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Pharmacology > Pain > Flashcards

Pain Flashcards

1
Q

Nociception Definition

A

-the physiological processes in response to a noxious stimulus

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2
Q

Allodynia Definition

A

-pain in response to a normally innocuous stimulus

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3
Q

Hyperalgesia Definition

A

-enhanced pain to a normally painful stimulus

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4
Q

What are 3 forms of pain?

A
  1. nociceptive
  2. inflammatory
  3. neuropathic
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5
Q

Draw the pain pathway

A

-opioids pain lecture

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6
Q

Referred Pain

A
  • pain from an area or organ that wasn’t initially damaged

- neighbouring sensory nerves sense the increased firing–> causes pain in areas adjacent to the joint

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7
Q

Opiate

A

-drugs derived from opium (morphine and codeine)

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8
Q

Opioid

A
  • agents with opiate like actions
  • synthetic drugs
  • proteins that mimic opiate actions (endorphins)
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9
Q

Narcotic

A
  • sleep inducing (pharmacological)

- drugs producing dependence (legal)

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10
Q

What are 3 properties of fentanyl?

A
  • highly selective mu opioid R agonist
  • long acting transdermal patch (peak effect=35 hr)
  • less nausea than morphine
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11
Q

What are 4 properties of Oxycodone?

A
  • semi-synthetic selective mu opioid R agonist
  • usually given with NSAID
  • sustained release oral formation (oxycontin, peak=3hrs)
  • drug of abuse (pill crushed and injected), crush proof tablet (oxecta)
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12
Q

What are the 4 opioid R subtypes and their actions?

A
  • mu
  • delta
  • kappa
  • ->inhibit neuronal depolarization
  • NOP–>neuronal depolarization
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13
Q

What are the endogenous ligands for each opioid R subtype?

A
  • mu-endomorphin
  • delta-enkephalin
  • kappa-dynorphin
  • NOP-nociceptin
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14
Q

What are the exogenous ligands for each opioid R subtype?

A
  • mu-morphine, codeine, heroin, fentanyl
  • delta-diprenorphine
  • kappa-etorphine
  • NOP-orphanin FQ
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15
Q

What are the opioid antagonists for each opioid R subtype?

A

mu-CTOP, DAMGO

  • delta-naltrindole
  • kappa-nor-BNI
  • NOP-nocistatin
  • naloxone is a non specific antagonist
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16
Q

What are the 4 sites of action of opioids

A
  1. periphery
  2. lamina II of dorsal horn (explain)
  3. supraspinal
  4. mesolimbic system
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17
Q

What causes up regulation of mu opioid Rs?

A

-acute inflammation
+MOR made in DRG
+axonal transportation of MORs +MOR in periphery & dorsal horn
+opioid analgesia

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18
Q

What are the 3 negative side effects of opioids?

A
  • severe constipation, somnolescence, cardio respiratory depression
  • tolerance
  • dependence
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19
Q

Explain opioid tolerance and its treatment

A

-increasing doses required to achieve therapeutic level
-minimized by start low and go slow
-occurs 2-3 weeks after frequent opioid use
Treatment
-rotation to another opioid
-recouple to a non opioid adjunct (e.g ketamine, cannabis)

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20
Q

Explain the mechanism of tolerance (GPCRKs)

A
  • arrestin binds and R is desensitized at surface

- arrestin bound Rs are internalized and recycled to cell surface OR degraded in lysosome

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21
Q

Explain physical dependence (physical abstinence syndrome)

A

Mild-lacrimation, sweating, yawning

severe-pain

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22
Q

Explain psychological dependence

A
  • compulsive drug seeking behaviour
  • occurs with drugs with mood enhancing properties
  • activates dopaminergic circuits
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23
Q

What is the treatment for dependence?

A
  • cessation of drug intake
  • naltrexone (opioid antagonist)
  • methadone (mu agonist, good oral availability, selective, long lasting/slow withdrawal)
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24
Q

Explain paradoxical opioid induced hyperalgesia

A
  • prolonged opioid use leads to an increase in pain
  • sensitization of peripheral nociceptors
  • sensitization of dorsal horn neurones
  • altered descending control mechanisms
  • glutamate R involvement–> coadminister glutamate antagonist
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25
Q

Polypharmacy with opioids

A
  • mu opioid Rs dimerize with CB1, opioid and cannabinoid have synergistic effect
  • opioid and low dose amphetamine (offset sedation)
  • opioid and antidepressant (useful for neuropathic pain)
26
Q

Future of opioid analgesia: peripherally restricted opioids

A
  • can target pain at the source
  • reduce sensitization of nociceptors
  • do not pass the BBB, less likely to cause addiction and centrally mediated side effects
27
Q

Future of opioid analgesia: Improve opioid R levels

A
  • inhibit beta arrestin activity-reduced R internalization
  • inhibit R degradation (protease inhibitors)
  • promote R recycling
28
Q

Describe prostaglandins

A
  • involved in causing inflammation and pain
  • produced by oxygenation of arachidonic acid in cell membranes
  • oxygenation occurs via COX1 and COX2
29
Q

Describe COX1

A
  • CONSTITUTIVELY EXPRESSED
  • found throughout the body
  • levels are relatively constant
  • involved in cell homeostasis
30
Q

Describe COX2

A
  • INDUCIBLE
  • found in inflamed tissue
  • present only transiently during inflammation or pain
  • short half life
  • promote inflammation and pain
31
Q

Draw the COX pathway

A

see NSAID lecture

32
Q

What are the physiological effects of prostaglandins on smooth muscle (2)?

A
  • vascular vasodilation

- GI contraction

33
Q

What are the physiological effects of prostaglandins on platelets (1)?

A

-aggregation, clotting responses

34
Q

What are the physiological effects of prostaglandins on kidneys (2)?

A
  • increases renin release

- increases glomerular filtration rate

35
Q

What are the physiological effects of prostaglandins on nervous system (2)?

A
  • peripheral sensitization

- central sensitization

36
Q

What are 4 types of NSAIDs?

A
  • acetlylsalicyclic acid (ASA) (anti platelet aggregation, shorter half life, less potent)
  • ibuprofen
  • naproxen
  • diclofenac
  • also non selective
37
Q

What are negative side effects of NSAIDs?

A

-prolonged use leads to GI damage and renal failure

38
Q

Explain the COX2 Hypothesis

A
  • COX2 inhibitors (Coxibs) would reduce inflammation induced prostaglandin production
  • preserve protective effects of COX1 pathway
39
Q

Why did the Coxib VIOXX fail?

A
  • it was too good at inhibiting COX2

- eg PGI2 is produced predominantly by COX2, causes vasodilation, platelet inhibition, protective of cardiomyocytes

40
Q

What are the recommendations for COX2 NSAID use?

A
  • patients at low risk of thrombotic events
  • prescribe lowest dose required to control symptoms (and maintain as long as possible)
  • add aspirin and a proton pump inhibitor to patients with increased risk of thrombotic events (aspirin for anti thrombotic effects, proton pump to prevent GI ulcerations)
41
Q

NSAID and opioid combinations

A
  • not possible to keep escalating NSAID dose, use in combo w/ opioid
  • FDA requires combination effect>individual components and NSAID>placebo
42
Q

What are the benefits of NSAID and opioid combinations (2)?

A
  • less propensity for opioid abuse

- highly effective analgesia while minimizing side effects of individual components

43
Q

Topical NSAIDs are primarily used for ? Benefits?

A

-arthritis pain
Benefits:
-target pain in the periphery, minimize centrally meditated side effects
-analgesia easily applied to superficial joints

44
Q

What are four topical NSAIDs approved by FDA?

A
  1. pennsaid
  2. solarez
  3. voltaren
  4. flector
    - contain diclofenac in differing concentrations
    - applied as either gel or patch
    - can produce local irritation due to vehicle
45
Q

What is the proposed mechanism of action of acetaminophen (5 steps)?

A
  1. deacetylated in the liver
  2. converted into endocannabinoid in the brain
  3. endocannabinoid can reduce pain at CB1 R
  4. endocannabinoid reinforces descending serotinergic pathway
  5. spinal release of 5HT inhibits pain transmission
46
Q

What are the benefits of acetaminophen (2)?

A
  • lacks side effects of ASA

- few drug interactions

47
Q

What are the adverse effects of acetaminophen (3)?

A
  • very few therefore safe up to 6g/day
  • overdose causes kidney necrosis and hepatotoxicity
  • hepatotoxicity may be potentiated in chronic alcoholics
48
Q

What are the 3 types of cannabinoids?

A
  • phytocannabinoids-derived from cannabis plant
  • synthetocannabinoids-man made
  • endocannabinoids-present naturally in the body (anandamide)
49
Q

What are the 2 cannabinoid Rs?

A
  • CB1, GPCR, located on peripheral and central nerves

- CB2, assoc. w/ immunocytes

50
Q

What is cannabis?

A
  • flowering plant
  • 3 species (sativa, indica, ruderalis)
  • oils secreted by trichomes of female plants
51
Q

What are the 3 sites of cannabinoid actions?

A
  1. peripheral nervous system-pain info no longer gets from the joint to the brain
  2. doral horn of the spinal cord
  3. supraspinal regions
52
Q

Describe cannabinoid actions at the spinal cord?

A
  • activation of CB1R on presynaptic terminal
  • inhibition of Ca flux
  • increased conductance of K ion channels, the neutron will hyper polarize making it more difficult to fire
  • decreased excitatory neurotransmitter release
53
Q

Draw the pathway for endocannabinoid degradation

A

-adjuncts pain lecture

54
Q

Prescription Cannabinoids-dronabinol

A

-synthetic THC
-oral capsule
approved for chemotherapy induced nausea, vomiting, anorexia associated with HIV AIDS

55
Q

Prescription Cannabinoids-Nabilone

A

-synthetic THC
-oral capsule
approved for chemotherapy induced nausea, vomiting, anorexia associated with HIV AIDS

56
Q

Prescription Cannabinoids-Nabiximols

A
  • oralmucosal spray
  • approved in canada for ms associated neuropathic pain, spasticity, advanced cancer pain
  • side effects-dry mouth, feelings of getting a little high
57
Q

Prescription Cannabinoids-herbal cannabis

A
  • various levels of CBs, terpenes, flavinoids
  • no formal approval
  • has to be heated to form chemical conversion
58
Q

Transient Receptor Potential Channels (TRPs)

A
  • named after the role of these channels in drosophila phototransduction
  • 6 families
  • molecular sensors of taste, temp and pain
59
Q

AMG517

A

-excellent TRPV1 antagonist candidate for treatment of inflammatory pain
oral bioavailability
-caused systemic TRPV1 blockade
-concentration dependent hypothermia

60
Q

Draw how capsaicin works on TRPV1

A

-adjuncts pain

61
Q

TRPM8

A
  • melastatin TRP family
  • non selective cation channel
  • expressed on 15% of small diameter sensory neurones
  • expression increases in models of neuropathic pain

Pharmacology (9 decks)

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