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Pharmacology > pharm exam 1-3 > Flashcards

pharm exam 1-3 Flashcards

1
Q

What is the study of pharmacology

A

the study of drugs and their interactions with the human body

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2
Q

What does the topic of pharmacology embrace

A

it embraces the knowledge of the source, physical and chemical properties, compounding, physiological actions, absorption, fate and excretion, and therapeutic use of drugs

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3
Q

A drug is defined as what?

A

any chemical agent that affects living protoplasm

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4
Q

What is an adverse drug reaction?

A

-any response to a drug in which is harmful and unintended-occurs at doses used in man for prophylaxis, diagnosis or treatment-side effects, drug allergies and drug interactions

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5
Q

What are the four main processes of pharmacokinetics?

A

Absorption, distribution, metabolism(biotransformation), and elimination of drugs

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6
Q

Pharmacokinetics is defined as what?

A

the action of the body on the drug. It is the study of the fate of drugs on the body

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7
Q

Why is it important to understand and apply pharmacokinetic principles?

A

it can increase the probability of therapeutic success and reduce the occurrence of adverse drug effects in the body

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8
Q

What is the tool used to design optimally beneficial drug therapy regimens?

A

proper drug, route of administration and dosing schedules

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9
Q

absorption is defined as

A

movement of a drug from its site of administration into the central compartment and the extent to which this occurs

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10
Q

If you have a solid dose form of a drug what must happen before the drug can be absorbed

A

there must be dissolution of the tablet or capsule thus liberating the drug

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11
Q

What are clinicians more concerned with when it comes to ADME?

A

bioavailability rather than absorption

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12
Q

What must occur in order for a drug to be absorbed?

A

it must be lipid soluble in order to have site access

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13
Q

Absorption occurs by what mechanisms

A

Active or passive transportIonized or non-ionized

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14
Q

What is active transport

A

against a concentration gradient and requires energy

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15
Q

what is passive transport

A

diffusion from higher to lower concentration

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16
Q

What is a site where there is a high probability for drug interactions

A

during movement through the GI tract

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17
Q

What is distribution

A

when a drug is transported to site where is reacts with various body tissues or receptors

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18
Q

After absorption or systemic administration where does a drug go

A

it is distributed into interstitial and intracellular fluids

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19
Q

What are the factors that affect distribution of a dug into tissue

A

Cardiac output, regional blood flow, capillary permeability and and tissue volume

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20
Q

What parts of the body would receive most of a drug

A

Initially Liver, Kidney, Brain and other well perfused organs

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21
Q

The second distribution phase is faster or slower?

A

slower

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22
Q

What parts of the body do the second distribution phase affect

A

it involves delivery to muscle, most viscera, skin and fat

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23
Q

Where does most of the drug get delivered from second phase distribution?

A

extravascularly

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24
Q

What are important factors that determine distribution

A

Lipid solubilityTransmembrane pH gradients

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25
Q

What happens when a drug is bound to plasma proteins and tissue macromolecules?

A

it limits the concentration of free drug

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26
Q

Lipid soluble drug have a high affinity for what

A

adipose tissue

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27
Q

Why do drugs get stored in the adipose tissue

A

there is low blood flow there creating a drug resivoir

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28
Q

What are highly lipid soluble class of drugs

A

Barbiturates, Phenothiazines, Benzodiazepines

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29
Q

What is the function of metabolism

A

to convert active lipid soluble compounds and convert them to inactive water soluble substances to be excreted by the kidneys

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30
Q

Where are most drugs metabolized?

A

in the liver, but it can also happen in the kidneys, lungs and intestinal tract

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31
Q

What happens during Phase I of metabolism

A

Hepatic microsomal enzymes first oxidize, demethylate and hydrolyze drugs

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32
Q

During what phase of metabolism do more drug interactions happen?

A

Phase I hepatic enzymes

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33
Q

Where do drug with a short half life and inactive metabolites get metabolized

A

they are metabolized during phase I which causes them to be less effected by drug interactions

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34
Q

What happens during Phase II of the metabolism

A

large water soluble substances(glucuronic acid, sulfate) are attached to the drug.

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35
Q

How many times may drugs circulate thru the phases of metabolism

A

drug can circulate through one or both phases multiple times until the water soluble characteristic is present

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36
Q

What are the important hepatic microsomal enzymes of Phase I metabolism

A

CYP 450

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37
Q

What is the CYP classification for enzymes

A

CYP #X##=family denoted by a numberX=subfamily denoted by letter or arabic numberX=individual gene denoted by a number

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38
Q

What are the CYP families primarily involved with drug metabolism?

A

CYP1,CYP2,CYP3,CYP4

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39
Q

How does enzyme inhibition effect the concentration of drugs?

A

It decreases the rate of metabolism of object drug by obstruction metabolizing enzymes.This leased to an increase in drug concentration

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40
Q

How would enzyme inhibition effect half life

A

it increases half life, which causes it to accumulate

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41
Q

What is the effect on the clearance of a drug when you induce an enzyme. What does this do to the concentration of the drug?

A

stimulates the increase in CYP 450 enzyme activitywhich increases the clearance of drug.This decreases the concentration of a drug

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42
Q

What is an example of a prototypical inducer

A

Phenobarbital it induces all enzymes

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43
Q

What is excretion/elimination?

A

process that removes the drug and its metabolites from the body

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44
Q

What are the primary ways drugs are excreted?

A

through the urine, feces, skin

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45
Q

How are drugs eliminated from the body?

A

they are eliminated either unchanged or converted to its metabolites

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46
Q

Excretory organs excluding the lungs eliminate what type of compounds more efficiently?

A

they eliminate polar compounds more efficiently that substances with high lipid solubility

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47
Q

What organ is the most important organ for excreting drugs and their metabolites?

A

the kidney

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48
Q

What happens to a drug when it is excreted through the feces?

A

substances are usually unabsorbed orally ingested drugs

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49
Q

how are unabsorbed drug metabolites excreted?

A

either in the bile or directly into the intestinal tract and not reabsorbed

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50
Q

why is excretion of drug through breast milk important?

A

because the excreted drugs are a potential source of unwanted pharmacological effects in a nursing infant

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51
Q

The lungs are important mainly for the excretion of what?

A

anesthetic gases

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52
Q

What are factors about a patient that can effect the basic pharmacokinetic principles

A

age, sex, weight, disease states and genetic factors

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53
Q

What is pharmacodynamics

A

action of the body on the drug

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54
Q

Pharmacodynamics is the study of what

A

biochemical and physiological effects of drugs and their mechanisms of action

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55
Q

What are the most common mechanism for drug interactions?

A

synergism, antagonism, altered cellular transport and effects on receptor sites

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56
Q

What is the benefit of understanding pharmacodynamics?

A

provides the basis for the rational therapeutic use of a drug and the design of a new superior therapeutic agents

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57
Q

What are the 4 most important parameters governing drug disposition are?

A

BioavailabilityVolume of distributionClearance Elimination

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58
Q

What is Bioavailability?

A

(F) The fractional extent to which a dose of drug reaches its site of action

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59
Q

What are factors that decrease bioavailability (F)

A

GI absorption 1st pass effect Metabolism (enzymes, active transport)

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60
Q

What is the route of administration based on

A

the understanding of the factors that decrease bio-availibility

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61
Q

What is volume of distribution?

A

it related the amount of drug in the body to the concentration (it doe not necessarily refer to an identifiable physiological volume but rather to the fluid volume that would be required to contain all of the drug in the body at the same concentration measured in the blood or plasma

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62
Q

What is half-life (t1/2)

A

the time is takes for the plasma concentration to be reduced by 50%

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63
Q

How many half life’s does it take to get to a steady state?

A

5

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64
Q

What does half life reflect in systemic concentration

A

reflects the decline of a systemic drug during a dosing interval at steady state

65
Q

Steady state is defined as

A

rate in = rate out

66
Q

In steady state the amount of drug in a given period is equal to what?

A

it is equal to the amount eliminated in that same period

67
Q

What is a drug interaction?

A

pharmacological result whether it is desired or undesiredthe effect of one drug is changed by another drug

68
Q

What are the classification of DI

A

PharmacokineticPharmacodynamic

69
Q

What types of DI are there

A

Drug-DrugDrug-FoodDrug-Disease

70
Q

What is a Pharmacokinetic DI

A

occurs when ADME of one drug is affected by another drug/agent

71
Q

What way does absorption effect drug interaction

A

through GI, pH, Binding, Increase or decrease in motility and changes in GI flora

72
Q

How does distribution affect drug interactions

A

drugs can interact with plasma proteins which can cause the drug to be bound vs unbound (free drug)

73
Q

What are factors that effect the elimination of drugs

A

Urinary pH and competitionexamples when you give a person probenecid and penicillin probenecid competes for excretion and thus the concentration of Penicillin in the body increases

74
Q

What is synergism/potentiation

A

they are additive effects between two or more drugs that result in a pharmacologic response that is greater than the sum of the individual responses to each drugex: beer+valium these two combined have higher than expected effects

75
Q

Antagonistic

A

are opposing effects. smaller effect than individual agentsEx: tenormin+sudafed

76
Q

what is a receptor

A

a molecule to which a drug bonds to bring about a change in function of the biologic system

77
Q

receptor site

A

specific region of the receptor molecule to which the drug binds

78
Q

What is an inert binding molecule or site

A

a molecule to which a drug may bind without changing any function

79
Q

spare receptor

A

does not bind drug when the drug concentration is sufficient to produce maxima effect

80
Q

Kd>EC50

A

this is present when there is spare receptor

81
Q

effector

A

component that accomplishes the biologic effect after the receptor is activated by an agonist

82
Q

efficacy, maximal efficacy Emax

A

the maximum effect that can be achieved with a particular drug regardless of does

83
Q

potency

A

the amount of drug needed to produce a given effect, determined mainly by the affinity of the receptor for the drug and number of receptors available

84
Q

What is a graded does curve

A

a graph of increasing response to increasing drug concentration or dose

85
Q

what is a quantal dose-response curve

A

a graph of the fraction of a population that shows a specified response at progressively increasing doses

86
Q

EC50

A

the concentration that causes 50% of the maximum effect or toxicity

87
Q

ED50

A

the dose that causes 50% of maximum effect or toxicity

88
Q

TD50 (TC50)

A

the median toxic dose or concetration at which toxicity occurs in 50% of cases

89
Q

LD50 (LC50)

A

the median lethal dose or concentration required to kill hald the members of a tested population after a specified test duration

90
Q

Kd

A

the concentration of a drug that binds 50% of the receptors in the system

91
Q

Bmax

A

maximal number of receptors bound

92
Q

agonist

A

a drug that activates its receptor upon binding

93
Q

partial agonist

A

a drug that binds to its receptor but produces a smaller effect at full dosase than a full agonist

94
Q

Allosteric agonist

A

a drug that binds to a receptor molecule without interfering with normal agonist binding but alters the response to normal agonist

95
Q

antagonist

A

pharmacologic antagonist that binds without activating its receptor and thereby prevents activation by agonist

96
Q

competitive antagonist

A

a pharmacologic antagonist that can be overcome by increasing the concentration of agonist

97
Q

Irreversible antagonist

A

a pharmacologic antagonist that cannot be overcome by increasing agonist concentration

98
Q

Physiologic antagonist

A

a drug that counter effects of another by binding to a different receptor and causing opposing effects

99
Q

chemical antagonist

A

a drug that counters effect of another by binding the agonist drug not the receptor

100
Q

Allosteric antagonist

A

a drugthat binds to a receptos molecule without interfering with normal antagonist binding but alters the response to the normal antagonist

101
Q

What is transmembrane diffiusion

A

a type of signaling mechanism when a a drug diffuese across a membrane and binds to intracellular receptor

102
Q

what is a transmembrane enzyme receptor

A

a receptor that is imbedded in the membrane where the outer domain provides the receptor function and inner domain provides the effector mechanism converting A to B

103
Q

What are ligand transmembrane receptors

A

receptors that spans through the cells membrane and after the outer receptor is activated by the appropriate ligand activating separate cytoplasmic tyrosine kinase molecule (JAKs) that phosphorylate STAT molecules

104
Q

What are transmembrane channels

A

are gated channels that are opend or close by binding of a drug to the receptor site

105
Q

What is a g protein coupled receptor

A

its a receptor that uses a coupling protein to activate a separate effector molecule

106
Q

What types of drugs are able to reach intracellular receptors

A

more lipid soluble or diffusable agents

107
Q

How do drugs effect intracellular receptors

A

they may cross the membrance and combine with an intracellular receptor that affects an intracellular effector molecule

108
Q

Are the receptor and effector are the same in the cell

A

NO, they may or may not be the same

109
Q

what type of transmembranse signaling do intracellular receptors need to activate them

A

there isnt a specialized transmembrane signaling device because the drugs that act on them pass through the membrane

110
Q

How do receptors located on membrane spanning enzymes function

A

drugs that affect them combine with a receptor site on the extracellular portion of the molecule and modify its intracellular activity

111
Q

what type of drug activates extracellualr receptor site

A

cytokine

112
Q

how do receptors located on membrane ion channels work

A

they bind to the receptor on the channel which causes the channel to open

113
Q

how do channel molecules act

A

they act as both a receptor and effector which will cause a change in transmembrane electrical potential

114
Q

How do receptors linked to G protein work

A

drug binds to receptors that are linked by coupling proteins to intracellular or membrane bound effectors when a G-coupled receptors bind agonist, the G protein is activated

115
Q

How are receptors regulated

A

by number, location and sensitivity

116
Q

how long can changes in receptor regulation occur

A

changes can occur over short period of time (minutes) or long periods (days)

117
Q

What is tachypylaxis

A

an acute decrease in the response to a drug after administration

118
Q

What does a frequent or continious exposure to agonist affect result in

A

short term reduction of receptor response

119
Q

what are the mechanism that can result in short term reduction of receptor response

A

The G proteins can be blocked which stops receptor activation and sensitization. Agonist receptor complexes may be internalized which will remove them from further activation by agonist. constant activation of the receptor effector could deplete the substrates needed to cause the effect.

120
Q

what is receptor down regulation

A

long term reduction in receptor number which occurs in response to continuous exposure to agonist

121
Q

what is receptor upregulation

A

it increases receptor number which occurs when receptor activation is blocked for long periods of time by pharacologic antagonists or denervation

122
Q

kinetic interaction

A

changes in effect are the result in the relationship between dose and the concentration. the pharmacologic effect has changed as a result in a change in drug concentration

123
Q

dynamic interaction

A

changes in effect are the result of changes in the relationship between the drug concentration and the effect. the pharmacologic effect had changed despite a lack of change in the drug concentration

124
Q

What is Bioavailability

A

measure of the amount of drug that reaches systemic circulation. measure of systemic drug exposure

125
Q

how is bio-availability measured

A

it is measured by making a graph of serum concentration vs. time where the area under the curve is the bioavailability. the pharmacokinetic parameter which quantifies drug exposure

126
Q

how is bioavailibility expressed

A

as a percentage or fraction of the drug administered which reaches systemic circulation

127
Q

what are the factors that affect bioavailability of a drug through oral administration

A

absorption characteristics of the drug and dose form amount of metabolism that occurs prior to drug reaching systemic circulation

128
Q

where can metabolism occur before it reaches systemic circulation

A

intestinal wall liver presence of interacting substrates drugs, food no food

129
Q

what is absolute bioavailability

A

is the term that describes the situation when one of the areas under the curve being compared is in a dose from with which there is and “absolute” (100%) absorption (IV doseage)

130
Q

relative availablility

A

is comparing the area under the curve from one dose form to another. it answers the question of how the two dose forms compare in terms of the relative amount of drug that reaches systemic circulation Neither drug form was administered IV

131
Q

What are salt form differences

A

dosing conversion (from on preparation to another) must account for differences in the extent of the absorption and the amount of drug contained in that formulation

132
Q

Cpmax

A

maximum concentration

133
Q

what does it mean if the concentration of an administered drug is high in relation to volume of distribution

A

the volume of distribution is low

134
Q

If an administered drug has a low concentration. what does that mean in terms of volume of distribution

A

the volume the drug appears to occupy is very large

135
Q

what does Cpmax= dose/vd

A

apparent volume of distribution

136
Q

what does understanding the physiologic volumes help us understand

A

tells us where the majority of the drug resides in the body

137
Q

what factors affect a drugs volume of distribution?

A

degree of lipid solubility degree of protein binding extent of tissue binding

138
Q

How would a drug with a high Vd look with lipid solubility, protein binding, tissue binding

A

higher lipid solubility lower protein binding greater tissue binding

139
Q

having knowledge of a drugs volume of distribution can assist us with what

A

determining drug doses and provide clinicians with a sense of the extent of a drug distribution into the spaces/areas. compartments of the body

140
Q

how can Vd be used to dertermine a drugs loading dose?

A

if you know the Vd of a drug you can calculate the dose required to achieve maximum concentration

141
Q

what is the extent of distribution

A

it is a function of drug characteristics and patient characteristics

142
Q

What factors will increase volume of distribution

A

durgs with higher lipid solubility lower protein binding greater tissue binding

143
Q

what are the two ways that drugs are eliminated from the body?

A

biotransformation excretion

144
Q

what is biotransformation

A

drug is chemically altered to for a metabolite that is more excretable than parent

145
Q

what is excretion

A

removal of a drug or metabolite from the body via an organ

146
Q

what is a prodrug

A

is when a parent drug has no activity and the metabolite does

147
Q

what enterohepatic circulation

A

a metabolite may be excreted into the small intestine via bile and then can get reabsorbed and re-enter systemic circulation

148
Q

what is the most common phase I reaction

A

oxidation

149
Q

what are the two parameters determing elimination rate

A

clearance elimination half life

150
Q

what is clearance

A

the volume of blood that is cleared of drug per time

151
Q

what is elimination half life

A

the time it takes for the concentration of drug to reduce by one hald

152
Q

what is the relationship between dose-serum concentration

A

there is a direct proportion between elimination rate to serum concentration. reffered to as a 1st order elimination so as the elimination rate of a drug increase so does the serum drug cocentration

153
Q

what is the realtionship for serum-dose concentration for oral drugs

A

they are not proportional because the % absorbed may decline with higher doese

154
Q

what is zero order elimination

A

it is when elimination is independent of dose

155
Q

what factors can affect steady state

A

anything that effects the input or output

156
Q

at steady state what is the relationship between the rate of the drug going into a patient and the rate leaving a patient at steady state

A

rate going in= rate going out the amount of drug eliminated over the dosing interval=the dose administered

157
Q

at steady state what is happening with regard to drug accumulation during steady state

A

the drug has reached equilibrium

158
Q

what determine how long it will take for a drug regimen to reach steady state?

A

dependent on its half life

Pharmacology (14 decks)

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