drugs basic Flashcards
pharmacology
study bio effect drugs on body
pharmacokinetics (4 components)
what happens to drugs in body
pharmadynamics
MOA, effects of body
med names
chemical - longest and used in research typicallygeneric - official name, always lower cased ex. acetomedafinetrade- brand name, easier to say, always capitalized
definitions
therapeutic effects - desired effectside effects- unintended effects, unavoidable, expectedtoxicities- harmful effectsadverse effects - unexpected and dangerous reactionallergic- unexpected, may be dangerous, immune response
what we need to know about meds
name (generic)classication (drug class)MOAcommon/serious side effectscontraindicationsnursing indications
drug approval
FDApreclinical - animal testingphase 1- healthy volunteer humansphase 2- volunteers with diseasephase 3- vast clinical market, must say side effectsphase 4- continued eval by FDA
controlled subs
schedule 1-5schedule 1 - not approvedschedule 2- narcotics, high potential abusesched 3- less pot abuse (non barb sedatives, nonamphetamines, stimssched 4- some pot abuse (sedatives, anti-anx)sched 5- low pot abuse - cough surrup
OTC meds
consumers must be able to diagnose own condition and monitor effectiveness easily
dietary supps
can only claim affect on body stucture and function, not med conditionadverse interactions- can incr toxicity pres med or cause decrease therapeutic effect
teratogens
congental malformatiopns dev fetusCat A- safeB- lack studiesC- no studies, animal studies riskD- poss risk fetus, dis with OBX- known risk, not outweigh benefits (Isotretinoin, Acutane)
pharmacogenomics
how genes affect response to drug
cellular adaption
changes body cell go through to permit survival and mx cell function- size/formatrophy- decrease shrink size- physiologic- developmental issue (birth)-pathologic- decrease workload change env conditions - blood supply, hormones++decreased protein synthesis and/or incre protein catabolismhypertrophy- incr size and function, mechanical stimuli- heart and kidneys most prone negative adaptation, hypertension w/ inc BPhyperplasia- incr # cells from incr rate cell division prolong injury++ turns into dysplasia- only cells have ability divide (skin, intestinal, glandular)- physiologic- pregnancy and wound healing-pathologic- cancersdysplasia- abnormal changes of mature cells - atypical hyperplasia- often with neoplastic growths, but NOT MEAN CANCEROUS - inflammation and chronic irritationmetaplasia- reversible replacement 1 type mature cell to another, can predispose to cancerneoplasia- abnormal cell growth, gene mutationanaplasia- cells diff to immature form or embryonic form (cancerous)
neoplasms- tumor
benign- differentiated immarture cells, unable to metastasize, grow slow, encapsulated, not cause severe probsmalignant/cancer - undifferentiated, more anaplastic, rapid growth, metastasize, no capsule
necrosis
irreversible, sweliing, burst cell, inflamationischemic necrosis- infarctioncan lead to gangrene and breading ground bacterialiquefactive necrosis- tissue w lots of lipids or number inflammatory cells
gangrene - disruption blood supply with bacteria
dry- blackened, dry, line demarcationwet- liquefacation, foul, rapid spread, extensive damage, systemic, no line demarcationgas- destroys connective tissues, gaseous bubbles, found in soil
infection
host take overlocalized- spec placesystemic- spread sev regionscausescommon- virus and bacteriavirus- only DNA/RNA must have host cells, covid, aids, flubacteria - much larger virus, single-celled, 1 strand DNA, reproduce inside/outside cell - strep, tb, utirarefungal - yeast infprotozoa- wet, malariahelminths - hook wormprion- only composed on protein- mad cow
modes transportation
must have reservoir to live and grow- humans, insects, envirdirect- kiss, sex, contact, dropletindirect- airborne- vehicle- food, water, blood - Hep A- vector- misquito- malaria
port entry organisms
oro and nasopharynx- airways, lungs, stomach and GIgenitourinary- sex, catheterskin- biggest barrier and biggest vulnerability if cut or not intacttranslocation- move bacteria across intestinal lining++PEROTINEAL CAVITY, blood streamblood- transfusion, needle sticksmaternal-fetal trans- cross placenta - zeka virus
stages infection
incubation- first get symptomsprodromal- onset nonspecific symptomsacute- get specific S/Sconvalescent- S/s get betterresolution- pathogen elimination
infectious process
injury- short per vasoconstriction - stop bleeding and invasion orgs, then prolonged VASODILATION- allow blood flow, bring immune cells, ++inflammation- warmth, redness, swellingincr permeability- fluid pulled out vascular space (blood vessel) and into place injuryimmigration leukocytes- neutrophils attack area, also eosinophils, NK cells, monocytesphagocytosis- leukocytes arrive and eat invaders - neutrophils and monocytes primaryexudate- leaky stuff from phagocytosis - 4 typessystematic symptoms- if not localized - FEVER- good- helps stim def mx to rid body orgs, slow bacteria virulent and divide, improved our immune syste- better neutrophil and macrophage func, improve antibody and T-cell activation
colonization- spec body site- not cause s/s, not sickinfection- cause s/s, have infection– incr temp, HR, RR–labs- culture and urinalysis
cultures– gram stain- blood, urine, body fluids, gram - more dangerous++culture and sensitivity- 24 hrs basic result, 72 id and pattern- says which antibiotic bacteria sensitive to+++ sputum, urine, blood, - skin contaminationurine- dipstick- pH 5-98 normalnitrates (normal negative)- bacteria change nitrate into nitritesluekocytes- normal negblood- (normal <5)
healthcare infections- nosocomial
MRSA- resistant spec drugCRE- resistant entire class medsMDRO- multi drug resistant org
superinfection- new infection occurs when treating diff infection- kill helpful flora+++ GI tract
– C Diff- extreme diarrhea, id with PCR, do not put on anti diarrhea medstx with Po/iv metronidazole or vancomycin- candidiasis- skin yeast infection, oral/vaginal, thrust when in mouthtx with antifungal
inflammation
ends with itisbegins healing process- detroys invaders, limits spread, prepares damage tissue for repairS/SLocalized- redness, swelling, heat, pain, loss function- causes- exogenous (trauma); endogenous (ischemia) ** acute only last 2 weeks
events inflammation
- tissue injury- vasodilation and vascular permeability- leukocyte recruitment (chemotaxis with neutrophils)- phagocytosis antigens exudates from phagocytosis (leaky fluid) x 4- serous- watery, low protein mild inflam- serosanguineous- pink-tinged, small amount RBC- purulent- severe inflammed w bacteria - abscesses req drainage- hemmorrhagic- most severe, lots RBC- -
systemic manifestations infection
driven by cytokines- fever, incr neutrophils, lethargy, muscle catabolism
specific adaptive immunity
major histocompatibility complex (MHC)- cluster genes chromosome 6 - human leukocyte antigen complex (name tag)proteins made by these genese are on cell surface, id as self and are MHC class 1 and IIrecognize/destroy foreign invadersretain memory (adaptive) - WBC - B cells (humoral) - body fluids- T-cells (cell mediated)- antigens on cellsMHC- proteins used to see self and non-self
humoral immunity = antibody immunity
B-cells- antibody mediated immunity- memory cells- remember antigen, puts name tag- plasma cells- secrete antibodies, bind to antigen
antibodies (immunoglobulins)
5 classesIgG- most common, bacteria and virusIgM- cytotoxic functions, new infectionsIgA- secretory functions, bodily fluidsIgD- stims B cells, B-cell helpersIgE- allergic rx, sig mast cell degranulation
immunity
passive- pass person to person , mother to fetus, injection antibodies- IgA- breastmilk, IgG- placentaactive- body’s own response through B-cells, active infection, vaccinestiter test confirms immunity
vaccines
traditional- inactive, killedattenuated- live, weakened form **not give to pregnant, weakened immune, chronic disease ** nasal flu vaccinetoxoids- inactive toxins stimulate production antitoxin *tetanusconjugate- protein/toxin from one attache to disease-causing org to stim response *H influenzamRNA- snip of genetic code ** covid vaccines
3 phases drug action1. pharmaceutic (dissolution)2. pharmacokinetic (what body does to drug)3. pharmacodynamic (what drug does to body)
- pharmaceutical- PO drugs only- disintegration and dissolution2. pharmacokinetic 4 processes1. absorption- GI, small intestine2. distribution- blood3. metabolism/biotransformation- liver4. excretion- kidneys
first pass effect
PO drugs onlymetabolism of drug before systemic circulation by liver- bioavailability is amount left after first pass
3 routes absorption
Enteral- PO- by way of GI–enteric coated breaks down small intestine not stomach– PO breaks down stomach, absorbed small intestine– SL, buccal, rectal - no first pass, highly vascular tissue2. parenteral- SQ, IM, IV, intrathecal, epidural,- no first pass and IV fastest3. topical (transdermal) - no first pass, slow - eyes skin, ears, nose , lungs
pharmacokinetics - distribution
movement drug through body and to target site ** need adequate blood circulation- disruptions - decreased blood flow - peripheral vascular disease, abscesses, tumorsblood brain barrier- brain very tight junctions, lipid-soluble only, alcohol, glucose can cross, not fully devel in infantsprotein binding effect- temp storage drug allows longer availabilitygoal- maintain steady free drug/unbound AKA Steady Stateonly UNBOUND drug is active and exert effects- reversible processAlbumin primary plasma protein and drug bindshypoalbuminemia- malnutrition, liver disease - incr free drug, overdose and toxicity to drug
pharmacokinetics - 3. metabolism
aka biotransformation- drug becomes inactivated - metabolite in LIVER- converts to water-soluble metabolite for kidney excretionCYP450 - enzyme metabolize drug, used by 1/2 drugs- substrate- drug uses 450 for metabolism- inducer- makes drug inactive, reduces amount drug body and therapeutic effect- inhibitor - slow drug metabolism, incr amount drug body, incr risk toxicity, decrease drug breakdown**grapefruit juice known CYP450 inhibitor meaning incr drug amount and lead to loxicity
pharmacokinetics - 4. excretion kidneys
elimination, gen only hydrophilic drug, must be water soluble kidneys through glomerular filtration, tubular secretion, tubular reabsorption- if drug heavily excreted and not reabsorbed, need frequent drug admin to keep steady statekidney disfunction - decr kidney = incr drug and toxicityrenal labs - blood urea nitrogen (BUN), creatineglomerular filtration rate (GFR)- best measure kidney function - GFR of drugs is related to free drug concentration in plasmahalf-life - time required drug decrease by 50%- takes 5 half lives for 97% elim and varies drug to drug- take 4-5 half-lives for steady state - control effective state - when intake drug =amount metabolised/excreted
around the clock dosing
goal maintain 50%used for chronic pain and PRN for breakthrough painonset - time takes drug elicit therapeutic effectspeak- time reach max therapeutic effectduration- time drug conc is sufficient to elicit therapeutic response
phase 3 drug action: pharmacodynamic- what drug does to body
drugs may incr/decr, replace, inhibit, destroy, protect, or irritate to cause response- exert multiple rather than single response - some desired, some not (side effects)receptors- proteins on cell surface- hormones and neurotransmitters interact w drugs to produce effects = drug-receptor complexagonist- stimulate, initiate desired effect, binds to receptorantagonist- inhibits/blocks, prevents/blocks nat substances (ligands) from binding to site to cause a response- receptor-less activation- chem/physical interaction ex- antacid
drugs worrisome
narrow therapeutic index- ratio - controls toxicityblack box warning- keeps drugs on market- package insert, product label, on magazine/advertising
adverse drug reaction
MED ERRORS, 3rd leading cause deathprevent errors1. restrict2. practice drug differentiation “tall man”3. use computerized systems4. make pt info accessible5. standardize and simplify6. apply reminders7. include pt therapy8. don’t use trailing zeros9. use leading zeros
high alert meds
heparininsulinopiodsinjectable KCLneuromuscular blocking agentschemotherapy drugs
drug interactions that increase therapeutic effect
- additive - 2 drugs same MOA- synergism/potentiation- 2 drug diff MOA but result combined effect greater than alone- displacement- moves 1 drug from protein-binding site to second drug - incr effect of displaced drug
drugs interactions decrease therapeutic effects
- antidote- given to antagonize toxic effect - narcan- decrease intestinal absorption- PO meds- activation CYP450 - incr metab rate drug
older adults and pharmacokinetics
hepatic- decrease drug metabolismGI- decrease absorption POcardiac- decrease circulation= decrease distributionrenal- drug excretion less completely
pathophysiology
patho- abnormal study disease and injury and how affect bodypathology- lab study of cells and tissues
disease
disrupt homeostasis- homeo- same- stasis- balance- physical, mental, social (autism)maintain equilibriumfeedback control group
causes disease - need susceptible host, conducive environment, and pathogen
intrinsic - genes, immunity, age, genderextrinsic- bacteria, virus, injury, bx, stressors, fungi
process disease
- ID - S/S2. occurrence- how often and when3. diagnosis- ID4. etiology- cause, what call5. prognosis- likelihood recovery
stages disease
- exposure- where?2. onset- sudden- insidious- slow, gradual (chronic)- latent- dormant- prodromal- indicates onset- manifestation- S/S3. Remission - not active4. convalescence- recovery
causes/type disease
idiopathic- unknownlatrogenic- caused by tx - MDROexacerbation- worsening disease - asthma
terminology
hypo- underhyper- over, abovepenia- lack of, deficiencycytosis- cells, increaseosis- process, condition, production/increase, invasion/infectionitis- inflammationpath- disease/suffering
cough
acute/chronicallergiessmokingmedssputumsystems: heart and lungsothers: pain (headache), swelling/edema, fever, fatigue, weight loss
