Exam 1- Principles, opioids, NSAIDS, GI, antiemetics, respir., antihistamines Flashcards
pharmacokinetics
what body does to drug
absorb, distribution, metabolism, excretion
pharmacodynamics
what drug actions on target cells
incl. adverse effects
absorption
pharmacokin.
enter body, absorbed into bloodstream
rate of absorp determined by onset of drug
extent determined by intensity or bioavailability of drug
distribution
pharmacokin
drug transp site of action
metabolism
pharmacokin
drug inactiv/biotransformed or changed
excretion
pharmacokin
drug eliminated
absorption rate and extent factors- iv v Po
changes via route
iv- 100%bioaval.
dosage needs be less than oral
oral- <70%, onset 1 hr
Im- onset 15-30min
Subq- onset 30-45min
absorption factors
blood flow site of admin ex. dec circ= dec absorb time GI function (acidity of stomach) Presence food and o/ drugs (can dec absorp) ex. antacids bind to o/ drugs
distribution factors
blood supply protein binding (if binds= inactivated/ effective) dec dosage if protein lvls low BBBarrier pregnancy
distribution intra-cellular transport
lipid pathway (drug dissol in lipid lyr) gated channels (mvmnt ions) carrier proteins
metabolism exceptions- metabolites
metabolites
by-product/ extra step before elimination
active or inactive
can build up and become toxic
metabolism exceptions- prodrugs
ex. codeine
distrib as inactive form
metab. actives
performed via liver
metabolism sites
liver- cytochrome p450 enzymes (cyp)
plasma, RBS’s, lungs, kidneys
hepatotoxicity
can inc exposure active drug
perform liver function test (LFT)
(alanine-aminotransferase) (aspartine-aminotransferase)
if lvls inc= dec dosage
metabolism factors- enzyme induction
enzyme induction
(drugs act. inc production metab. enzymes)
1-3 wks after introduction
dec effectiveness bc dec active form
same drug gets metab by many diff types of enzymes
metabolism factors- enzyme inhibition
dec drug metab enzymes= inc active drug
(in risk toxicity)
Ex. use drug A w/ cyp enzymes and use drug B w/ cyp inhib
drug A not metab as well
metabolism factors- first pass effect
major metab on 1st pass thru liver
dec distrib drug
excretion sites
kidneys, bile/feces
impaired excretion
dec renal function
in risk drug accum
(assoc. w/ unchanged or active drugs)
Excretion factors
blood-uria nitrogen bun inc= dec renal func creatinine byprod musc contraction, inc w/ dec kid. function gfr
minimum effective concentration
mec
baseline lvl before action occurs
toxic conc
lvl which drug causes harm
therapeutic conc.
gap btw b/ extremes
can be monitored
if range narrow drugs prone accum.
assess for peak / trough lvls
peak-drawn after drug given (1hr)
trough- before give drug
(results can alter dosage interval or conc)
serum half-life
time requir drug conc dec 50% determined by rate metab/excretion (if impaired= inc 1/2 life= inc accum; mre prone toxicity) dosage= freq 1/2 life steady state conc.
receptor theory/ action types
act. inactiv of intracellular enzymes
changes in perm of cell mem to ions
modif. syn release or inactivation of neurohorm
agonist
act cell receptor
antagonist
block act. receptor
ex. beta-blocker w/ cardiac
drug-related variables- dosage, admin. route, drug-drug interactions
dosage
admin. route (iv v. subq)
diff. in absorp and distribution
drug diet interaction
food slow absorp
ex. monoamine oxidase inhib drugs act. release
neurotrans= inc sympath response= in bp
drug-related variables- drug-drug interactions contin., synergistic effects, displacement
additive effects
2 sub w/ similar actions
ex. sedative, meds and alcohol
synergistic
2 opposing actions wrk together
ex. Tylenol and hydrocodone (better pain relief together)
displacement
protein affinitydrug-metabolizing enzymes-overdose
act. charcol
narcan
acetyl-cystiene
patient-related variables- age, body weight
age
pregnancy/ fetus= organ immaturity
children 1-12
older adults >65 yrs
dec total body water (water sol drugs mre concen)
dec serum albumin (inc affects bc dec protein)
metabolism dec bc dec liver func= inc risk toxicity
dec renal fun (inc drug accumm)
polypharmacy- drug interactions, 7x inc adverse drug event
body weight
weights mre= inc dose bc lrgr distrib area
patient-related variables- genetics, ethnicity
genetics
rapid metab- need higher doses, drug converted to inactive quicker (less active floating around)
slow metab- dec doses, drug slowly inactiv
ethnicity
african a= need inc doses cardiac meds
lwr doses Ca channel blockers/diuretics
asians= inc sensitivity to everything
patient-related variables- gender, tolerance
wmn respond diff
smaller size/weight, inc body fat %, dec muscle tissue, smaller blood vol, horm fluctuations
tolerance
chronic drug users higher tolerance for certain chemicals
side effect
undesir response when drug at therapeutic lvl
ex. htn meds cause vasodil and can lead hypotension
toxicity
undesir response to elevated drug lvl
inc risk= elderly, peds, ppl w/ dec liver and renal func
(not at therapeutic lvl)
idiosyncratic and paradoxical reaction
idiosyncratic- not common or unexpected bc genetic disposition
ex. paralytic last sev hours instead of 1
paradoxical- opposite of intended rxn
ex. caffeine calms adhd instead of stimulates
pain def
unpleasant sensation that usually indicates tissue damage
*if not controlled can interfere w/ ADLs and QOL
thalamus
relay station for incoming sensory stimuli
pain stim pathway
nociceptors, spinal cord, brain stem, thalamus, neurons
causes pain
chem and physical
types pain
acute- <3 mon, sharp
chronic- >3mon, w/ visible signs distress
cancer- acute or chronic
neuropathic- damage to cns, burning, usually chronic
visceral- organs, not localized, deep and dull
somatic- damage skin, bone or muscle, localized, sharp, throbbing
opioid analgesics pain management
mod- severe, chronic
nonopioid pain management
acute and chronic
mild to mod
neuropathic or bone
opioid general chara
relieve pain by inhib pain sign transm from periphery to brain
well absorbed
metab in liver and can produce metabolites excreted in urine
pain recep locations
brain, spinal cord, periph tissues, GI tract
types- Mu, Kappa, and Delta (usually Mu in CNS)
opioid effects- cns and gi
cns- analgesia, depression/sedation, respir depression, n/v, pupil constriction, euphoria
GI effects- slow motility, constop, bowl/biliary spasm, delayed perstalsis
black box warning
assigned by FDA for majority opioids
indicate pot fatal adverse effects/ risk abuse
ex. fentanyl, hydromorp, methadone, morphine and oxycodone
= high risk abuse and overdose to respir depression
opioid use- gi- operative and pain
pain- burns, cancer, L and D, acute MI
gi- cramping, diarrhea
unproductive cough
pre/post op- sedation, antianxiety, anesthesia induction
opioid contraindications
existing respir depression
< 12 rr- hold (exception palliative care)
chronic lung dis (rel)
if respir dep. occurs dec lung vol from beginning makes it worse
liver or kidney dis
monitor metabolism function
prostatic hypertrophy
cause urinary retention worsens w/ opioids
inc ICP
if respir depression happens, inc co2, vasodil, inc blood vol brain, inc icp more
known hypersensitivity to opioids- (absolute)
avoid all known allergies
morphine- max analgesia times
iv- 10-20 min IM- 30 min Po- 60 min SubQ- 60-90 min * determines when need reassess for pain
morphine- metab and use
mod to severe
given Po, IV
iv push, drip (cont infusion, only for severe/chronic ex cancer), PCA
metab in liver
biotransformed, chem becomes inactive (if no metabolites are produced)
excreted by kidneys
impaired function= prolonged sedation
hydrocodone
combo w/ acetomin (don’t exceed 4g limit)
route- oral only
used post procedure pain
*no titrating up
codeine
weak pro-drug
innactive upon admin, activated after metab
up 25% ppl dont have converting enzymes (rxn is unpredictable)
fentanyl
most potent, quick acting, less n/v
route- iv, transderm, transmucosal
dosed in microg
use- procedures, drip/patch cancer pain
hydromorphone
potent
no active metabolites
effective for severe pain
opioid-naive route considerations
transderm patch- only ppl been on opioids >2 wks
released meds hourly for 3 days
*use gloves and witness disposal
transmuc- used brkthrough, severe, chronic pain
immed relief, dose could be lethal for reg person
meperidine
"demeral" act metab, prone toxicity avoid w/ elderly *not favorable L/D?
Methadone
longer duration of action
use- severe, chronic, pain and addiction trtmnt
less peaks/valleys (prevents total withdrawl)
can delay repolarization of ventricle
*QRS can land on T-wave causing caridac arrest from ventricular tachycardia
*use tele on pt
oxycodone
alone or w/ acetomin as percocet short acting (percocet or oxyIR (immed release) long acting (oxycontin)
opioids- adverse effects
RESPIR DEPRESSION
EXCESSIVE SEDATION
hypotension
vasodil dec bp (common w/ morphine) hold if bp 90-100
n/v
constipation
stimulant lax most effective/ preventative measure
miosis
urinary retention- tightening of sphincter
assessment of pt receiving opioids
LOC and RR b/a admin
IV admin- capno or contin. ox
monitor bp b/a admin
ensure saftey- ex. bed rails, non-skid socks
prevent/treat constipation
have resuscitation equipment and naloxone
naloxone
use- trt respir depression caused by opioid overdose/ adverse rxn
routes- iv, im, subq, intranasal
overdose- 0.4-2 mg iv
resp depression- 0.1-0.2mg iv repeat q 2 min until desired effect
ex. of partial agonist (no matter dose, still bind w/ no effect)
shorter half-life- 45 min
drug selection
least potent, least invasive
pain assessment key
dosing guidelines opioids
if dose range ordered start w/ smaller dose
dosages change w/ diff opioids
reduced dose for pts alrdy recieving cns depress. (antianxiety, antidep, antihista etc)
intermittent/brkthru pain use prn dosing
severe, acute give parenteral opioid at onset
premed prior painful act
common opioid potency list
fentanyl, hydromorphone, morphine, hydrocodone, oxycodone, codeine
opioid tolerance, dependence and addiction
tol- lrg dose for same effect
dependence- withdrawl symptoms if taken away after 2wks, *normal occurrence w/ chronic use
addiction- pattern of contin use despite physical, psycho and social harm (tol can contribute)
opioid use in opioid tolerant pt
s/s of withdrawal occur if adeq dosage not maintained
opioid use older adults/ children
adults- inc risk resp depres, excess sedation and confusion
kids- use age-approp assessment tools ex FACES
avoid im injections
inc assessment for adverse effects needed
non-pharmaco. interven should used
ex anti-prostaglandin drugs
nsaids non-steroidal anti-inflamm drugs ex. aspirin ibuprofen ketorolac (iv aspirin) indomethacin celecoxib
Aspirin
low dose- cox1 inhib, used as blood thinner
moderate dose- non-selective cox1+2 inhib, used to dec pain and fever
adverse effects- rapid absorb= gastric toxicity
anticoag= inc bleeding time
dec renal vasodil= renal insufficiency
inc risk Reyes syndrome in kids
inc risk GI bleed in elderly
prostaglandin use w/ nsaids
block act. prostaglandins (which contrib to inflammation)
prostaglandin act. -
inc platelet aggregation
stim hypothal inc temp
inc pain sensitivity
inc mucous production GI tract
encourage vasodil afferent arteriole in glomerulus
nonselective cox inhib
block cox 1 and 2
ex. ibupofen
selective cox inhib
ex. celecoxib bind cox2 enzyme benefits- don't anticoag inc risk stroke, heart attack *similar chemically to sulfa drugs (allergy notice)
cox inhib patho
bind cox enzymes, prevent arachidonic acid accessing catalytic site enzymes, inhib prostaglandin syn
NSAID USE
inflammation disorders- degen. joint dis, OsteoArth, RA
pain- mild-mod, surgery or mild trauma
fever- Aspirin not used in kids!! (causes encephal)
suppress platelet aggregation- 1x/day for MI/ stroke prevention
NSAID potential conseq effects
peptic ulcer dis
gi bleeding disorders
impaired renal function- nephrotoxicity
hypersensitivity
children/ aspirin (Reyes)
pregnancy + aspirin or ketoralac
caution w/ asa, (x2 bleeding for at least week after admin) never use Ketoralac
tinnitus
rash/ itching
non-aspirin- inc risk mi/cva (celecoxib)nsaid-considerations
allergies
adverse effects (bleeding and renal function)
give w/ food dec gi irritation
ensure hydrated (meds already cause vasoconstriction of blood to glomerulus)
nsaid interactions
dec effects antihtn (diuretics, ace inhib and beta blockers)
inc effect anticoags
combo w/ herbal supp ex ginkgo/ ginseng- inc risk bleeding
acetaminophen benefits and cons
pros- not cause n/v, bleeding or anticoag
treat mild- mod pain and fever (acts on hypothal to vasodil and inc sweating to lwr body temp and inc blood flow = dec bp)
cons- no anti-inflamm, metab in liver (produce toxic metabolite)
role of glutathione
converts toxic metabolites to urine to be excreted
acetaminophen overdose depletes
acetamin adverse effects
n/v, abdom pain, diarr, constipation, STEVENS JOHNSON SYNDROME (allergic rxn where skin sheds)
acetamin hepatoxicity
single lrg dose- 10-15g as little as 6g
excessive doses- 3-4g/ day for year or 5-8g/day for weeks
4g for alcoholics (inc toxic metab and dec glutathione)
acetamin toxicity
s/s nonspecific
24-48hrs after overdose liver tests inc
manif- jaundice, vomiting, cns stim, delirium, coma
trtmnt- act charcoal w/in 4hrs
acetylcysteine- oral or iv
most benef 8-10hrs, max 36hrs
(mimicks glutathione) cannot reverse damage done
chondroitin and glucosamine
delay brkdwn joint cart, stim synth of new cart
used to treat OA
capsicum
cayenne
topical route
do not use in preg
reduce pain by depleting subst. P (mediator in transm pain impulses)
peptic ulcer dis- patho, complications
upper GI dis. charac by erosion gut wall
common cause- h pylori
locations- lesser curvature stomach and duodenum
complications- hemorrhage, perforation, Gi bleeding, sepsis, hemorr stroke
patho- imbal btw mucosal barrier + aggressive factors
peptic ulcer dis- s/s
asymptomatic
epigastric pain
n/v, hemaemesis (coffee or bright red)
bloating, melena (drk tarry)
peptic ulcer dis- aggressive factors
h pylori- gram neg, colonize in stomach
NSAIDS- inhib prostaglandin
acid
pepsin- digestive proteins that can irrit if no barrier
smoking- delay healing, inc risk reaccur, dec secretion bicarb, inc gastric emptying- inc acid lvl in duodenum
physiologic stress after op- inc cortisol (dec viscosity mucus barrier), vasoconstric, ischemia gi mucosa, inc sympath n system- inc acid production
peptic ulcer dis- defensive factors
mucus- secreted by gi mucosal cells
bicarb- excr frm epith cells stomach, wrk neutralize H+ ions that penetrate mucus
blood flow
prostaglandins- stim secretion mucus/bicarb, promote vasdil for GI circ.
GERD- cause, contrib factors, s/s
regurgitation gastric contents into esophagus
cause- incompetent low esoph sphincter (LES)
factors- meds (ccb/ nitrates) relax sphinc, hiatal hernia, gastric distention, recumbent postion (inc p in stomach and force on sphincter)
s/s- heartburn
drug categories- GERD
antisecretory- H2, PPI
mucosal protectants
antacids- neutralizers
antibiotics- amoxicillin, tetracyclin (used if h pylori ulcer present)
histamine 2 receptor antagonists
gerd
cimetidine, ranitidine, famotidine, nizatidine
suppres secretion acid by blocking h2 recep
h2 (promote secretion acid)
cimetidine
h2 antag absorb dec by antacids (sep by 1hr) inhibits hepatic metab of o/ drugs half life- 2hrs 70% excreted in urine *use cautiously w/ renal impairmnt
cimetidine- effects
confusion, cv dysrhyth w/ iv, pneumonia (if inc pH, inc bac growth of stomach), diarr, n, gynecomastia (bind to androgen recep to block), agranulocytosis, aplastic anemia (dec wbc and rbc production- inc risk infection/ anemia)
famotidine
h2 antag
not inhib cyp 450 enzymes (no drug-drug metab interactions)
ranitidine
h2 antag
weak cyp 450 inhib (few drug interactions)
antacids/ food not inhib absorb
not bind androgen recep (no gynecomastia)
cimetidine- considerations
avoid antacids admin w/in 1 hr
monitor renal fun and AE
check d-d intactions (inhibits some metab o/ d)
proton pump inhibitors- action, examples
omeprazole, esomeprazole, lansoprazole, pantoprazole (clincial)
action- bind gastric proton pump prevent release acid
*drug choice for gerd and ulcers/erosion trtmnt
90% effectiveness and faster acting compared to H2
omeprazole- absob, metab, half life
absorp- brkn down by gastric acid, dont crush!!
well absorbed after Po
metab- use cautiously in liver dis
half life- 30- 1hr extended release
omeprazole- adverse effects
not commonly used gi prophylaxis anymore
gi- abdom pain, constip, diarrh, flatulence, n
respir- pneum.
ms- fractures (long term use dec Ca absorp bc Ca needs high acidic environment for brkdwn)
rebound acid hypersecre if drug dc
hypomagnesemia (needs high acidic environ)
inc risk c diff- inc ph = inc bac growth
PPI interactions rt- absorp/ metab
seperate frm PPI at least 1 hr
absorp- hiv/aids drugs- atazanzvir, delavirdine, nelfinavir
antifungal- ketoconazole, itraconazole
metabo- clopidogrel (anti platelet aggreg)
clopidogrel
used prevent clots (coronary/ cerebral)
pro drug (needs metab to activate)
PPI can inhibit metab enzymes
cause drug be ineffective
*pantoprazole least inhibitiveh2 blockers/ ppi pt ed
smoking cessation (delay healing and inc reaccur) inc fluid/ fiber intake to dec constip avoid alch, nsaids, foods inc gi irritation report s/s gi bleeding report confusion/ hallucinations = accum toxicity
sucralfate
mucosal protectant creates gel when exposed acid anti-ulcer agent low AE *not dec acid secretion or neutralize acid *flush feeding tube b/a
sucralfate- admin, AE, interactions
admin- Po or oral suspension
1 hr before meals and at bedtime
minimal systemic absorption
AE- constipation
interactions- antacids, h2, ppi dec effectiveness
needs <4 pH to work
dec absorp digoxin, warfarin, phenytoin (admin 2hrs apart)
antacid- aluminum
low ANC (effectivn) slow onset, long duration AE- constip, lowers Phosph bc binding
antacid- Mg
high ANC
rapid onset/ long duration
AE- diarrh, accum easy in renal impairment!
antacid- Ca
high ANC
rapid onset/long duration
AE- acid rebound, constip, flatulence, bleching (co2 produced in gi tract)
* best option for renal impairment
constipation cause
irreg colon function stool not soft, formed or eliminated w/out straining poor diet dysfun anal sphincter (spinal c injury) slow intestinal transit meds ex. opioids
fiber func for elimination
absorbs h20, softens feces and inc mass
inc mass= inc p on intestines= stim perstalsis
bulk forming lax
action- softens fecal mass and inc bulk
considerations- used for temp trtmnt
AE- gas/bloating, esophageal obstruction (take at least 8 oz water)
surfactant/ stool softeners
action- lower surface tension= facilit penetration water into feces
used prevent constip
AE- cramps, diarrh
stimulant lax
action- inc h2o and electro vol in intest lumen
most commonly abused
AE- mild cramping, diarrh, dehydra
osmotic lax
action- draw water into lumen
AE- Mg toxicity, dehydration, fluid vol retention/ overload
diarrhea def, s/s, complications
stools excessive vol and fluidity
s/s- gi dis, infection, inflamm, ibs
complications- dehydra, electrolyte depletion
diarrhea- opioid trtmnt- action, AE
diphenoxylate w/ atropine (lomotil)
loperamide- doesnt cross BBB
action- activate opioid recep in gi tract
dec intestinal motil, reduces fluid in feces
AE- drowsiness, constip
atropine- blurred vision, dry m, urinary retention
diarrhea- bismuth subsalicylate
pepto bismol
absorbs h2o in intestin
forms protective coating over intestine mucosa
*avoid w/ ppl allergy to aspirin
may blacken stool/ tongue bc rxn w/ sulfur
emetic response
reflex by act. of vomiting center (grp neurons in meduall oblongata)
direct and indirect
emetic response- direct
exposure noxious stim. or stim frm inner ear
ex. motion sickness
emetic response- indirect
chemoreceptor trigger zone (CTZ) act by
signals via vagal n from stomach/ sm in
direct action certain meds (cancer, opioids)
antiemetics- serotonin receptor antagonists
ondanstron
most effective preventing/treating chemo induced n/v
action- block serot. recep in ctz
AE- headache, diarrh, dizziness
inc risk CV v-fib and v-tach
not block dopamine recep (no extrapyramidal effects (abnorm mvmnts))
antiemetics- substance P/ Neuorkinin antagonist
aprepitant
action- block neurokinin recep for sub P in ctz (ctz then cant activ vomiting center)
benefit- prolonged duration action
prevents delayed chemo induced n/v
problem- pot drug interactions dt effect metabolizing liver enzymes
AE- fatigue, hiccups, dizziness, diarr
antiemetics- dopamine antagonists- phenothiazines
*not reccom for pt parkinsons dis
prochlorperzine and promethazine (can be irr to tissue and veins)
block dopamine 2 recep in ctz
use- trt post op n/v
Po, IM, IV, rectal
AE- hypotension, sedation, anticholinergic effects (blurred v, dry mouth, urinary retention)
antiemetics- dopamine antagonists- metoclopramide
“reglan”blocks dopamin recep in ctz and enhances acetylchol
inc perstalsis and gastric emptying
Po and iV
admin 30 min b4 meals
* caution for gi obstruction (inc p on intest wall cause ischemia and perforation- metoclopramide exaber o2 requirements for intestinal wall)
AE- sedation, diarr, tardive dyskinesia
motion sickness- antihistamines-moa-ae
dramamine, antivert
block recep for acetylchol and H1 in the pathway that connects inner ear to vomiting center
AE- drowsiness, blurred v, dry m, urinary retention
motion sickness- scopolamine
muscarinic acetylchol antag
most effective for motion sickness
Po, subq, transdermal patch
action- suppress nerve traffic in neuronal pthway connects vestibular apparatus of inner ear to vomiting center
AE- dry m, blurred vision and urinary retention
asthma def and significance
obstructive airway disorder
results- airway inflamm, bronchial hyper-responsiveness, episodic reversible airway obstruction
sig- 12.7 dollars/year, 22-24 million ppl, 1.5 ED visits each year
asthma risk factors
exposure to air poll, allergens, tobacco smoke
recurrent respir tract infections
esophageal reflux
hygiene hypothesis (early exposure microbial diversity dec asthma)
obesity
asthma triggers
environm factors- allergens occupational exposure food/food additives drugs (nsaids, antib) dis/conditions (cold, covid) exercise, emotional stress, sudden changes weather
patho of classes meds used treat asthma
corticosteroids- inhib reponse antigens
antihistamines- inc secretion thickness
bronchodil- (Long and short acting) after response
inflam and bronchospasms cause
wheezing and shortness breath
asthma treatment goals
min symptoms
improve QOL
dec need urgent trtmnt
improve pulmonary function test ( incentive spir)
dec inflamm that leads to airway remodeling
asthma control- environm
avoid allergens/ o triggers
asthma control- pharmacotherapy
short acting beta 2 agonists (albuterol)
located in sm musc airway- promote bronchodil
diff than beta 1!! (sympath nerv. system)
inhaled corticosteroids
leukotriene modifiers (montelukast)
long acting beta 2 agonists (salmeterol)
intermittent asthma (exercise induced) treat w
SABA
stair step asthma meds
SABA ICS ICS med dose ICS med AND LABA/ LEUKOTRIENE ICS high AND LABA OR LEUKO ICS high AND LABA OR LEUKO AND ORAL CORTICOSTEROID
benefit of ICS vs oral CS
no systemic side effects
can use lower dose
COPD def and sig, risk factors
def- preventable and treatable dis. w/ airflow limitation that isnt completely reversible
sig- 32 million ppl, 4th leading cause death
risk- exposure tobacco smoke, dust, chem, genetics
incl chronic bronchitis and emphysema
COPD patho
exposure irritants, inflamm cells migrate to lungs
progressive lung damage
end result- airway obstruction, air trapping, bronchospasm, hypoxemia, hypercapnea
diff btw bronchitis and emphysema
bronch- hypertrophy mucus-secreting glands in upper airway
emphys- deterioration alveoli
CPOD treatment goals
prevent dis progression relief symp improv exercise tol improv health status prevent exacerb reduction mortality
COPD management- non-pharmacologic
smoking cessation (inc 2nd hand)
risk factor reduction- flu vaccine
pulmonary rehab- improves QOL, perform and dyspnea
COPD trtmnt pharmacotherapy
bronchodil- beta 2 agonists, methylxanthines, anticholinergics and corticosteroids
beta 2 agonist- action
bronchodil
active beta 2 recep in sm muscl lung= bronchodil and relief bronchospasm
suppress histamine release
use- acute attacks SABA or long term use LABA
beta 2 antagonist types
SABA- albuterol (proventil, ventolin)
LABA- salmeterol (serevent)
oral beta 2- albuterol and terbutaline
SABA admin
nebulizer or metered dose inhaler
preferred bc route delivers highest conc directly to bronchioles
LABA-duration
long term control beta 2
delayed onset
q12 hr
beta 2 agonist adverse effects
saba- (albuterol) tachyc, angina, tremor can start to effect beta 1 recep laba- (salmeterol) never used alone, body can become tolerant
methylxanthines
bronchodil
used mainly copd
med- theophylline
theophylline moa- absorp- metab
moa- relaxes sm musc bronchi
blocks adenosine
absorb- Po slow, only avaliable sustained-release
metab- via liver
inc= smoking (dec half life 50%), drug interactions (can require inc dose for same effect)
dec= chf, liver dis, prolonged fever, age, geriatric/neonates, drug interactions
theophylline- adverse effects and trtmnt
small therapeutic range 10-20 mcg/mL, goal 5-15
assess for s/s toxicity
mild tox- n/v, diarr, insomnia, restlnessness
serious tox- VF, seizures, death d/t cardiopulm collapse
trtmnt- d/c drug, admin activated charcoal
theophylline interactions
caffeine- dec metab and intesify effects
phenytoin, rifampin and phenobarbitol- dec lvls
cimetidine (h2 recep)- inc lvls
anticholinergic moa
bronchodil
ipratropium bromide (atrovent) inhaled
moa- binds ach recep and prevents binding
prevents bronchoconstriction
atrovent adverse effects
dry mouth, irritation pharynx
inc intraocular p (glycoma caution)
avoid use Combivent if pt peanut allergy
inhaled corticosteroids
long term use
reduces exacerbations, dec airway remodeling, PREVENTATIVE
anti-inflamm
prostaglandin inhib
types ICS
fluticasone propionate (flovent)
beclomethasone diproprionate (beclovent)
budesonide (pulmicort)
flunisolide (aerospan)
ICS- moa, adverse effects
moa- block late phase rxn to allergen, reduce airway hyper responsive, inhib inflamm cell migration/activation
ae- pharyngeal irritation, coughing, dry mouth, oral fungal infections
ICS- nursing implications
caution w/ psychosis, fungal infections, aids, tb, diab, glaucoma, osteoporosis, peptic ulcer dis (inhib prostag), renal dis, chf, edema
pt rinse/gargle water prevent dev oral fungal infections (thrush)
Leukotriene modifiers moa
montelukast
block leukot action, dec inflamm, bronchoconstriction and mucus prodution
moa- block inflamm in lungs, prevent vascular perm, dec inflamm cell migration/action, prevent leukotrienes fr attaching to recep on cells in lungs
*used after ICS NOT for fast acting emergencies
montelukast- therapeutic use and adverse effects
prevent/ trtmnt asthma ppl > 1
prevention exercise induced >15 yrs
relief allergic rhinitis
ae- churg strauss syndrome (inflamm blood v) suicidal thoughts, drug interaction w/ phenytoin (anti-seizure)
leukotriene nursing implications
assess liver function
limit alcoh
preventative** not used to treat after the fact
general implications- respir agents
avoid exposure conditions cause bronchospasms (smoking, allergens)
adequate fluid intake (dec thickening of secretions)
avoid excessive fatigue, heat, caffeine (methylxanthine- theophylline)
allergic rhinitis- def, manif, management
inflamm disorder affects upper/lwr airways and eyes
manif- runny nose, congestion, itchy eyes, sneezing
management- control allergens, decongestant, antihistamine, intranasla corticosteroid (seasonal allergies), immunotherapy (gradual exposure allergens)
decongestant- use , cause, dosage forms
use- excessive nasal secretions, inflammed/ swollen nasal mucosa
cause- allergies, upper respir infections (cold)
dosage- oral (systemic), inhaled/ topical
oral decongestant
prolonged effects, delayed onset
less potent effect, no rebound congestion
ex sudafed
topical decongestant
prompt onset, potent, rebound congestion
ex. sinex
decongestant- moa, ae
moa- stimulation alpha 1 recep in sm musc vessels = constriction capillaries, tissues shrink and nasla secretions in swollen mucous mem beter able drain, dec stuffiness
ae- topical (sprays) rebound cong, stinging, drying nasal mucosa
oral- peripheral vasoconstriction (inc bp) tachycard, urinary retention, cns stim (nervousness, tremors, headache)
*can be used make meth
antihistamines
compete w histamine. for recep sites
h1and 2 blockers
h2- acid secretion
h1- antihistamine
antihistamines- moa, uses
moa- blocks histamine= dec vasodil, respir secretions, cap permeability
*better dec s/s than reversing
uses- cold, anaphylaxis, allergic rhinitis, insect bite, urticaria (itching)
motion sickness and sleep aid
traditional antihis
first gen
work peripherally and centrally
anticholinergic effects (more effective than nonsedating drugs)
ex. benadryl
ae- dry mouth, constipation, changes ision, pupil dilation, mild drowsiness
peripheral acting antihis
fewer cns side effects
longer duration action
ex. allegra/Claritin
dec drowsiness
antihistamine pt education
not reccom for elderly, due to excessive sedation, confusion or hypotension w/ 1st gen
avoid cns dep and alcoh
mouth care and sucking on hard candy redue dry mouth
