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

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

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
Q

receptor theory/ action types

A

act. inactiv of intracellular enzymes
changes in perm of cell mem to ions
modif. syn release or inactivation of neurohorm

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26
Q

agonist

A

act cell receptor

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27
Q

antagonist

A

block act. receptor

ex. beta-blocker w/ cardiac

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28
Q

drug-related variables- dosage, admin. route, drug-drug interactions

A

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

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29
Q

drug-related variables- drug-drug interactions contin., synergistic effects, displacement

A 
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
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30
Q

drug-metabolizing enzymes-overdose

A

act. charcol
narcan
acetyl-cystiene

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31
Q

patient-related variables- age, body weight

A

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

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32
Q

patient-related variables- genetics, ethnicity

A

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

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33
Q

patient-related variables- gender, tolerance

A

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

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34
Q

side effect

A

undesir response when drug at therapeutic lvl

ex. htn meds cause vasodil and can lead hypotension

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35
Q

toxicity

A

undesir response to elevated drug lvl
inc risk= elderly, peds, ppl w/ dec liver and renal func
(not at therapeutic lvl)

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36
Q

idiosyncratic and paradoxical reaction

A

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

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37
Q

pain def

A

unpleasant sensation that usually indicates tissue damage

*if not controlled can interfere w/ ADLs and QOL

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38
Q

thalamus

A

relay station for incoming sensory stimuli

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39
Q

pain stim pathway

A

nociceptors, spinal cord, brain stem, thalamus, neurons

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40
Q

causes pain

A

chem and physical

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41
Q

types pain

A

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

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42
Q

opioid analgesics pain management

A

mod- severe, chronic

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43
Q

nonopioid pain management

A

acute and chronic
mild to mod
neuropathic or bone

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44
Q

opioid general chara

A

relieve pain by inhib pain sign transm from periphery to brain
well absorbed
metab in liver and can produce metabolites excreted in urine

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45
Q

pain recep locations

A

brain, spinal cord, periph tissues, GI tract

types- Mu, Kappa, and Delta (usually Mu in CNS)

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46
Q

opioid effects- cns and gi

A

cns- analgesia, depression/sedation, respir depression, n/v, pupil constriction, euphoria
GI effects- slow motility, constop, bowl/biliary spasm, delayed perstalsis

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47
Q

black box warning

A

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

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48
Q

opioid use- gi- operative and pain

A

pain- burns, cancer, L and D, acute MI
gi- cramping, diarrhea
unproductive cough
pre/post op- sedation, antianxiety, anesthesia induction

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49
Q

opioid contraindications

A

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

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50
Q

morphine- max analgesia times

A 
iv- 10-20 min
IM- 30 min
Po- 60 min
SubQ- 60-90 min
* determines when need reassess for pain
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51
Q

morphine- metab and use

A

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

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52
Q

hydrocodone

A

combo w/ acetomin (don’t exceed 4g limit)
route- oral only
used post procedure pain
*no titrating up

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53
Q

codeine

A

weak pro-drug
innactive upon admin, activated after metab
up 25% ppl dont have converting enzymes (rxn is unpredictable)

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54
Q

fentanyl

A

most potent, quick acting, less n/v
route- iv, transderm, transmucosal
dosed in microg
use- procedures, drip/patch cancer pain

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55
Q

hydromorphone

A

potent
no active metabolites
effective for severe pain

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56
Q

opioid-naive route considerations

A

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

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57
Q

meperidine

A 
"demeral"
act metab, prone toxicity
avoid w/ elderly
*not favorable 
L/D?
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58
Q

Methadone

A

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

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59
Q

oxycodone

A 
alone or w/ acetomin as percocet
short acting (percocet or oxyIR (immed release)
long acting (oxycontin)
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60
Q

opioids- adverse effects

A

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

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61
Q

assessment of pt receiving opioids

A

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

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62
Q

naloxone

A

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

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63
Q

drug selection

A

least potent, least invasive

pain assessment key

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64
Q

dosing guidelines opioids

A

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

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65
Q

common opioid potency list

A

fentanyl, hydromorphone, morphine, hydrocodone, oxycodone, codeine

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66
Q

opioid tolerance, dependence and addiction

A

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)

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67
Q

opioid use in opioid tolerant pt

A

s/s of withdrawal occur if adeq dosage not maintained

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68
Q

opioid use older adults/ children

A

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

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69
Q

ex anti-prostaglandin drugs

A 
nsaids
non-steroidal anti-inflamm drugs
ex. aspirin
ibuprofen
ketorolac (iv aspirin)
indomethacin
celecoxib
70
Q

Aspirin

A

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
Q

prostaglandin use w/ nsaids

A

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

72
Q

nonselective cox inhib

A

block cox 1 and 2

ex. ibupofen

73
Q

selective cox inhib

A 
ex. celecoxib
bind cox2 enzyme
benefits- don't anticoag
inc risk stroke, heart attack
*similar chemically to sulfa drugs (allergy notice)
74
Q

cox inhib patho

A

bind cox enzymes, prevent arachidonic acid accessing catalytic site enzymes, inhib prostaglandin syn

75
Q

NSAID USE

A

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
Q

NSAID potential conseq effects

A 
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
Q

nsaid-considerations

A

allergies
adverse effects (bleeding and renal function)
give w/ food dec gi irritation
ensure hydrated (meds already cause vasoconstriction of blood to glomerulus)

78
Q

nsaid interactions

A

dec effects antihtn (diuretics, ace inhib and beta blockers)
inc effect anticoags
combo w/ herbal supp ex ginkgo/ ginseng- inc risk bleeding

79
Q

acetaminophen benefits and cons

A

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
Q

role of glutathione

A

converts toxic metabolites to urine to be excreted

acetaminophen overdose depletes

81
Q

acetamin adverse effects

A

n/v, abdom pain, diarr, constipation, STEVENS JOHNSON SYNDROME (allergic rxn where skin sheds)

82
Q

acetamin hepatoxicity

A

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
Q

acetamin toxicity

A

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
Q

chondroitin and glucosamine

A

delay brkdwn joint cart, stim synth of new cart

used to treat OA

85
Q

capsicum

A

cayenne
topical route
do not use in preg
reduce pain by depleting subst. P (mediator in transm pain impulses)

86
Q

peptic ulcer dis- patho, complications

A

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
Q

peptic ulcer dis- s/s

A

asymptomatic
epigastric pain
n/v, hemaemesis (coffee or bright red)
bloating, melena (drk tarry)

88
Q

peptic ulcer dis- aggressive factors

A

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
Q

peptic ulcer dis- defensive factors

A

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
Q

GERD- cause, contrib factors, s/s

A

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
Q

drug categories- GERD

A

antisecretory- H2, PPI
mucosal protectants
antacids- neutralizers
antibiotics- amoxicillin, tetracyclin (used if h pylori ulcer present)

92
Q

histamine 2 receptor antagonists

A

gerd
cimetidine, ranitidine, famotidine, nizatidine
suppres secretion acid by blocking h2 recep
h2 (promote secretion acid)

93
Q

cimetidine

A 
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
Q

cimetidine- effects

A

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
Q

famotidine

A

h2 antag

not inhib cyp 450 enzymes (no drug-drug metab interactions)

96
Q

ranitidine

A

h2 antag
weak cyp 450 inhib (few drug interactions)
antacids/ food not inhib absorb
not bind androgen recep (no gynecomastia)

97
Q

cimetidine- considerations

A

avoid antacids admin w/in 1 hr
monitor renal fun and AE
check d-d intactions (inhibits some metab o/ d)

98
Q

proton pump inhibitors- action, examples

A

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
Q

omeprazole- absob, metab, half life

A

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
Q

omeprazole- adverse effects

A

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
Q

PPI interactions rt- absorp/ metab

A

seperate frm PPI at least 1 hr
absorp- hiv/aids drugs- atazanzvir, delavirdine, nelfinavir
antifungal- ketoconazole, itraconazole
metabo- clopidogrel (anti platelet aggreg)

102
Q

clopidogrel

A 
used prevent clots (coronary/ cerebral)
pro drug (needs metab to activate)
PPI can inhibit metab enzymes
    cause drug be ineffective
*pantoprazole least inhibitive
103
Q

h2 blockers/ ppi pt ed

A 
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
Q

sucralfate

A 
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
Q

sucralfate- admin, AE, interactions

A

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
Q

antacid- aluminum

A 
low ANC (effectivn)
slow onset, long duration
AE- constip, lowers Phosph bc binding
107
Q

antacid- Mg

A

high ANC
rapid onset/ long duration
AE- diarrh, accum easy in renal impairment!

108
Q

antacid- Ca

A

high ANC

rapid onset/long duration
AE- acid rebound, constip, flatulence, bleching (co2 produced in gi tract)
* best option for renal impairment

109
Q

constipation cause

A 
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
Q

fiber func for elimination

A

absorbs h20, softens feces and inc mass

inc mass= inc p on intestines= stim perstalsis

111
Q

bulk forming lax

A

action- softens fecal mass and inc bulk
considerations- used for temp trtmnt
AE- gas/bloating, esophageal obstruction (take at least 8 oz water)

112
Q

surfactant/ stool softeners

A

action- lower surface tension= facilit penetration water into feces
used prevent constip
AE- cramps, diarrh

113
Q

stimulant lax

A

action- inc h2o and electro vol in intest lumen
most commonly abused
AE- mild cramping, diarrh, dehydra

114
Q

osmotic lax

A

action- draw water into lumen

AE- Mg toxicity, dehydration, fluid vol retention/ overload

115
Q

diarrhea def, s/s, complications

A

stools excessive vol and fluidity
s/s- gi dis, infection, inflamm, ibs
complications- dehydra, electrolyte depletion

116
Q

diarrhea- opioid trtmnt- action, AE

A

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
Q

diarrhea- bismuth subsalicylate

A

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
Q

emetic response

A

reflex by act. of vomiting center (grp neurons in meduall oblongata)
direct and indirect

119
Q

emetic response- direct

A

exposure noxious stim. or stim frm inner ear

ex. motion sickness

120
Q

emetic response- indirect

A

chemoreceptor trigger zone (CTZ) act by
signals via vagal n from stomach/ sm in
direct action certain meds (cancer, opioids)

121
Q

antiemetics- serotonin receptor antagonists

A

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
Q

antiemetics- substance P/ Neuorkinin antagonist

A

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
Q

antiemetics- dopamine antagonists- phenothiazines

A

*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
Q

antiemetics- dopamine antagonists- metoclopramide

A

“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
Q

motion sickness- antihistamines-moa-ae

A

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
Q

motion sickness- scopolamine

A

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
Q

asthma def and significance

A

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
Q

asthma risk factors

A

exposure to air poll, allergens, tobacco smoke
recurrent respir tract infections
esophageal reflux
hygiene hypothesis (early exposure microbial diversity dec asthma)
obesity

129
Q

asthma triggers

A 
environm factors- allergens
occupational exposure
food/food additives
drugs (nsaids, antib)
dis/conditions (cold, covid)
exercise, emotional stress, sudden changes weather
130
Q

patho of classes meds used treat asthma

A

corticosteroids- inhib reponse antigens
antihistamines- inc secretion thickness
bronchodil- (Long and short acting) after response

131
Q

inflam and bronchospasms cause

A

wheezing and shortness breath

132
Q

asthma treatment goals

A

min symptoms
improve QOL
dec need urgent trtmnt
improve pulmonary function test ( incentive spir)
dec inflamm that leads to airway remodeling

133
Q

asthma control- environm

A

avoid allergens/ o triggers

134
Q

asthma control- pharmacotherapy

A

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
Q

intermittent asthma (exercise induced) treat w

A

SABA

136
Q

stair step asthma meds

A 
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
Q

benefit of ICS vs oral CS

A

no systemic side effects

can use lower dose

138
Q

COPD def and sig, risk factors

A

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
Q

COPD patho

A

exposure irritants, inflamm cells migrate to lungs
progressive lung damage
end result- airway obstruction, air trapping, bronchospasm, hypoxemia, hypercapnea

140
Q

diff btw bronchitis and emphysema

A

bronch- hypertrophy mucus-secreting glands in upper airway

emphys- deterioration alveoli

141
Q

CPOD treatment goals

A 
prevent dis progression
relief symp
improv exercise tol
improv health status
prevent exacerb
reduction mortality
142
Q

COPD management- non-pharmacologic

A

smoking cessation (inc 2nd hand)
risk factor reduction- flu vaccine
pulmonary rehab- improves QOL, perform and dyspnea

143
Q

COPD trtmnt pharmacotherapy

A

bronchodil- beta 2 agonists, methylxanthines, anticholinergics and corticosteroids

144
Q

beta 2 agonist- action

A

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
Q

beta 2 antagonist types

A

SABA- albuterol (proventil, ventolin)
LABA- salmeterol (serevent)
oral beta 2- albuterol and terbutaline

146
Q

SABA admin

A

nebulizer or metered dose inhaler

preferred bc route delivers highest conc directly to bronchioles

147
Q

LABA-duration

A

long term control beta 2
delayed onset
q12 hr

148
Q

beta 2 agonist adverse effects

A 
saba- (albuterol)
tachyc, angina, tremor
can start to effect beta 1 recep
laba- (salmeterol)
never used alone, body can become tolerant
149
Q

methylxanthines

A

bronchodil
used mainly copd
med- theophylline

150
Q

theophylline moa- absorp- metab

A

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

151
Q

theophylline- adverse effects and trtmnt

A

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

152
Q

theophylline interactions

A

caffeine- dec metab and intesify effects
phenytoin, rifampin and phenobarbitol- dec lvls
cimetidine (h2 recep)- inc lvls

153
Q

anticholinergic moa

A

bronchodil
ipratropium bromide (atrovent) inhaled
moa- binds ach recep and prevents binding
prevents bronchoconstriction

154
Q

atrovent adverse effects

A

dry mouth, irritation pharynx
inc intraocular p (glycoma caution)
avoid use Combivent if pt peanut allergy

155
Q

inhaled corticosteroids

A

long term use
reduces exacerbations, dec airway remodeling, PREVENTATIVE
anti-inflamm
prostaglandin inhib

156
Q

types ICS

A

fluticasone propionate (flovent)
beclomethasone diproprionate (beclovent)
budesonide (pulmicort)
flunisolide (aerospan)

157
Q

ICS- moa, adverse effects

A

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

158
Q

ICS- nursing implications

A

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)

159
Q

Leukotriene modifiers moa

A

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
Q

montelukast- therapeutic use and adverse effects

A

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)

161
Q

leukotriene nursing implications

A

assess liver function
limit alcoh
preventative** not used to treat after the fact

162
Q

general implications- respir agents

A

avoid exposure conditions cause bronchospasms (smoking, allergens)
adequate fluid intake (dec thickening of secretions)
avoid excessive fatigue, heat, caffeine (methylxanthine- theophylline)

163
Q

allergic rhinitis- def, manif, management

A

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)

164
Q

decongestant- use , cause, dosage forms

A

use- excessive nasal secretions, inflammed/ swollen nasal mucosa
cause- allergies, upper respir infections (cold)
dosage- oral (systemic), inhaled/ topical

165
Q

oral decongestant

A

prolonged effects, delayed onset
less potent effect, no rebound congestion
ex sudafed

166
Q

topical decongestant

A

prompt onset, potent, rebound congestion

ex. sinex

167
Q

decongestant- moa, ae

A

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

168
Q

antihistamines

A

compete w histamine. for recep sites
h1and 2 blockers
h2- acid secretion
h1- antihistamine

169
Q

antihistamines- moa, uses

A

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

170
Q

traditional antihis

A

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

171
Q

peripheral acting antihis

A

fewer cns side effects
longer duration action
ex. allegra/Claritin
dec drowsiness

172
Q

antihistamine pt education

A

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

336 Pharmacology (5 decks)

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