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Advanced Pharmacology > Pharm exam 1 > Flashcards

Pharm exam 1 Flashcards

1
Q

what are the 3 levels of prescriptive authority?

A
  • full- no physician oversight
  • reduced- need oversight to prescribe
  • restricted- need oversight to prescribe, diagnose, and treat
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2
Q

3 phases of drug testing before approval

A

phase 1- test healthy subjects
phase 2- pt. with targeted disease/disorder
phase 3- controlled and uncontrolled clinical trials for safety/efficacy

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3
Q

legend drugs

A

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

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4
Q

bioavailability

A

% 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.

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5
Q

types of immune mediated ADRs

A

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)

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6
Q

most common herbal preparations for:
anxiety
insomnia
depression

A

anxiety- kava, mugwort, wormwood, pill-bearing spurge, passionflower
insomnia- melatonin, chamomile, mugwort, valerian,
depression- St Johns wort

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7
Q

most common herbal preparations for:
confusion/forgetfulness
constipation
indigestion

A

confusion/forgetfulness- ginko, ginseng, chaparral
constipation- cascara, senna, castor bean
indigestion- caraway, licorice, papaya enzyme

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8
Q

most common herbal preparations for:
arthritis
muscle/ligament pain
headache/migraine

A

arthritis- glucosamine and chondroitin
muscle/ligament pain- wintergreen oil and liniments
headache-migraine- feverfew

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9
Q

factors that influence metabolism of a drug

A

age, liver disease, pregnancy, genetics, time of day, environment, diet, alcohol, drug interactions

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10
Q

two types of chemical reactions in the liver that prep and tag molecules for excretion

A

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

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11
Q

prodrug

A

administered inactive (or significantly less active) and becomes active when metabolized

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12
Q

pharmacodynamics

A

the effects of drugs on the body; drug receptor interaction and activity, dose response relationship, and drug potency/efficacy

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13
Q

dose response curve

A

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

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14
Q

potency

A

how much drug is needed (dose or concentration) to produce biological response

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15
Q

efficacy

A

the ability of a drug to produce a max effect at any dosage

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16
Q

pharmacokinetics

A

absorption, distribution, metabolism, and excretion of drugs; movement of drugs throughout the body

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17
Q

peak blood levels

A

rapid absorption leads to higher peak blood levels and greater risk of toxicity

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18
Q

absorption

A

movement of drug from site of administration into the blood

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19
Q

distribution

A

movement of absorbed drug in bodily fluids throughout the body to target tissues

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20
Q

free drug

A

drugs not bound to protein in circulation (active drugs)

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21
Q

drugs in bound states?

unbound states?

A
  • bound- travel

- unbound- cross membranes. more drug eliminated if unbound

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22
Q

what are the only drugs that cross the blood brain barrier?

A

lipid soluble

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23
Q

metabolism(biotransformation)

A

chemical change of a drug structure to:

  • enhance excretion
  • inactivate the drug
  • increase therapeutic action
  • activate a prodrug
  • increase/decrease toxicity
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24
Q

rational drug selection WHO 6 step model

A
  1. define pt. problem
  2. specify therapeutic objective
  3. collaborate with pt.
  4. pick treatment
  5. educate pt.
  6. monitor effectiveness (passive-teach, active-follow ups)
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25
Q

Medicare Part D

A
  • started in 2004
  • covers 75% after $250 deductible met
  • patient pay 25% for RX between $250 and $2,250
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26
Q

“donut hole” of medicare part D

A
  • patient pay 100% between $2,250-$5,100

- covered 100% after $5,100

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27
Q

half life of a drug

A

how long it takes or half of the dose to be metabolized and eliminated from the bloodstream

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28
Q

first pass metabolism

A

the concentration of a drug is greatly reduced before it reaches systemic circulation

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29
Q

low plasma proteins (low albumin) has what effect on drug binding?

A

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

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30
Q

inhibitors?

inducers?

A
  • inhibitors may decrease metabolism of substrates, which leads to increased drug effect
  • inducers may increase metabolism of substrates, which leads to decreased drug effect
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31
Q

what cytochrome dose grapefruit juice affect, and how dose grapefruit juice affect it?

A
  • CYP34A

- inhibits CYP34A, which can cause an increase in blood levels of some drugs

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32
Q

agonists

A
  • produce receptor stimulation

- can cause receptors to decrease in response to receptor stimulation

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33
Q

antagonists

A
  • 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
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34
Q

how long does it take to reach steady state blood levels?

A

4-5.5 HALF lives

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35
Q

how long does it take to totally eliminate drug from body?

A

4-5.5 lives

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36
Q

class 1 scheduled drugs

A
  • no accepted medical use

- heroin, LSD, marijuana, mescaline, peyote

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37
Q

class 2 scheduled drugs

A
  • 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
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38
Q

what instances may class 2 schedules drugs be electronic?

A
  1. hospice
  2. nursing home
  3. IV meds at home
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39
Q

class 3 scheduled drugs

A
  • 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
40
Q

class 4 scheduled drugs

A
  • same as class 3 (phone RX ok, rewritten after 6 months or 5 refills)
  • pentazocine, propoxyphene, phentermine, benzo’s. meprobamate
41
Q

class 5 scheduled drugs

A

OTC: loperamide, diphenoxylate

42
Q

what decreases verapamil effectiveness?

A

Ca and Vit D

43
Q

contraindications for ACE, ARB, DRI

A

ABSOLUTE contraindications

  1. bil. renal artery stenosis
  2. angioedema
  3. 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
44
Q

drug of choice for patients that are young, caucasian, HF, or post MI

A

ACE/ARB

45
Q

ACE

A

“-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)
46
Q

ARB

A

“-tan” losartan, valsartan

  • angiotensin II receptor blocker
  • renoprotective
  • can suppress progression of diabetic neuropathy
47
Q

DRI

A

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
48
Q

how do ACEIs affect lithium?

A

increase serum lithium levels and sx of toxicity

49
Q

ARBs and antacids

A

avoid or separate doses by 1 hour

50
Q

Beta blockers (MOA, what do they treat?)

A

“-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
51
Q

ADRs of beta blockers

A
  • sexual dysfunction
  • depression
  • fatigue
  • increased cholesterol
  • increased glucose
52
Q

greatest beta 1 selective blocker?

A

atenolol

53
Q

contraindications for BB

A
  • NOT for asthma patients
  • AV block
  • may precipitate or exacerbate type 2 DM
54
Q

Ca Channel Blockers: type 1

A
  • diltiazem, verapamil
  • nondihydropyridine
  • targets heart: decreases firing at SA, slows AV conduction
55
Q

Ca Channel Blockers: type 2

A

“-pine” amlodipine, nifedipine

  • dihydropyridine
  • targets blood vessels
56
Q

Ca Channel Blockers MOA

A
  • 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
57
Q

Ca Channel Blockers contraindications

A

unstable angina- can cause tachycardia

2nd or 3rd degree blocks

58
Q

Digoxin

A
  • 10% of people have bacteria in gut that deactivates
  • narrow therapeutic window
  • not extensively metabolized and largely excreted unchanged by kidneys
59
Q

Digoxin MOA

A
  • 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
60
Q

half life of Digoxin

A

36-48 hours

61
Q

Digoxin used in?

A
  • A fib
  • paroxysmal SVT (bc it slows AV conduction)
  • HF (not 1st line but for pt with severe systolic dysfunction for inotropic action)
62
Q

signs of Dig toxicity

A
  • yellow vision
  • green halos
  • atrial arrhythmia
  • atrial tachycardia
63
Q

Digoxin ADRs

A
  • GI
  • fatigue
  • disorientation/hallucination
  • CV reactions are extension of effect of Dig: bradycardia, junctional and AV arrhythmia, bigeminy, PVC’s
64
Q

Amiodarone special monitoring

A
  • periodic CXR
  • TSH
  • ophthalmic exams
  • pulmonary function tests q3-6 months
65
Q

anti-arrhythmic classes

A
  1. sodium channel blockers
  2. beta blockers
  3. potassium channel blockers
  4. calcium channel blockers
66
Q

Nitrates MOA

A

DILATION of venous vessels results in decreased afterload, venous pooling and decreased venous return to the heart, and decreased LV end diastolic pressure (preload)

67
Q

Nitrate ADRs

A
  • orthostatic hypotension
  • increased IOP (avoid in closed angle glaucoma)
  • syncope
  • tachycardia
  • headache (may need to change . for pt with persistent HA)
68
Q

Peripheral Vasodilators

A
  • 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
69
Q

most potent peripheral vasodilator?

A

minoxidil

70
Q

what do NSAIDs do to peripheral vasodilators?

A

decrease their effectiveness

71
Q

what medication can cause a lupus like syndrome?

A

hydralazine (peripheral vasodilator)

72
Q

HDL, LDL, and TG goal

A

HDL 45 men, 55 women
LDL varies 70-160
TG less than 150

73
Q

what is the only antilipidemic that can be used in active liver disease?

A

bile acid sequesterants

74
Q

Niacin

A

-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”

75
Q

Fibric acid derivatives

A
  • gemfibrozil, fenofibrate
  • mainly for triglyceride lypolysis (can decrease TG by 50% or more)
  • decrease LDL 15-20%
  • increase HDL by 15-25%
76
Q

bile acid sequesterants

A
  • 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%
77
Q

Ezetimbe (Zetia)

A
  • blocks absorption of cholesterol at intestinal border
  • decrease LDL 12%
  • booster WITH statin, or for statin intolerant
78
Q

HMG-CoA reductase inhibitor MOA

A
  • 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)
79
Q

how do statins interact with Digoxin?

A

statins increase Dig levels

80
Q

3 types of diuretics and examples

A
  • thiazide: hydrochlorothiazide, chlorthalidone, metolazone
  • loop: bumex and furosemide
  • K+ sparing: spironolatone, amiloride, eplerenone, triamterene
81
Q

what is important to monitor with all diuretics?

A

electrolytes with creatinine clearance of <25-30 min

82
Q

ADRs of diuretics

A
  • gynecomastia in males
  • renal calculi
  • gout
83
Q

Contraindications/ADRs of thiazide diuretics

A
  • 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
84
Q

diuretic for pregnant women?

A

spironolactone

85
Q

what increases bradykinin?

A
  • bradykinin is a vasodilator (BP drops)

- ACEIs increase bradykinin by inhibiting its degradation

86
Q

initial drugs of choice for HNT

A

nonblacks- thiazide diuretic, ACEI, ARB, CCB

blacks- CCB, thiazide diuretic

87
Q

treatment of women of childbearing age with HTN

A
  • BB drug of choice

- labetalol, nifedipine, methyldopa

88
Q

document what before starting statin in african american?

A

CK

89
Q

dietary therapy for hyperlipidemia

A
  • 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
90
Q

pharm mgmt for angina

A
  • aspirin
  • nitrates (nitro and isorsorbide)
  • beta blockers
  • CCB
  • ACEI
  • statins
91
Q

stage A HF

A
  • 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.
92
Q

stage B HF

A

ACEI in all, BB in most

93
Q

stage C HF

A

ACEI and BB in all, in addition to diuretics/spironolactone and digoxin

94
Q

stage D HF

A

Stage C treatments plus dobutamine, possible ventricular assist device, transplantation, hospice

95
Q

post MI medications

A
  • BB
  • ACEI
  • aldosterone antagonists
  • lipid lowering therapy
  • antiplatelet therapy
96
Q

Decrease afterload

A 
CCB
ACEI
ARB
NITRATES
BB
97
Q

Decreases preload

A

ACEI
ARB
NITRATES
SPIRONOLACTONE

Advanced Pharmacology (3 decks)

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