Drug Interactions Flashcards by Neil Srivastava

Define Pharmacology

The study of the effects of drugs

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Define Pharmakinetics

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

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Define Pharmacodynamics

How the drug affects the body

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Name two neurotransmitters

Each

Serotonin

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What are auto acids

Local Hormones

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Name two auto acids

Cytokines

Histamines

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Name two hormones

Testosterone

Hydrocortisone

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How do ligand-gated ion channels function

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

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Give an example of a ligand-gated ion channels

Nicotinic ACh receptors

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How do G protein-coupled receptors function

M3 receptor couples with Gq and Phospholipase C
Second Messenger IP3 or DAG
Beta-2-adrenoreceptor couples with Gq and Adrenal Cyclase to give cAMP

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What do kinase-linked receptors respond to

Growth Factors

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What is a kinase

Another word for phosphorylation

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Define protein dimerisation

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

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How do kinase-linked receptors function

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

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How do cytosolic receptors function

Modify gene transcription

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What are messenger molecules for cytosolic receptors

Steroids

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What is the role of zinc fingers

Recognise discrete regions of DNA

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What is a zinc finger

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

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How does an allergy effect histamine levels

Increased levels

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How does Parkinsons effect dopamine

Decreased

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How does myasthenia graves effect receptors

Loss of nicotinic ACh receptors

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What is Mastocytosis

Increase in C-kit receptors

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Define receptor potency

Measure of how well a drug works

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What is an EC50

Concentration that gives half the maximal response

Define agonist

A compound that binds to a receptor and activates it

How can we compare drug potencies on a graph

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

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

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)

Formula for intrinsic activity

Emax of partial agonist / Emax of full agonist

Define antagonist

A compound that reduces the effect of an agonist

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

The affinity

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

Atropine - Antag Muscarine - Agon

Name the antagonist/agonist for NAChR

Curare - Antag | Nicotine - Agon

How much of all genes express G coupled receptors

How many drugs target G could receptors

30%

Examples of ligands

Light Energy Lipids Proteins

When are G protein couples receptors activated

When bound to GDP

When are G protein coupled receptors not active

When bound to GTP

Binding to a H1 receptor does what

Inflammation

Binding to a H2 receptor does what

- Contraction of Ileum | - Gastric acid secretion from parietal cells

Binding to a H3 receptor does what

CNS disorders

What does binding to H4 receptors do

Inflammation

What is the antagonist to H2 receptors

Mepyramine

How does Mepyramine effect H2 receptors

- Reversed contraction of ileum | - No effect on acid secretion

Define affinity

How well a ligand binds to a receptor

Define efficacy

How well a ligand activates a receptor

What is the efficacy of antagonists

Zero because the receptor is not activated

What is the irreversible antagonist of beta adrenoreceptors

BAAM

How does receptor reserve differ from full and spare agonists

Full - can have receptor reserve as maximal response seen with less than 100% occupancy Partial - Maxmal response not seen even with 100% occupancy

What factors effect drug action (4)

1. Affinity 2. Efficacy 3. Receptor number 4. Signal amplification

What happens during allosteric modulation

Binding of ligand to allosteric site

What is the orthosteric site

Where agonists usually bind to

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

Increased tolerance and desensitisation

What is isoprenaline

Non-selective Beta adrenoreceptor agonist

What is the selective agonist to beta adrenoceptor

Salbutamol

What is the result of salbutamol

Opens up medium and large airways for the lungs

When is isoprenaline used

For bradycardia and heart block (NOT asthma)

What is desensitisation of receptors

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

Where are G-protein coupled receptors found

EUKARYOTES