Pharmacology Test 1

Front 1

acetaminophen

Back 1

tylenol aka APAP

Front 2

what act was passed in 1938?

Back 2

the food drug and cosmetic act, modern history of us drug regulations, experimental requirements

Front 3

purpose of a new drug application?

Back 3

must be submitted to the FDA before marketing for approval

Front 4

In what year was efficacy data required?

Back 4

1962, must prove the efficacy along with safety of a drug

Front 5

phase one of clinical testing

Back 5

clinical pharmacology/establish safety of drug

Front 6

phase 2 of clinical testing

Back 6

clinical investigations-establish efficacy and what dose is needed

Front 7

phase 3 of clinical testing

Back 7

clinical trials! verify efficacy w/ more specific barriers, end points, detecting side effects and % compared to placebo

Front 8

phase 4 of clinical testing

Back 8

post marketing studies, only step that doesn't have to be completed before NDA; looking at other diseases drug could help with or notice additional adverse rxns

Front 9

how long/how much does a drug take to be developed?

Back 9

10-15 years, 400-800 million dollars

Front 10

1 kg = ? lbs

Back 10

2.2

Front 11

1 ml = ? cc

Back 11

1 mL = 1 cc

Front 12

1 gram = ? mg

Back 12

1 gram = 1000 mg

Front 13

what is mylanta used for?

Back 13

anti-acid

Front 14

what drug rxn should you be aware of with mylanta?

Back 14

mylanta has electrolytes that can bind to the antibiotic ciproflaxn and make it a different size compound (don't take min/vit with cipro either)

Front 15

what does cc stand for?

Back 15

cubic centemeter

Front 16

30 cc = 30 mL = 30 g

Back 16

all equal to one oz (ounce)

Front 17

how many mL is one dram?

Back 17

4 mL= 1 dram
dram=dr

Front 18

how many mg is one grain equal too?

Back 18

60 mg= 1 grain
grain=gr

Front 19

how many oz is one pound?

Back 19

16 oz= 1 pound

Front 20

how many mL are in a teaspoon?

Back 20

5 mL=1 tsp=5 cc

Front 21

how many mL are in a table spoon?

Back 21

15 mL= 1 tbsp

Front 22

how many ounces are in a cup?

Back 22

8 oz=1 cup=240 mL

Front 23

pharmacodynamics

Back 23

Biochemical & physiological effects of drugs and mechanisms of action study of how drug effects body

Front 24

Pharmacokinetics

Back 24

Study of how the body absorbs, distributes, metabolizes and excretes drugs
study of body's effect on drugs

Front 25

what is teratology?

Back 25

How drugs taken during pregnancy can cause fetal morphology

Front 26

what is an example of a category X drug for pregnancy?

Back 26

Accutane (retinols) used for acne treatment

Front 27

what is the TI of a drug?

Back 27

therapeutic index/margin of safety

Front 28

what is the therapeutic index ratio for humans?

Back 28

TD1/ED1
minimum toxic dose/minimum therapeutic dose
high # = safe:)

Front 29

what doe drug specificity mean?

Back 29

the receptor must be able to recognize drug for it to work

Front 30

what do drug receptor complexes do?

Back 30

produce a biochemical or physiologic response

Front 31

what are the general effects of drug binding?

Back 31

Release of NT, hormone or endogenous chemicals
Change electrical potential or membrane permeability
Cause cascade effect

Front 32

what is an agonist?

Back 32

Drug that combines with a receptor and activates that receptor
*same response as endogenous chemical or stimulates release of endogenous chemical

Front 33

epinephrine

Back 33

adrenergic agonist
give to pts to increase HR/BP

Front 34

antagonist

Back 34

Drug that combines with a receptor used by an endogenous chemical and blocks or diminishes the response of the endogenous agent or blocks release of NT or inhibits signaling of released NT.

Front 35

atropine

Back 35

cholinergic antagonist

Front 36

what is a partial agonist?

Back 36

has affinity but low efficacy
binds but elicits less response and blocks receptor for more effective drug

Front 37

butorphenol (stadol) u and K activity

Back 37

bind to opioid receptors for pain relief but not as well as morphine would-less addictive and no high

Front 38

competitive antagonism

Back 38

agonist and antagonist compete for the same receptor site.

Front 39

Non-competitive antagonism

Back 39

agonist and antagonist bind at different sites on the same receptor
ex- binds and changes receptor configuration so agonist can't bind

Front 40

what is efficacy?

Back 40

The magnitude of the maximum effect (predefined)

Front 41

what is potency?

Back 41

If the dose of drug A is less than drug B to achieve the same response – Drug A is more potent. (1mg vs. 100mg)

Front 42

what is tolerance?

Back 42

Reduced response to the same dose or increased dose needed for the same response
happens with narcotics/nitroglycerin/pain relievers

Front 43

what causes tolerance?

Back 43

•Change in receptor sensitivity
•Change in pharmacokinetics of drug
doesn't occur with all drugs

Front 44

dependence

Back 44

ADDICTION need for drug
can be psychological or physiological

Front 45

allergy
ABCD

Back 45

hypersensitivity!
adverse immune reaction that results from a previous exposure to a particular chemical or one that is structurally similar.

Front 46

type 1 allergy

Back 46

Anaphylactic rxns, histamine released, IgE response
urticaria, rash, vasodilation, hypotension, edema, inflammaion, rhinitis, asthma, tachycardia

Front 47

type 2 allergy

Back 47

B for BLOOD CELLS-ANEMIA
cytolytic rxns w/ IgG and IgM, effect cells and circ sys=hemolytic anemia, thrombocytopenia, granulocytopenia

Front 48

examples of type 2 allergies?

Back 48

quinidine, Methyldopa
These autoimmune reactions to drugs usually subside within several months after drug discontinuation

Front 49

type 3 allergy

Back 49

C is for Complexes/rash-
IgG mediated, immune complexes are deposited in the vascular endothelium=serum sickness occurs

Front 50

symptoms of type 3 allergy

Back 50

erythema multiforme, arthritis, nephritis, CNS abnormalities, myocarditis and systemic lupus erythematosus.
ex: sulfonamide antibiotics

Front 51

type 4 allergy

Back 51

DELAYED hypersensitivity
mediated by T cells/WBC
antigen+ lymphokines=inflam rxn
ex poison ivy, antibiotics, benzocaine

Front 52

idiosyncratic rxn

Back 52

Unusual response to a drug, usually caused by genetic differences in metabolism or immunologic mechanisms.

Front 53

how do drugs cross the membrane?

Back 53

passive diffusion, facilitated diffusion, active transport, pinocytosis

Front 54

passive diffusion?

Back 54

down concentration gradient, most common

Front 55

what determines a drugs ability to diffuse across the membrane?

Back 55

more lipid soluable-crosses easier
non electrolytes-related to lipid sol
electrolytes-based on pH

Front 56

facilitated diffusion

Back 56

passes with concentration gradient, but it requires a transporter (i.e. carrier protein). still uses no E

Front 57

Active transport

Back 57

against concentration gradient and requires E

Front 58

Pinocytosis

Back 58

formation and movement of vesicles (packages) across membranes, requires energy

Front 59

absorption

Back 59

the rate at which a drug leaves its site of administration and the extent to which it occurs

Front 60

bioavailability

Back 60

extent (%) to which a drug reaches its site of action or a biological fluid that has access to that site

Front 61

first pass effect

Back 61

occures with oral drugs!
Drugs that are well absorbed from the G.I. tract and are metabolized in the liver, have decreased bioavailability in systemic circulation

Front 62

what are factors that modify absorption?

Back 62

drug solubility (solutions>suspensions>capsules>tablets), circulation at site, absorbing surface area, astric emptying time, intestinal motility,
food

Front 63

what effect does food have on drug absorption?

Back 63

can delay effects or reduce the drug absorption so usually suggest to take drugs on empty stomach (or with food if drug upsets stomach)

Front 64

enteral routes of administration?

Back 64

ie GI tract-
oral (PO)
sublingual (SL) good for high lipid
rectal (PR)- if oral not possible but abs is unpredicatble

Front 65

parenteral route of administration

Back 65

IV, IM, SQ or SC (subcutaneous)

Front 66

topical route of drug administration?

Back 66

cream, lotions, eye drops
"local"

Front 67

transdermal route of drug administration?

Back 67

absorbed through skin into systemic system

Front 68

Oral administration

Back 68

Safest Easiest, Cheapest. Absorption in first third of the small intestine. BUT some drugs can’t be absorbed

Front 69

what are some negatives to oral administration?

Back 69

too irritating,
destroyed by acids or enzymes in G.I. Tract
altered by food or chemicals.

Front 70

IV parenteral administration

Back 70

no absorption phase, accurate, immediate, irreversible, must be aqueous.

Front 71

IM parenteral administration

Back 71

onset is slower and duration is longer than IV, absorption is delayed and is related to vascularity

Front 72

subcutaneous (SC/SQ) parenteral administration

Back 72

onset is slower and duration is longer than IM because fat is less vascular than muscle

Front 73

distribution

Back 73

is the delivery of drug from circulation to tissues and its movement through compartments (BBB and placental)

Front 74

what is a reservoir

Back 74

drug protein binding sites

Front 75

drugs must be xxxx to be active

Back 75

free/unbound and then must bind to the right receptor

Front 76

what is the BBB?

Back 76

Blood-Brain Barrier- memebrane that separates the blood from the cerebro-spinal fluid and brain. more restrictive than any other membrane and the brain is highly lipophilic

Front 77

because bbb is lipophilic CNS depressants xxx and antibiotics xxxx

Back 77

depressants- concentrate in brain
antibiotics- dont pass into bbb

Front 78

placental barrier

Back 78

membrane separating the blood from the placenta- LESS restrictive than most

Front 79

what does meningitis do to the BBB?

Back 79

the inflammation to the meninges decreases the restrictiveness of the BBB so antibiotics can get in

Front 80

what is the bodies natural response to drugs?

Back 80

wants to convert any chemical into inactive/water soluble form for excretion. Most biotransformations occur in the liver

Front 81

what is a prodrug?

Back 81

needs to undergo a transformation in the body to be active

Front 82

phase 1 of metabolism

Back 82

Non-synthetic! oxidation reduction rxns, hydrolysis
cyt P450!
BREAKS DOWN COMPOUNDS

Front 83

Phase II of metabolism

Back 83

synthetic- conjugation (glucuronidation, sulfonation) to make more polar/water soluble and easier to excrete

Front 84

all phases of metabolism are ______

Back 84

enzymatic

Front 85

where can metabolism occur?

Back 85

LIVER, gi tract, lungs, skin, kidneys

Front 86

CYP450

Back 86

Main phase I enzyme system involved in the oxidative metabolism of drugs, chemicals and some endogenous substances

Front 87

CYP3A4

Back 87

predominant isoform: 50% of CYP-mediated metabolism
benzos/HIV drugs/Ca channel blckr
DONT drink FJ bc inhibits CYP3A4=toxicity

Front 88

CYP2D6

Back 88

second most common isoform: 30% of CYP-mediated metabolism,
psychotropics, codeine, beta-blockers

Front 89

CYP2C9

Back 89

third most common isoform: 10%
phenytoin, warfarin, NSAIDs

Front 90

Pharmacogenomics

Back 90

the general study of all of the many different genes that determine drug behavior

Front 91

Pharmacogenetics

Back 91

refers to the study of inherited differences (variation) in drug metabolism and response.

Front 92

SNP on CYP2D6?

Back 92

most studied* Affects metabolism of psychotropics, codeine, β-blockers and antiarrhythmics
7% white, 1-3% black

Front 93

what effect does a SNP on CYP2D6 have on codeine metabolism?

Back 93

codeine is a prodrug that must be activated first by CYP2D6 so if mutation then no activation=no efficacy on that person

Front 94

what effect does a mutation on the CYP2C9 have?

Back 94

affects phenytoin and warfarin metabolism so can't metabolize them and thus toxicity

Front 95

phenytoin

Back 95

anti-seizure drug

Front 96

warfarin

Back 96

anti-coagulant drug, if CYP2C9 mutation then increase risk of bleeding, easy bruising, gums bleeding
NARROW theraputic index

Front 97

what is INR

Back 97

international normalized ratio to monitor bleeding time-checks for blood levels and watch when pt on warfarin so that they don't blled out

Front 98

Alcohol and aldehyde dehydrogenase in Asians is decreased →

Back 98

increase in cancer in upper respiratory tract

Front 99

G6PD deficiency in 14% African Americans →

Back 99

RBC hemolysis with sulfa drugs

Front 100

N-acetyltransferse → “slow acetylators” more common in middle east population
phase 2 metabolism

Back 100

therefore increase risk of INH (isoniozine, TB drug) induced ADRs
can't metabplize drugs as efficiently

Front 101

transport protein polymorphism?

Back 101

p-glycoprotein normally promotes movement of drugs towards GI tract/kidney for excretion so mutation=decreased elimination and toxicity

Front 102

routes of drug excretion?

Back 102

kidney, feces, breast milk

Front 103

How is excretion in the kidney controlled?

Back 103

pH related!
more alkaline pee=more weak acid excreted
more acidic pee= more weak base excreted

Front 104

clearance

Back 104

rate at which drug is eliminated from the body

Front 105

Steady state

Back 105

when the rate of administration = clearance

Front 106

how long does it take to reach steady state?

Back 106

4-5 half lives

Front 107

Half life

Back 107

the amount of time it takes for the concentration of a drug to be reduced by half

Front 108

what are some clinical applications of the half life?

Back 108

determining dosing intervals
determining how long for a drug to reach its steady state
determining how long for a drug to be completely eliminated from the body

Front 109

elimination half life

Back 109

how long it takes a drug to leave the body once you stop taking it

Front 110

synergism

Back 110

combined effect of two drugs is greater than the sum

Front 111

Potentiation

Back 111

an inactive drug increases the effect of another

Front 112

Induction

Back 112

one drug increases the drug-metabolizing enzyme activity of another

Front 113

Inhibition

Back 113

metabolism or excretion of one drug is blocked by another

Front 114

Unbinding

Back 114

one drug displaces another from a protein binding site that its not supposed to be on. (More unbound drug = more activity)

Front 115

elderly are _____ to anticholergic drug side effects such as______. why?

Back 115

more susceptible to anticholenergic effects such as dry mouth/constipation bc produce less saliva and are prone to constipation already

Front 116

creatinine

Back 116

by product of muscle production, should eliminate 100%
elevated creatinine in serum=decrease in urine

Front 117

what are normal creatinine levels?

Back 117

0.6-1.2 serum creatinine
100-120 creatinine clearance
100 percent should be eliminated with urine

Front 118

what does the creatinine levels give insight too?

Back 118

the glomular filtration rate of the kidney- increased serum creatinine levels=kidney dysfunction

Front 119

category A for teratogens

Back 119

studied in women fail to show a risk, the SAFEST

Front 120

category B for teratogens

Back 120

something bad happened in animals but was not shown in women

Front 121

category C for teratogens

Back 121

something bad happened in animals, but no tests done in humans

Front 122

category D for teratogens

Back 122

there is evidence of fetal risk and only used in life threatening situations ex epilepsy meds

Front 123

category X for teratogens

Back 123

caused fetal abnormalities and benefits NEVER out weigh the risk to child
ex accutane

Front 124

what are some drugs that require special attention in the elderly?

Back 124

Analgesics Anticholinergics
Anticoagulants Antidepressants
Antidiabetics Antihpertensives
Antipsychotics
Beta blockers
Digoxin
H2 antagonists
Hypnotics/anxiolytics OTCs

Front 125

Name 4 Teratogens

Back 125

1) Amphetamines
2)Diethylstilbestrol
3)Ethanol
4)Thalidomide

Front 126

amphetamine effect on fetus

Back 126

- abn development/bad in school

Front 127

Diethylstilbestrol effect on fetus

Back 127

vaginal adenosis and vaginal adenocarcinoma

Front 128

ethanol effects on fetus

Back 128

fetal EtOH syndrom, nerudevel defects

Front 129

thalidomide effects on fetus

Back 129

phocomelia (abnormalities to the face, limbs, ears, nose, vessels and many other underdevelopments)

Front 130

what drugs are contraindicated in neonates?

Back 130

sulfonamides, antihistamines and ceftriaxone abx
cause kernicterus

Front 131

what drugs are contraindicated in children?

Back 131

aspirin (Ryes syndrome)
fluoroquinolones (ONLY for conjunctivitis, anthrax and cystic fibrosis)
tetracyclines-yellow teeth

Front 132

Rye's syndrome

Back 132

lowers blood sugar, fatty liver, encephalopathy
RASH*VOMITING*LIVER DAMAGE

Front 133

kernicterus

Back 133

excessive jaundice, can be caused by sulfonamides and ceftriaxone abx in neonates

Front 134

fxn of ANS

Back 134

Regulates activity of smooth muscle, exocrine glands, cardiac tissue and certain metabolic activities HOMEOSTASIS
involuntary

Front 135

how many efferent neurons does the ANS have

Back 135

2-postganlionic and preganglionic neurons

Front 136

what is the primary NT of the sympathetic NS?

Back 136

Norepinephrine

Front 137

what is the primary NT of the parasympathetic NS?

Back 137

Acetylcholine (ACH)

Front 138

what are the general effects of the parasympathetic NS?

Back 138

SLUDGE
salivation, lactation, urination, defication, gi and erection
(decrease HR and bronchioconstriction)

Front 139

what are the general effects of the sympathetic system?

Back 139

increase HR, bronchiodilation, mydriasis, opposite of para basically
EJACULATION

Front 140

when is it okay to use aspirin in children younger than 15 years old?

Back 140

Kawasakis and juvinile rheumatoid arthritis

Front 141

when is it okay to use fluoroquinolones in children?

Back 141

for bac. conjunctivitis, anthrax and cystic fibrosis

Front 142

where are muscurinic receptors located?

Back 142

both in parasymoathetic and and the sympathetic (sweat glands only) and the CNS

Front 143

direct agonists....

Back 143

Activate postsynaptic receptors

Front 144

Indirect agonists

Back 144

Stimulate release of NT
Inhibit reuptake of NT
Inhibit metabolism of NT

Front 145

Direct antagonists

Back 145

Block postsynaptic receptors

Front 146

Indirect antagonists

Back 146

Inhibit synthesis of NT
Prevent vesicular storage of NT
Inhibit release of NT

Front 147

organophosphate poisoning

Back 147

augmented cholinergic NT at central and peripheral synapses- produces extreme SLUDGE, siezures. respiratory depression, coma, parlysis

Front 148

treatment for organophosphate poisoning?

Back 148

use atropine (ACh inhibitor) and pralidoxime (regenerate ACh)

Front 149

what are the CNS side effects of using muscarinic receptor antagonist?

Back 149

sedation, confusion, altered mental status
ex if want to help stomach pain could get all that^

Front 150

always use a ______ and NEVER use a ______ zero

Back 150

always use a leading zero and never use a trailing zero!

Front 151

GTT

Back 151

drops

Front 152

AS

Back 152

left ear

Front 153

AD

Back 153

right ear
"auricle droit"

Front 154

AC

Back 154

before meals

Front 155

what do you do if you make an error on a written Rx?

Back 155

cross it out with ONE line and initial it

Front 156

Schedule I (C-I)

Back 156

very high potential for abuse - no current therapeutic use. heroin, hallucinogenic substances (LSD, mescaline, peyote)

Front 157

Schedule II (C-II)

Back 157

high potential for abuse with severe liability to cause psychic or physical dependence. Morphine, codeine, amphetamines, barbiturates, methylphenidate, oxycodone

Front 158

what are CII on in NYS?

Back 158

benzodiazepines (in NYS), anabolic steroids (in NYS),

Front 159

Schedule III (C-III)

Back 159

less potential for abuse than C-I or C-II. Vicodin, Tylenol with codeine tabs, some cough preparations

Front 160

Schedule IV (C-IV)

Back 160

still less abuse potential than I, II and III. phenobarbital, some cough preparations

Front 161

Schedule V (C-V)

Back 161

least potential for abuse - Lomotil

Front 162

what are the two types of drugs that can only be orally prescribed in emergency situations?

Back 162

CII and BDZs and Rx must then say authorization for Emergency Dispensing

Front 163

what are the supply and refill limits for CII?

Back 163

30 day supply and ZERO (O) refils

Front 164

what is the supply and refill limits for CIII-CV

Back 164

30 day supply with up to FIVE (5) refills

Front 165

what does the diagnostic code A stand for?

Back 165

pAnic disorder

Front 166

diagnostic codes on Rx

Back 166

for prescribing more than a 30-day supply of controlled substances

Front 167

what does the diagnostic code B stand for?

Back 167

ADD

Front 168

what does the diagnostic code C stand for?

Back 168

Chronic debilitating neurological conditions characterized as a movement disorder or exhibiting seizure, convulsive or spasm activity

Front 169

what does the diagnostic code D stand for?

Back 169

pain for patients with chronic/incurable Diseases

Front 170

what does the diagnostic code E stand for?

Back 170

Narcolepsy
E-asy to fall aslEEp

Front 171

what does the diagnostic code F stand for?

Back 171

Hormone deficiency states in males; gynecologic conditions that are responsive with anabolic steroids or chorionic gonadotropin; metastatic breast cancer in women; anemia and angioedema

Front 172

what equation is used to measure Creatinine clearance?

Back 172

Cockcroft-Gault equation

Front 173

what are organophosphates?

Back 173

irreversible cholinesterase inhibitors

Front 174

nondepolarizing neuromuscular blocking agents

Back 174

Competitive antagonist of ACH at nicotinic muscle receptors (takes ACH place on receptor)
paralysis/relaxation
Atracurium, pancuronium, vecuronium

Front 175

depolarizing neuromuscular blocking agents

Back 175

Causes “persistent” depolarization, constant stimulation-flacid paralysis
Succinylcholine