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PHRM 845 > exam 5 pain > Flashcards

exam 5 pain Flashcards

1
Q

what are the two types of pain?

A

acute and chronic

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2
Q

what are the types of chronic pain?

A

Nociceptive: inflammatory like OA, RA
neuropathic: central or peripheral
visceral: inflammatory like internal organs, IBS
mixed: lower back and cancer

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3
Q

what is opioid induced hyperalgesia?

A

chronic opioid use can lead to more pain
it can cause a secondary pain pathway

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4
Q

what is clinical assessment of pain?

A

pain is an emotion and impacts mood

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5
Q

what is the pain circuitry?

A

Pain starts at trauma and travels to the spinal cord
Then travels to the brain where the signal is read
Then travels back down to the spinal cord to act on CNS

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6
Q

what are the peripheral receptors and channels involved in pain signalling?

A

temperature sensitive: TRP, TRPV for heat and TRPM for cold
acid sensitive: acid sensing ion channel (ASIO) –> activated by H+ and conducts Na+
chemical irritant senstive: histamine and bradykinin

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7
Q

What is the main ion channel responsible for conduction of pain signal

A

Na 1.8

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8
Q

What are the three different pain fibers that transduce different pain signals?

A

Alpha-B fibers
Alpha-delta fibers
C- fibers

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9
Q

A-B fibers function?

A

not pain producing - so just touch and pressure
fastest, 35-75m/s

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10
Q

alpha-delta function?

A

pain and cold
myelinated
first pain, reflex arc
fast

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11
Q

C fibers function?

A

pain, temperature, touch, pressure
unmyelinated
slowest
second pain –> dull, aching

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12
Q

What is substance P?

A

Plays a role in heightening pain response
repeated stimuli reduces firing threshold
increased expression of pain receptors leads to sensitization –> since it sends more signals to spinal cord
functions: vasodilation, degranulation of mast cells, release of histamine, inflammation of prostaglandins

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13
Q

what is the spinal pain cicuirtry?

A

nerve damage causes nerve degeneration (neuroma)
neuroma causes spontaneous afferent activity and spinal sensitzation

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14
Q

what is spinal sensitization?

A

it leads to non painful stimulus becoming painful due to increased AMPA and NMDA receptor

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15
Q

what is spontaneous afferent activity?

A

it leads to spontaneous dysesthesias (shooting and burning pain)

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16
Q

Whtat is the brain pain circuitry?

A

high expression of opioid receptors in the brain stem along descending pathway
mu opioid receptor in the brain plats important role in pain signal

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17
Q

what are the two types of opium alkaloids?

A

Phenanthrenes - three ring structures
Benzylisoquinolones

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18
Q

what are the differences between opiates and opioids?

A

opiates are naturally occuring (morphine)
opioids are general term like synthetics (fentanyl)

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19
Q

What does 3 position substitutions ether or ester produce?

A

decreases the potency
seen in codeine

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20
Q

what is the function of 6 position?

A

increases activity seen in hydromorphone or hydrocodone

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21
Q

what is the function of the 14 position OH?

A

increases the potency seen in oxycodone

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22
Q

what type of receptors are opioid receptors?

A

GPCR
open GIRK postassium channels that normally maintain membrane potential
drugs hyperpolarize

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23
Q

what is the Mu opioid receptor and what are it’s therapuetic uses?

A

beta-endorphins (endogenous morphine)
uses: acute pain treatment, sedation, antitussive
not as effective for chronic pain

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24
Q

what is the presynaptic action of mu opioid receptors?

A

inhibit Ca+ channels to to decrease neurotransmitter release

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25
Q

what is the postsynaptic activity of mu opioid receptors?

A

activate GIRK channel releases efflux of K+ that causes hyperpolarization

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26
Q

What are opioid induced side effects?

A

they are on target effects
respiratory depression, constipation, addction, urinary retention, N/V, mioisis
pruritus due to opioid inducing histamine receptors

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27
Q

would you use opioids as anti-diarrheal?

A

Yes, some opioids are formulated to specifically act on the Gi

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28
Q

what is the kappa opioid receptor?

A

dynorphins are the natural ligand
activation causes dysphoric effects

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29
Q

why are kappa opioids thought to be less addictive?

A

activation of K opioid receptor causes dysphoric effects
there is a reduction in DA release
this can be used in combo with mu opioid receptor agonists to reduce addiction potential

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30
Q

are there any delta opioid receptor agonists approved?

A

none approved by FDA

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31
Q

what is the mechanism for opioids leading to addiction?

A
  1. Opioid binds mu receptor
  2. GI singaling inhibits neurotransmitter release
  3. Less GABA to activate GABA-a
  4. Less inhibition of dopamine neuron activity
  5. Increase in DA release
  6. Increased activation of DA receptors
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32
Q

What are the pharmacokinetics of morphine and phenanthrenes?

A

they are readily absorbed
go through first pass metabolism
hepatic metabolism: CYP3A4 and CYP2D6
glomerular filtration

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33
Q

which opioids are pro drugs?

A

heroin, codeine, tramadol

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34
Q

which opioids do not produce active metabolites?

A

methadone and fentanyl

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35
Q

Which drugs are metabolized by CYP3A4?

A

drugs beginning with NOR are created from 3A4
nor metabolites are deactivated and less active

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36
Q

What is the plasma concentration of an UM taking a prodrug?

A

increased plasma concentrations
higher ADRs

37
Q

what is the plasma concentration of a PM taking a a prodrug?

A

no therapeutic effect

38
Q

what is fentanyl’s potency?

A

very potent
100x morphine
50x heroin

39
Q

what are the opioids related to fentanyl?

A

Sufentanil, remifentanil, alfentanil
used for anesthesia and sedation
breakdown by plasma esterases due to ester linkage

40
Q

what are the common opioids?

A

hydromorphone: no active metabolites
morphine
hydrocodone
oxycodone

41
Q

what are the non-phenanthrene opioids?

A

tramadol, meperidine, methadone

42
Q

what is tramadol?

A

has SNRI properties
mild opiate analgesic

43
Q

what is meperidine?

A

used to treat rigors (shivering)
not recommended

44
Q

what is methadone?

A

used for opioid dependence
pronlonged QTc
NMDA antagonist to also reduce pain signal

45
Q

what are other clinically used opioids that are non analgesic?

A

cough/antitussive: codeine and dextromethorphan
anti-diarrheal: loperamide and lomotil

46
Q

what is bupennorphine?

A

partial mu agonist
weak K and delta agonist
used for opiod replacement therapy

47
Q

what are medications used for constipation?

A

senna: irritates colon to force contraction
PEG
dioctyl sodium

48
Q

how is methadone used for opioid dependence?

A

Full mu receptor agonist
Slow acting
Accumulation with repeated dose
NMDA antagonist

49
Q

how is buprenorphine used for opioid dependence?

A

Mu opioid partial agonist
Blocks full agonist effect of heroin and oxycodone
Provides some activation
Subutex has abuse potential

50
Q

how is naltrexone used for opioid dependence?

A

antagonist
will cause withdrawal due to antagonism
decent oral bioavailability

51
Q

what is the difference between naloxone and naltrexone?

A

naltrexone is orally administered and has medium half life
naxolone has limited oral bioavailability and a short half-life

52
Q

what is Naloxone?

A

Limited oral bioavailability
Short half life
Rapid onset
Repeated every 2-5 minutes if not concoius

53
Q

what is neonatal abstinence syndrome?

A

Drug is passed through placenta and after birth, baby suffers from withdrawal
Heroin and other opiates: Serious withdrawal in baby and Seizures can occur in babies born to methadone users

54
Q

what is the treatment of neonatal abstinence syndrome?

A

Nonpharm: swaddling, hypercaloric formula, frequent feedings, rehydration
Pharm: Morphine, SL buprenorphine, methadone, clonidine can be useful

55
Q

what are the uses of NSAIDs?

A

Analgesia: chornic pain, myalgias, inflammation
Anti-inflammatory: bursitis, tendonitis, OA, RA, gout
Antipyretic
ASA to reduce risk of MI

56
Q

What are three phases of inflammation?

A

Acute: vasodilation –> increased permeability
Subacute: infiltration of neutrophil
Chronic: proliferation

57
Q

what are eicosanoids?

A

arachidonic acid metabolites

58
Q

what is NSAID mechanism?

A

inhibit COX in AA pathway
decreases in TXA, PGE, PGI
PGI protects stomach lining –> why NSAIDs can cause upset stomach/ulcers

59
Q

Which NSAID is irreversible?

A

aspirin

60
Q

what are the therapuetics of aspirin?

A

prophylaxis for anticoagulation
no tolerance development to analgesic effects
risk of reyes syndrome in children

61
Q

what is aspirin poisoning?

A

mild effects: vertigo and tinnitus
CNS effects: respiratory alkalosis and metabolic acidosis

62
Q

what is the treatment of aspirin poisoning?

A

reduce salicylate
dextrose and sodium bicarbonate to trap and excrete

63
Q

what are arylproprionic acids NSAIDs?

A

potent reversible COX inhibitors
ibuprofen 2hr t1/2
naproxen 14hr 1/2

64
Q

what are arylacetic acid derivatives?

A

diclofenac: can be gel, increased risk peptic ulcer
indomethacin: potnet reversible inhibitors of PG biosynthesis, high side effects
sulindac: less toxic derivative indomethacin

65
Q

what are enolic acids?

A

meloxicam and piroxicam
reversible competitive inhibitors
meloxicam low doses is Cox2 selective

66
Q

what are the ADRs of NSAIDs?

A

renal function: inhibitrs PGE2 synthesis so water retention and edema
bleed risk
inhibits uterine motility

67
Q

what are NSAID CIs?

A

Avoid: CKD, PUD, hx GI bleed
CV risk
Interfere with wound healing
Asthma exacerabtions

68
Q

What are the therapuetic uses of APAP?

A

highly effective analgesic and antipyretic
no GI toxicity
overdose can cause hepatic necrosis

69
Q

what are ADRs of APAP?

A

more renal toxicity than ASA + NSAIDs
dose dependent necrosis
increase in toxic metabolites NAPQI

70
Q

why are COX 2 not used anymore?

A

they had reduce ulcer risk and GI bleeds but are no longer used due to risk of clots, stroke, and heart attacks

71
Q

what are functions of sodium channel blockers?

A

local anesthetics
psychiatric drugs
SNRIs

72
Q

what are local anesthetics?

A

lidocaine
bupivacaine
benzocaine: esters gave higher allergy risk

73
Q

what are the sodium channel blockers that psychiatric drugs?

A

anticonvulsants: lamotrigine, carbamazepine
TCA: amitriptyline and nortriptyline

74
Q

what are sodium channel blockers with SNRI function?

A

SNRIs increase NE and can act on A2 receptors to provide analgesia
duloxetine and venlafaxine
milnacipran does not have Na channel function

75
Q

what are Ca channel blockers?

A

gabapentin and pregabalin
Cav1,2 selective
not metabolized
no drug-drug interactions

76
Q

what is schedule 1?

A

no medical use
high abuse potential
marijuana, THC, LSD

77
Q

what is a C2?

A

high abuse potential
has medical use
morphine, cocaine, PCP, opioids

78
Q

what is C3?

A

medical use
moderate abuse
ketamine, buprenorphine, marinol

79
Q

what is the MOA of cocaine and amphetamines?

A

block DAT which causes an efflux of DA into the synapse
results in accumulation of DA

80
Q

what are substances that act on ion channels? and what receptors?

A

nicotine: ionotropic acetylcholine receptor agonist
PCP/ketamine: ionotropic NMDA receptor antagonist
BZD,BARB: GABAa PAM

81
Q

what is the DA hypothesis of addiction?

A

pleasurable events release DA
DA is important for assigning value to reward prediction

82
Q

what are limits of DA hypothesis?

A

DA is not required for reward learning
DA does not cause liking, is only a predictor of outcome

83
Q

what is the glutamate hypothesis of addiction?

A

Glutamate can increase DA activity in Nuclues accumbens
DA controls glutamate activity in amygdala

84
Q

why does drug use induce long term changes to neuronal plasticity?

A

Rewarding substances cause increases in glutamatergic AMPA receptors

85
Q

What is physical dependence?

A

the body needs more drug and has built tolerance
body withdrawals w/o drug

86
Q

what is psychological dependence?

A

mental urge to take drug to function
craving even without withdrawals

87
Q

what are the types of withdrawal symptoms?

A

emotional
physical: goose bumps
dangerous: alcohol and tranquilizers, grand mal seizures, delirium tremens

88
Q

substance use disoder criteria

A

mild 2-3
mod 4-5
severe 6+

89
Q

what is drug reward and its relation to postive or negative reinforcement?

A

Drug is rewarding and produces positive reinforcement
Negative reinforcement: reward by escaping negative stimulus or event

PHRM 845 (9 decks)

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