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Foundations- KML > Week 4: Pharmodynamics- Nordgren > Flashcards

Week 4: Pharmodynamics- Nordgren Flashcards

0
Q

toxicology

A

deals with adverse side effects on living systems (science of poisons)

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1
Q

Definition of pharmocology

A

study of substances (drugs) that interact with living species through chemical properties

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2
Q

drug receptor

A

cellular macromolecule that interacts with a drug ==> initiates a series of biochemical events

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3
Q

functions of a receptor

A

1) recognition of drug (ligand)- the receptor binds to drug/ligand
2) signal transduction- transfer of info

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4
Q

agonist

A

drug that activates molecular, biochemical, and physiological events associated with that interaction

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5
Q

pharmacologic dogma

A

a drug may increase or decrease cell function, but does not initiate new cell function

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6
Q

do drugs bind covalently with the receptor

A

no- if have such a strong interaction they will never let go

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7
Q

most receptors are…

A

proteins (enzymes)

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8
Q

transduction mechanisms can… (3 things)

A

alters receptor function (conformational change)
generate 2nd messenger (can lead to signal cascade)
impacts gene transcription

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9
Q

4 transduction mechanisms

A

1) G protein coupled receptor signal
2) ligand-gated ion channel
3) receptors as enzymes
4) receptors regulating nuclear transcription

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10
Q

most common type of transduction mechanism

A

g proteins

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11
Q

G protein coupled receptors (GPCRs)

A

most common drug receptor group

regulate 2nd messengers

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12
Q

ligand-gated ion channels

A

open up channel and allow ions to flow through
ligand binds ==> channel opens ==> ions flow through and down electrochemical gradient (can lead to depolarization of the membrane)

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13
Q

receptors as enzymes

A

when receptors bind they dimerize and form the perfect physical site for binding
can be inactivated or activated by ligand binding (kinases and phosphatases)

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14
Q

receptors regulating nuclear transcription

A

receptors have the ability directly bind to DNA regulate expression of adjacent genes
when receptor binds to ligand ==> chaperone will be inactivated

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15
Q

attributes of receptor-mediated processes

A

1) highly compartmentalized (receptor location and specificity)
2) self limiting on short time scale (bind then dissociate)
3) organized into opposing systems
4) provide opps for signal aplification
5) operate through a relatively small number of 2nd messengers (1 2nd messenger can signal different things depending on what is bound to the receptor)

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16
Q

many drug-drug interactions can be explained by this distinctive attribute or receptor-mediated biological processes:

A

a large number of different receptors may operate through a much smaller number of 2nd messenger systems

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17
Q

3 ways drugs can work by not interacting with receptors:

A

1) drugs interacting chemically with small molecules
2) drugs producing physiochemical effects
3) drugs that target rapidly dividing cells

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18
Q

cell-cell specific drugs functions

A

toxic to cells that are diving
include structural analogs that act by interfering with DNA/RNA
bind to DNA and cause strand breaks

19
Q

occupancy theory

A

tissues responding to drugs often exhibit a saturable response- at some point you can keep adding drugs and nothing will happen

20
Q

function of dose response curves

A

help us find 1/2 maximal effect

help us find what does we need to get max response

21
Q

EC50

A

the [ ] of drug producing 50% of the maximal response and is an estimate of drug’s Kd

can also be written as ED50- the dose of drug producing 50% of the maximal response

22
Q

affinity

A

describes the ability of a drug to form a complex with a receptor
characterized as 1/Kd
greater the affinity the lower the drug [ ] req’d to produce an effect

23
Q

potency

A

relative position of dose-response curve

24
Q

efficacy or intrinsic activity

A

the ability of a drug-receptor complex to produce a response

25
Q

full agonist

A

drug capable of inducing a maximum response

26
Q

partial agonist

A

drug that produces less than maximal response

27
Q

antangonist

A

drug which inhibits the action of an agonist

28
Q

pure antagonist

A

drug that binds to receptor that induces no response and has zero efficacy

29
Q

competitive curve

A

competes for binding
dose response shifts to right
can still get same response- just need more drug
slope does not change

30
Q

non-competitive antagonist

A

irreversible
maximal response reduced
slope reduced
apparent affinity changes little, if at all

31
Q

compound A has a higher potency than compound B. What does this say about their response curves in relation to one another

A

the dose-response curve for A is well to the left of the that for B

32
Q

compound A is said to be a non-competitive antagonist of compound B. What is true about this?

A

adding A reduces the response of the system to a fixed does of B and the addition of more B will not bring back the full response

33
Q

physiological antagonism

A

involves interactions b/t regulatory pathways mediated by different receptors
ex: to affect your BP you can do stuff to your glucose levels

34
Q

partial agonist

A

cant be explained by occupancy theory

may act like an antagonist when in the presence of a full agonist

35
Q

inverse agonist

A

cant be explained by occupancy theory
without an antagonist present, it acts like an agonist but with an antagonist present it levels everything out (guessing i have no idea)

36
Q

two state model

A

believes that the receptor exists in an active and inactive form
equilibrium exists b/t the 2
agonist ==> binds to active form ==> shift equilibrium to active form
inverse agonist ==> binds to inactive form ==> shift equilibrium to inactive form
partial agonist- small preference for active form
antagonist- does not preferentially bind to either form and does not alter the equilibrium b/t the active and inactive form of the receptor

37
Q

spare receptors

A

occupancy of small % of receptors elicits a maximal response ==> system behaves like it has “spare” receptors (more than it needs)

38
Q

quantal dose effect

A

all or none response
population response
cant be used to determine Kd or max efficacy

39
Q

median effective dose (ED50)

A

dose producing effect on 50% of pop

40
Q

hyperrecative

A

<ED50

dont need a lot of the drug to react

41
Q

hyporeactive

A

> ED50

need a lot of the drug to react

42
Q

tolerance

A

a form of hyporeactivity induced by repeated administration

43
Q

tachyphylaxis

A

form of hyporeactivity induced rapidly after only a few doses

44
Q

therapeutic index and what its numbers mean

A

measure of relative safety
high the number, safer it is
LD50- how much drug it takes to kill 50%
ED50- how much drug it takes to effect 50%

Foundations- KML (13 decks)

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