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Year 2 > Drug Interactions > Flashcards

Drug Interactions Flashcards

1
Q

Define Pharmacology

A

The study of the effects of drugs

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2
Q

Define Pharmakinetics

A

How the body affects the drug; Absorption, Distribution, Metabolism and Excretion

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3
Q

Define Pharmacodynamics

A

How the drug affects the body

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4
Q

Name two neurotransmitters

A

Each

Serotonin

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5
Q

What are auto acids

A

Local Hormones

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6
Q

Name two auto acids

A

Cytokines

Histamines

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7
Q

Name two hormones

A

Testosterone

Hydrocortisone

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8
Q

How do ligand-gated ion channels function

A

Binding of AcetylCholine opens pores and allows cations to move into cell

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9
Q

Give an example of a ligand-gated ion channels

A

Nicotinic ACh receptors

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10
Q

How do G protein-coupled receptors function

A
  1. M3 receptor couples with Gq and Phospholipase C
  2. Second Messenger IP3 or DAG
  3. Beta-2-adrenoreceptor couples with Gq and Adrenal Cyclase to give cAMP
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11
Q

What do kinase-linked receptors respond to

A

Growth Factors

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12
Q

What is a kinase

A

Another word for phosphorylation

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13
Q

Define protein dimerisation

A

Where two molecules join together via covalent or non-covalent bonds

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14
Q

How do kinase-linked receptors function

A
  1. Extracellular lingand binding causes dimerisation
  2. Allows tyrosine in cytoplasm to be trans-phosphorylated, spreading signal through plasma membrane
  3. Tyrosine residue creates binding site for SH2 and PTB (phosphotyrosine binding proteins)
  4. Initiates signal transduction pathways
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15
Q

How do cytosolic receptors function

A

Modify gene transcription

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16
Q

What are messenger molecules for cytosolic receptors

A

Steroids

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17
Q

What is the role of zinc fingers

A

Recognise discrete regions of DNA

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18
Q

What is a zinc finger

A

They bind different parts of the DNA together to modify gene transcription (the sequence)

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19
Q

How does an allergy effect histamine levels

A

Increased levels

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20
Q

How does Parkinsons effect dopamine

A

Decreased

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21
Q

How does myasthenia graves effect receptors

A

Loss of nicotinic ACh receptors

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22
Q

What is Mastocytosis

A

Increase in C-kit receptors

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23
Q

Define receptor potency

A

Measure of how well a drug works

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24
Q

What is an EC50

A

Concentration that gives half the maximal response

25
Q

Define agonist

A

A compound that binds to a receptor and activates it

26
Q

How can we compare drug potencies on a graph

A

If compound A is further to the left of the graph than compound B, it is more potent

27
Q

How do we distinguish between a full agonist and a partial agonist

A

On a graph, a full agonist hits 100% whilst a partial hits a peak/plateau lower than 100%

We refer to this as ‘efficacity’ in exams (e.g. Compound A is more efficacious than B)

28
Q

Formula for intrinsic activity

A

Emax of partial agonist / Emax of full agonist

29
Q

Define antagonist

A

A compound that reduces the effect of an agonist

30
Q

What does activity of receptor depend on after being bound to by an antagonist

A

The affinity

31
Q

Name an antagonist\agonist to MAChR (Muscarinic ACH receptor)

A

Atropine - Antag

Muscarine - Agon

32
Q

Name the antagonist/agonist for NAChR

A

Curare - Antag

Nicotine - Agon

33
Q

How much of all genes express G coupled receptors

A

4%

34
Q

How many drugs target G could receptors

A

30%

35
Q

Examples of ligands

A

Light
Energy
Lipids
Proteins

36
Q

When are G protein couples receptors activated

A

When bound to GDP

37
Q

When are G protein coupled receptors not active

A

When bound to GTP

38
Q

Binding to a H1 receptor does what

A

Inflammation

39
Q

Binding to a H2 receptor does what

A
  • Contraction of Ileum

- Gastric acid secretion from parietal cells

40
Q

Binding to a H3 receptor does what

A

CNS disorders

41
Q

What does binding to H4 receptors do

A

Inflammation

42
Q

What is the antagonist to H2 receptors

A

Mepyramine

43
Q

How does Mepyramine effect H2 receptors

A
  • Reversed contraction of ileum

- No effect on acid secretion

44
Q

Define affinity

A

How well a ligand binds to a receptor

45
Q

Define efficacy

A

How well a ligand activates a receptor

46
Q

What is the efficacy of antagonists

A

Zero because the receptor is not activated

47
Q

What is the irreversible antagonist of beta adrenoreceptors

A

BAAM

48
Q

How does receptor reserve differ from full and spare agonists

A

Full - can have receptor reserve as maximal response seen with less than 100% occupancy

Partial - Maxmal response not seen even with 100% occupancy

49
Q

What factors effect drug action (4)

A
  1. Affinity
  2. Efficacy
  3. Receptor number
  4. Signal amplification
50
Q

What happens during allosteric modulation

A

Binding of ligand to allosteric site

51
Q

What is the orthosteric site

A

Where agonists usually bind to

52
Q

What is the consequence of continuous, repeated and high conc. of an agonist

A

Increased tolerance and desensitisation

53
Q

What is isoprenaline

A

Non-selective Beta adrenoreceptor agonist

54
Q

What is the selective agonist to beta adrenoceptor

A

Salbutamol

55
Q

What is the result of salbutamol

A

Opens up medium and large airways for the lungs

56
Q

When is isoprenaline used

A

For bradycardia and heart block (NOT asthma)

57
Q

What is desensitisation of receptors

A
  1. Become uncouples (no interaction with G protein)
  2. Receptor internalised in vesicle of cell
  3. Receptor is degraded
58
Q

Where are G-protein coupled receptors found

A

EUKARYOTES

Year 2 (155 decks)

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