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PHRM 845 > exam 5 pain > Flashcards

exam 5 pain Flashcards

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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
what is the postsynaptic activity of mu opioid receptors?
activate GIRK channel releases efflux of K+ that causes hyperpolarization
26
What are opioid induced side effects?
they are on target effects respiratory depression, constipation, addction, urinary retention, N/V, mioisis pruritus due to opioid inducing histamine receptors
27
would you use opioids as anti-diarrheal?
Yes, some opioids are formulated to specifically act on the Gi
28
what is the kappa opioid receptor?
dynorphins are the natural ligand activation causes dysphoric effects
29
why are kappa opioids thought to be less addictive?
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
30
are there any delta opioid receptor agonists approved?
none approved by FDA
31
what is the mechanism for opioids leading to addiction?
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
32
What are the pharmacokinetics of morphine and phenanthrenes?
they are readily absorbed go through first pass metabolism hepatic metabolism: CYP3A4 and CYP2D6 glomerular filtration
33
which opioids are pro drugs?
heroin, codeine, tramadol
34
which opioids do not produce active metabolites?
methadone and fentanyl
35
Which drugs are metabolized by CYP3A4?
drugs beginning with NOR are created from 3A4 nor metabolites are deactivated and less active
36
What is the plasma concentration of an UM taking a prodrug?
increased plasma concentrations higher ADRs
37
what is the plasma concentration of a PM taking a a prodrug?
no therapeutic effect
38
what is fentanyl's potency?
very potent 100x morphine 50x heroin
39
what are the opioids related to fentanyl?
Sufentanil, remifentanil, alfentanil used for anesthesia and sedation breakdown by plasma esterases due to ester linkage
40
what are the common opioids?
hydromorphone: no active metabolites morphine hydrocodone oxycodone
41
what are the non-phenanthrene opioids?
tramadol, meperidine, methadone
42
what is tramadol?
has SNRI properties mild opiate analgesic
43
what is meperidine?
used to treat rigors (shivering) not recommended
44
what is methadone?
used for opioid dependence pronlonged QTc NMDA antagonist to also reduce pain signal
45
what are other clinically used opioids that are non analgesic?
cough/antitussive: codeine and dextromethorphan anti-diarrheal: loperamide and lomotil
46
what is bupennorphine?
partial mu agonist weak K and delta agonist used for opiod replacement therapy
47
what are medications used for constipation?
senna: irritates colon to force contraction PEG dioctyl sodium
48
how is methadone used for opioid dependence?
Full mu receptor agonist Slow acting Accumulation with repeated dose NMDA antagonist
49
how is buprenorphine used for opioid dependence?
Mu opioid partial agonist Blocks full agonist effect of heroin and oxycodone Provides some activation Subutex has abuse potential
50
how is naltrexone used for opioid dependence?
antagonist will cause withdrawal due to antagonism decent oral bioavailability
51
what is the difference between naloxone and naltrexone?
naltrexone is orally administered and has medium half life naxolone has limited oral bioavailability and a short half-life
52
what is Naloxone?
Limited oral bioavailability Short half life Rapid onset Repeated every 2-5 minutes if not concoius
53
what is neonatal abstinence syndrome?
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
what is the treatment of neonatal abstinence syndrome?
Nonpharm: swaddling, hypercaloric formula, frequent feedings, rehydration Pharm: Morphine, SL buprenorphine, methadone, clonidine can be useful
55
what are the uses of NSAIDs?
Analgesia: chornic pain, myalgias, inflammation Anti-inflammatory: bursitis, tendonitis, OA, RA, gout Antipyretic ASA to reduce risk of MI
56
What are three phases of inflammation?
Acute: vasodilation --> increased permeability Subacute: infiltration of neutrophil Chronic: proliferation
57
what are eicosanoids?
arachidonic acid metabolites
58
what is NSAID mechanism?
inhibit COX in AA pathway decreases in TXA, PGE, PGI PGI protects stomach lining --> why NSAIDs can cause upset stomach/ulcers
59
Which NSAID is irreversible?
aspirin
60
what are the therapuetics of aspirin?
prophylaxis for anticoagulation no tolerance development to analgesic effects risk of reyes syndrome in children
61
what is aspirin poisoning?
mild effects: vertigo and tinnitus CNS effects: respiratory alkalosis and metabolic acidosis
62
what is the treatment of aspirin poisoning?
reduce salicylate dextrose and sodium bicarbonate to trap and excrete
63
what are arylproprionic acids NSAIDs?
potent reversible COX inhibitors ibuprofen 2hr t1/2 naproxen 14hr 1/2
64
what are arylacetic acid derivatives?
diclofenac: can be gel, increased risk peptic ulcer indomethacin: potnet reversible inhibitors of PG biosynthesis, high side effects sulindac: less toxic derivative indomethacin
65
what are enolic acids?
meloxicam and piroxicam reversible competitive inhibitors meloxicam low doses is Cox2 selective
66
what are the ADRs of NSAIDs?
renal function: inhibitrs PGE2 synthesis so water retention and edema bleed risk inhibits uterine motility
67
what are NSAID CIs?
Avoid: CKD, PUD, hx GI bleed CV risk Interfere with wound healing Asthma exacerabtions
68
What are the therapuetic uses of APAP?
highly effective analgesic and antipyretic no GI toxicity overdose can cause hepatic necrosis
69
what are ADRs of APAP?
more renal toxicity than ASA + NSAIDs dose dependent necrosis increase in toxic metabolites NAPQI
70
why are COX 2 not used anymore?
they had reduce ulcer risk and GI bleeds but are no longer used due to risk of clots, stroke, and heart attacks
71
what are functions of sodium channel blockers?
local anesthetics psychiatric drugs SNRIs
72
what are local anesthetics?
lidocaine bupivacaine benzocaine: esters gave higher allergy risk
73
what are the sodium channel blockers that psychiatric drugs?
anticonvulsants: lamotrigine, carbamazepine TCA: amitriptyline and nortriptyline
74
what are sodium channel blockers with SNRI function?
SNRIs increase NE and can act on A2 receptors to provide analgesia duloxetine and venlafaxine milnacipran does not have Na channel function
75
what are Ca channel blockers?
gabapentin and pregabalin Cav1,2 selective not metabolized no drug-drug interactions
76
what is schedule 1?
no medical use high abuse potential marijuana, THC, LSD
77
what is a C2?
high abuse potential has medical use morphine, cocaine, PCP, opioids
78
what is C3?
medical use moderate abuse ketamine, buprenorphine, marinol
79
what is the MOA of cocaine and amphetamines?
block DAT which causes an efflux of DA into the synapse results in accumulation of DA
80
what are substances that act on ion channels? and what receptors?
nicotine: ionotropic acetylcholine receptor agonist PCP/ketamine: ionotropic NMDA receptor antagonist BZD,BARB: GABAa PAM
81
what is the DA hypothesis of addiction?
pleasurable events release DA DA is important for assigning value to reward prediction
82
what are limits of DA hypothesis?
DA is not required for reward learning DA does not cause liking, is only a predictor of outcome
83
what is the glutamate hypothesis of addiction?
Glutamate can increase DA activity in Nuclues accumbens DA controls glutamate activity in amygdala
84
why does drug use induce long term changes to neuronal plasticity?
Rewarding substances cause increases in glutamatergic AMPA receptors
85
What is physical dependence?
the body needs more drug and has built tolerance body withdrawals w/o drug
86
what is psychological dependence?
mental urge to take drug to function craving even without withdrawals
87
what are the types of withdrawal symptoms?
emotional physical: goose bumps dangerous: alcohol and tranquilizers, grand mal seizures, delirium tremens
88
substance use disoder criteria
mild 2-3 mod 4-5 severe 6+
89
what is drug reward and its relation to postive or negative reinforcement?
Drug is rewarding and produces positive reinforcement Negative reinforcement: reward by escaping negative stimulus or event

PHRM 845 (9 decks)

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