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203 Cards in this Set
- Front
- Back
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analgesia receptors in the dorsal spinal cord
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mu
delta |
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analgesia receptors in the ventral spinal cord
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kappa
delta |
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analgesia receptors in the PAG, thalamus, cortex, limbic areas
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mu
kappa delta |
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why resp depression
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mu receptors in the medulla
which regulates breathing |
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most deadly se of opioids
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resp depression
|
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t/f
opioids increases the response to CO2 |
f
decreases doesn't change response to PO2 |
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what causes euphoria /dysphoria w/ opioids
|
mu
kappa delta in mesolimbic areas |
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miosis due to which receptors and where
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mu
kappa edinger-westphal nucleus (cranial nerve 3) |
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why during resp depression thre's mydriasis pupils
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due to decreased O2 they will dilate
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sedation due to
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mu
kappa |
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sedation due to inhibiton/excitation of the ----
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inhibition
locs ceruleus |
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sedation due to inhibition of -----
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NE
locus cerelus on ascending. . .directly on NE cell bodies |
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muscular rigidity due to
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mu
kappa delta |
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muscular rigidity due mu, delta, and kappy receptors on the
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niagrostriatal tract
causes catalepsy |
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why antitussive activity
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suppression of medullary cough center
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t/f
antitussive actions due to mu, kappy, delta activity |
f
not mediated by those receptors also naloxone insenstitive |
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nausea due to the ---- receptors in the ----
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mu
ctz |
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nausea worse in ---- pt
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ambulators
give phenergan . . .antimuscarinic |
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due to the ---- receptors in the hypothalamus hormone release is affected. . . what are the effects
|
mu
decreased testosteroe and estrogen disruption of the menstrual cycle |
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why convulsant activity
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due to possible inhbition of gaba
or metabolites occurs mostly in kids |
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decreased transmission of u, k and delta in the
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in descending
due to gaba |
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increased transmission of u, k, and delta inthe
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PAG
RAS |
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due to elevated CO2 there's increased ---- bl flow which will lead to increased -----
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cerebral (to get rid of the CO2)
CSF this will increase ICP (opiods will add to this) |
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opiods are couple to the G-
which will increase/decrease camp |
1
decrease camp. . .opens K channels, leads to hyperpolarization also decreased Ca channels |
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constipation due to -- receptors in the --- and ---
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mu
stomach intestine |
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mu causes decreases gi ---, icreased ---, and decreased ----
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motility
tone secretions |
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constipation due to the loss of --- to ----
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urge
defecate |
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biliary will have -- pressure so there epigastric distress
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increased
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t/f
direct effects on hr and bp |
f
no direct effects |
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hypotension possibly due to
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histamine's vasodilation peripherally
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effects of histamine
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flushing
itching |
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|
which has more histamine effects
morphine or fentanly |
morphine
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which receptors will have spasmogenic effect on sm muscle
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mu
delta |
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will --- labor, ---- effects of oxytocin
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prolong
inhibit |
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--- voiding reflex, increases ---, --- ADH
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inhibit
tone increases (decreased urination) |
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supress/stimulate lymphocyte activity
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suppress
decrease killer cells |
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receptors mediate immune system
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mu
delta direct and indirect effects |
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which receptor causes resp depression and euphoria
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mu
increases DA |
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which recpetor will inhibit DA
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K
|
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rank from more lipophilic to least
heroin, morphine, codeine |
heroin>codeine>morphine
|
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opioid onset of action determined by
--- of administration ---- solubility |
route
lipid (the more the faster into brain) |
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t/f
most m-like not well absorbed orally |
f
well absorbed orally |
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t/f
m-like have significant first pass metabolism |
t
|
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t/f
m-like have low protein binding |
f
significant protein binding |
|
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metabolism of morphine like:
--- by liver |
glucorinated by liver
N or O methylated |
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t/f
only inactive metabolites for m-like |
f
inactive and active |
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how are metabolites excreted
|
urine
|
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indications for acute pain for m-like
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sx
MI trauma |
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indications for chronic pain for m-like
|
post-op
terminal illness |
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ci for m-like
-- injury --- depression --- pain ----- alleryg/---- impaired -- fx --- disease |
head
resp chronic pregnancy allergy/asthma liver renal |
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why are m-like ci in pregn
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decreased protein binidng and bbb in fetus
|
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why is m-like cied w/ chronic pain
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due to increased tolerance
|
|
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what diseases will you avoid to due potential of resp depression w/ m -like
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emphysema
kyphosciolosis age obesity |
|
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how can m-like exacerbate allergy/asthma
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due to increased histmine
|
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impaired liver and kidney fx will lead to accumulation of
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drug or active metabolite
|
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type of m-like w/ most abuse
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lipophilic
full agonist |
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which population has decreased protein binding
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fetus
young kids so they will have more effects |
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cns depressants will cause sedation, etc
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bzd
barbiturates ethanol |
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cns depress and opioids will increase ---, -- and --- ---
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sedation
euphoria resp depression |
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cns depress and opioids have what type of moa
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pk
pd |
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maoi and antidepressnats w/ mACH or H1 will cause --- and --- -----
will increase ---- and increase risk of -------- |
sedation
resp depression analgesia risk of seizures |
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t/f
increased NE and 5HT levels will help w/ analgesia |
t
|
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why an increased risk of sizures w/ maoi, antidepressants
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due to gaba inhibition
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|
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which antipsychotics will increase sedation adn resp depression
|
mACH or H1 receptor
block D2, alpha, 5HT2A/2C so might need to increase dose |
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why increase dose w/ pt's using antipsychotics
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block D2, alpha, 5HT 2A/2C
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|
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amphetamine increase -- and ----
but decreases ----- |
euphoria
analgesia sedation |
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whhy an increased chance of abuse w/ amphetamine
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due to increase in D2
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antihistamines will increase -- and some increase ------
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analgesia
sedation (less w/ 2nd gen antihistamines) |
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why give nsaids w/ opioids
|
different moa
synergistic increased K conductance decreases prostaglandins |
|
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which is used more for analgesia
ssri's nssri's |
nssri's
|
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alpha 2 agonist used in combo w/ opiates to tx
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spinal pain
|
|
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toxicity can cuase
|
stupor
coma very low resp rate symmetrical pinpoint pupils |
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w/ toxicity what do you give
|
naloxone and ventilate
|
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why monitor resp even after naloxone given
|
short t1/2
resp depression can reoccur so monitor drip/pt |
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|
morphine, hydromorphone, oxymorphone have --- 1st pass metabolism
|
significant
2-6 fold less potent orally |
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morphine, hydromorphone, oxymorphone --% bound to plasma proteins
|
35
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t/f
morphine, hydromorphine, oxymorphone . . . a lot crosses the bbb |
f
very little |
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what morphine metabolite is acitve
|
morphine -6 glucorindate
|
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active metabolite in brain is ---
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morphine
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heroin is more --- soluable
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lipid
|
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why does meperidine have less GI, sm muscle, biliary effects
|
better ability to x bbb
so might be safer may be ssri, so watch for syndrome |
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this m-like suppresses withdrawal symptoms, less euphoria
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methaodone
|
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methadone has low --- development
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tolerance
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methadone used for -- and --- withdrawal
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mild
protracted |
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why is methadone used to tx withdrawal
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long t1/2 . . . 15-40 hrs
less 1st pass effect |
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how is LAAM different from methadone
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longer duration of action
|
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where are NE and 5HT found
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substantia gelatinosa
|
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ne and 5ht activates ---
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enkephalons
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ne and 5ht have direct/indirect effects to inhibit pain signals
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direct
|
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u and delta inhibit
|
sub p
decrease Ca and Camp |
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k and delta will increase ----- ----
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k conductance. . .hyperpolarization
|
|
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what's 100-1000 x morphine potenecy
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fentanyl
sufentanil remifentanyl |
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fentanyl, sufentanil, remifentanyl has low/high resp depression
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low
probably due to it's ease of crossing the bbb |
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fentanyl, sufentanil, remifentanyl has a long/short duration of action
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short
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fentanyl, sufentanil, remifentanyl are very -- soluable
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lipid
|
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fentanyl, sufentanil, remifentanyl crosses the bbb easily/w/ difficulty
|
easily
so also leaves rapidly. . . shorter duration of action and prob why there's less resp depression |
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t/f
fentanyl, sufentanil, remifentanyl has no histamine release |
t
|
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fentanyl, sufentanil, remifentanyl causes marked ---
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rigidity
|
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codeine, oxycodone, hydrocodone has more/less 1st pass metabolism
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less
|
|
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codeine, oxycodone, hydrocodone has --- effects w/ nsaids
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synergistics
good for pain relief |
|
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codeine, oxycodone, hydrocodone are good ----
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antitussants
|
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why r codeine, oxycodone, hydrocodone good as outpt
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less 1st pass which has better efficacy
|
|
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levorphanol has less/more first pass
|
less
|
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levorphanol has more/less nausea
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less
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levorphanol is the parent drug of
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dextromorphan (which has no opiate activity by itself)
|
|
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propoxyphene similar to --- w/o the ---- effect
|
codeine
antitussant |
|
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propoxyphene has very good/bad bioavailability orally
|
very good
|
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which route should you not give propoxyphene
why |
iv/sq
irritating to veins |
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why is naloxone mixed w/ certain opioids
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cuz it's inactive orally
so if abusers crush and inject/snort they will not get high |
|
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why is codeine an effective pain med
|
possibly cuz codeine is metabolized to morphine by cyp 2d6
and the morphine might be the active agent |
|
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why do mixed action opiates have less addiction, resp depression, constipation
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cuz less mu activity
mu usu causes resp depression, euphoria, and constipation |
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what receptor has no or little effects on resp rate, gi, and has opposite effects on the mesolimbic activity
|
kappa
|
|
|
receptors of pentazocine
partial --- full --- agonist |
mu
kappa |
|
|
pentazocine has less:
------ ----- ------ |
resp depression
euphoria constipation |
|
|
pentazocine compounded w/
|
naloxone
|
|
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what does pentazocine cause at high doses
|
dysphoria
|
|
|
pentazocine high doses can cause an increae in
|
bp
hr |
|
|
nalbuphine receptors:
--- antagonist full --- agonist |
mu
kappa |
|
|
nalbuphine causes less ----- and ---
but the same ------- as pentazocine |
resp depression
dysphoria constipation |
|
|
pentazocine will activate the descending --- and ---
|
ne
5ht |
|
|
t/f
nalbuphine is a mu antagonist so there will be no resp depression |
f
there's some, possibly due to the coupling of receptors/dimers or due unknown activity of delta |
|
|
butorphanol receptors
|
partial mu
full kappa agonist |
|
|
butorphanol cause less:
|
resp depression
dysphoria |
|
|
butorphanol causes increases in
|
bp
|
|
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buprenorphine receptors
|
partial mu
full kappa antagonist |
|
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buprenorphine has full kappa ----
|
antagonist
|
|
|
buprenorphine used to tx
|
chronic pain
addiction tx it has an increased affinity to mu and slow dissociation rate |
|
|
buprenorphine combined w/
|
naloxone
|
|
|
t1/2 of buprenorphine
duration |
3 hrs
72 hrs so good for chronic pain and addiction tx |
|
|
tramadol receptor
|
partial mu
|
|
|
tramadol has -- to --- like efficacy
|
meperidine
codeine |
|
|
tramadol has minimal --- --- or ----
|
resp depression
constipation |
|
|
tramadol has less--- and ---
|
tolerance
dependence |
|
|
tramadol also inhibits ---- and ---
|
NE transporters
5HT transporters . . . don't combine w/ ssri's or maoi will also help increase mood |
|
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tramadol only partly blocked by
|
naloxone
|
|
|
spiradoline is a selective --- agonist
|
kappa
|
|
|
spiradoline can cause too much ----- and not enouugh -----
|
dysphoria
analgesia (not used, this is an example of effects of the dimer theory) |
|
|
naloxone has --- ---- for opiate effects
|
competitive antagonism
|
|
|
naloxone used to tx
|
opiate overdose
|
|
|
naloxone can precipate --- syndrome
|
abstinence
|
|
|
t/f
in the absence of opiates naloxone can cause resp depression |
f
no effects |
|
|
t/f
naloxone has effects only on exogenous opioid actions |
f
also has effects on endogenous |
|
|
route naloxone should be given
|
iv only
|
|
|
why must you adminster naloxone continuously
|
short t1/2
|
|
|
t/f
naloxone and nalterexone can cause liver toxicity if used long term |
t
|
|
|
t/f
the slower you remove the naloxone the more severe the withdrawal s/s |
f
the faster you remove the naloxone cuz less time for body to adjust |
|
|
which has a longer duration naloxone or naltrexone
|
naltrexone
|
|
|
naltrexone used to tx acute/chronic opiate effects
|
acute
(such as overdose) |
|
|
naltrexone will decrease the cravings of
|
etoh
|
|
|
naltrexone has less/more first pass
|
less
t1/2= 24 hrs so can be used as outpt |
|
|
this antagonist is a pure mu antagonist
|
nalmefene
|
|
|
nalmefene has less -- toxicity
|
liver
|
|
|
this antag might work against compulsive gambline, shopping
|
nalmefene
|
|
|
nalmefene has more/less 1st pass
and longer/shorter t1/2 |
less
longer |
|
|
dextromethorphan only rxed for --- cough
|
nonuseful
|
|
|
t/f
receptors of dextromethorphan are the same as the opiate receptors |
f
distinct |
|
|
t/f
dextromethorphan has high abuse potential and high toxicity |
f
low |
|
|
dextromethorphan is a -- antagonist, blocks --- tolerance
|
NMDA
opiate |
|
|
dextromethorphan may have --/-- effects
|
NE
5HT |
|
|
at hight conc dextromethorphan might be ----due to the blockade of ---
|
hallucinogenic
NMDA |
|
|
due to the blockage of nmda --is decreased
|
glutamate
so less tolerance |
|
|
t/f
naloxone has effects only on exogenous opioid actions |
f
also has effects on endogenous |
|
|
route naloxone should be given
|
iv only
|
|
|
why must you adminster naloxone continuously
|
short t1/2
|
|
|
t/f
naloxone and nalterexone can cause liver toxicity if used long term |
t
|
|
|
t/f
the slower you remove the naloxone the more severe the withdrawal s/s |
f
the faster you remove the naloxone cuz less time for body to adjust |
|
|
diphenoxylate is combined w/ ---- to counteract abuse
|
atropine
due to antimuscarinic effects, abusers will be hesitant |
|
|
t/f
diphenoxylate very soluable |
f
insoluable so exposed to gi, no absorbed by cns |
|
|
diphenoxylate is a -- agonist
|
mu
|
|
|
t/f
loperamide crosses the bbb |
f
|
|
|
loperamide is a -- agonist
|
mu
|
|
|
diphenoxylate is combined w/ ---- to counteract abuse
|
atropine
due to antimuscarinic effects, abusers will be hesitant |
|
|
t/f
diphenoxylate very soluable |
f
insoluable so exposed to gi, no absorbed by cns |
|
|
diphenoxylate is a -- agonist
|
mu
|
|
|
t/f
loperamide crosses the bbb |
f
|
|
|
loperamide is a -- agonist
|
mu
|
|
|
loperamide has --- abuse potential
|
no
even when crushed |
|
|
loperamide is ---- lasting
|
long
|
|
|
less effect the more you take
|
tolerance
|
|
|
what influences tolerance
PD or PK |
PD
opioids not affected by cyp chronically |
|
|
opioids have more tolerance to
|
euphria
analgesia resp depression sedation nausea (can be good, say effects usu wear off) endocrine sm. muscle |
|
|
opioids have less tolerance to
|
miosis
antitussive constipation biliary |
|
|
tolerance due to
--- of receptors to -- proteins increased --- activity changes to ---, --- neurotransmission |
uncoupling
g proteins adenylate cyclase activity NE NMDA |
|
|
uncoupling of G proteins due to possible ---
|
phosphorylation . . . increase AC due to Gi downregulation
|
|
|
how will sedation be offset
|
due to an increase in NE. .. ascending inhibited by opiates
|
|
|
day 1 abstinece syndrome s/s
|
lacrimation
runny nose sweating yawning insomnia increased hr and bp (increase in autonomic, opposite of opiate) |
|
|
1-2 days of abstinence
|
PLUS. . .
mydriasis anorexia gooseflesh tremor |
|
|
2-3 days of abstinence syndrome
|
PLUS . . .
cramps diarrhea chills vomiting sneezing |
|
|
7-10 days of abstinence syndrome
|
over but protracted withdrawal syndrome
|
|
|
dependence due to
decreased efficacy of --- opioids increased ---- -- activity overall downregulation of --- -- adrenergic receptors in the PAG and LC |
endogenous
AC Alpha-2 |
|
|
why a decrease efficacy of endogenous opioids
|
due to use of exogenous
|
|
|
abuse worse for --- agonist vs -- agonist
|
full
partial |
|
|
abuse liability worse for more --- soluable
|
lipid
|
|
|
put in order of more to least lipid soluble
mepridine methadone fentanyl morphine heroin |
fentanyl > heroin > meperidine > morphine > methadone
|
|
|
nonabusers can use which tx
|
cold turkey
decrease dose every several days |
|
|
abuser can tx dependence by
|
sub detox: methadone, buprenorphine
long acting aciting antagonist: naltrexone clonidine |
|
|
long acting antag: nalrexone alleviates --- cravings via --- process
|
environmental
extinction |
|
|
what should be done before long-acting opiate antagonist used
|
wean off the drug first
|
|
|
clonidine activates alpha 2 adrenegic --- in the ---
|
autoreceptors
LC |
|
|
clonidine decreases ---- hyperactivity
|
NE
|
|
|
clonidine alleviates ----symptoms but not -------
|
withdrawal
cravings |
|
|
what dependence tx suppresses cravings
|
substitiution detox
|
|
|
know last chart
|
knowl ast chart
|
