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Semester 2 > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

1906 Pure Food and Drug Act

A

Products must be accurately labeled

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2
Q

1938 Food, Drugs, and Cosmetic Act

A

Demo of safety before release into market

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3
Q

1951 Humphrey-Durham Amendment

A

Established Prescriptions for certain drugs (pot harmful, complicated instructions)

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4
Q

1962 Drug Amendments

A

Safety and required demo of efficacy (thalidomide)

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5
Q

Clinical Testing Phases

A

I (safe, kinetics), II (does it work in pts.), III (double blind)

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6
Q

Quantal dose-response curves

A

How many people (all or none?)

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7
Q

What do Quantal dose-response curves predict?

A

Population frequency

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8
Q

Graded dose-response curve

A

How much effect?

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9
Q

What does a graded dose response curve predict?

A

Population response magnitude

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10
Q

ED50

A

dose producing a defined effect in 50% pop (quantal dose-response)

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11
Q

EC50

A

Concentration producing 50% of the maximal effect (graded dose-response curve)

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12
Q

LD50

A

dose of a drug that will produce a lethal (not actually lethal, highly toxic) effect in half pop

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13
Q

TD50

A

dose of a drug that will produce a toxic effect in half the population

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14
Q

TI

A

ratio of LD50 to ED50

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15
Q

Drugs with large TIs are ____

A

very safe

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16
Q

TI =

A

LD50/ED50

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17
Q

vitamins/supplements/”natural products” can cause____

A

liver injury

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18
Q

What are the concerns of regulating dietary supplements?

A

effectiveness, contain whats listed, contaminated, contain prescription drugs but not reported

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19
Q

1994 Dietary Supplement Health and Education ACt

A

accurately labeled

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20
Q

2006 Dietary Supplement and NonPresciption Drug Consumer Protection Act

A

must report serious adverse effects post marketing, burden of proof is with FDA

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21
Q

Whats an example of drug regulation for supplements?

A

DMAA - amphetamine derivative marketed as dietary supplement (adverse effects: arrhythmia and heart attacks)

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22
Q

What makes a drug unsafe?

A

Receptors -which bind, action, where located
Interactions
Who is taking (kids, preg, elderly, genetics)

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23
Q

safer drugs often have greater _____

A

organ and receptor selectivity

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24
Q

Drugs interaction with ___

A

other drugs, dietary constituents, herbal remedies

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25
Q

What does a narrow therapeutic window mean?

A

Small changes in amount can lead to toxicity

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26
Q

What do things that result in drug interactions commonly effect?

A

PK of drug: CYPs and drug metabolism

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27
Q

If a drug demonstrates receptor selectivity, it means ____

A

at rel low drug conc, it primarily acts at one receptor/receptor subgroup; but increasing the drug conc will result in reduced selectivity

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28
Q

Factors influencing receptor selectivity

A

drug solubility , drug and receptor structure, and chemical forces influencing drug-receptor interaction

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29
Q

Beta-2 Adrenergic Binding Pocket is a _____

A

dynamic interaction, dynamic conformation change

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30
Q

What is the importance of a covalent bond in receptor phamacology?

A

The ligand - receptor complex is essentially permanent

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31
Q

most receptors have ____ bonds

A

ionic (reversible interactions)

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32
Q

What are types of drug targets?

A

Receptors, Ion channels (anti-epileptics), enzymes (ACE inhibitors), transporters (SSRIs)

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33
Q

What are different types of receptors?

A

Ligand-gated ion channels, G-protein coupled receptors, kinase-linked receptors, nuclear receptors

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34
Q

Target 1 (a subunit examples)

A

adenylyl cyclase (Gs, Gi), Phospolipase C (Gq)

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35
Q

Target 2 (bg subunit) examples

A

K+ channel, Ca++ channel, PI3 K

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36
Q

Gs action?

A

activates adenylyl cyclase

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37
Q

what inhibits cAMP

A

phosphodiesterases

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38
Q

Gi action?

A

inhibits adenylyl cyclase

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39
Q

Gq action?

A

activates phospholipase C

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40
Q

What does the G-protein Beta/Gamma Subunits target?

A

K channel, calcium channel, PI3 Kinase

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41
Q

What are some other drug targets?

A

Chemical & physiochemical mechanisms, DNA/RNA and the ribosome, Biopharmaceuticals, gene therapy

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42
Q

Desensitization

A

diminished response after continuous application to repeated exposure to an agonist

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43
Q

What can desensitization be observed as?

A

decrease in potency (right shift in curve), decrease in efficacy
at any single conc, see reduced response

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44
Q

What does desensitization look like at the receptor level?

A

Reduction in receptor responsiveness

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45
Q

Tolerance

A

reduction in response to repetitive use of same drug can be overcome by increasing dose

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46
Q

Drug resistance:

A

reduced effectiveness of drug usually in reference to microorganisms or population of cancer cells

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47
Q

what are diminishing drug effects due to

A

altered metabolism of drugs, exhaustion of mediators, phys adaptations, active etrusion from cells, change in receptors, down-regulation and loss of receptors

48
Q

with continued activation of the receptor, the system responds by:

A

decreasing responsiveness

49
Q

What does increased receptor responsiveness result from

A

chronic reduction of receptor stimulation, tissue response to pathological conditions

50
Q

with continued block of the receptor, the system responds by

A

increasing responsiveness

51
Q

when withdrawing pt from a drug, what should you do?

A

TAPER the dose

52
Q

long term stimulation of the receptor is likely to cause

A

desensitization and/or down-regulation

53
Q

long term blockage of the receptor is likely to cause

A

up regulation and/or sensitization

54
Q

placebo

A

dosage form devoid of active ingredient

55
Q

written prescriptions are required for

A

Schedule II drugs

56
Q

Agonist drug

A

active site of similar shape to the endogenous ligand so binds to the receptor and produces the same effect

57
Q

Antagonist drug

A

close enough in shape to bind to the receptor but not close enough to produce an effect; takes up receptor space and prevent endogenous ligand from binding

58
Q

Where is the most accurate part of a Dose response curve

A

middle of curve - EC50

59
Q

dose

A

amount of drug administered to person (in vivo)

60
Q

concentration

A

amount of drug per unit volume

61
Q

Occupation of a drug is governed by

A

affinity

62
Q

Activation of a drug is governed by

A

efficacy

63
Q

efficacy

A

ability of ligand-receptor complex to produce an effect

64
Q

affinity

A

interaction of a ligand and a receptor

65
Q

agonist

A

ligand which binds to a receptor and produces no effect one its own by will reduce the effect of an agonist

66
Q

an agonist has ___ and an antagonist has ___

A

efficacy, no efficacy

67
Q

affinity is ____ upon activation of the receptor

A

independent

68
Q

the stronger a drug is bound to a receptor (higher affinity), the ____ the Kd

A

smaller

69
Q

A high affinity means ____

A

you need less drug to occupy 50% of receptors

70
Q

the higher the affinity, the smaller the ____

A

Kd

71
Q

potency

A

how much of a drug is needed to generate a response

72
Q

How can a low potency drug still be effective?

A

need more of it

73
Q

efficacy

A

how much a response is generated

74
Q

low ____ drugs cannot reach maximal response

A

efficacy

75
Q

the response is maximal when ____

A

all receptor sites have been occupied

76
Q

orthosteric

A

ligand binds at the same site as endogenous ligand

77
Q

allosteric

A

ligand binds at a site distinct from endogenous ligand binding site

78
Q

positive allosteric modulator

A

has no effect by itself but enhances orthosteric ligand affinity or efficacy

79
Q

a positive allosteric modulator/enhancer ____ the effect of an antagonist

A

potentiates

80
Q

allosteric agonist

A

mediates receptor activation on its own at site distinct from orthosteric site

81
Q

neutral allosteric ligand

A

binds allosteric site without affecting orthosteric site but blocks action of other allosteric modulator (blocks ability of anything else to bind)

82
Q

Allosteric antagonist (negative allosteric modulator)

A

reduces orthosteric ligand affinity or efficacy

83
Q

Examples of positive allosteric modulators

A

barbiturates, benzodiazepines, alcohol (enhance effect of GABA)

84
Q

example of neutral allosteric ligand

A

flumazenil (doesnt impact GABA, inhibits binding of other allosteric modulators)

85
Q

example of allosteric antagonist

A

picrotoxin

86
Q

synergism

A

effect two drugs are greater than in ind. effects add together

87
Q

drug potentiation

A

a drug without an effect of its own increases the effect of a second drug

88
Q

additive effects

A

1+1=2

89
Q

agonist effect blocked in a _____ manner by antagonist

A

dose-dependent

90
Q

types of noncompetitive allosteric sties

A

reversible and irreversible

91
Q

what are nonreceptor antagonists

A

chemical, pharmacokinetic, physiological antagonists

92
Q

competitive (reversible) antagonism

A

a ligand that reduces the action of another ligand by blocking access to its binding

93
Q

competitive (reversible) antagonism binds at

A

the same site or overlapping site as the endogenous ligand

94
Q

how can an agonist bind with competitive antagonists

A

increase dose (antagonist reversibly binds)

95
Q

competitive (reversible) antagonist cause ____ change in efficacy but ___ change in potency

A

no, reduction

96
Q

how does a competitive (R) antagonist shift the agonist log concentration-effect curve

A

shifts to the right without changing slope or maximum

97
Q

competitive irreversible antagonist

A

a ligand which binds to agonist binding site and dissociates very slowly or not at all thus decreasing the action of the agonist

98
Q

what does a competitive irreversible antagonist do the action of the agonist

A

decreases it

99
Q

allosteric antagonism

A

ligand which binds a site on the receptor distinct from the orthosteric ligand binding site and reduces the agonist effect

100
Q

how does allosteric antagonism prevent reduces agonist effect

A

preventing the receptor from full conformational change

101
Q

a competitive antagonist will cause ____ potency and ____ efficacy

A

reduced, not change

102
Q

a noncompetitive/I competitive antagonist will _____ potency and ____ efficacy

A

reduce/not change/ reduce

103
Q

partial agonist as antagonist

A

effect of adding a partial agonist when the receptor is occupied by a full gonist

104
Q

what does a partial agonist do

A

decrease max effect of agonist (not get full effect)

105
Q

what is a partial antagonist good for (example)

A

withdrawal (opiods)

106
Q

chemical antagonism

A

combines with agonist in solution so that the agonist is no longer able to interact with receptor (antiacids, chelating agents, and neutralizing bodies)

107
Q

pharmacokinetic antagonism

A

reduces concentration of the agonist

108
Q

how does pharmacokinetic antagonism reduce the concentration of the agonist

A

by decreasing rate of absorption, increasing metabolic degradation, increasing rate of renal excretion, ion trapping

109
Q

medication administered for allergic reaction

A

epinephrine

110
Q

what are the effects of epinephrine

A

vasoconstricts and bronchodilates

111
Q

effects of histamine

A

vasodilates and bronchoconstricts

112
Q

The swallowing center is located where?

A

Medulla of brain stem

113
Q

Dehydration has what effect on salivary flow?

A

inhibits

114
Q

What “glands” in small intestine secrete alkaline mucus?

A

brunners

115
Q

Most water and electrolyte recovery occurs in what GI section?

A

LI

Semester 2 (6 decks)

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