Pharmacodynamics

therapeutic effect

the ability of a drug to effect physiological, biochemical, or pathological mechanisms in order to treat or prevent a disease

selectivity

the ability of a drug to work on a specific area

etiological treatment

the drug is able to fight the disease itself and heal the patient

symptomatic treatment

the drug eases symptoms of the disease but doesn't cure the patient. Most drugs fall into this category

minimum effective concentration

MEC

lag time

the time from when a drug is administered until it starts being active. The time until it reaches the MEC

duration of action

the time in which drug concentration is above the MEC and the drug is active

additive effect

the effect of two drugs together is equal to the sum of the effects of each drug on its own. E(A+B) = Ea + Eb

synergistic effect

the effect of two drugs together is greater than the effect of the sum of each drug on its own E(a+b) > Ea + Eb

receptors, enzymes, ion channels, transporters

types of link sites for drugs

ligand

a chemical secreted from a drug that a receptor knows how to identify and connect to

mediators

chemicals that act when they are close to there release source

neurotransmitters

mediators of neurons

hormones

proteins excreted from glands to the bloodstream and act on sites that are far away from there release source

time responsive curve

shows the effect of the drug in relation to time

Maximal Peak Effect

after the drug reaches this on the time responsive curve the effect of the drug will decrease and the curve will start turning downwards

Dose responsive curve

this curve shows the effect of the drug in percentages

Emax

sign for maximum intensity of the drug on the dose responsive curve. It is dependent on the concentration of the drug that is next to the receptor

EC50

the concentration of the drug that gives 50% of the maximum effect. It is easier to decipher than Emax since that number is very close to 0 since the curve is a logarithm

affinity

the level of interaction between a drug and its receptor. It is dependent on the concentration of the drug by the receptor and the Kd

Kd

the dissociation constant. The ability of a ligand to seperate from a receptor

inversely proportional

the relationship between affinity and the Kd is ____

efficacy

the ability of a drug to cause an effect after it connects to a receptor. The ability of the drug to activate the receptor

Potency

the concentration of drug required in order to achieve a desired effect. It is a greater the smaller the required dose is

ED50

the dosage of drug that causes a clinical effect in 50% of the population

TD50

the dosage of drug that causes side effects or toxic effects in 50% of the population

LD50

the dosage of drug that is lethal to 50% of the population

Therapeutic Index

TD50/ED50. The number indicated how many times a larger of an effective dose will likely be toxic

Therapeutic window range

the difference between when a drug is safe and when it becomes toxic. It is displayed on a curve and the wider that curve is the safer the drug is

TW

MTC- MEC

minimum toxic concentration

MTC

agonist

a drug that connects to a receptor and activates it

antagonist

a drug that attaches to a receptor and doesn't activate it. Therefor it inhibits an agonist from being able to attach to the receptor

full agonist

an agonist that is able to have a maximal effect on a receptor

partial/antagonist agonist

an agonist that is able to cause a partial effect on the receptor. Can also act as an inhibitor since it prevents a full agonist from attaching to the receptor and achieving maximal effect.

competitive antagonist

antagonist that in its presence a larger dosage of agonist will need to be given in order to achieve the same desired effect. It effects the potency but not the efficacy of the drug.

noncompetitive antagonist

antagonist that attaches to a different site on the receptor than the agonist changing the shape of the receptor and preventing the agonist from connecting. This effects the efficacy but not the potency of the drug.

down regulation

During chronic treatment with an agonist the body doesn't like that the receptors are constantly being activated so it brings receptors into the cell decreasing the amount on the membrane.

higher dosage

in order to fix the problem of down regulation a _________ must be given

up regulation

During chronic treatment with an antagonist the body will start producing more receptors since the drug is blocking all the other ones. It will cause over activity of the antagonist because it will then connect to the new receptors

lower dosage

in order to fix the problem of up regulation a ________ must be given

desensitization

a decreased response of the body to a drug that requires increases of dosage in order to reach desired effects

tachyphylaxis

the effect of a drug occurs within seconds and it is quickly excreted from the body thus decreasing its overall effect.

hypersensitization

When chronic treatment of a drug causes an oversensitivity to the drug to develop. A lower dosage must be given to prevent toxicity. It is caused by up regulation

ligand gated ion channels

molecules connect to the receptor and cause re/depolarization causing the ion channels to open and a change in concentration which will lead to a specific effect in milliseconds

ionotropic receptors

the type of receptors in ligand gated ion channels

G protein coupled receptors

these receptors cause opening of ion channels or are stimulated by an enzyme to open ion channels causing an effect in seconds

metabotropic receptors

another name for G protein coupled receptors

kinase-linked receptors

a ligand connects to the receptor, causing phosphorylation, gene transcription, protein synthesis, and a desired effect within hours

nuclear receptors

a receptor located inside the cell. It achieves its desired a effect within a few hours

ion channel blockers

prevent passage of ions by physically blocking the receptor on the ion channel

false substrate

enters the enzyme and makes it work but the product that it makes is useless. Therefore it is an inhibitor because it prevented the enzyme from creating a useful product

substrate analog

enters the enzyme and blocks its ability to work

false substrate

a molecule that has no effect. It attaches to the transporter and busies it so it cant work on something else that will actually have an effect