Exam 1- Principles, opioids, NSAIDS, GI, antiemetics, respir., antihistamines Flashcards

(172 cards)

1
Q

pharmacokinetics

A

what body does to drug

absorb, distribution, metabolism, excretion

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2
Q

pharmacodynamics

A

what drug actions on target cells

incl. adverse effects

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3
Q

absorption

A

pharmacokin.
enter body, absorbed into bloodstream
rate of absorp determined by onset of drug
extent determined by intensity or bioavailability of drug

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4
Q

distribution

A

pharmacokin

drug transp site of action

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5
Q

metabolism

A

pharmacokin

drug inactiv/biotransformed or changed

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6
Q

excretion

A

pharmacokin

drug eliminated

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7
Q

absorption rate and extent factors- iv v Po

A

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

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8
Q

absorption factors

A
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
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9
Q

distribution factors

A
blood supply
protein binding (if binds= inactivated/ effective)
dec dosage if protein lvls low
BBBarrier
pregnancy
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10
Q

distribution intra-cellular transport

A
lipid pathway (drug dissol in lipid lyr)
gated channels (mvmnt ions)
carrier proteins
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11
Q

metabolism exceptions- metabolites

A

metabolites
by-product/ extra step before elimination
active or inactive
can build up and become toxic

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12
Q

metabolism exceptions- prodrugs

A

ex. codeine
distrib as inactive form
metab. actives
performed via liver

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13
Q

metabolism sites

A

liver- cytochrome p450 enzymes (cyp)

plasma, RBS’s, lungs, kidneys

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14
Q

hepatotoxicity

A

can inc exposure active drug
perform liver function test (LFT)
(alanine-aminotransferase) (aspartine-aminotransferase)
if lvls inc= dec dosage

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15
Q

metabolism factors- enzyme induction

A

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

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16
Q

metabolism factors- enzyme inhibition

A

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

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17
Q

metabolism factors- first pass effect

A

major metab on 1st pass thru liver

dec distrib drug

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18
Q

excretion sites

A

kidneys, bile/feces

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19
Q

impaired excretion

A

dec renal function
in risk drug accum
(assoc. w/ unchanged or active drugs)

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20
Q

Excretion factors

A
blood-uria nitrogen
bun inc= dec renal func
creatinine
byprod musc contraction, inc w/ dec kid. function
gfr
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21
Q

minimum effective concentration

A

mec

baseline lvl before action occurs

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22
Q

toxic conc

A

lvl which drug causes harm

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23
Q

therapeutic conc.

A

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)

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24
Q

serum half-life

A
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.
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25
receptor theory/ action types
act. inactiv of intracellular enzymes changes in perm of cell mem to ions modif. syn release or inactivation of neurohorm
26
agonist
act cell receptor
27
antagonist
block act. receptor | ex. beta-blocker w/ cardiac
28
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
29
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 affinity ```
30
drug-metabolizing enzymes-overdose
act. charcol narcan acetyl-cystiene
31
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
32
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
33
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
34
side effect
undesir response when drug at therapeutic lvl | ex. htn meds cause vasodil and can lead hypotension
35
toxicity
undesir response to elevated drug lvl inc risk= elderly, peds, ppl w/ dec liver and renal func (not at therapeutic lvl)
36
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
37
pain def
unpleasant sensation that usually indicates tissue damage | *if not controlled can interfere w/ ADLs and QOL
38
thalamus
relay station for incoming sensory stimuli
39
pain stim pathway
nociceptors, spinal cord, brain stem, thalamus, neurons
40
causes pain
chem and physical
41
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
42
opioid analgesics pain management
mod- severe, chronic
43
nonopioid pain management
acute and chronic mild to mod neuropathic or bone
44
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
45
pain recep locations
brain, spinal cord, periph tissues, GI tract | types- Mu, Kappa, and Delta (usually Mu in CNS)
46
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
47
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
48
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
49
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
50
morphine- max analgesia times
``` iv- 10-20 min IM- 30 min Po- 60 min SubQ- 60-90 min * determines when need reassess for pain ```
51
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
52
hydrocodone
combo w/ acetomin (don't exceed 4g limit) route- oral only used post procedure pain *no titrating up
53
codeine
weak pro-drug innactive upon admin, activated after metab up 25% ppl dont have converting enzymes (rxn is unpredictable)
54
fentanyl
most potent, quick acting, less n/v route- iv, transderm, transmucosal dosed in microg use- procedures, drip/patch cancer pain
55
hydromorphone
potent no active metabolites effective for severe pain
56
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
57
meperidine
``` "demeral" act metab, prone toxicity avoid w/ elderly *not favorable L/D? ```
58
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
59
oxycodone
``` alone or w/ acetomin as percocet short acting (percocet or oxyIR (immed release) long acting (oxycontin) ```
60
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
61
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
62
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
63
drug selection
least potent, least invasive | pain assessment key
64
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
65
common opioid potency list
fentanyl, hydromorphone, morphine, hydrocodone, oxycodone, codeine
66
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)
67
opioid use in opioid tolerant pt
s/s of withdrawal occur if adeq dosage not maintained
68
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
69
ex anti-prostaglandin drugs
``` nsaids non-steroidal anti-inflamm drugs ex. aspirin ibuprofen ketorolac (iv aspirin) indomethacin celecoxib ```
70
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
71
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
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nonselective cox inhib
block cox 1 and 2 | ex. ibupofen
73
selective cox inhib
``` ex. celecoxib bind cox2 enzyme benefits- don't anticoag inc risk stroke, heart attack *similar chemically to sulfa drugs (allergy notice) ```
74
cox inhib patho
bind cox enzymes, prevent arachidonic acid accessing catalytic site enzymes, inhib prostaglandin syn
75
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
76
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) ```
77
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)
78
nsaid interactions
dec effects antihtn (diuretics, ace inhib and beta blockers) inc effect anticoags combo w/ herbal supp ex ginkgo/ ginseng- inc risk bleeding
79
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)
80
role of glutathione
converts toxic metabolites to urine to be excreted | acetaminophen overdose depletes
81
acetamin adverse effects
n/v, abdom pain, diarr, constipation, STEVENS JOHNSON SYNDROME (allergic rxn where skin sheds)
82
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)
83
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
84
chondroitin and glucosamine
delay brkdwn joint cart, stim synth of new cart | used to treat OA
85
capsicum
cayenne topical route do not use in preg reduce pain by depleting subst. P (mediator in transm pain impulses)
86
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
87
peptic ulcer dis- s/s
asymptomatic epigastric pain n/v, hemaemesis (coffee or bright red) bloating, melena (drk tarry)
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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
89
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.
90
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
91
drug categories- GERD
antisecretory- H2, PPI mucosal protectants antacids- neutralizers antibiotics- amoxicillin, tetracyclin (used if h pylori ulcer present)
92
histamine 2 receptor antagonists
gerd cimetidine, ranitidine, famotidine, nizatidine suppres secretion acid by blocking h2 recep h2 (promote secretion acid)
93
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 ```
94
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)
95
famotidine
h2 antag | not inhib cyp 450 enzymes (no drug-drug metab interactions)
96
ranitidine
h2 antag weak cyp 450 inhib (few drug interactions) antacids/ food not inhib absorb not bind androgen recep (no gynecomastia)
97
cimetidine- considerations
avoid antacids admin w/in 1 hr monitor renal fun and AE check d-d intactions (inhibits some metab o/ d)
98
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
99
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
100
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
101
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)
102
clopidogrel
``` used prevent clots (coronary/ cerebral) pro drug (needs metab to activate) PPI can inhibit metab enzymes cause drug be ineffective *pantoprazole least inhibitive ```
103
h2 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 ```
104
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 ```
105
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)
106
antacid- aluminum
``` low ANC (effectivn) slow onset, long duration AE- constip, lowers Phosph bc binding ```
107
antacid- Mg
high ANC rapid onset/ long duration AE- diarrh, accum easy in renal impairment!
108
antacid- Ca
high ANC rapid onset/long duration AE- acid rebound, constip, flatulence, bleching (co2 produced in gi tract) * best option for renal impairment
109
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 ```
110
fiber func for elimination
absorbs h20, softens feces and inc mass | inc mass= inc p on intestines= stim perstalsis
111
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)
112
surfactant/ stool softeners
action- lower surface tension= facilit penetration water into feces used prevent constip AE- cramps, diarrh
113
stimulant lax
action- inc h2o and electro vol in intest lumen most commonly abused AE- mild cramping, diarrh, dehydra
114
osmotic lax
action- draw water into lumen | AE- Mg toxicity, dehydration, fluid vol retention/ overload
115
diarrhea def, s/s, complications
stools excessive vol and fluidity s/s- gi dis, infection, inflamm, ibs complications- dehydra, electrolyte depletion
116
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
117
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
118
emetic response
reflex by act. of vomiting center (grp neurons in meduall oblongata) direct and indirect
119
emetic response- direct
exposure noxious stim. or stim frm inner ear | ex. motion sickness
120
emetic response- indirect
chemoreceptor trigger zone (CTZ) act by signals via vagal n from stomach/ sm in direct action certain meds (cancer, opioids)
121
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))
122
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
123
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)
124
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
125
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
126
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
127
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
128
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
129
asthma triggers
``` environm factors- allergens occupational exposure food/food additives drugs (nsaids, antib) dis/conditions (cold, covid) exercise, emotional stress, sudden changes weather ```
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patho of classes meds used treat asthma
corticosteroids- inhib reponse antigens antihistamines- inc secretion thickness bronchodil- (Long and short acting) after response
131
inflam and bronchospasms cause
wheezing and shortness breath
132
asthma treatment goals
min symptoms improve QOL dec need urgent trtmnt improve pulmonary function test ( incentive spir) dec inflamm that leads to airway remodeling
133
asthma control- environm
avoid allergens/ o triggers
134
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)
135
intermittent asthma (exercise induced) treat w
SABA
136
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 ```
137
benefit of ICS vs oral CS
no systemic side effects | can use lower dose
138
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
139
COPD patho
exposure irritants, inflamm cells migrate to lungs progressive lung damage end result- airway obstruction, air trapping, bronchospasm, hypoxemia, hypercapnea
140
diff btw bronchitis and emphysema
bronch- hypertrophy mucus-secreting glands in upper airway | emphys- deterioration alveoli
141
CPOD treatment goals
``` prevent dis progression relief symp improv exercise tol improv health status prevent exacerb reduction mortality ```
142
COPD management- non-pharmacologic
smoking cessation (inc 2nd hand) risk factor reduction- flu vaccine pulmonary rehab- improves QOL, perform and dyspnea
143
COPD trtmnt pharmacotherapy
bronchodil- beta 2 agonists, methylxanthines, anticholinergics and corticosteroids
144
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
145
beta 2 antagonist types
SABA- albuterol (proventil, ventolin) LABA- salmeterol (serevent) oral beta 2- albuterol and terbutaline
146
SABA admin
nebulizer or metered dose inhaler | preferred bc route delivers highest conc directly to bronchioles
147
LABA-duration
long term control beta 2 delayed onset q12 hr
148
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 ```
149
methylxanthines
bronchodil used mainly copd med- theophylline
150
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
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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
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theophylline interactions
caffeine- dec metab and intesify effects phenytoin, rifampin and phenobarbitol- dec lvls cimetidine (h2 recep)- inc lvls
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anticholinergic moa
bronchodil ipratropium bromide (atrovent) inhaled moa- binds ach recep and prevents binding prevents bronchoconstriction
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atrovent adverse effects
dry mouth, irritation pharynx inc intraocular p (glycoma caution) avoid use Combivent if pt peanut allergy
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inhaled corticosteroids
long term use reduces exacerbations, dec airway remodeling, PREVENTATIVE anti-inflamm prostaglandin inhib
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types ICS
fluticasone propionate (flovent) beclomethasone diproprionate (beclovent) budesonide (pulmicort) flunisolide (aerospan)
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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
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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)
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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
160
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)
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leukotriene nursing implications
assess liver function limit alcoh preventative** not used to treat after the fact
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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)
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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)
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decongestant- use , cause, dosage forms
use- excessive nasal secretions, inflammed/ swollen nasal mucosa cause- allergies, upper respir infections (cold) dosage- oral (systemic), inhaled/ topical
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oral decongestant
prolonged effects, delayed onset less potent effect, no rebound congestion ex sudafed
166
topical decongestant
prompt onset, potent, rebound congestion | ex. sinex
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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
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antihistamines
compete w histamine. for recep sites h1and 2 blockers h2- acid secretion h1- antihistamine
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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
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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
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peripheral acting antihis
fewer cns side effects longer duration action ex. allegra/Claritin dec drowsiness
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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