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GMS 6551 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Choosing diseases

A

-government incentives target orphan diseases
-target diseases that have a large market (make profit; cancer, heart disease)–rare diseases won’t make money
-pharma is made of companies and the first order of buisness is money

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2
Q

drug target (most common)

A

enzymes
receptors

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2
Q

Drug target

A

enzymes
receptor
other proteins
dna
rna

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3
Q

selectivity

A

target determines side effects
BEST=bacterial
-easier to target non-human proteins & mutated cancer proteins (make sure normal protein is unaffected)

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4
Q

Assay development

A

-test drugs to see if they work
in vitro
in vivo
ex vivo

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5
Q

in vitro

A

-test tube
-cell culture (not an entire organism)

FAST & INEXPENSIVE
-clean system (test just what is in tube)

Disadvantage: test tube not a cell or animal
–1st round of testing

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6
Q

in vivo

A

living animals (mice, rats, rabbits)

Disadvantage: expensive, animals may suffer, regulations, complex systems

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7
Q

ex vivo

A

tissues out of living animals

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8
Q

lead compound

A

natural products
chemical banks
rational drug design

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9
Q

natural products

A

plants
algae
bacteria
fungi

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10
Q

chemical banks

A

thousands/ millions
-pharma companies

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11
Q

rational drug design

A

use logic to cut down brute work
-utilize side effect
-alter natural ligand (antihistamine)

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12
Q

Molecular Docking

A

-fast, cheap (free)
-crystal structures of proteins known
-program calculates chemical attraction

disadvantage: skips ALOT of details like
conformations-proteins changing shape
cell membrane-cant cross, can never go inside cell and hep protein

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13
Q

Structural Activity Relationships (SAR)

A

-optimize lead compound
-makes drug better
-eliminates unneeded functionalization

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14
Q

pharmokinetics

A

absorption
distribution
metabolism
excretion

what body does to drug
(dosage, circulation, and site of action)

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15
Q

Hepatitis C virus

A

old treatment cheap, less effective and toxic
–new treatment is effective, safe but very expensive

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16
Q

cancer treatments

A

increases life by days, costs hundreds to thousands

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17
Q

pharma companies

A

motivated by money
-may not have patients best interest at heart

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18
Q

pharmacology

A

study of how chemical substances interact and modulate living systems

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19
Q

pharmacodynamics

A

what it does to biologic system of body (ex: relieve pain, etc.)

pharmacological effect
—mechanism
—potency
—efficacy
—toxicity

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20
Q

pharmacogenetics

A

how genetic makeup impacts interaction of drug

-each person’s unique reaction

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21
Q

toxicology

A

adverse effects of drug and molecules

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22
Q

drug

A

any substance that interacts and modulates a living system

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23
Q

agonist

A

drug ACTIVATES biologic response

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24
Q

antagonist

A

drug INHIBITS biologic response (NO response)

-by binding to receptor it will prevent binding of agonist

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25
Q

drug action targets

A

receptors
enzymes

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26
Q

pharmacotherapeutics

A

clinical response
-efficacy and toxicology

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27
Q

chemical name

A

chemical structure
ex: n-acetyl-p-aminophenol

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28
Q

non-proprietary name

A

chemical or pharmacological class
-generic name
ex: acetaminophen

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29
Q

proprietary name

A

trade name
-marketing name (catchy)
–made once determined medicine is profitable
ex: tylenol, tempra (can have several)

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30
Q

drug classification

A

chemical properties
mechanism of action
disease/ condition
abuse potential
–otc drugs
–prescription drugs
–orphan drugs

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31
Q

chemical properties

A

benzodiazepines
sulfonamides

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32
Q

mechanism of action

A

-ACE inhibitor (angiotensin converting enzyme)
-calcium channel blocker
-carbonic anhydrase inhibitors

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33
Q

disease/condition

A

analgesics
antidepressants
antihypertensives

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34
Q

Drug classification

A

Schedule I-V

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35
Q

schedule I

A

HIGH
-heroin, LSD, marijuana
-no currently accepted medical use
-CANNOT BE PRESCRIBED

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36
Q

schedule II

A

HIGH
-morphine, amphetamines, high dose, codeine
-no refills, requires written prescription (IN PERSON)

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37
Q

schedule III

A

MODERATE
-ketamine, low dose codeine
-5 refills max within 6 months

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38
Q

schedule IV

A

LOW
-benzodiazepines
-5 refills max, within 6 months

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39
Q

schedule V

A

LOWEST
diphenoxylate

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40
Q

translational research

A

moving knowledge and discovery gained from basic sciences to application in clinical and community settings
-encompasses a bidirectional continuum (move around and follow trajectory)
t0-t4

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41
Q

translational research continuum

A

public health
basic research
pre-clinical research
clinical research
clinic implementation

ALL CENTERED AROUND PATIENT INVOLVEMENT

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42
Q

t0

A

define mechanisms underlying health or disease (identify opportunities and approaches to a health problem)
–yields knowledge about defining mechanisms targets or lead molecules

BASIC RESEARCH QUESTION

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43
Q

t1

A

test basic research findings for clinical effect (discovery of candidate health application)
–yields knowledge about new methods of diagnosis, treatment, and prevention

PHASE I AND II CLINICAL TRIALS, OBSERVATIONAL STUDIES

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44
Q

t2

A

test new inventions under controlled environments (health application to evidence based practice guidelines)
–yields knowledge about efficacy of interventions in optimal settings

PHASE III CLINICAL TRIALS–OBSERVATIONAL STUDIES–EVIDENCE SYNTHESIS AND GUIDELINE DEVELOPMENT

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45
Q

t3

A

explore ways of applying guidelines in general practice (practice guidelines to health practices)
–yields knowledge about how interventions work in REAL WORLD settings

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46
Q

t4

A

study influences on the health of populations (practice to population health impact)
–research ultimately results in improved global health

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47
Q

multidisciplinary

A

diverse backgrounds
-additive, complementary, independent, sequential

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48
Q

interdisciplinary

A

different expertise working together to integrate knowledge
-interactive, combine, integrate

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49
Q

transdisciplinary

A

holistic
-new methodologic or conceptual frameworks

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50
Q

unmet health need

A

FDA: condition whose treatment or diagnosis is not addressed adequately by available therapy

-does not need to have a treatment for a disease

-immediate need for defined population and long-term need for society

-may arise due to budget constraints, low socioeconomic status (underserved individuals)

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51
Q

determining treatment unment health need

A

priority
-treating patients not on any other treatments
-treating patients who will get the largest health gain

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52
Q

t0 objectives

A

identify functional significance of genomic polymorphisms
try preclinical methods: animal modes/ human physiological studies, human blood or cell lines, computational models

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53
Q

therapeutic modalities

A

intervention used to heal someone

Drugs: small molecules, biologics, devices, diagnostics

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54
Q

Drug (FDA)

A

substance recognized by official pharmacopoeia/ formulary

-intended for use in diagnosis, cure, mitigation, treatment, or prevention of disease

-substance intended to affect the structure or any function of body

-substance intended for use as component of medicine NOT device, component, part or accessory of device

-biological products

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55
Q

small molecules

A

most drugs are
-weight 900 Da
-organic molecules, natural products, full/semi synthetic
-have oral bioavailability, cross biological membranes

–have well defined chemical structure

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56
Q

Biologics

A

vaccines, blood & blood components, allergenics, somatic cells, gene therapy, tissues, recombinant and therapeutic proteins

-isolated from variety of natural sources and produce what small molecules cant provide

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57
Q

proteins

A

antibody, large proteins

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58
Q

biologics delivery method

A

-viral vectors (gene therapies)
-nanoparticles

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59
Q

top selling

A

humira- adalimumab
enbrel- etanercept
remicade- imflixamab

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60
Q

medical device

A

instrument, apparatus, implement, machine, contrivance, implant which is:

-intended for use in the diagnosis of disease or other conditions, or in cure, mitigation, treatment, or prevention of disease, in man or other animals

-affect the structure or any function of the body of man or other animals which does not achieve any of its primary intended purposes through chemical action within or on the body of man or other animals NOT DEPENDENT UPON being metabolized for treatment of any of its primary intended purposes

61
Q

Class I

A

least regulatory control (general controls)

-bandages, exam gloves

62
Q

Class II

A

general controls with special controls

-acupuncture needles, powered wheelchair, infusion pump, surgical drapes

63
Q

Class III

A

above & requires pre-market approval (PMA)

supports or sustains life

-pacemaker, defibrillators

64
Q

premarket notification

A

“similar devices”
-how does it differ and is it safe & effective
-documented lab data but human data not required
-clearance v approval (cant say FDA approved)

65
Q

pre-market approval

A

completely new or Class III
-laboratory and clinical data needed
-more time, money, and documentation

66
Q

diagnostics

A

used to determine whether or not a condition is present in an individual

tissue biopsy: detect tumor, analyze drug response
breathalyzer: alcohol
blood: PSA, glucose, electrolytes
urine: hCG (pregnancy)

considerations:
qualitative v quantitative
invasive v non invasive
accuracy v precision
sensitivity v specificity

67
Q

invasive v non invasive

A

stand alone or part of series of tests

68
Q

accuracy

A

how close measured value to standard or known value

69
Q

precision

A

degree to which several measurements provide answers very close to each other

70
Q

sensitivity

A

probability that individual with disease tests positive

71
Q

specificity

A

probability individual without the disease will test negative

72
Q

efficacy

A

maximum response produced by a drug

73
Q

potency

A

concentration or dose of drug that produces 50% maximal response

74
Q

partial agonist

A

will not produce an effect as large as a full agonist

-more potent agonist (lower log value) but will produce a response larger than less potent

75
Q

competitive antagonist inhibition

A

competes with agonist for a spot
-affinity of drug for receptor decreases as well as potency

–if you add more agonists (more potent) they will outcompete the antagonists

76
Q

non-competitive (allosteric) inhibition

A

bind at different site (besides main site) which may change the receptors response to the agonist

CHANGES EFFICACY OF THE RECEPTOR

-no competition so potency of agonist WILL NOT CHANGE

-

77
Q

Desensitization (chronic agonist)

A

receptor continually activated by agonist and internalized by cells causing the receptors to get degraded (less available) causing down regulated

gonadotropin releasing hormone (GnRH)

78
Q

Supersensitivity (chronic agonist)

A

to compensate for continuous blocking ( & lack of activation) cell will put more receptors on its surface
causing receptors to get up regulate

ex: propranolol

79
Q

Gonadotropin

A

-downregulation
-controls release of lutenizing hormone (LH)
-has pulsatile release
-continuous treatment of leuprolide will cause desensitization (decrease in testosterone= prostate cancer growth)

80
Q

leuprolide

A

agonist for GnRH receptor used to treat prostatic cancer

-get constant activation of receptors, which they will eventually downregulate (degradation) producing less of the lutenizing hormone

81
Q

luteinizing hormone

A

stimulates testosterone synthesis

82
Q

graded concentration response

A

for therapeutic efficacy, which is important for clinical use

83
Q

quantal dose response

A

all or none response
-take number of responders out of study and give those who didn’t have a higher dosage (add accumulated of responders)

84
Q

quantal dose responsive curve

A

therapeutic index
-effective dose: which 50% of individuals exhibit the therapeutic effect (increases heart rate)

toxid dose: which 50% of individuals exhibit toxic effect vomiting

85
Q

therapeutic index (TI)

A

TD50/ED50

86
Q

enteral administration

A

-oral
-sublingual
-rectal

87
Q

oral

A

non-invasive (excellent for repeating dosing)

-undergoes first-pass metabolism (digestive)

88
Q

sublingual

A

place under tongue and is absorbed
-rapid entry of permeable drugs
–NO FIRST PASS metabolism

89
Q

Rectal

A

oral administration is impractical

partial first pass metabolism

90
Q

parenteral administration

A

intravenous
subcutaneous
intramuscular
topical
transdermal
inhalation

91
Q

intravenous

A

rapid and complete distribution (go everywhere quickly)

92
Q

subcutaneous

A

slow absorption
-hypodermis injection

93
Q

intramuscular

A

larger volume than subcutaneous
-use slow release formulations (if you want absorbed slow)

if muscle has larger blood supply drugs will be absorbed quicker

94
Q

topical

A

directly where we want it
-localized
-rapid reuptake through mucous membranes

95
Q

transdermal

A

eyes, skin, etc.
-sustained release
-potential for irritation

96
Q

inhalatation

A

-efficient for anesthesia
-initially localized to pulmonary system

97
Q

bioavailability

A

-absorbability of a drug
-usually measured in percentage

100% bioavailability will never happen with oral formulation

compared to IV, oral has a delay in plasma concentration and it does not get as high

98
Q

passive absorption

A

diffusion (high to low concentration)
-dependent on membrane permeability and concentration gradient

99
Q

membrane permeability

A

smaller drugs are reabsorbed faster
-lipophilicity increases absorption
-

100
Q

neutral molecules

A

absorbed faster than ionized

101
Q

factors influencing absorption

A

-membrane permeability
-gastric emptying
-formulation

102
Q

gastric emptying

A

fatty foods will delay gastric emptying

103
Q

formulation

A

-coatings (enteric ones abosorbed in intestine not stomach)
-hydrogels
-sustained v controlled release

104
Q

sustained release

A

constant, same amount released overtime

105
Q

controlled release

A

over a period of time amount tapers off

106
Q

single compartment (drug distribution)

A

distribute evenly throughout body

107
Q

unequal distribution

A

-between organs
-metabolize before pure equilibrium
-many drugs bind to plasma proteins
-sequesters drug in plasma
-potential for drug interactions

108
Q

Phase 1

A

usually involves “activation” of molecule so it can be conjugated with more polar group (liver ER but can occur in other tissues such as GI tract)

-oxidation
-epoxidation
-o and n dealkylation
-reduction
-dehalogenation (Br and Cl)
-hydrolysis (esters and amides)

109
Q

Phase II (conjugation)

A

biotransformation into more polar form, readily excreted in urine and feces

-Acetylation
-Glucouronidation
-Sulfation
-Glutathionation

110
Q

factors affecting drug metabolism

A

-age (max efficacy at 50)
-change in diet
-chronic drug use cause synthesis of larger amounts of biotransformation
-genetic differences

111
Q

non renal excretion

A

-bile (largest non-renal route)
-lung
-saliva
-milk
-sweat

112
Q

renal excretion

A

-glomerular filtration
-active tubular secretion (ion secretion)
-passive reabsorption: (drugs in top 2 steps reach the distal tubule and passively diffuse out of kidney into blood supply and get remetabolized

113
Q

glomerular filtration

A

most drugs are passively filtered into nephron

-renal blood flow (20% cardiac output)
-Plasma protein binding
-such drug is not reabsorbed or additionally secreted, then its clearance would be about 125 ml/minute (GFR)

114
Q

active tubular secretion

A

some drugs are secreted into nephron
-the clearance of such drug can be as high as 600ml/minute

-OAT and OCT (non-specific)
-important for protein bound drugs

115
Q

passive reabsoprtion

A

many drugs passively reabsorbed in the course of urine formation

-drug ionization will affect the extent of this passive reabsorption (move to from higher to lower concentration)

ion trapping (trapping ionized drug can be exploited to speed up removal)

116
Q

biliary excretion

A

active transport systems for basic and acidic compounds are an elimination of ionized compounds and their metabolites

-glucuronides
-high MW weight conjugates

117
Q

entero heptatic recycling

A

-gut bacteria unconjugate metabolites which get transported back to liver

(similar to recovery of bile salts drugs excreted in bile)

activated charcoal interrupts recycling (speed up removal of drug)

118
Q

lungs

A

eliminates gases and volatile substances
ex: gas anesthetics, alcohol

119
Q

factors affecting lung excretion

A

blood flow
rate of respiration
solubility in blood

120
Q

milk

A

-lactic secretions rich in fat and protein
-unionized drug diffuses through mammary epithelium
ex: anti-cancer drugs, lithium

121
Q

saliva

A

-unionized drug secreted passively
-cause bitter taste in mouth

ex: caffeine, alcohol

122
Q

sweat

A

-very minor
-alcohol, salicylic acid

123
Q

steady state

A

rate of drug infusion= rate of elimination at therapeutic dose

124
Q

non-saturating elimination

A

first order (reverse linear)
-more drug in body, elimination will be faster

-glomerular filtration
-diffusion and ion trapping
-active renal secretion
-metabolic enzymatic processes

elimination= -kel[drug]
follows an exponential decay

125
Q

half life (t1/2)

A

0.693/kel

126
Q

Vd (volume of distribution)

A

dose (mg) /plasma concentration (mg/L)

127
Q

doubling dosage

A

increases duration of time by approximately one half life

128
Q

saturating elimination

A

zero order (completely linear, as time increases drug concentration decreases)

RARE

catalysis= kcat[enzyme]

129
Q

first order processes

A

reach a plateau with repeated doses, avoid reaching toxic levels

130
Q

zero order processes

A

start constant and go above toxic level with repeated dosages, very unpredictable and cannot reach plateau

131
Q

plateau

A

time determined by Kel
-describes the decrease in drug when the drug administration is haltered

132
Q

loading dose

A

avoids slow rise of drug to therapeutic level

-most stable for it to be the largest dose and then give smaller maintenance doses

=Vd*[drugs]

133
Q

clearance

A

the relationship between drug concentration and rate of drug elimination from the body

=kel * Vd or (0.693/t(1/2))*Vd

134
Q

maintenance dose

A

Cl[drugs]Tm

135
Q

phase IV variability

A

-due to large population of patients studied
-increased diversity/ heterogeneity in patient population (variation in drug pharmacokinetics and pharmacodynamics)

136
Q

sources of individuality

A

condition of state of being
environmental
genetic
drug combinations (drug interactions)

137
Q

children

A

newborn/ infants

-drug distribution
-lower plasma proteins (more free drug availabile)
-lower P450 enzymes
-lower GFR

138
Q

elderly

A

-lower GFR
-lower P450
-changes in PD

139
Q

p450 induction

A

charcoal broiled foods
-broccoli/sprouts

140
Q

p450 inhibitors

A

grape fruit juice, topical fruits

-higher levels of drug in patient
-prevents activation of drug from pro-active state

141
Q

Codeine

A

prodrug conversion to morphine
-poor metabolizer (low analgesia)
-ultra rapid metabolizer

142
Q

drugs may

A

-inhibit metabolism of other drugs (increase half life)
-stimulate metabolism of other drugs
-displace other drugs from albumin binding sites (increase in free v bound drug)
-inhibit oral absorption of other drugs

143
Q

pharmacokinetics

A

study of genetic basis for variation in drug response
affects:
-pharmacokinetics
-pharmacodynamics

144
Q

isoniazid

A

treatment of tuberculosis
-modification of drug by acetylation (phase II liver metabolism)
-variation in genetic alleles for NAT affecting drug half life
-can alter therapeutic and adverse reactions

145
Q

primaquine

A

antimalarial drug forms reactive metabolites inactivated by reduced form of GSH

-can cause hemolytic anemia (lysis of red blood cells)

occurs primarily in patients with deficiency in glucose-6-phosphate dehydrogenase

146
Q

warfarin

A

inhibitor of vitamin K epoxide reductase (VKORC1)

-recycles oxidized vitamin K to its reduced form

147
Q

chronic myelogenous leukemia

A

malignant hematopoietic stem cell disorder
-expression of tyrosine kinase essential for maintaining oncogenic state
-95% cases associated with Philadelphia chromosome

148
Q

imatinib

A

inhibits Bcr-Abl tyrosine kinase present in philadelphia chromosome

149
Q

tamoxifen

A

prodrug
-polymorphism in CYP2D6 lead to lower therapeutic levels of active drug causing relapse

pharmacodynamic: missing estrogen receptor

150
Q
A
151
Q
A

GMS 6551 (1 decks)

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