Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology 1A > Key Defintions > Flashcards

Key Defintions Flashcards

1
Q

How would you define the term ‘drug’ in Pharmacology?

A

A substance with a known chemical structure that produces a biological effect when administered to a living organism.

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

How would you define the term ‘drug target’ in Pharmacology?

A

A molecule in the body that is intrinsically associated with a
particular disease process and that could be targeted by a drug to give a therapeutic effect.

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

What is meant by the ‘central dogma’ in biology?

A

“DNA makes RNA, and RNA makes protein”
The flow of genetic information within a biological system

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

GLUDAP

List 6 types of Post-Translational Modification.

A
  1. Glycosylation
  2. Lipidation
  3. Ubiquitination
  4. Disulfide Bond
  5. Acetylation
  6. Phosphorylation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name 4 common drug targets.

A
  1. Receptors
  2. Ion Channels
  3. Enzymes
  4. Carrier Molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 4 types of intercellular signalling and their characteristics?

A
  1. Contact-Dependent
  2. Paracrine - Mediator molecules produced by a signalling cell.
  3. Synaptic
  4. Endocrine - hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ach

Give an example of a signalling molecule that produces a variety of cellular responses.

A

Acetylcholine binds to heart muscle cells, causing decreased rate and force of contraction.
Acetylcholine binds to skeletal muscle cells / smooth muscle cells, causing contraction of the muscle.
Acetylcholine binds to salivary gland cells, causing secretion.

Due to different acetylcholine receptors on different types of cells.

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

What are the 4 types of GPCRs and what do they do?

A

Gs(α) Activates adenylyl cyclase.
Gi(α) Reduces activity of adenylyl cyclase.
Gq(α) Activates phospholipase C (PLC), opens Ca2+ channels.
Gi(βγ) Can bind to K+ channels.

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

What type of functions are most GPCRs in the human genome involved in?

A

Sensory Functions

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

Think ports

What are the 3 types of transporter protein?

A

Uniport (A moves with conc. gradient).
Symport (A and B both move with conc. gradient)
Antiport (A moves with conc. gradient, B moves against it)

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

Give 5 reasons that drugs are taken.

A
  1. To produce a cure
  2. To suppress symptoms
  3. To prevent a disease or symptom
  4. To diagnose a disease
  5. For recreational reasons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why mights drugs show side effects and toxicity?

A
  1. Drugs are insufficiently selective
  2. Target site may underlie many processes.
  3. The prolonged use of the drug may lead to long-term or permanent changes in structure and function.
  4. Lack of knowledge of disease process.
  5. Patient variability
  6. Drug interactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define the terms agonist and antagonist.

A

Agonist - A drug that evokes a response.
Antagonist - A drug that prevents the action of another drug, can be naturally occurring (e.g. hormone or transmitter).

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

What is the Law of Mass Action?

A

Rate of chemical reaction is directly proportional to concentration of reactants.

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

Quantitative measure of affinity

What is the KD of a drug?

A

Concentration of drug that occupies 50% of receptors at equilibrium.

It is inversely proportional to the affinity of the drug.

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

What is the Receptor Occupancy Equation?

A

P = [D] / ([D]+KD)

P is proportion of receptors that have drug molecule bound to them.

D is drug

17
Q

What do binding curves show and how are they usually presented?

A

[D] on x-axis
P (proportion of receptors that have drug molecule bound to them) on y-axis.
Usually [D] is logged, giving a sigmoidal curve.

From this we can estimate (RT) and KD

18
Q

What is RT?

A

Total number of receptors.

19
Q

What is meant by the term ‘efficacy’?

A

Efficacy refers to the ability of a drug to activate the drug-receptor complex to elicit a response. Agonists have efficacy, antagonists do not.

20
Q

What is meant by the term ‘potency’?

A

Potency is the relative amount of drug is needed to produce a particular response.

21
Q

What is meant by Emax?

A

Maximum response, receptors are saturated with drug.

22
Q

What is the EC50 of a drug?

A

the concentration of drug that gives 50% of maximal response.

23
Q

What is efficacy?

Why might the EC50 be much lower than the KD for a drug?

A

Efficacy amplifies the effect of the binding of one drug molecule to one receptor.
You don’t have to occupy all the receptors to get the maximum response.
This will vary depending on the efficacy of the agonist and the number of receptors.

Binding curve will be rightward of the functional response curve.

24
Q

What is meant by the receptor reserve?

A

the proportion of receptors that are excess to producing a maximum response (Emax).

25
Q

What is the difference between partial and full agonists?

A

Full agonists have high efficacy and can evoke a maximum tissue reposnse.
Partial agonists have low efficacy, cannot evoke maximum tissue response, so they occupy all receptors to evoke their maximum response - no receptor reserve.

Partial agonist concentration-response curves and binding curves are superimposible.

26
Q

What is a rough measure of the receptor reserve?

A

KD / EC50

27
Q

What effect will reducing the receptor number have on the concentration-response curve?

A

It will shift to the right.

Binding curve will not be affected.

28
Q

More β2 receptors in the bronchi than in the heart.

Salbutamol is a partial agonist that binds to β2 adrenoreceptors. How is this useful therapeutically?

A

magnitude of the effect of a partial agonist is dependent on receptor number
Bronchi smooth muscle has an abundance of β2 receptors, while the heart has very few.
Salbutamol can evoke a significant relaxation of bronchi smooth muscle with little or no effect on heartx airway without having much effect on heart rate.

29
Q

Mu-opioid agonists are very good analgesics but also have severe side effects.
Buprenorphine is partial agonist at mu-opiod receptor.
What is the therapeutic value of using Buprenorphine as an analgesics rather than an opiod such as heroin?

A

Side effects of Mu-opiods agonist include dependence, addiction and respiratory depression.
Buprenorphine has a very high affinity for Mu-opiod receptor but low efficacy - much less side effects. High affinity means it binds for a long time.

30
Q

What are the 3 types of antagonism?

A

Competitive: Binds at agonist binding site.
Non-Competitive: Inhibits agonist binding in a different way to binding to agonist binding site.
Uncompetitive:

31
Q

What effects do competitive reversible antagonists have on concentration response curve?

A

Curve shifts rightwards, no change in Emax</max>.

No change because we can saturate with agonist.

32
Q

What is KB?

A

The equilibrium constant for the antagonist.

33
Q

What are problems with using a Schild plot?

A

It can take several hours and biological preparations can fail.

34
Q

What is 1 advantage and 1 disadvantage of using the Gaddum-Schild Equation to estimate KB?

A

It is quick - only requires 2 conc-response curves to be produced.
Might not ensure the antagonist would produce parallel shifts with no change in Emax.

35
Q

Lower HR

Give an example of a therapeutic use of competitive antagonism.

A

Propanolol competitively inhibits β-adrenoreceptor to lower heart rate.

36
Q

What are the 2 types of competitive irreversible antagonism?

A
  • Allosteric Modulator (antagonist binds to another site, saturable effect).
  • Binds, antagonising response later in pathway.
37
Q

What is the therapeutic mechanism of action of antisense oligonucleotides?

A

Suppression of expression of a harmful gene.

Pharmacology 1A (5 decks)

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