Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Basic Mechanisms > Flashcards

Basic Mechanisms Flashcards

1
Q

Therapeutic effects of aspirin?

A

Analgesic, antipyretic, anti platelet aggregation, anti inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Side effect of aspirin and why?

A

GI bleeding, inhibits COX 1, protects stomach wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Morphine therapeutic effects

A

Analgesic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Side effects of morphine

A

Respiratory depressant, constipation, vomiting, addictive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why side effects and toxicity?

A

Not selective enough, widespread target, structure function change, lack of knowledge, patient variability, drug interactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do patients vary drug wise?

A

Genes, age, pregnancy, disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Admin routes for drugs (7.3)

A

Oral, suppository, sublingual, topical, transdermal patch, inhalation, injection (IV, IM, SC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is pharmacokinetics?

A

The way the body deals with drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are pharmacodynamics?

A

The effect of drugs on the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Reasons normal drugs can be toxic

A

Elderly, renal/hepatic impairment, poor metabolism, drug interaction, enzyme inhibition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Reasons drugs may be ineffective

A

Rapid metabolism, enzyme induction, poor compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where do drugs act?

A

MITCh - membrane receptors, intracellular enzymes, transporters, ion channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Targets for drug action

A

MITCh, plus nucleic acids, and miscellaneous (lipids eg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Receptor super families

A

Ionotropic, metabotropic, tyrosine kinase, dna linked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

H1 action and antagonist use

A

Contracts bronchi, antagonist is anti allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

H2 action and antagonist use

A

Stimulates gastric acid secretion, antagonist is anti ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Possible drug problems?

A

Selectivity, patient variability, lack of knowledge, idosyncratic, drug reactions, structure function change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What has affinity?

A

Agonists and antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What has efficacy?

A

Only agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is k+1?

A

Association rate, D+R -> DR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is k-1?

A

Dissociation rate, DR -> D+R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is affinity?

A

Binding of D to R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Kd?

A

Dissociation constant, conc of drug that occupies 50% of receptors
Kd = [D] [R] / [DR]

24
Q

What does a lower Kd mean in terms of affinity?

A

Higher affinity

25
Q

Fractional receptor occupancy equation (P)

A

P = [D] / [D] + Kd

26
Q

What does potency depend on?

A

Affinity and efficacy

27
Q

What is efficacy?

A

Ability of drug to activate receptor

28
Q

What is EC50?

A

The conc of drug which elicits half of the max response

29
Q

Why is Kd not equal to EC50?

A

Due to amplification, EC50 always lower (on left)

30
Q

What does distance between EC50 and Kd curves show?

A

Efficacy, less distance less efficacy

31
Q

What is the receptor reserve determined by?

A

Efficacy

32
Q

What effect does decreasing receptor no. have on curve?

A

Shift to right - less chance of collision

33
Q

What affects position of conc response curve?

A

Affinity, efficacy, receptor no.

34
Q

What is potency?

A

How much drug needed to produce a particular response

35
Q

What is receptor reserve,

A

Total no of receptors - no occupied

36
Q

What needs to happen to decrease max response

A

Lose more than receptor reserve

37
Q

What is partial agonism?

A

Max response is less than full response of tissue. Needs to fill all receptor to achieve it’s max. Low efficacy. EC50 close to Kd

38
Q

Example of clinically used partial agonist

A

Salbutamol, full in lungs, partial in heart. Less side affect

39
Q

What is a competitive antagonist

A

Competes with ligand for ligand binding site and blocks, usually reversible, overcome by increase in agonist

40
Q

What is non competitive antagonism

A

Binds to a site separate to agonist site, modifies site to prevent agonist binding, normally irreversible.

41
Q

What is uncompetitive antagonism

A

Binds to and active form of the receptor, doesn’t interfere with agonist binding (use dependant). Blocks later in pathway. Eg meantime in alzheimers

42
Q

Effect of competitive agonist of curve

A

Shift to right, no decrease in max

43
Q

How do you calculate dose ratio?

A

Conc of agonist with antagonist / conc of agonist alone producing same response

44
Q

What is the gaddum schild equation to calculate Kb?

A

Dose ratio = 1 + ([antagonist] / Kb)

45
Q

What is Kb?

A

Dissociation conc of antagonist

46
Q

What does schild plot involve

A

Y axis is log(DR-1), x axis is log [B], plot results of several CR curves, extend line to xaxis - gives Kb. Slope must be 1

47
Q

Examples of competitive antagonists

A

Propranolol, haloperidol, atropine, ranitidine, d-tubocurarine.

48
Q

What is a competitive irreversible antagonist

A

Binds irreversible to receptor at agonist binding site, shifts curve to right and then a decrease in max

49
Q

What is physiological antagonism?

A

One drug antagonises another via and independent molecular target eg NA and ACh

50
Q

What is constitutive activity?

A

At resting level, R cycling between active and inactive without A bound.

51
Q

What does agonist do (constitutive activity)

A

Stabilise receptor in active formation

52
Q

What does antagonist do? (ca)

A

Brings back to constitutive resting level

53
Q

What does inverse agonist do?

A

Has negative efficacy, prevents constitutive cycling, keeps R inactive

54
Q

How is tolerance useful sometimes?

A

In trycyclic antidepressants, adaptive down regulation of receptors after inc of NA/ serotonin in synapse, increases firing rate and serotonin release

55
Q

What is tachyphylaxis?

A

Desensitisation of receptor if too much of drug too quickly

Pharmacology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions