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Semester 3 FS Exam 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Pharmacology

A

study of how a drug interacts with the body
mechanism of a drug with a focus of how it is counteracting the disease
how is the drug interacting with teh body

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2
Q

Toxicology

A

studying toxicity and harmful effects

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3
Q

Pharmacy

A

focused to the clinical distribution and preparation - need to have clinical license to distribute and work with patients

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4
Q

Pharmacokinetics

A

Focussed on processes that affect drug concentration in the body
What is the body doing to the drug
absorp, distribution, metab, elimination

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5
Q

Pharmacodynamics

A

What is the drug doing to the body - inc or dec HR..

Talking about receptors and signaling pathways that get activated

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6
Q

Drug nomenclature - Chemical name

A

nobody really uses this

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7
Q

Drug nomenclature - generic name

A

Every chemical has a generic name that never changes - more useful to look at generic name vs trade name

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8
Q

Drug nomenclature - trade name

A

company holds a patent on it but they expire and change so you can have multiple trade names for the same compound

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9
Q

Prescription drugs

A

drugs whose sale is restricted and available only with rx from licensed provider

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10
Q

All rx drugs in US are controlled by

A

FDA - they decide if a drug requires an rx or not

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11
Q

State decides

A

who can prescribe the drug

PAs differ at state level

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12
Q

Schedule 1 drugs

A

High abuse potential, no medical use

Cant get licensed for sched 1

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13
Q

Schedule 2 drugs

A

High abuse potential, have medical use - potential for physiological and physical dependence (morphine)

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14
Q

Schedule 3 drugs

A

less abuse potential than 1 or 2, have medical use, low potential for physical dependence but high potential for psychological dependence (annabolic steroids)

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15
Q

Schedule 4

A

Less abuse potential than 3, have medical use, little potential of dependence

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16
Q

Shcedule 5

A

less abuse potential than 4, have medical use, limited dependence

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17
Q

Pattern for schedule

A

Abuse potential becomes less and there is some medical use for drug as you go down

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18
Q

OTC medications - non prescription OTC meds

A

Drugs that can be sold without directions for safe use by the public

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19
Q

OTC meds - Variation

A

Packaged differently - from drug and therapeutic standpoint they are the same drug but might just have difference in flavor or something

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20
Q

Monitoring OTCs

A

Nonprescription drugs advisory committee of US FDA

Responsible for making recommendations on the removal of medications from OTC and addition of any to OTC

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21
Q

OTCs have to be given significant consideration when treating a patient since:

A
  1. be a useful therapeutic option for patient
  2. may exacerbate a medical condition
  3. interact with another OTC or rx med
  4. Be used inappropriately
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22
Q

Drug development - First

A

Identification of a new compound - drug combo, new target, drug modification, mass screening

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23
Q

Drug development - Second

A

Experimentation - drug characterization (molecular, cellular) Toxicity (minimal lethal dose animal testing)

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24
Q

Drug Development - Third

A

Clinical testing

Phases

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25
Q

Drug development - Phase 1

A

Limits of safe dosing range

Subjects are low - goal is about the safety

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26
Q

Drug development - Phase 2

A

Does it work?

More subjects - is it doing what it is supposed to do

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27
Q

Drug development - phase 3

A

Well controlled, more patients, see if it is working as expand population and still monitoring safety

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28
Q

Drug development - phase 4

A

monitoring while being sold - postmarketing surveillance

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29
Q

Drug classification - Drug action

A

Classification based on therapeutic action can result in a broad range of descriptiveness
Ex - antiviral agents
It is very broad and there is no ability to generalize the mechanism of action or side effects with this classification

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30
Q

Drug classification - Molecular target

A

Dependent upon an understanding of the molecular target, can include receptors or enzymes
Ex - beta blockers
Need to understand physiology

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31
Q

Drug classsification - molecular target - what can be predicted

A

broad distinctions like use, action, side effects

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32
Q

Drug classification - Drug source

A

Based on natural source of the drug

This name gives no indication of how it works or what the physiological target might be

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33
Q

Drug classification - chemical nature

A

specific chemical name is rarely used but a broader grouping can provide info on structure, action, or use - grouping like steroid, barbituates..

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34
Q

Drug classification - generic name

A

can be derived from chemical name and provides some indication for what class the drug belongs to

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35
Q

Pharmacokinetics

A 
Absorption
Distribution
Metabolism
Elimination
What the body does to a drug
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36
Q

Pharmacodynamics

A

Drug targets or receptors effects

What the drug does to the body

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37
Q

Drug absorption

A

The movement of an agent from the site of administration into the circulation

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38
Q

Three types of administration

A

Enteral
Parenteral
Topical

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39
Q

Enteral includes

A 
Anytime you are using the GI tract to deliver the drug 
Oral
Sublingual
Buccal
Rectal
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40
Q

Enteral - Oral

A

Taking pill - use stomach or intestine
Easiest and best compliance
First organ after absorbed is liver - could lose up to 8-% of the drug by this time so typically oral dose is higher because you are expecting to lose some with liver metabolism

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41
Q

Enteral sublingual

A

under the tongue

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42
Q

Enteral Buccal

A

btw cheek and gum

Goes straight to venous system - not as convenient and compliance is lower

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43
Q

Enteral Rectal

A

Good if targeting that tissue
Can also be good if want to use enteral but pt cant swallow
compliance is low and drug is not completely absorbed

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44
Q

Parenteral

A 
You have to pierce the skin 
Intravenous
Intramuscular
Subcutaneous
Intrathecal 
Epidural
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45
Q

Parenteral - IV

A

most direct - put drug directly into circulation

Administer exact amount - mistakes cant be made though

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46
Q

Parenteral - IM

A

painful

can get away with a single dose though and have it diffuse over time

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47
Q

Parenteral Subcutaneous

A

insulin is common - cant do orally because stomach would digest

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48
Q

Parenteral Epidural and Intrathecal

A

ways to target nervous system - subarachnoid or epidural space - very targeted nerve block

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49
Q

Topical

A 
putting drug on surface that is generally the target tissue - can be internal too though 
Topical
Transdermal
Inhalational
Otic/Optic
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50
Q

Topical - transdermal

A

applying a drug to the skin but hoping it goes through the skin and into the blood
BC path
Patch behind ear

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51
Q

Topical - inhalational

A

breathing in - target might be mucous membrane of lungs but could also be systemci

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52
Q

Topical - otic/optic

A

eye drops or ear drops - targeting that site specifically

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53
Q

How are most drugs transported

A

passivelt

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54
Q

Ionized vs non-ionized forms

A

Non ionized form more readily cross membranes

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55
Q

Pronated vs unpronated

A

pronated form of a weak acid is nonionized

unpronated form of a weak base is nonionized

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56
Q

Weak acid - absorbed when

A

pronated (nonionized form)

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57
Q

Weak base - absorbed when

A

unpronated (nonionized form)

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58
Q

Hendersen Hasselbalch equation is used to determine

A

ration of ionized to non-ionized forms

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59
Q

HH ratio is dependent upon

A

the pH (acidity) of the environment and the pKa (pH at which 50% of the drug is ionized and 50% is nonionized)

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60
Q

HH equation

A

log (proton/unproton) = pKa - pH

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61
Q

pKa is defined as

A

the point at which half is protonated and half is unprtonated

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62
Q

If pH is less than pKa which form dominates

A

protonated

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63
Q

If pH is more then pKa which form dominates

A

unprotonated

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64
Q

The more hydrogen ions there are around, (the more acid that is around) the more likely

A 
HA is to form
More acidic (lower pH) --> protonated will form
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65
Q

Weak acids are protonated (HA) in

A

lower pH of the stomach

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66
Q

Weak bases are nonprotonated in the

A

higher pH of the intestines

67
Q

Weak acids are more readily absorbed from the

A

stomach (low pH)

68
Q

Weak bases are more readily absorbed from the

A

intestines (high pH)

69
Q

GI contents impact absorption - why take some on empty stomach

A

so that you can get the max absorption and you can reach the therapeutic effect
even presence of just liquids can reduce absorption by 60%

70
Q

GI contents impact absorption - why take with a meal

A

you can slow down the transit time in the GI tract
You can get more absorption if you keep it in the stomach longer - same effect just get higher concentration in the blood if taken with meal

71
Q

Drug distribution

A

the process by which a drug leaves the circulation and enters the tissues perfused by the blood

72
Q

Factors that impact distribution

A

Cardiovascular factors (CO, blood flow, capillary perm, plasma protein binding)
Tissue binding
Drug molecular size
Lipid solubility

73
Q

Drug distribution - cardiovascular factors - Cardiac output

A

The greater the CO the more you are moving blood through the body so the quicker you will distribute it

74
Q

Drug distribution - cardiovascular factors - regional blood flow

A

The more vascularized the tissue, the more the drug has access to the tissue

75
Q

Drug distribution - cardiovascular factors - capillary permeability

A

impacts the acess that the drug has to tissue

76
Q

Drug distribution - cardiovascular - binding to plasma proteins

A

as drugs stick to plasma proteins in the blood some stick more than others and the stickier ones will be less distributed because get trapped in blood

77
Q

Drug distribution - tissue binding

A

once a drug is distributed to the tissue it can get help in that environment

78
Q

Drug distribution - drug molecule size

A

if it is a large drug may have more difficulty accessing the tissue

79
Q

Drug distribution - lipid solubility

A

the more lipid soluble the easier it is to cross membrane and barriers

80
Q

Drug metabolism/biotransformation

A

can be categorized as phase 1 and phase 2 biotransformation

Reactions can covernt a parent compound into an active or inactive metabolite

81
Q

Drug metabolism - biotransformation primarily occurs where? What is the goal

A

liver

goal is to take compound and make it hydrophilic (inc water solubility) to make it easier for kidney to excrete

82
Q

Phase 1 of biotransformation

A

Generate a more polar molecule by exposing a functional group on the parent compound

83
Q

Phase 2 of biotransformation

A

rxs yield a more water soluble conjugated product to be excreted
Stick a bulky group on it to make it water soluble

84
Q

Biotransformaion - lineality

A

not a very linear process
some are just eliminated, some start at phase 2 and some go 1 and then 2
Some even require the transformation before being distributed

85
Q

First pass effect

A

drug absorbed by stomach or intestine will first be carried to the liver by the portal vein - drug can be inactivated before even reaching the intended target

86
Q

First pass effect - impaired liver function

A

May have to take a lower dose because they’ve lost some of the first pass effect so more will get into circulation - danger of reaching toxic level

87
Q

Drug elimination - two types

A

Renal

Fecal

88
Q

Drug elimination - Renal

A

Primary mechanism of drug elimination
Dependent on several processes - Glomerular filtration rate
- Binding to plasma proteins
- Alkalinization or acidification of urine

89
Q

Drug elimination - Fecal

A

Hepatic secretion into bile

Enterocyte-mediated secretion

90
Q

Drug concentration - bioavailability

A

the amount of a drug that reaches the systemic circulation

91
Q

The bioavailability of a drug adminstered through IV will be

A

100% - direct administration into the blood

92
Q

What impacts the bioavailability of a drug

A

absorption, metabolism, distribution and elimination

93
Q

Most bioavailability to least

A 
IV
IM
SC
Oral
Rectal
Inhalation
Transdermal
94
Q

Drug concentration - half life

A

The time it takes for the concentration of a drug in the plasma tod ec by 50% (so 50% is gone)

95
Q

What half life for most of drug to be gone

A

4th or 5th half life

96
Q

Drug concentration - steady state

A

the point during a dosing regimen when elimination of a drug is equal to the bioavailability
About 4 or 5 half lives

97
Q

When administering multiple doses why does conc plateua instead of continuing to inc

A

Dosing at every half life - by the 4th or 5th dose, the entire first dose is gone so you arent adding to that first dose anymore

98
Q

Drug concentration - the time to reach steady state conc is

A

NOT dependent on the dose or the frquency of doses - will always be the 4th or 5th half life

99
Q

The actual steady state concentration

A

is determined by dose and dosing frquency

100
Q

If you do not have time to wait for the 4 or 5 half lives - what can you do

A

IV administration or can give a loading dose (high dose on first day)

101
Q

Drug receptors

A

Recognize and bind other molecules (ligands/drug/hormone)
Propgate regulatory signals following ligand binding
Modulate ongoing cellular function

102
Q

Drug receptrs - 5 types

A

Intracellular
Receptors with intrinsic enzymatic activity
Receptors that directly associate with intracellular enzymes
Ligand gated ion channel
7 membrane spanning receptors

103
Q

Drug receptors - intracellular receptors

A

The drug or ligand has to diffuse the membrane to get to the receptor - has to be lipophilic
Drug binds to receptor and intracellular receptor goes into nucleus to change gene expression

104
Q

Drug receptor - receptors with intrinsic enzymatic acitvity

A

Drug binds to these receptors and brings them together (like an on switch) when they come together they act with substrates in the cell that are changed in some way to elicit a function - get some type of cellular change as result

105
Q

Drug receptor - receptors that directly associate with intracellular enzymes

A

drug binds to a receptor and turns on an associated enzyme

106
Q

Drug receptor - Ligand gated ion channel

A

Drug binds to receptor and you change opening or closing of the receptor and the movement of ions across it

107
Q

Drug receptor - 7 transmembrane receptors

A

Weaves in and out of membrane 7 times - G coupled protein receptors
Coupled with G protein that goes on to impact another molecule like cascade of events

108
Q

Do all drugs bind to a receptor to elicit response?

A

no, but most do

Some we arent targeting receptors though like tums - we are taking it to neutralize and dec aciditiy

109
Q

Drug receptors - Receptor numbers

A

dynamic process - the number of receptors can change

110
Q

Drug receptors - Downregulation

A

Decrease in the number of receptors

Continued stimulation of the receptor and the receptor will go away

111
Q

Drug receptors - Upregulation

A

Increase in number of receptors
Continued exposure to an inhibitor - you might have to inc dose because now you have more receptors to response and if you are blocking a response you now have more receptors to block

112
Q

Dissociation constant (Kd)

A

There will be one for every drug

It will tell us a point where there is a mixture of half of your receptors bound to your drug and half are not

113
Q

Dissociation constant defines

A

a drugs affinity
Tells us how sticky the drug is - how tightly that drug is to the receptor
The faster you reach Kd, the more affinity a drug has - so you need less drug to bind half of the receptors

114
Q

EC50 =

A

concentration of drug that produces a half maximal effect/response

115
Q

Drug response - go on forever?

A

No, there is a saturation effect

A drug response is saturable - there is a max effect

116
Q

Potency

A

A measurement of drug dose used to compare the relative affinity and effectiveness of two or more drugs
Usually done by comparing EC50 of two or more agents
Comparing which drug takes less conc to create a half max response

117
Q

Potency is a

A

comparison

118
Q

Efficacy

A

The max effect a drug can induce (Emax)

119
Q

Agonist

A

A drug or ligand that binds to a receptor and produces a molecular, cellular, or physiological response
Agonists stimulate a response

120
Q

Antagoist

A

A drug or ligand that binds to a receptor and inhibits the response produced by an agonist
Antagonists block a response
Two types

121
Q

Two types of antagonists

A

Competitive and Noncompetitive

122
Q

Competitive antagonist

A

Agonist and antagonist compete for the same binding site - only one can win though
Shift to the right in EC50
Max effect still achievable

123
Q

Noncompetitive antagonist

A

Agonist and antagonist bind to different sites
Dec in max effect because you are knocking out some of the receptors (structurally changed some of the receptors so that the normal hormone doesnt recognize it anymore)

124
Q

Partial agonist

A

A drug that produces a lower maximal response as compared to the agonist
Allows you to reduce responses without blocking them

125
Q

ED50

A

Median effective dose
Dose at which 50% of individuals exhibit a specific quantal effect
Dose where 50% get the effect

126
Q

TD50

A

Median toxic dose

Dose at which a specific toxic effect occurs in 50% of the individuals tested

127
Q

LD50

A

Median lethal dose
Dose that is lethal for 50% of individuals tested
This is experimentally defined with animals

128
Q

TI

A

Therapeutic Index
Indicator of safey
The ratio of TD50/ED50
The greater the ratio (or the window btw) the safer the drug is because there is more room for error

129
Q

Tolerance

A

Decrease in drug response following repeated administration of the drug

130
Q

Causes for tolerance

A

changes in pharmacokinetic parameters, pharmacodynamic parameters, or behavioral changes

131
Q

Sensitization

A

Reverse tolerance

Increase in drug response following repeated exposure to a drug

132
Q

Senxitization is seen more with

A

durg drug interactions - maybe one is blocking the metabolism of another so there is more drug available and person has larger response to it - more sensitization
Shift to the left on dose curve

133
Q

Additive effect

A

Occurs when two drugs given in combination produce a response that is consistent with each agents potency
20 + 20 = 40

134
Q

Synergistic effect

A

Response that is magnified beyond the sum of either agents agents potency
20 + 20 = 90

135
Q

Advantage to synergistic effect

A

You can use a lower dose of the synergistic combination to get your desired therapeutic effect and lower dose means less adverse effects

136
Q

Varations of drug response - genetic - Polymorphism

A

Variation in the genetic code present at an allele frequency of grater than or equal to 1% - so it is showing up over and over again

137
Q

Types of polymorphism

A

Single nucleotide polymorphisms (SNP)

Insertions/Deletions (Indels)

138
Q

Single nucleotide polymorphisms

A

1 SNP every 300 - 1000 base pairs

There is a change in one base in a DNA coding but it is showing up at a frequency of more than 1%

139
Q

Insertions/Deletions

A

Less frequent than SNPs

An insertion or deletion of chunk of material that may or may not code for anything but it disrupts the coding

140
Q

Pharmacogenetics

A

The study of the genetic basis for variations in drug response

141
Q

Monogenic

A

Expression of a single gene results in a single phenotype

142
Q

Multigenic

A

Networks of genes acting together to create a single phenotype

143
Q

Recessive trait

A

Phenotype exhibited when a non functional allele occurs on both the maternal and paternal chromosome
Both mom and dad have bad copy and this gives child adverse outcome when processing drug

144
Q

Dominant trait

A

Phenotype exhibited when a non-functional allele occurs n either the maternal or paternal chromosome You only need a bad allele from either mom or dad and it gives you the bad response - outcome is no metabolism of the drug and toxicity can be huge

145
Q

Co-dominant trait

A

Heterozygotes display an intermediate phenotype as compared to wild type and homozygotes Intermediate type where you have some in between response
Reduction in metabolism by maybe 50%

146
Q

Genetic testing can be helpful because

A

it can tell you if a drug will end up causing someone more harm - it may work well for some but harm others
Better to know that to treat everyone the same

147
Q

Monogenic vs. Multigenic

A

Monogenic (low, intermediate, high)

Multigenic - not as simple to break down into categories - can be very difficult to manage

148
Q

Codeine

A

Therapeutic effect of codeine depends on CYP2D6 metabolism to morphine

149
Q

Variations in drug repsponse - Disease - Absorption

A

Tissue damage or alteration caused by disease can impact how a drug is absorbed
Ex: GI tract - if there is a dec in absorption of nutrients then probably not absorbing drug either

150
Q

Variations in drug response - Disease - Metabolism and Elimination

A

Disease of tissue involved in metabolism and elimination can impact the pharmacokinetic parameters of a drug

151
Q

Variations in drug response:

A
  1. Genetics
  2. Disease
  3. Drug interactions
  4. Age
  5. Sex
  6. Environment
152
Q

Variations in drug response - drug interactions - Ciproflocacin and Ca

A

Some drug interactions can prevent the absorption of both the drug and the nutrient
distribution

153
Q

Variations in drug response - drug interactions - Phenytoin and protein

A

Some drug interactions will alter the protein free and protein bound fractions of the drug thus increasing the free drug availability or drug

154
Q

Variations in drug response - drug interactions - Ethinyl estradiol

A

Inc the metabolism and dec the bioavailability - so the drug is less effective

155
Q

Variations in drug response - drug interactions - Simvastatin

A

decrease in metabolism - patient at greater risk of experiencing adverse effects or altered therapeutic effects

156
Q

Variations in drug response - drug interactions - Lithium

A

Competition btw sodium and lithium can result in changes in excretion of the cations

157
Q

Variations in drug response - drug interactions - Monoamine oxidase inhibitors

A

Drug interactions can increase the action of MAOIs

158
Q

Variations in drug response - drug interactions - Warafin

A

Inhibitory effect of warafarin can be overcome by excessive vit K - vit K can alter the actions of warfarin by reducing its effect

159
Q

Variations in drug response - Age

A

Pharmacokinetic and pharmacodynamic parameters will differ in geriatric and pediatric populations

160
Q

Variations in drug response - Age - Peds

A

Changes occur related to enzyme/protein expression patterns, body composition, and blood flow

161
Q

Variations in drug response - Age - Geriatrics

A

Decline in organ function, more likely to be ill and taking medication, population is more susceptible to variations in a drug response due to drug interactions or disease

162
Q

Variations in drug response - sex

A

Men and women differ with respect to body composition and thus the distribution of drugs may differ
Also there are difference in organ function and enzyme expression that can impact pharmacokinetics

163
Q

Variations in drug response - Environment

A

Occupational exposure
Diet
Stress
Smoking/alcohol intake

Semester 3 FS Exam 1 (2 decks)

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