Drug
chemical that can affect a living process
Pharmacology
the study of drugs and their interactions with living systems
Clinical pharmacology
study of drugs in humans
Therapeutics
use of drugs to diagnose, prevent, or treat disease/prevent pregnancy
Effectiveness
does it elicit the response for which it is given
Selectivity
causes only the response for which it is given
Reversible action
subside after a certain amount of time
Predictability
how will patient respond
Chemical stability
shelf life
Pharmacokinetics
extend of movement depends on the ability of drugs to pass to and from the major spaces of the body
Absorption
movement of a drug from the site of administration into the blood
Bioavailability
amount of active drug that reaches the systemic circulation from its site of administration
Distribution
movement of drugs throughout the body
Metabolism
enzymatic alteration of drug structure, mainly in the liver by the cytochrome P450 system
Excretion
removal of drugs from the body
Pharmacodynamics
the study of biochemical and physiological actions of drugs and the molecular mechanisms by which those effects are produced
Plasma drug levels
predictive of therapeutic and toxic responses
Minimum effective concentration (MEC)
plasma drug level at which therapeutic effects will occur
Toxic concentration
level at which toxic effects occur
Therapeutic range
falls between the MEC and toxic concentration, depends on the drug
Drug half life
time required for the drug in the body to decrease by half
Plateau
steady level of drug has been achieved (drug eliminated = dose administered)
Peak
highest level of drug
Trough
lowest level of drug
Loading doses
used when plateau must be achieved quickly
Maintenance
smaller doses used when plateau is achieved
Graded response
patient response gets more intense with increased dosing
Max efficacy
largest effect a drug can produce
Potency
amount of drug given to elicit an effect (higher potency = less drug for big response)
Drug receptors
chemical sites in the body at which the drug interacts
Affinity
strength of attraction between a drug and its receptor
Intrinsic activity
ability of a drug to activate a receptor upon binding
Agonists
activate receptors (high affinity/intrinsic activity) and mimic the action of endogenous regulators
Partial agonist
moderate intrinsic activity, less effect than a full agonist
Antagonists
prevent receptor activity (high affinity/NO intrinsic activity) and block the actions of endogenous molecules
Noncompetitive antagonist
bind irreversibly ot receptors, decrease available receptors
Competitive antagonist
receptor blockade by competing with agonists, higher concentration wins if equal affinity
Desensitization
cell becomes less responsive due to continuous exposure to agonist
Hypersensitivity
continuous exposure of cell receptors to antagonist
Therapeutic index
ratio between average effective dose and average lethal dose
Tolerance
decreased responsiveness to a drug as a result of repeated drug administration
Pharmacodynamic tolerance
long term administration, adaptive processes occur
Metabolic tolerance
accelerated drug metabolism caused by drug interactions
Tachyphylaxis
form of tolerance, reduction in drug response is caused by repeated doses within hours
Pharmacogenetics
study of genetically inherited conditions that affect drug interactions
Intensification/potentiative
one drug intensifies the other
Reduction/inhibitory
one drug reduces the other
Side effect
minor effect that is nearly unavoidable (such as nausea)
Toxicity
dosage exceeds the amount the body can eliminate
Anaphylaxis
most serious reaction, medical emergency, systemic that closes airways and causes swelling
Idiosyncratic
abnormal/unusual response
Paradoxical
opposite of intended
Iatrogenic
disease that occurs as result of drugs
Physical dependence
state in which the body has adapted to prolonged exposure so that abstinence syndrome results if discontinued
Carcinogenic
causes cancer
Teratogenic
causes birth defects
Neurotoxicity
brain sensitive to small amounts of substances
Hepatotoxicity
liver is susceptible to toxicants as it is the main site of metabolism
Nephrotoxicity
highly susceptible because high vascularization, usually acute tubular necrosis
Immunotoxicity
immunosuppression or destruction of components
Cardiotoxicity
irregularity of rhythms and conduction, heart damage, depression of function
Ototoxicity
affects cranial nerve VIII, auditory damage on structures of the ear like the cochlea
Levothyroxine
synthetic T
Liothyronine
synthetic T3
Liotrix
synthetic T4 AND T3
Armour thyroid
T4, T3, and iodine