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Therapeutics III > Exam 5 (final) - Barker's lectures > Flashcards

Exam 5 (final) - Barker's lectures Flashcards

1
Q

describe opioid induced hyperalgesia

A

worsened pain due to chronic opioid use

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2
Q

pain is an ________ and impacts mood because of this

A

emotion

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3
Q

pain begins with stimulus in _______ and signals to the _____

A

periphery, brain/CNS

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4
Q

temperature sensitive receptors and channels involved in pain

A

TRP (transient receptor potential cation channel)
TRPV (vanniloid) = heat (and spice like capsaicin)
TRPM (melastatin) = cold (like menthol)

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5
Q

glutamates’ role in pain

A

glutamate in the major excitatory neuron in brain
-plays a role in conduction in spinal cord

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6
Q

A beta fibers

A

non-noxious (non-pain producing)
faster (35-75m/s)

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7
Q

A gamma fibers

A

pain, cold receptors
fast (2-35m/s)
respond to “first pain” such as sharp object

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8
Q

C-fibers

A

respond to pain, temp, touch, pressure, itch
-“second pain” (dull, aching)
slow (0.5-2m/s)

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9
Q

what is substance P

A

neuropeptide released when there is an injury causing a chain of events

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10
Q

substance P chain of events (4 steps)

A
  1. vasodilation
  2. degranulation of mast cells
  3. release of histamine
  4. inflammation and prostaglandins
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11
Q

neuropathic pain sensitization description (spinal)

A

neuropeptides (CGRP and substance P) –> PLC –> PKC –> more excitable AMPA and NMDA receptors, and more expression and sensitivity
-possibly leads to ectopic action potentials

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12
Q

where does NSAID inhibition occur along signaling pathway

A

on afferent neuron just after injury signal is starting to be sent down afferent neuron

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13
Q

mu opioid receptor expression in the brain leads to what effects of opioids

A

altered mood
sedation
reduction in emotional reaction

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14
Q

morphine, codeine and thebaine are part of what structural class

A

phenanthrenes

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15
Q

3 position substitutions lead to _____

A

decreased potency - codeine

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16
Q

6 position substitutions lead to ______

A

increased activity - hydromorphone or hydrocodone (from codeine)

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17
Q

14 position OH leads to _______

A

increased potency - oxycodone

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18
Q

N-allyl substitutions leads to _____

A

antagonist activity - nalaxone or naltrexone

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19
Q

buprenorphine has substitution on which spot of the opioid structure to allow for partial agonism

A

N-allyl

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20
Q

what 3 opioid receptors are responsible for analgesia effects and side effects of opioids

A

mu
kappa
delta

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21
Q

presynaptically, mu agonists (opioid agonists) bind to ______ receptors causing an inhibition of _____ channels and a ______ in neurotransmitter release

A

mu opioid, calcium, decrease

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22
Q

postsynaptically, mu agonists (opioid agonists) bind to ______ receptors causing activation of ______ so that _____ can leave the neuron, preventing conduction to CNS

A

mu opioid, GIRK channel, potassium

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23
Q

efflux of K+ by GIRK is called ________

A

hyperpolarization

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24
Q

opioid induced side effects are mostly ____ effects (on-target or off-target)

A

on target

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25
Q

opioid induced side effects include (6)

A

-respiratory depression
-constipation
-pruritis (itch - note this is not allergic rxn but can be -bad enough to where pts must switch opioids)
-addiciton
-urinary retention
-NV

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26
Q

would you use opioids as an anti-diarrheal?

A

yes, you can, and some have been designed to stay out of the CNS so no analgesic effects occur (act only in GI tract to slow motility)

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27
Q

role of kappa opioid receptor

A

-reduce DA release, meaning reduction in abuse potential
-counterbalance mu opioid receptor effects

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28
Q

role of delta opioid receptor

A

reduce anxiety and depression
treat alcoholism
side effects: seizures
no FDA approved drugs for this yet

29
Q

depressants (just like stimulants) can cause DA release. How?

A
  1. opioid drug binds presynaptic mu receptor
  2. less GABA to activate GABA-A
  3. shuts off inhibition of DA neuron activity
  4. increased DA release and therefore activation of DA receptors
30
Q

in general, IV dosing looks like what on a conc./half life graph?

A

quick initial peak in about 6 minutes, then drops off quick

31
Q

in general, IM/SQ dosing looks like what on a conc./half life graph?

A

high initial peak (not as high as IV) in about 30 minutes, then drops off (slower than IV)

32
Q

in general, PO/PR dosing looks like what on a conc./half life graph?

A

lower initial peak in about 60 minutes, drops off slower than other forms

33
Q

morphine bioavailability is ____%

A

25

34
Q

morphine is metabolized by CYP _____ and _____

A

2D6 and 3A4

35
Q

what three opioids are prodrugs

A

heroin
codeine
tramadol

36
Q

codeine is metabolized to _________

A

hydrocodone
morphine

37
Q

heroin is metabolized to _________

A

morphine

38
Q

CYP3A4 makes opioids starting with ______

A

nor
-norhydrocodone
-noroxycodone
-noroxymorphone

39
Q

when UM of codeine is given normal dose, they will have _______ serum concentrations of morphine

A

increased (by ~50%) (most common in north africa)

40
Q

when PM of codeine is given normal dose, they will have _______ serum concentrations of morphine

A

decreased (most common in caucasian)
-no effect

41
Q

tramadol may have properties similar to what other drug class?

A

SNRIs

42
Q

meperidine has a toxic metabolite that leads to neurotoxicity (nervousness, tremors, twitching, seizures). which metabolite is it and what is it metabolized by?

A

normeperidine, 3A4

43
Q

blocking of NMDA does what? what drug is this effect seen in?

A

blocks conduction of pain signals
methadone

44
Q

3 drugs used to prevent constipation with opioids

A

Senna
-colonic contraction/increased fluid secretion
PEG (MiraLAX)
-stool softener
docusate
-stool softener

45
Q

difference between opioid tolerance and opioid induced hyperalgesia

A

tolerance = needs increased dose to have effect on pain
induced hyperalgesia = due to prolonged opioid use, increased dose with have no effect on pain

46
Q

methadone is a _____ _______

A

full agonist

47
Q

methadone is a ______ antagonist

A

NMDA

48
Q

methadone action is _____ and _____

A

slow and long

49
Q

buprenorphine is a ______ ______

A

partial agonist

50
Q

naltrexone is a ________

A

antagonist

51
Q

effects on baby if mother was on opioids during pregnancy

A

baby has withdrawal up to 4-6 months after birth
-seizures seen in methadone users
-opioids present in breast milk

52
Q

treatment of neonatal abstinence syndrome

A

non-pharm:
-more calories
-observe temp, weight (gain or loss), sleep
-rehydrate

pharm:
-morphine 0.4mg/mL
-SL buprenorphine
-methadone 0.05-0.1mg/kg/dose q6h

53
Q

NSAIDs are COX inhibitors by what pathway

A

arachadonic acid pathway

54
Q

COX-1 or COX-2 selective NSAIDs show fewer GI side effects

A

COX-2
-reduce ulcers
-reduce GI bleed

55
Q

aspirin MOA

A

irreversibly inhibits COX-1/2 by acetylation

56
Q

other NSAIDs MOA

A

competitive (reversible) inhibition of COX-1/2

57
Q

which has longer half life ibuprofen or naproxen?

A

naproxen (14hr)
ibuprofen (2hr)

58
Q

NSAID CI

A

CKD
PUD
Hx of GI bleed
increase CV risk
-also known to cause asthma exacerbations

59
Q

opioids receptors

A

mu, kappa, delta

60
Q

LSD, mushrooms receptors

A

5HT2a, 5HT2c

61
Q

marijuana, K2, spice receptors

A

CB1

62
Q

GHB receptors

A

GABA-B

63
Q

caffeine receptors

A

adenosine

64
Q

cocaine, amphetamine receptors

A

DAT
-NE, 5HT secondary

65
Q

MDMA, ecstasy receptors

A

monoamine transporters

66
Q

alcohol receptors

A

dirty (lots of them)
-GABA
-5HT

67
Q

nicotine receptors (ion channels)

A

Ach R
-agonist

68
Q

PCP, ketamine receptors (ion channels)

A

NMDA R
-antagonist

69
Q

benzos, barbiturates receptors (ion channels)

A

GABA-A
-positive allosteric modulators

Therapeutics III (22 decks)

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