Term
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Definition
Response to acute stimulus that damages tissues.
Recognizes: injury, inflammation, cancer
Unrecognized: trigeminal neuralgia, peripheral neuropathy, chronic pain |
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Term
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Definition
Nociceptive: localized, stabbing, aching
Neuropathic: regional, burning, tingling
Psychogenic: pain that is caused increased or prolonged by mental, emotional or behavioral factors. |
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Term
| Nociceptive Afferent Neurons |
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Definition
Unmyelinated C fibers and finely myelinated A delta fibers w/sensory endings in tissue.
A Delta: produces sharp, intense well localized discomfort
C fiber: dull burning diffuse pain
NOCICEPTIVE AFFERENTS are stimulated by Mechanical, Thermal or Chemical stimuli |
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Term
| Important Excitatory Transmitters for Pain (Afferent Nociceptive Neurons) |
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Definition
Substance P: slow depolarizing response in postsynaptic cell. Leads to Ca influx and activates NO synthesis. Acts peripherally producing inflammation.
Nitric Oxide (NO): enhances pain perception and transmission by unknown mechanisms. |
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Term
| Substance P and Neurokinin A (NKA) |
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Definition
| Released from central and peripheral nerve terminals. Trigger inflammatory response. Responses vary; smooth muscle (GI, bronchials) constriction, blood vessels constrict/dilate and increased permeability leading to edema. |
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Term
| Other transmitters for pain |
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Definition
Bradykinin: response to tissue injury. inflammatory mediator, sensitizing nociceptor peripheral terminals reducing pain threshold. ENHANCED by prostaglandin E and F
Prostaglandin E & F: released during inflammatory states and ischemia. do not cause pain, just enhance pain effects of other chemicals.
**Aspirin-type drugs inhibit prostaglandins and decrease pain
Histamine, lactic acid, and K+ |
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Term
| Centrally Acting Neurotransmitters of Pain |
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Definition
Glutamate - involved in fast synaptic transmission
GABA - released by interneurons, inhibiting some excitatory impulses @ dorsal horn, **interrupt ascending pain impulses
Norepinephrine, ATP, Serotonin |
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Term
| Opiate and Opioid Peptides |
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Definition
| Opioid: any substance that produces morphine-like effects that are blocked by morphine antagonist naloxone. |
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Term
| Opiates vs Opioid Peptides |
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Definition
Opiates: naturally occurring opioids in plants
Opioid Peptides: endorphins and enkephalins found in humans
- B-endorphin
- Met-encephalin - modulate ascending pain impulses
- Leu-encphalin - modulate ascending pain impulses
- Dynorphin - mainly in interneurons
- Nocicephin - produces pain |
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Term
| Opiate Receptors (refer to table in assignment 3) |
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Definition
Mediate pharmacologic action of opiates. Centrally and peripherally located.
**G-protein linked:
K+ channels open (increased influx of K+), leads to decrease Ca2+ influx, DECREASING SUBSTANCE P AND GLUTAMATE |
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Term
| M.O.R.P.H.I.N.E.S. Mnemonic |
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Definition
Miosis (pin point pupil)
Orthostatic hypotension
Respiratory depression
Physical dependency
Histamine release
Increased ICP (intracranial pressure)
Nausea
Euphoria
Sedation |
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Term
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Definition
Treatment of choice for severe pain
Decrease calcium influx @ presynaptic terminal of noci C and A delta fibers.
**prevents substance P and glutamate release. Increase K+ influx, hyperpolarization and decrease nerve transmition. Inhibits GABAergic transmission in brain. |
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Term
| Opioid Analgesic Classification |
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Definition
Strength of interaction with receptor (typically mu "mew")
Receptor category
- agonist - agonist/antagonist
- partial agonist
Chemically
Regulatory - DEA |
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Term
| Strong Opioid Agonist Meds |
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Definition
Morphine (Duramorph)
Fentanyl (Sublimaze)
Hydromorphone (Dilaudid)
Meperidine (Demerol)
Methadone (Dolophine)
Oxycodone (Percocet, OxyContin)
Hydrocodone (Vicodin, Lortab) |
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Term
| Strong Opioid Agonist MOA |
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Definition
Strong affinity for Mu receptors, less for delta or kappa.
Similar pharmacodynamics effects.
Differ in analgesic potency and pharmacokinetics.
Some combine with non-opioid analgesics for additive effect. |
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Term
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Definition
#1 Fentanyl
Diamorphine (heroin)
Hydromorphone
Levorphanol
Morphine |
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Term
Strong Opioid Agonists
Morphine |
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Definition
| Potent metabolite, can develop tolerance with repeated use. |
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Term
Strong Opioid Agonists
Fentanyl |
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Definition
Much more potent than morphine
**Transdermal patch, heat increases drug delivery from patch |
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Term
Strong Opioid Agonists
Methadone |
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Definition
Potent as morphine but longer duration of action. Inactive metabolites allow for analgesia to wear off b4 physical withdrawal develops.
**used for opioid addiction pts to assist w/withdrawal process. Taper doses. LONG TERM not favorable, cardiomyopathy risk. |
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Term
Strong Opioid Agonists
Hydrocodone/oxycodone |
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Definition
Acetaminophen component blah blah blah
hydro = Vicodin
oxy = Percocet |
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Term
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Definition
For moderate/mild pain
Codeine (also has acetaminophen combo)
- virtually no pain relieving activity; used for antitussive. cross-sensitivity w/morphine allergies
Tramadol " "
Tapentadol |
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Term
Opioid Agonists-Antagonists
(partial mixed agonists) |
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Definition
Interact with kappa and delta receptors, also partially with mu receptors.
*used in patients that cannot tolerate morphine's effects
*Butorphanol (Stadol) - injection, nasal spray
*Nalbuphine (Nubain) - injection
Tramadol/Tapentadol
All have less abuse potential |
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Term
Opioid Agonists-Antagonists
Tramadol/Tapentadol |
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Definition
Tramadol (Ultram)/ Tapentadol (Nucynta)
- less abuse potential
- has acetaminophen
- mu and kappa receptor agonist
norepinephrine and serotonin reuptake, so caution with other drugs affecting serotonin/norepinephrine such as
Antidepressants |
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Term
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Definition
Reverses respiratory depression nd coma in opioid overdose.
Competitive antagonist for all receptors but highest affinity for mu.
IV
Produces withdrawal in those physically dependent, but not healthy pts. |
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Term
| Adverse Effects of Opioids |
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Definition
CNS: miosis, rigidity, nausea/vom, euphoria, sedation/drowsy/depression, impaired reasoning, respiratory depression.
Peripheral: constipation, urinary retention, biliary colic, bronchoconstriction, rash/itch
Other: hyperthermia (mu agonist); hypothermia (kappa agonist), hypotension |
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Term
| CNS Adverse Effects of Opioids |
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Definition
Respiratory depression - occurs at usual doses (depressed response to CO2)
Cough suppression
Miosis - reddened eyes from cerebral vessel dilation
Nausea/vomiting
Truncal rididity |
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Term
| Peripheral ADE's of Opioids |
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Definition
Constipation, urinary retention, bronchospasm
Biliary colic
Rash |
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Term
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Definition
Immunosuppression
Hormones:
- decrease in cortisol, FSH, testosterone and estrogen
-- decreased libido, increased aggression, amenorrhea, galactorrhea |
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Term
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Definition
Symptoms peak after 24-72 hrs after last dose.
- anxiety irritability
- chills/hot flashes, runny nose
- diarrhea, stomach cramps
- insomnia, yawning
- sweating/shivering, tachycardia
- nausea and vomiting |
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Term
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Definition
Elderly pts who may fall
Pts prone to pneumonia
Rash/hypersensitivity
AIDS patients w/suppressed immunity
Children
Abuse/dependence tendencies and family theft issues |
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Term
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Definition
PT must be prepared for ADR in patients who recently start opioids: drowsiness/dizinness/impaired cognition. Tolerance develops with many Sx's but miosis, and constipation are long lasting.
General precautions for patients:
- avoid driving or using machinery
- increased fall risk
- unsteady gait (use railings): getting up and down, quick movements
- impaired cognition. no important decisions.
**Patches: AVOID HEAT and certain types of imaging.
Schedule therapy when opioid will reach peak analgesic action.
**Impaired ability of pt to report pain, and respiratory depression should be considered with exercise program.
Respiratory: watch respirations, skin color, exertion level. |
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Term
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Definition
Many drugs in this class.
fen, enac or xen generic name
OTC or Rx for MUSCULOSKELETAL PAIN/INJURY, OR Tx OF INFLAMMATORY CONDITION (RA)
MOA: most work by blocking prostaglandin synthesis |
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Term
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Definition
In nearly every tissue
Released w/injury, inflammation, or tumor
Several types (A-F, H & I). Derived from fatty acids.
Acted on by COX |
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Term
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Definition
| Vasodilation. vasodilation or constriction of bronchioles. Platelet aggregation. PAIN PRODUCTION. Increase CO and capillary permeability. increase body temp. |
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Term
| Cycloosygenase (COX) Enzyme System |
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Definition
2 isoforms of COX enzyme
Cox-1: platelets, kidneys, stomach
Cox-2: synoviocytes, endothelial cells, macrophages
**NSAIDS are COX inhibitors
Selective
- Celecoxib (Celebrex)
Non-selective
- Aspirin, ibuprofen, naproxen |
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Term
| Aspirin (acetylsalicylic acid) |
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Definition
Widely used analgesic, antipyretic and anti-inflammatory
Blocks PG synth by irreversibly blocking COX-1 and 2
Benefits: raises body temp, decrease synth of PG's that sensitize nociceptors, and block PG-induced vascular permeability.
**Increased bleeding time so be alert of bleeding/bruising |
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Term
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Definition
GI problems: blocking cox-1 affects PGI2, leading to discomfort, bleeding, hemorrhage, ulcers.
Renal: blocks PG's that lead to decrease excretion of electrolytes, increasing water retention leading to HTN.
Can also get diarrhea, nausea, vom |
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Term
| NSAIDs (nonselective cox inhibitors) |
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Definition
| More potent than aspirin, vary in effects. Not cardioprotective like aspirin. Mixed tolerances to adverse effects. |
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Term
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Definition
COX-2 induced by inflammation or surgery.
Do not cause renal and GI complications like other NSAIDs and Aspirin.
No antithrombic effects (good post op)
Improve ROM in patients after orthopedic surgery |
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Term
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Definition
| Chronic use negatively affects satellite cells crucial for hypertrophy and strengthening. Intermittent use is preferred. |
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Term
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Definition
Affect BP and BP meds
Increase risk of bleedin w/warfarin
Loss of cardio protection w/COX-2 inhibition.
Compete against aspirin, so timing of doses is important. |
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Term
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Definition
MOA: inhibits PG synthesis via COX-2, NO and substance P. Central and peripherally acting.
Standard for osteoarthritis.
Potential for liver toxicity. |
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Term
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Definition
Bruising, complaints of GI Sx Nausea/vom/diarrhea
Ask about timing of low dose aspirin w/other NSAIDs
Chronic acetaminophen effects
Need for increased meds after PT
Increased pain tolerance can lead to injury |
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Term
| Neuropathic Pain/Neuropathy |
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Definition
Associated w/disease or injury to PNS or CNS. (diabetes, immunodeficiency, ischemia, cancer, MS).
Sustained noxious input alters way body processes noxious stimuli.
Mediators are cytokines, PG's and leukotrienes, and neuropeptides (bradykinin substance P) |
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Term
| Clinical signs of neuropathic pain |
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Definition
Stimulus-independent pain:
- shooting pain, shock-like, aching
- crushing, burning, electrical shock-like
*all related to nerve compression
Stimulus-dependent
- mechanical, chemical, thermal
- hyperalgia, mechanical central pain from repetitive stimuli |
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Term
| Neuropathic Pain/Neuropathy cont.. |
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Definition
Multiple agents are often used.
1) Antidepressants
2) Anticonvulsants
and others like lidocaine |
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Term
| Cancer-related pain control |
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Definition
1st line: NSAIDS
2nd line: weak opioids
3rd line: strong opioids
require higher doses of opioids than normal.
Common regimen: long acting opioid + breakthrough meds (opioid/NSAIDs/APAP which is acetaminophens) + corticosteroids for inflammation. bisphosphonates for bone pain. |
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