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326 pharm 1 > htn > Flashcards

htn Flashcards

1
Q

pharmacology

A

study bio effect drugs on body

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2
Q

pharmacokinetics (4 components)

A

what happens to drugs in body

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3
Q

pharmadynamics

A

MOA, effects of body

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4
Q

med names

A

chemical - longest and used in research typicallygeneric - official name, always lower cased ex. acetomedafinetrade- brand name, easier to say, always capitalized

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5
Q

definitions

A

therapeutic effects - desired effectside effects- unintended effects, unavoidable, expectedtoxicities- harmful effectsadverse effects - unexpected and dangerous reactionallergic- unexpected, may be dangerous, immune response

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6
Q

what we need to know about meds

A

name (generic)classication (drug class)MOAcommon/serious side effectscontraindicationsnursing indications

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7
Q

drug approval

A

FDApreclinical - animal testingphase 1- healthy volunteer humansphase 2- volunteers with diseasephase 3- vast clinical market, must say side effectsphase 4- continued eval by FDA

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8
Q

controlled subs

A

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

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9
Q

OTC meds

A

consumers must be able to diagnose own condition and monitor effectiveness easily

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10
Q

dietary supps

A

can only claim affect on body stucture and function, not med conditionadverse interactions- can incr toxicity pres med or cause decrease therapeutic effect

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11
Q

teratogens

A

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)

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12
Q

pharmacogenomics

A

how genes affect response to drug

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13
Q

cellular adaption

A

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)

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14
Q

neoplasms- tumor

A

benign- differentiated immarture cells, unable to metastasize, grow slow, encapsulated, not cause severe probsmalignant/cancer - undifferentiated, more anaplastic, rapid growth, metastasize, no capsule

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15
Q

necrosis

A

irreversible, sweliing, burst cell, inflamationischemic necrosis- infarctioncan lead to gangrene and breading ground bacterialiquefactive necrosis- tissue w lots of lipids or number inflammatory cells

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16
Q

gangrene - disruption blood supply with bacteria

A

dry- blackened, dry, line demarcationwet- liquefacation, foul, rapid spread, extensive damage, systemic, no line demarcationgas- destroys connective tissues, gaseous bubbles, found in soil

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17
Q

infection

A

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

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18
Q

modes transportation

A

must have reservoir to live and grow- humans, insects, envirdirect- kiss, sex, contact, dropletindirect- airborne- vehicle- food, water, blood - Hep A- vector- misquito- malaria

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19
Q

port entry organisms

A

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

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20
Q

stages infection

A

incubation- first get symptomsprodromal- onset nonspecific symptomsacute- get specific S/Sconvalescent- S/s get betterresolution- pathogen elimination

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21
Q

infectious process

A

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

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22
Q

colonization- spec body site- not cause s/s, not sickinfection- cause s/s, have infection– incr temp, HR, RR–labs- culture and urinalysis

A

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)

23
Q

healthcare infections- nosocomial

A

MRSA- resistant spec drugCRE- resistant entire class medsMDRO- multi drug resistant org

24
Q

superinfection- new infection occurs when treating diff infection- kill helpful flora+++ GI tract

A

– 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

25
Q

inflammation

A

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

26
Q

events inflammation

A
  • 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- -
27
Q

systemic manifestations infection

A

driven by cytokines- fever, incr neutrophils, lethargy, muscle catabolism

28
Q

specific adaptive immunity

A

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

29
Q

humoral immunity = antibody immunity

A

B-cells- antibody mediated immunity- memory cells- remember antigen, puts name tag- plasma cells- secrete antibodies, bind to antigen

30
Q

antibodies (immunoglobulins)

A

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

31
Q

immunity

A

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

32
Q

vaccines

A

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

33
Q

3 phases drug action1. pharmaceutic (dissolution)2. pharmacokinetic (what body does to drug)3. pharmacodynamic (what drug does to body)

A
  1. pharmaceutical- PO drugs only- disintegration and dissolution2. pharmacokinetic 4 processes1. absorption- GI, small intestine2. distribution- blood3. metabolism/biotransformation- liver4. excretion- kidneys
34
Q

first pass effect

A

PO drugs onlymetabolism of drug before systemic circulation by liver- bioavailability is amount left after first pass

35
Q

3 routes absorption

A

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

36
Q

pharmacokinetics - distribution

A

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

37
Q

pharmacokinetics - 3. metabolism

A

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

38
Q

pharmacokinetics - 4. excretion kidneys

A

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

39
Q

around the clock dosing

A

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

40
Q

phase 3 drug action: pharmacodynamic- what drug does to body

A

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

41
Q

drugs worrisome

A

narrow therapeutic index- ratio - controls toxicityblack box warning- keeps drugs on market- package insert, product label, on magazine/advertising

42
Q

adverse drug reaction

A

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

43
Q

high alert meds

A

heparininsulinopiodsinjectable KCLneuromuscular blocking agentschemotherapy drugs

44
Q

drug interactions that increase therapeutic effect

A
  • 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
45
Q

drugs interactions decrease therapeutic effects

A
  • antidote- given to antagonize toxic effect - narcan- decrease intestinal absorption- PO meds- activation CYP450 - incr metab rate drug
46
Q

older adults and pharmacokinetics

A

hepatic- decrease drug metabolismGI- decrease absorption POcardiac- decrease circulation= decrease distributionrenal- drug excretion less completely

47
Q

pathophysiology

A

patho- abnormal study disease and injury and how affect bodypathology- lab study of cells and tissues

48
Q

disease

A

disrupt homeostasis- homeo- same- stasis- balance- physical, mental, social (autism)maintain equilibriumfeedback control group

49
Q

causes disease - need susceptible host, conducive environment, and pathogen

A

intrinsic - genes, immunity, age, genderextrinsic- bacteria, virus, injury, bx, stressors, fungi

50
Q

process disease

A
  1. ID - S/S2. occurrence- how often and when3. diagnosis- ID4. etiology- cause, what call5. prognosis- likelihood recovery
51
Q

stages disease

A
  1. exposure- where?2. onset- sudden- insidious- slow, gradual (chronic)- latent- dormant- prodromal- indicates onset- manifestation- S/S3. Remission - not active4. convalescence- recovery
52
Q

causes/type disease

A

idiopathic- unknownlatrogenic- caused by tx - MDROexacerbation- worsening disease - asthma

53
Q

terminology

A

hypo- underhyper- over, abovepenia- lack of, deficiencycytosis- cells, increaseosis- process, condition, production/increase, invasion/infectionitis- inflammationpath- disease/suffering

54
Q

cough

A

acute/chronicallergiessmokingmedssputumsystems: heart and lungsothers: pain (headache), swelling/edema, fever, fatigue, weight loss

326 pharm 1 (23 decks)

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