Pharmacology part 3: Final Flashcards
what are 2 types of analgesics
opiods and nonopiods
what are 2 types of antinflammatory agents
NSAIDS and glucocorticoids
function of opioids
alter pain perception
used with moderate to severe pain
indicated for use in chronic or acute pain
common opioids
codeine
fentanyl
hydrocodone
meperidine
morphine
oxycodone
propoxyphene
tramadol
what is an opioid agonist
binds to receptor and stimulates
strong and moderate types
what is an opioid antagonist
receptor blocker
how does a mixed agonist/antagonist opiod work
stimulates some receptors while blocking others
good for pts with addictive potential
where can opioids act
at pre/post synaptic neurons on brainstem or on peripheral neurons right in the joints to decrease excitability
where do opioids primarily react
brain and spinal cord
what are 3 ways opioids control pain
decreased synaptic activity in ascending pain pathways
decreased sensitivoty of sensory neurons that send painful impulses to cord
activate descending anti-pain pathways
minor adverse effects of opioids
sedation
mood changes
confusion
N&V
constipation
serious adverse effects of opioids
orthostatic hypotension
respiratory depression
potential for tolerance, dependence, and addiction
what is opiod tolerance
need more drug to achieve same effect
begins at 1st dose
obvious after 2-3 weeks
lasts up to 1-2 weeks after stop taking
what is opioid physical dependence
onset of withdrawal if drug is suddenly stopped
can begin 6-10 hours after last dose and peaks at 2-3 days
symptoms last about 5 days
NOT addiction
symptoms of phsycial dependence
body aches
gooseflesh
fever/shivers
N&V
diarrhea
cramps
uncontrollable yawn
weak/fatigue
leg cramps/tremors
sneezing/runny nose
loss of appetote
sweating
tachycardia
what is opioid addiction
chronic relapsing disease characterized by compulsive drug seeking and use despite negative consequences and by ling lasting changes in brain
risks of opioid addiction is low if…
only used for a limited period of time (i.e. 3-7 days)
dosage matches pt pain level
pt has no hx of substance abuse
pt doesn’t not misuse opioid
what is chronic opioid analgesic therapy (COAT)
more than 90 days continuous therapeutic use
misues can occur in 21-29% pts
tolerance/dependence likely but addiction is only estimated to 8-12%
what is the role of a patient controlled analgesia
patient activates pump and self administers a small amount of opioid
pump is programmed to prevent overdose
benefits of PCA
may allow better pain control with fewer side effects
increased pt satisfaction
requires pt awareness and cognitive ability
what is opioid induced hyperalgesia
opioids may be ineffective or increase pain in certain patients
possible mechanism = opioids turn on nociceptive pathways that use glutamate
more likely in pts with hx of addiction
rehabilitaion concerns for opioids
be alert for orthostatic hypotension
monitor signs of respiratory depression
monitor pain levels and watch out for hyperalgesia
watch for signs of abuse/overdose
characteristics of NSAIDs
analgesics
anti inflammatory
anti coagulant
mechanism of NSAIDS
inhibits prostoglandins by oxyclyonase
*prostoglandins cause fever, inflammation, and pain when cell is injured
examples of over the counter NSAIDS
asprin
ibuprofen
naproxen
ketoprofen
examples of prescription NSAIDS
fenoprofen
piroxicam
major difference between over the counter and prescription NSAIDS is what
the cost
side effects and rehab concerns for NSAIDS
gastric irritation
liver/kidney damage
cardio problems (increase BP and cause cardiac/stroke)
impair bone/cartilage healing
overdose can cause hearing loss, tinnitis, HA, or confusion
describe type COX-1 enzyme
normal in certain cell types
produce prostoglandins to protect cell
i.e. in stomach, kidneys, and platelets
describe COX-2 enzyme
induced when cell is injured
synthesizes PG to mediate pain and inflammation
i.e. like RA
function of COX-2 selective drugs
inhibit synthesis of PGs in pain and inflammation
they spare production of beneficial PGs in the stomach, kidneys, and platelets
can decrease pain and inflammation with less toxicity compared to other drugs
concern with COX-2 inhibiting drugs
evidence that they promote infarction
can cause heart attack or stroke
some drugs have been recalled
only COX-2 drug remaining on market
celebrex
mechanism in which COX-2 inhibiting drugs promote infarction
normal body = nalance between PGs that cause vasodilation and vasoconstriction
COX-2 selsctive drugs = inhibit the dilators and allow constricting PGs to dominate
characteristics of acetaminophen
analgesic and antipyretic effects
no GI irritaion
no anti inflammatory or anti coagulant effects
high dose = liver toxicity
how can acetampnophen be liver toxic
too much byproduct of benzo can build up and damage liver due to not enough GSH
signs of liver toxicity
yellow skin
loss of appetite
bleeding/bruising
N&V
fever
how can acetominaphen combined with opiods be beneficial
allows better overall pain control with low overdose
what are anti infalmmatory steroids
aka glucocorticoids or adrenocorticosteroids
powerful antiinflammatory and immunosupressive agents
common anti inflammatory steroids
betamethasone
cortisone
dexamethasone
hydrocortisone
paramethasone
prednisolone
prednisone
how do the anti inflammatory effects of anti inflammatory steroids
act on inflammatory cells
drug binds to glucocorticoid receptor in cytoplasm
drug receptor travels to nucleus and decreases expression of inflammatory proteins and increases expression of antiinflammatory proteins
administration methods of anti-inflammatory steroids
oral = for systemic; regular maintenance dose; dose packs
injection = intra articular; 3-4 per year
other = inhalation, topical, nasal, ophthalmic, otic, etc
primary problem with anti inflammatory steroids as well as other concerns
catabolic effect on bone, muscle, ligament, tendon, and skin
other = salt/water retention, increased infextion, gastric ulcers, glucose intolerance, glaucome. adrenal supression
