Pharmacology

Front 1

Pharmacodynamics

Back 1

Affect of the drug on the body

Front 2

Pharmacokinetics

Back 2

Affect of the body on the drug

Front 3

Indication/Contra-indication

Back 3

Indication = condition where drug is helpful

Contraindication = condition in which drug not safe

Front 4

Antagonist, Agonist

Back 4

Agonist - stimulates recepttor action

Antagonist - blocks receptor action

Front 5

Reversible vs Irreversible drugs

Back 5

Reversible - dissociates from receptor leaving receptor still functional

Irreversible - drug does not dissociate, bound drug and receptor internalized and broken down, not able to be used again until new drug synthesized

Front 6

Use dependant drugs

Back 6

Only exert effects on activated receptors.

Front 7

Drug half life

Back 7

time taken for a 50% decrease in the drug concentration of the plasma. determined by Vd and clearance

Front 8

Explain solubility of ionised vs unionised drugs

Explain effects of pH on acidic/basic drugs

Back 8

Ionized - water soluble

Unionized - lipid soluble

Acidic - ionized in basic enviro/unionized in acidic

Basic - ionized in acidic enviro/unionized in basic

So you want a basic drug in a basic enviro/acidic drug in acidic enviro for movement across membranes

Front 9

Ligand-gated ion channels

Back 9

Time – milliseconds

Ligand (drug) binds to ion channel -> conformational change in structure -> opens channel -> ions pass through channel tointerior/exterior of cell -> hyperpolarization/depolarization

Front 10

G protein coupled receptors

Back 10

Time – seconds. V. common. Ligand binds tomembrane bound receptor. Part of receptor inside cell bound to G protein (αβγ)with GDP attached to α subunit. Ligand binds receptor site -> G protein changesconfirmation, GTP replaces GDP on α subunit. activated α subunit seperates fromβγ subunits -> α subunitactivates target. If 2 targets – βγ subunits activate other target. cAMP may act as secondary messenger to signal furtherintracellular events.

Front 11

Kinase-linked receptors

Back 11

Time – hours. Membrane receptors respond mainly to protein mediators eg. Cytokines Ligand binds receptor -> receptors undergo dimerization (2 receptorscome together – coupling). -> Phosphorylation inside cell – addition of phosphategroups to end of receptors inside cell -> intracellular effects due tophosphorylation.

Front 12

Intracellular/Nuclear Receptors

Back 12

Time – hours (involves protein synthesis). Receptors that regulate gene transmission -> up/down regulation of protein synthesis

Ligand diffuses through membrane à cytoplasm. Ligand binds -> inactivated receptor (eg. Transcriptonfactor). Ligand + receptor migrate -> nucleus and are ACTIVATED.

Complex ->transcription of DNA à protein synthesis

Front 13

Volume of distribution

Back 13

Volume ofdistribution: volume of fluid required to contain the total amount of drug inthe body at the same concentration as is present in the plasma.

Drugs with Vdsimilar to plasma conc – most of drug remains in plasma. High Vd = low plasmaconc. -> slower elimination.

Vd = dose/plasmaconcentration.

Half life directlyproportional to Vd – Vd determines elimination rate, which determines halflife.

Front 14

2 phases of metabolism

Back 14

1. Oxidation, reduction, hydrolysis or hydration by enzyme eg. cytochrome p450

2. Conjugation– synthesis of bond between drug and metabolite (exogenous substrate) -> polar molecule that can move through waterto be excreted, and is less biologically active.

Front 15

Loading dose

Back 15

High initial dose that gets plasma concentrationto therapeutic range. Dose then tapered in order to maintain plasmaconcentration in therapeutic range.

Front 16

Steady State

Back 16

level we aim to keep plasma conc. at for greatertherapeutic effects, but decreased side effects. generally takes 4-5 half lives. Drugs with high half life may require loading dose.

Front 17

Clearance

Back 17

sum of metabolism andelimination. Relates plasma conc. of drug to eliminationrate – efficiency of drug elimination from body. High clearance -> low half life. High plasma conc -> fast elimination rate.