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325 patho > mod 1 > Flashcards

mod 1 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 typically

generic - official name, always lower cased
ex. acetomedafine

trade- brand name, easier to say, always capitalized

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5
Q

definitions

A

therapeutic effects - desired effect

side effects- unintended effects, unavoidable, expected

toxicities- harmful effects

adverse effects - unexpected and dangerous reaction

allergic- 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)
MOA
common/serious side effects
contraindications
nursing indications
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7
Q

drug approval

A

FDA

preclinical - animal testing
phase 1- healthy volunteer humans
phase 2- volunteers with disease
phase 3- vast clinical market, must say side effects
phase 4- continued eval by FDA
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8
Q

controlled subs

A

schedule 1-5

schedule 1 - not approved
schedule 2- narcotics, high potential abuse
sched 3- less pot abuse (non barb sedatives, nonamphetamines, stims
sched 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 condition

adverse interactions
- can incr toxicity pres med or cause decrease therapeutic effect

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11
Q

teratogens

A

congental malformatiopns dev fetus

Cat A- safe
B- lack studies
C- no studies, animal studies risk
D- poss risk fetus, dis with OB
X- 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/form

atrophy- decrease shrink size
- physiologic- developmental issue (birth)
-pathologic- decrease workload change env conditions - blood supply, hormones
++decreased protein synthesis and/or incre protein catabolism

hypertrophy- incr size and function, mechanical stimuli
- heart and kidneys most prone negative adaptation, hypertension w/ inc BP

hyperplasia- 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- cancers

dysplasia- abnormal changes of mature cells - atypical hyperplasia
- often with neoplastic growths, but NOT MEAN CANCEROUS - inflammation and chronic irritation

metaplasia- reversible replacement 1 type mature cell to another, can predispose to cancer

neoplasia- abnormal cell growth, gene mutation
anaplasia- 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 probs

malignant/cancer - undifferentiated, more anaplastic, rapid growth, metastasize, no capsule

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15
Q

necrosis

A

irreversible, sweliing, burst cell, inflamation
ischemic necrosis- infarction
can lead to gangrene and breading ground bacteria
liquefactive 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 demarcation

wet- liquefacation, foul, rapid spread, extensive damage, systemic, no line demarcation

gas- destroys connective tissues, gaseous bubbles, found in soil

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17
Q

infection

A

host take over
localized- spec place
systemic- spread sev regions

causes
common- virus and bacteria
virus- only DNA/RNA must have host cells, covid, aids, flu
bacteria - much larger virus, single-celled, 1 strand DNA, reproduce inside/outside cell - strep, tb, uti

rare
fungal - yeast inf
protozoa- wet, malaria
helminths - hook worm
prion- only composed on protein- mad cow
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18
Q

modes transportation

A 
must have reservoir to live and grow
- humans, insects, envir
direct- kiss, sex, contact, droplet
indirect- 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 GI

genitourinary- sex, catheter

skin- biggest barrier and biggest vulnerability if cut or not intact

translocation- move bacteria across intestinal lining
++PEROTINEAL CAVITY, blood stream

blood- transfusion, needle sticks

maternal-fetal trans- cross placenta - zeka virus

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20
Q

stages infection

A 
incubation- first get symptoms
prodromal- onset nonspecific symptoms
acute- get specific S/S
convalescent- S/s get better
resolution- 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, swelling

incr permeability- fluid pulled out vascular space (blood vessel) and into place injury

immigration leukocytes- neutrophils attack area, also eosinophils, NK cells, monocytes

phagocytosis- leukocytes arrive and eat invaders - neutrophils and monocytes primary

exudate- leaky stuff from phagocytosis - 4 types

systematic 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 sick

infection- 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 contamination

urine- dipstick- pH 5-98 normal
nitrates (normal negative)
- bacteria change nitrate into nitrites
luekocytes- normal neg
blood- (normal <5)
23
Q

healthcare infections- nosocomial

A

MRSA- resistant spec drug
CRE- resistant entire class meds
MDRO- 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 meds
tx with Po/iv metronidazole or vancomycin

  • candidiasis- skin yeast infection, oral/vaginal, thrust when in mouth
    tx with antifungal
25
Q

inflammation

A

ends with itis
begins healing process
- detroys invaders, limits spread, prepares damage tissue for repair

S/S
Localized- 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 II

recognize/destroy foreign invaders
retain memory (adaptive) - WBC
- B cells (humoral) - body fluids
- T-cells (cell mediated)- antigens on cells

MHC- 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 classes
IgG- most common, bacteria and virus
IgM- cytotoxic functions, new infections
IgA- secretory functions, bodily fluids
IgD- stims B cells, B-cell helpers
IgE- allergic rx, sig mast cell degranulation
31
Q

immunity

A

passive- pass person to person , mother to fetus, injection antibodies
- IgA- breastmilk, IgG- placenta

active- body’s own response through B-cells, active infection, vaccines

titer test confirms immunity

32
Q

vaccines

A

traditional- inactive, killed
attenuated- live, weakened form **not give to pregnant, weakened immune, chronic disease ** nasal flu vaccine
toxoids- inactive toxins stimulate production antitoxin *tetanus
conjugate- protein/toxin from one attache to disease-causing org to stim response *H influenza
mRNA- snip of genetic code ** covid vaccines

33
Q

3 phases drug action

  1. pharmaceutic (dissolution)
  2. pharmacokinetic (what body does to drug)
  3. pharmacodynamic (what drug does to body)
A
  1. pharmaceutical- PO drugs only
    - disintegration and dissolution
  2. pharmacokinetic 4 processes
  3. absorption- GI, small intestine
  4. distribution- blood
  5. metabolism/biotransformation- liver
  6. excretion- kidneys
34
Q

first pass effect

A

PO drugs only
metabolism 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 tissue
  1. parenteral- SQ, IM, IV, intrathecal, epidural,
    - no first pass and IV fastest
  2. 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, tumors

blood brain barrier- brain very tight junctions, lipid-soluble only, alcohol, glucose can cross, not fully devel in infants

protein binding effect- temp storage drug allows longer availability
goal- maintain steady free drug/unbound AKA Steady State
**only UNBOUND drug is active and exert effects
- reversible process

**Albumin primary plasma protein and drug binds

hypoalbuminemia- 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 excretion

CYP450 - 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 state

kidney disfunction - decr kidney = incr drug and toxicity

renal labs - blood urea nitrogen (BUN), creatine
**glomerular filtration rate (GFR)- best measure kidney function - GFR of drugs is related to free drug concentration in plasma

half-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 pain

onset - time takes drug elicit therapeutic effects
peak- time reach max therapeutic effect
duration- 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 complex
agonist- stimulate, initiate desired effect, binds to receptor
antagonist- 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 toxicity

black box warning- keeps drugs on market- package insert, product label, on magazine/advertising

42
Q

adverse drug reaction

A 
MED ERRORS, 3rd leading cause death
prevent errors
1. restrict
2. practice drug differentiation "tall man"
3. use computerized systems
4. make pt info accessible
5. standardize and simplify
6. apply reminders
7. include pt therapy
8. don't use trailing zeros
9. use leading zeros
43
Q

high alert meds

A 
heparin
insulin
opiods
injectable KCL
neuromuscular blocking agents
chemotherapy 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 metabolism
GI- decrease absorption PO
cardiac- decrease circulation= decrease distribution
renal- drug excretion less completely

47
Q

pathophysiology

A

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

48
Q

disease

A

disrupt homeostasis

  • homeo- same
  • stasis- balance
  • physical, mental, social (autism)

maintain equilibrium
feedback control group

49
Q

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

A

intrinsic - genes, immunity, age, gender

extrinsic- bacteria, virus, injury, bx, stressors, fungi

50
Q

process disease

A
  1. ID - S/S
  2. occurrence- how often and when
  3. diagnosis- ID
  4. etiology- cause, what call
  5. 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/S
  3. Remission - not active
  4. convalescence- recovery
52
Q

causes/type disease

A

idiopathic- unknown
latrogenic- caused by tx - MDRO
exacerbation- worsening disease - asthma

53
Q

terminology

A 
hypo- under
hyper- over, above
penia- lack of, deficiency
cytosis- cells, increase
osis- process, condition, production/increase, invasion/infection
itis- inflammation
path- disease/suffering
54
Q

cough

A 
acute/chronic
allergies
smoking
meds
sputum

systems: heart and lungs

others:
pain (headache), swelling/edema, fever, fatigue, weight loss

325 patho (3 decks)

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