may decrease metabolism of substrates, which leads to increased drug effect
- inducers may increase metabolism of substrates, which leads to decreased drug effect
what cytochrome dose grapefruit juice affect, and how dose grapefruit juice affect it?
- CYP34A
- inhibits CYP34A, which can cause an increase in blood levels of some drugs
agonists
- produce receptor stimulation
- can cause receptors to decrease in response to receptor stimulation
antagonists
- drugs that occupy receptors without stimulating them and prevent other molecules from stimulation also
- can cause receptors to upregulate in response to decrease receptor stimulation
how long does it take to reach steady state blood levels?
4-5.5 HALF lives
how long does it take to totally eliminate drug from body?
4-5.5 lives
class 1 scheduled drugs
- no accepted medical use
- heroin, LSD, marijuana, mescaline, peyote
class 2 scheduled drugs
- written RX only, no refills
- expired if not filled in 72 hours
- narcotics: morphine, codeine, opium, oxy, methadone
- stimulants: cocaine, amphetamine, methylphenidate
- depressants: phenobarb, secobarb
what instances may class 2 schedules drugs be electronic?
- hospice
- nursing home
- IV meds at home
class 3 scheduled drugs
- phone RX ok
- must be rewritten after 6 months or 5 refills
- narcotics: codeine in combo with non-narcotic ingredients over 90mg/tab, hydro not over 50mg/tab
- stimulants: benzphetamine, chlorpheniramine, diethylpropion
- depressants: butabarbitol
class 4 scheduled drugs
- same as class 3 (phone RX ok, rewritten after 6 months or 5 refills)
- pentazocine, propoxyphene, phentermine, benzo’s. meprobamate
class 5 scheduled drugs
OTC: loperamide, diphenoxylate
what decreases verapamil effectiveness?
Ca and Vit D
contraindications for ACE, ARB, DRI
ABSOLUTE contraindications
- bil. renal artery stenosis
- angioedema
- pregnancy
also hyperkalemia;
- risk of hyperkalemia increases in HF
- check serum K+ prior to initiating therapy and within 1 week to note trends
- beware of concurrent use with K+ supplements
drug of choice for patients that are young, caucasian, HF, or post MI
ACE/ARB
ACE
“-pril” lisionpril, catopril
- angiotensin converting enzyme inhibitor (stops conversion of angiotensin I to angiotensin II)
- renoprotective, can be used for kidney protection in DM pts
- dry cough (bc ACEIs prevent breakdown of bradykinin)
ARB
“-tan” losartan, valsartan
- angiotensin II receptor blocker
- renoprotective
- can suppress progression of diabetic neuropathy
DRI
Aliskiren-Tekturna
- direct renin inhibitor (impacts renin levels with subsequent angiotension I and II reduction)
- NOT renoprotective
- not for DM pt. with GFR <60
- poorly absorbed with high fat meals
how do ACEIs affect lithium?
increase serum lithium levels and sx of toxicity
ARBs and antacids
avoid or separate doses by 1 hour
Beta blockers (MOA, what do they treat?)
“-olol” metoprolol, atenolol, propanolol, sotalol
- act by occupying beta receptor sites
- tx for HF, post MI, and asymptomatic LV dysfunction
- also used for essential tremor, migraines, hyperthyroidism
- can cause rebound tachycardia
- rise slow: ortho hypotension
ADRs of beta blockers
- sexual dysfunction
- depression
- fatigue
- increased cholesterol
- increased glucose
greatest beta 1 selective blocker?
atenolol
contraindications for BB
- NOT for asthma patients
- AV block
- may precipitate or exacerbate type 2 DM
Ca Channel Blockers: type 1
- diltiazem, verapamil
- nondihydropyridine
- targets heart: decreases firing at SA, slows AV conduction
Ca Channel Blockers: type 2
“-pine” amlodipine, nifedipine
- dihydropyridine
- targets blood vessels
Ca Channel Blockers MOA
- block the influx of Ca in smooth mucles prolonging vascular smooth muscle relaxation and decreaing transmembrane Ca content
- relaxes arterial smooth muscle but have little effect on venous beds resulting in significant reduction in afterload but limited effects of preload
Ca Channel Blockers contraindications
unstable angina- can cause tachycardia
2nd or 3rd degree blocks
Digoxin
- 10% of people have bacteria in gut that deactivates
- narrow therapeutic window
- not extensively metabolized and largely excreted unchanged by kidneys
Digoxin MOA
- Potent inhibitors of Na-K-ATPase system “the sodium pump” resulting in Na and Ca buildup in the cell and increased velocity and shortening of cardiac muscle
- Negative chronotropic effects, slowed conduction and automaticity (negative dromotropism) through the AV node more than the Purkinje fibers
half life of Digoxin
36-48 hours
Digoxin used in?
- A fib
- paroxysmal SVT (bc it slows AV conduction)
- HF (not 1st line but for pt with severe systolic dysfunction for inotropic action)
signs of Dig toxicity
- yellow vision
- green halos
- atrial arrhythmia
- atrial tachycardia
Digoxin ADRs
- GI
- fatigue
- disorientation/hallucination
- CV reactions are extension of effect of Dig: bradycardia, junctional and AV arrhythmia, bigeminy, PVC’s
Amiodarone special monitoring
- periodic CXR
- TSH
- ophthalmic exams
- pulmonary function tests q3-6 months
anti-arrhythmic classes
- sodium channel blockers
- beta blockers
- potassium channel blockers
- calcium channel blockers
Nitrates MOA
DILATION of venous vessels results in decreased afterload, venous pooling and decreased venous return to the heart, and decreased LV end diastolic pressure (preload)
Nitrate ADRs
- orthostatic hypotension
- increased IOP (avoid in closed angle glaucoma)
- syncope
- tachycardia
- headache (may need to change . for pt with persistent HA)
Peripheral Vasodilators
- hydralazine, aprezoline, minoxidil
- directly relax and dilate arterial smooth muscle
- absorbed well orally
- can cause tachycardia and NA/Water retention so used cautiously in CVD pts
most potent peripheral vasodilator?
minoxidil
what do NSAIDs do to peripheral vasodilators?
decrease their effectiveness
what medication can cause a lupus like syndrome?
hydralazine (peripheral vasodilator)
HDL, LDL, and TG goal
HDL 45 men, 55 women
LDL varies 70-160
TG less than 150
what is the only antilipidemic that can be used in active liver disease?
bile acid sequesterants
Niacin
-inhibition of free fatty acid release from adipose tissue
decreases LDL 10-15%
increases HDL 20-30
-some contain tartrazine, so avoid in patients with aspirin allergy
-“lost its luster”
Fibric acid derivatives
- gemfibrozil, fenofibrate
- mainly for triglyceride lypolysis (can decrease TG by 50% or more)
- decrease LDL 15-20%
- increase HDL by 15-25%
bile acid sequesterants
- colestipol, cholestyramine
- exchange chloride ions for bile acids promoting bile acid excretion, and enhanced conversion of cholesterol to bile acid
- decrease LDL by 10-35%
- increase HDL by 5%
Ezetimbe (Zetia)
- blocks absorption of cholesterol at intestinal border
- decrease LDL 12%
- booster WITH statin, or for statin intolerant
HMG-CoA reductase inhibitor MOA
- block synthesis of cholesterol in liver by inhibiting HMG-CoA reductase activity and increase affinity for LDL receptors
- decreases LDL 25-63%
- increase HDL 8-17%
- may cause muscle aches and myalgia (monitor CK)
how do statins interact with Digoxin?
statins increase Dig levels
3 types of diuretics and examples
- thiazide: hydrochlorothiazide, chlorthalidone, metolazone
- loop: bumex and furosemide
- K+ sparing: spironolatone, amiloride, eplerenone, triamterene
what is important to monitor with all diuretics?
electrolytes with creatinine clearance of <25-30 min
ADRs of diuretics
- gynecomastia in males
- renal calculi
- gout
Contraindications/ADRs of thiazide diuretics
- sulfa allergy!
- replace thiazide with loop if GFR <30
- photosensitivity (can last years)
- glucose intolerance-HYPERGLYCEMIA
- hepatic dysfunction
- older adults- hypotension and tinnitus
- diminished effect on warfarin
- decreased renal excretion of lithium
diuretic for pregnant women?
spironolactone
what increases bradykinin?
- bradykinin is a vasodilator (BP drops)
- ACEIs increase bradykinin by inhibiting its degradation
initial drugs of choice for HNT
nonblacks- thiazide diuretic, ACEI, ARB, CCB
blacks- CCB, thiazide diuretic
treatment of women of childbearing age with HTN
- BB drug of choice
- labetalol, nifedipine, methyldopa
document what before starting statin in african american?
CK
dietary therapy for hyperlipidemia
- reduce saturated fats to <7% of calories
- consume 2gm/day plant sterols (fruits, veggies)
- dietary cholesterol intake of <200mgday
- soluble fiber 10-25 gm/day
- dietary fiber 20-30 gm/day
- increase monosaturated (good) fats
pharm mgmt for angina
- aspirin
- nitrates (nitro and isorsorbide)
- beta blockers
- CCB
- ACEI
- statins
stage A HF
- Lifestyle modification: dyslipidemia, diabetes, hypertension (diuretics or angiotensin-converting enzyme inhibitors - ACEIs)
- ACEIs are drug of choice in patients with diabetes.
- Angiotensin II receptor blockers (ARBs) are considered in ACEI-intolerant patients, but more expensive.
stage B HF
ACEI in all, BB in most
stage C HF
ACEI and BB in all, in addition to diuretics/spironolactone and digoxin
stage D HF
Stage C treatments plus dobutamine, possible ventricular assist device, transplantation, hospice
post MI medications
- BB
- ACEI
- aldosterone antagonists
- lipid lowering therapy
- antiplatelet therapy
Decrease afterload
CCB ACEI ARB NITRATES BB
Decreases preload
ACEI
ARB
NITRATES
SPIRONOLACTONE
