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Drugs Brain And Behaviour > Lecture 3- Pharmacodynamics > Flashcards

Lecture 3- Pharmacodynamics Flashcards

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1
Q

What is pharmacodynamics

A

-Subfield of pharmacology
-The study of the biochemical effects of drugs and their mechanism of action

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2
Q

Drugs do not produce unique biological effects- instead they

A

Modify the rate of ongoing cellular events

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3
Q

Agonists are drugs that

A

-Cause a biological response
-Have intrinsic activity

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4
Q

What do receptors mediate

A

-The effects of endogenous ligands
-Not the effects of drugs

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5
Q

Drug receptor interactions usually involve which kind of bond

A

Non covalent- weak bonds

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6
Q

Affinity:

A

Kd: Rate of dissociation

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7
Q

Lower K values indicate

A

Low dissociation and high affinity

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8
Q

What is intrinsic activity

A

Degree to which a ligand activates receptors

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9
Q

Principles of Drug-Receptor interactions

A

-The magnitude of the drug effect is proportional to the number of receptors occupied
-Law of Mass Action

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10
Q

What is Law of Mass Action

A

A drug produces maximal effect when all receptors are occupied

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11
Q

After a certain point adding more drug

A

-Does not increase observed drug effect- ED 100
-May continue to increase other drug effects at other receptors

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12
Q

ED 50

A

-Effective dose
-Dose that produces response in 50% of subjects

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13
Q

TD 50

A

-Toxic dose
-Dose that produces a given toxic effect in 50% of subjects

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14
Q

LD 50

A

-Lethal Dose
-Dose that kills 50% of subjects

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15
Q

Therapeutic index equation

A

TI = TD50 / ED50

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16
Q

Safety margin equation

A

Safety margin = LD50 - ED50

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17
Q

What are two main characteristics of agonists

A

-Potency (How much drug is needed to produce an effect)
-Efficacy (Maximum effect)

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18
Q

More potent means

A

They reach 100% elevation of pain threshold at a lower dose than other drugs

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19
Q

Affinity is the inverse of

A

Dissociation

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20
Q

Affinity does not determine

A

The maximum possible effect because at high doses lots of drug molecules are available to take the place of dissociated ones

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21
Q

Why do some drugs have higher efficacy than others

A

-They may act by different mechanisms at different receptors
-They may have more or less intrinsic activity at the same receptor, once bound

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22
Q

Antagonists produce their effect by

A

Blocking the action of an antagonist or an endogenous ligand at the same receptor

23
Q

How do competitive antagonists affect the dose response curve

A

Shifts the dose response curve to the right

24
Q

Competitive antagonist effect can be overcome by

A

Increasing the dose of agonist

25
Q

Competitive antagonists bind to

A

Same receptor site as agonist and competes for available binding sites

26
Q

How do Non-competitive antagonists affect the dose effect curve

A

Shift the curve to the right and change it’s shape by reducing the maximum effect

27
Q

Non competitive antagonists can NOT be overcome by

A

Increasing the dose of the agonist as there is a decrease in maximum effect

28
Q

Non competitive antagonists make receptors

A

Unavailable for drug action

29
Q

What are the effects of alpha bungarotoxin

A

-Irreversible binding to acetylcholine receptor
-Paralysis
-Respiratory failure

30
Q

Irreversible antagonists form

A

Long lasting bond

31
Q

Recovery after irreversible antagonists

A

Synthesis of new receptors

32
Q

Partial agonists have what effects

A

Intermediate levels of intrinsic activity at a receptor compared to a full agonist

33
Q

What do partial agonists do in the presence of a full agonist

A

-Antagonise
-Can act as a competitive antagonists by competing for binding sites

34
Q

Partial agonists intrinsic activity can cause

A

Ceiling effect as the have lower intrinsic activity

35
Q

Inverse agonist affect the does-effect curve how

A

Produce a descending dose effect curve

36
Q

Inverse agonists produce

A

-An effect opposite to that of the endogenous ligand or one produced by an agonist

37
Q

How are inverse agonists possible

A

Some receptors have substantial endogenous activity even when ligands are not bound

38
Q

What is tolerance

A

Drug effect gets smaller

39
Q

What effect does tolerance have on the margin of safety

A

Reduces margin of safety as desired effect requires a higher dose which is closer to lethal dose

40
Q

Types of tolerance

A

-Acute tolerance
-Protracted tolerance
-Cross-tolerance

41
Q

What is acute tolerance

A

Drug effect decreases rapidly within a single session

42
Q

What is protracted tolerance

A

Drug effect decreases with repeated administration

43
Q

What is cross tolerance

A

Drug effect decreases with repeated administration of another drug

44
Q

In many cases tolerance reflects

A

Homeostatic adaptations of the body, trying to return to normal despite presence of the drug

45
Q

What is pharmacokinetic tolerance

A

Changes can be be pharmacokinetic/metabolic such as enzyme induction

46
Q

What is pharmacodynamic tolerance

A

-Changes occur to receptors and their corresponding signalling pathways
-E.g receptors may have fewer in number or change intracellular location

47
Q

Behavioural tolerance

A

Learning factors can influence such as setting

48
Q

What is sensitisation

A

If a drug effect gets bigger

49
Q

Examples of cross sensitisation

A

-Cocaine and amphetamine
-Stress can lead to drug sensitivity

50
Q

Sensitisation and tolerance is not to a

A

Drug but to a drug effect

51
Q

Withdrawal symptoms are typically

A

Opposite to the acute effects of the drug

52
Q

While tolerance is reversible, withdrawal symptoms are

A

Transient

53
Q

Tolerance and withdrawal are not necessary for

A

Addiction

Drugs Brain And Behaviour (8 decks)

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