week one Flashcards
pathopharmacology
study of biological effects of drugs introduced to the body that cause some sort of change
pharmacodynamics
mechanism of action or affect on the body
chemical name of drug
long, used for research
generic name
official name, lowercase
trade name
brand, easier to remember
prototype
model drug that others in its class are compared to
therapeutic drug effect
intended effect of a drug
drug side effects
unintended, unavoidable
drug toxicities
harmful drug effects
adverse drug rxn
unexpected or dangerous
allergic reaction
unexpected and involves the immune system
preclinical trial
lab animals to test for therapeutic/adverse effects
Phase I drug study
human volunteers
Phase II study
tested on pt with the disease
Phase III study
clinical market with close observation
Phase IV studies
continued monitoring by FDA
Schedule I drug
no medical use, heroin
schedule II drug
medical use with high abuse potential
Schedule III drug
less abuse potential, testosterone
Schedule IV
Some abuse potential, xanax
schedule V
low abuse, cough suppressant w codeine
dietary supplement restriction
only allowed to claim effect on body structure, NOT treatment
herbal med interactions
increase toxicity or reduce therapy
teratogen
causes congenital malformations
FDA pregnancy risk A
safe for fetus
pregnancy risk category B
not enough studies to decide
pregnancy risk C
animal studies show potential harm
Fda pregnancy risk level D
possible fetal risk
pregnancy risk x
known risk, outweigh any benefits
pharmacogenomics
how genes effect our response to drugs
pathophysiology
study of disease and injury
pathology
study of cells and tissues
disease overview
disruption in homeostasis physical, mental, or social
intrinsic disease factors
genes, immunity, age, gender
extrinsic disease factors
bacteria, behavior, injury, fungi, stress, virus
steps in disease process
identification, occurrence, diagnosis, etiology, prognosis
disease stages
exposure, onset, remission, convalescence
insidious
slowly progressing
latent
inactive but able to return
prodromal
symptoms before full disease
idiopathic disease
cause is unknown, only theories
latrogenic disease
from health procedure or some type of medical cause
exacerbation
worsening of disease
hypo
under
hyper
more
penia
lack of
cytosis
increase in cells
osis
process or condition
itis
inflammation
pathy
disease or suffering
overview pharmaceutic phase
dissolution
pharmacokinetic phase overview and steps
drug moving through body and what body does to drug
absorption, distribution, metabolism, excretion
pharmacodynamic phase overview
what the drug does to body (MOA)
first pass effect
metabolism of drug before systemic circulation
enteral absorption
via GI tract in some way
Enteric coated meds
intended to break down small intestine
SL, buccal, rectal
no first pass effect
parenteral
subq, IM, Iv, etc, fastest, no first pass effect
transdermal route
application to surfaces, no first pass
distribution phase
movement of drug through the body
blood brain barrier
cells in capillary walls that have very tight junctions, drugs must be lipid soluble or have transport system to cross
metabolism part of pharmacokinetic phase
method by which drugs are inactivated into a metabolite
liver is the major site, can be excreted by kidneys
CYP 450
isoenyme that metabolizes drugs
CYP 450 substrate
drug uses it for metabolism
CYP 450 inducer
speeds up metabolism
CYP 450 inhibitor
slows metabolism
excretion phase of pharmacokinetic phase
elimination of drug from the body, only hydrophilic drugs are excreted effectively
kidney lbs
BUN, creatinine, GFR
half life
time it takes for concentration to decrease by one half, 4-5 half lives for steady state
goal of around the clock dosing
maintain 50% concentration
onset
time it takes for drug to elicit therapeutic response
peak
time it takes for drug to reach max therapeutic response
duration
time drug concentration is sufficient to elicit effect
pharmacodynamic receptors
chemicals interact with drugs to produce effect
agonist
stimulates/activates
initiates therapeutic effect
antagonist
inhibits/ blocks other chemicals
receptorless activation
through chemical or physical interactions with small molecules
narrow therapeutic index
small window of target range
black box
very dangerous
high alert meds
insulin, heparin, opiod, potassium chloride, neuromuscular blocking, chemo
additive drug effect
2 drugs with similar MOA
synergism
different moa, but result in combined drug effect greater of one alone
activation interaction that increases
activates drug metabolizing enzyme in liver and decreases metabolism
displacement
moves one drug from plasma protein binding sites via second drug, increases effect
antidote
antagonize toxicity
consequences of hepatic changes in older adults
metabolized more slowly
consequences of cardiac changes in older adults
bad circulation
consequence of GI change in older adults
decreased absorption
consequences of renal changes in old adults
drugs are excreted less completely
inflammation
occurs with cell injury, protective mechanism that begins healing
inflammation process
injury, vasodilation, leukocyte recruitment
phagocytosis
serous exudate
watery, mild
serosanguineous exudate
pink tinged fluid, small amount of rbc
purulent exudate
sever inflammation with bacterial infection
hemorrhagic exudate
lots of rbc, most severe
cytokines lead to
fever, neutrophils, lethargy, muscle catabolism
major histocompatibility complex
cluster of genes that make proteins. go on cell surfaces to identify self
specific adaptive immunity
recognizes foreign invaders and destroys
b and t cells
humoral immunity
b cells, memory cells and plasma cells
passive immunity
transfer of plasma with antibodies to someone without them
mother of fetus
injection of antibodies
active immunity
protected state due to body response
vaccine
traditional vaccine
inactivated or killes
attenuated
weakened organisms
toxoids
inactivated toxins
conjugate vaccine
protein attached to disease causing organism to stimulate response
normal urinalysis pH
5.0-9.0
atrophy
shrinking in cell size
physiologic atrophy
development issue
pathologic atrophy
related to change in environmental conditions
hypertrophy
increase in size of cell
hyperplasia
increase in cell number, pathologic consistent with cancer
dysplasia
abnormal change in size and shape of cells. associated with cancer but is not cancer
metaplasia
replacement of one cell type to another
neoplasia
cell growth is not responding to normal regulatory processes
necrosis
irreversible, swelling and burst of cell
gangrene
dead tissue breeds bacteria