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HLSC 222- midterm 1 > pharmacodynamics > Flashcards

pharmacodynamics Flashcards

1
Q

Dose- response relationship

A

relationship between size of an administered dose and intensity of response produced

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2
Q

What does graded dose response mean

A

as dose increases, response becomes progressively larger

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3
Q

maximal efficacy

A

largest EFFECT drug can produce
- for the SAME doses, which drug has the LARGER EFFECT

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4
Q

How is maximal efficacy indicated on a dose response curve

A

the height of a curve

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5
Q

what is a problem with high efficacy when treating a patient?

A

it is hard to match the response intensity to patient needs

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6
Q

Relative Potency

A

AMOUNT of drug required to elicit an effect
- how much drug do we need to elicit the same effect

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7
Q

what are 3 points about potency

A

(1) rarely important drug characteristic
(2) Implies nothing about Maximal efficacy
(3) “this drug produces its effect at low doses”

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8
Q

Receptors

A

chemical sites in body that most drugs interact with to produce its effect

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9
Q

Equation for interaction between a drug and receptors

A

D + R <– –> D - R COMPLEX –> RESPONSE

D= drug
R= receptors

binding of a drug is reversible
receptor can only be on or off

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10
Q

what happens when a drug binds to a receptor?

A

mimic or block actions of endogenous regulatory molecules
- increase of decrease activity controlled by receptor

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11
Q

what do drugs do for the body

A

help the body help itself

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12
Q

what are the 4 primary receptor families

A

a) cell- membrane embedded receptor
b) ligand- gated ion channels
c) G protein- coupled receptor systems
d) transcription factors

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13
Q

Cell-membrane embedded receptors

A
  • spans cell membrane
  • ligand-domain located on cell surface
  • enzyme catalytic site located on inside of cell
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14
Q

what happens when a drug binds to cell-membrane embedded receptors?

how quickly does it respond

A

activates enzyme = increase activity

response occurs in seconds

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15
Q

what receptor does insulin use

A

cell-membrane embedded receptors

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16
Q

Ligand- Gated Ion Channel function

how fast does it happen

A

regulate ion flow in and out of cells
- specific to ion

milliseconds

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17
Q

what act through ligand-gated ion channels?

A

several neurotransmitters (acetylcholine and GABA)

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18
Q

G Protein -Coupled Receptor System components

A
  • receptor
  • G protein
  • effector
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19
Q

G Protein- Coupled Receptor System function

how fast

A

drug/endogenous ligand activates receptor which activated G Protein –> activates effector

rapid response

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20
Q

Transcription factors

A

situated on DNA in nucleus
- activated by lipid-soluble ligands

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21
Q

how do transcription factors differ from the other

A

(1) receptors are within cell not on surface
(2) responses from activation are delayed –> because transcription of RNA

22
Q

How fast does transcription factors act

A

hours or days

23
Q

Selectivity

A

only elicit responses for which it is given

24
Q

why is there no such thing as wholly selective drugs

A

all drugs cause side effects

25
Q

what does it mean when a drug is more selective

A

fewer side effects because the drug reacts with fewer specific receptors for that drug.

26
Q

what are there receptors for

A

(1) each neurotransmitter
(2) each hormone
(3) molecules that regulate physiological processes (histamine, prostaglandins, leukotrienes)

27
Q

why is selective drug action possible

A

due to many types of receptors

28
Q

if a drug only acts with one receptor and regulates one process

A

drug effect will be limited

29
Q

if drugs interact with several receptors

A

drug will elicit a drug effect will be wide

30
Q

can a drug selectively turn on single processes of a receptor?

A

no, if the receptor is activated ALL processes are activated.

Ex) opioid receptors modulate pain, but also respiration and bowel motility
- morphine for pain will also cause respiratory depression and constipation

31
Q

does selectively guarantee safety

A

NO
EX) botulinum toxin selective for one receptor but causes paralysis of respiratory muscles –> death

32
Q

what are the theories of drug- related interaction

A

(1) Simple Occupancy Theory
(2) Modified Occupancy Theory

33
Q

Simple Occupancy Theory (SOT)

A

(1) intensity of drug response is proportional to number of receptors occupied by the drug

(2) maximal response will occur when all available receptors are occupied

34
Q

What does SOT assume

A

all receptors are identical with

(1) ability to bind to receptor
(2) ability to influence receptor function

35
Q

What factors does Modified theory take into account?

A

Affinity and Intrinsic activity

36
Q

Affinity

is it reflected in efficacy or potency?

A

strength of attraction between drug and receptor

potency
- high affinity = effective at low doses = very potent

37
Q

Intrinsic Activity

is it reflected in efficacy or potency?

A

ability of a drug to ACTIVATE a receptor

Efficacy
-high intrinsic activity cause intense receptor activation = high efficacy

  • intensity of response is still related to number of receptors occupied
38
Q

Antagonists

A

Drugs block action of endogenous molecules

  • prevents activation of the receptors by agonist
39
Q

Agonists

A

Drugs mimic action of endogenous molecules

  • activate receptor (decreases or increases receptor activity depending on what the endogenous molecules does to the receptor)
40
Q

does agonists have affinity or high intrinsic activity?

A

BOTH
- binds and activates

41
Q

Explain how antagonist response is determined

A

Determined by how much Agonist is present

  • if there is no agonist present, administering antagonist has no effect
42
Q

Noncompetitive (insurmountable) Antagonists (NA

A

bind IRREVERSIBLY
- reduce number of receptors available for agonists
- reduces TOTAL number of receptors available for
- if enough NA is present, agonist effect will be completely blocked

43
Q

Competitive (Surmountable) Antagonists (CA)

A

REVERSIBLY binds

  • binding to endogenous molecules or CA is due to which is present in highest conc.
  • MAX response of agonist is not reduced
    –> increase amount of agonist required to produce a given intensity of response
44
Q

Partial Agonists

A
  • moderate intrinsic activity
  • Maximal effect of a partial agonist is lower than that of a full agonist
45
Q

What can happen to a cell that is subject to continuous activation/ inhibition

A

(1) can change number of receptors on their surface

(2) change sensitivity to agonist molecules

45
Q

what happens when a receptor is continually exposed to an agonist

A
  • will become less responsive (desensitized, refractory, or down-regulated)
  • destruction of receptors
46
Q

What happens to receptors with continuous exposure to antagonist

A

cell will become more responsive (hypersensitivity, supersensitive, up-regulated)

-synthesis of more receptors

47
Q

what are examples of drugs that don’t involve receptors?

A

Antacids: neutralize gastric acidity by chemical reaction stomach acid

Antiseptics: precipitating bacterial proteins

Saline laxatives: draws water into intestinal lumen via osmotic effect

48
Q

What is ED50

A

Average Effective Dose
The dose at middle frequency distribution

standard dose

49
Q

Therapeutic Index (TI)

A

measure of drugs safety

ratio of drugs LD50 to ED50

50
Q

LD50

A

the dose that is lethal to 50% of animals treated

HLSC 222- midterm 1 (10 decks)

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