the ability of a drug to effect physiological, biochemical, or pathological mechanisms in order to treat or prevent a disease
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selectivity
the ability of a drug to work on a specific area
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etiological treatment
the drug is able to fight the disease itself and heal the patient
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symptomatic treatment
the drug eases symptoms of the disease but doesn't cure the patient. Most drugs fall into this category
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minimum effective concentration
MEC
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lag time
the time from when a drug is administered until it starts being active. The time until it reaches the MEC
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duration of action
the time in which drug concentration is above the MEC and the drug is active
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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
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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
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receptors, enzymes, ion channels, transporters
types of link sites for drugs
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ligand
a chemical secreted from a drug that a receptor knows how to identify and connect to
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mediators
chemicals that act when they are close to there release source
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neurotransmitters
mediators of neurons
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hormones
proteins excreted from glands to the bloodstream and act on sites that are far away from there release source
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time responsive curve
shows the effect of the drug in relation to time
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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
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Dose responsive curve
this curve shows the effect of the drug in percentages
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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
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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
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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
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Kd
the dissociation constant. The ability of a ligand to seperate from a receptor
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inversely proportional
the relationship between affinity and the Kd is ____
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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
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Potency
the concentration of drug required in order to achieve a desired effect. It is a greater the smaller the required dose is
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ED50
the dosage of drug that causes a clinical effect in 50% of the population
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TD50
the dosage of drug that causes side effects or toxic effects in 50% of the population
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LD50
the dosage of drug that is lethal to 50% of the population
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Therapeutic Index
TD50/ED50. The number indicated how many times a larger of an effective dose will likely be toxic
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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
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TW
MTC- MEC
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minimum toxic concentration
MTC
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agonist
a drug that connects to a receptor and activates it
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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
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full agonist
an agonist that is able to have a maximal effect on a receptor
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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.
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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.
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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.
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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.
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higher dosage
in order to fix the problem of down regulation a _________ must be given
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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
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lower dosage
in order to fix the problem of up regulation a ________ must be given
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desensitization
a decreased response of the body to a drug that requires increases of dosage in order to reach desired effects
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tachyphylaxis
the effect of a drug occurs within seconds and it is quickly excreted from the body thus decreasing its overall effect.
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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
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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
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ionotropic receptors
the type of receptors in ligand gated ion channels
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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
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metabotropic receptors
another name for G protein coupled receptors
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kinase-linked receptors
a ligand connects to the receptor, causing phosphorylation, gene transcription, protein synthesis, and a desired effect within hours
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nuclear receptors
a receptor located inside the cell. It achieves its desired a effect within a few hours
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ion channel blockers
prevent passage of ions by physically blocking the receptor on the ion channel
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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
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substrate analog
enters the enzyme and blocks its ability to work
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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
Studied by 12 people
