pain management Flashcards
Describe the classification schemes of pain relating to duration, intensity, and origin of the pain.
acute: short duration, resolves, Pain is directly related to the resolution or healing of tissue damage. Acute pain is primarily nociceptive - somatic more common than visceral. Chronic: longer duration, persists beyond normal healing time (neuropathic), related to chronic dz, wihtout identifiable cause or associated with cancer
severity intensity of pain
0 No pain,Relaxed, calm expression
1-2 Least pain, Stressed, tense, expression
3-4 Mild pain, Guarded movement, grimacing
5-6 Moderate pain, Moaning, restless
7-8 Severe pain, Crying out
9-10 Excruciating pain, Increased intensity of above0 No pain,Relaxed, calm expression
1-2 Least pain, Stressed, tense, expression
3-4 Mild pain, Guarded movement, grimacing
5-6 Moderate pain, Moaning, restless
7-8 Severe pain, Crying out
9-10 Excruciating pain, Increased intensity of above0 No pain,Relaxed, calm expression
1-2 Least pain, Stressed, tense, expression
3-4 Mild pain, Guarded movement, grimacing
5-6 Moderate pain, Moaning, restless
7-8 Severe pain, Crying out
9-10 Excruciating pain, Increased intensity of above
Compare and contrast the components of nociceptive pain vs neuropathic pain emphasizing those aspects that are most relevant to targeting pharmacotherapy.
Nociceptive: “Normal” pain resulting from activation of nociceptive nerve fibers. Can be somatic (skin, bone, joint, CT, muscle) or visceral. Neuropathic: persists and has become disengaged from noxious stimuli or the healing process. Result of nerve damage and abnormal operation of nervous system.
Nociceptive: “Normal” pain resulting from activation of nociceptive nerve fibers. Can be somatic (skin, bone, joint, CT, muscle) or visceral. Neuropathic: persists and has become disengaged from noxious stimuli or the healing process. Result of nerve damage and abnormal operation of nervous system.
Nociceptive: “Normal” pain resulting from activation of nociceptive nerve fibers. Can be somatic (skin, bone, joint, CT, muscle) or visceral. Neuropathic: persists and has become disengaged from noxious stimuli or the healing process. Result of nerve damage and abnormal operation of nervous system.
nociceptive pain is described as…
throbbing and well localized (somatic) or referred/ well localized (visceral)
neuropathic pain is described as…
burning, tingling, shock-like or shooting, with an exaggerated response to normal painful stimuli (hyperalgesia) and/or a painful response to normally nonnoxious stimuli (allodynia)
nociceptive pain is carried by what fibers
Ad and C fibers > DRG > synapsing at dorsal horn projection neurons > spinothalamic tract or spinobulbar tract > somatosensory cortex (location and intensity) or limbic system (emotional and motivational aspects) respectively
Peripheral sensitization
Tissue inflammation may change chemical environment at terminals of nociceptor. Damaged cells release-synthesize proinflammatory mediators that can directly activate the terminal and produce pain or render the terminal hypersensitive to subsequent stimuli.
central sensitization
NMDA receptor is central to the amplification of synaptic transfer from terminal to dorsal horn neurons. Initial sensitization is activity dependent, then later sustained by transcriptional changes (via COX-2, BDNF, substance P, NK1).
ectopic activity
Increased excitability of injured sensory neurons can generate pacemaker-like ectopic discharges that result in sensory inflow that is independent of any peripheral stimuli.
Principle of chronic pain management
mainly neuropathic pain: Non-opioid and adjuvant medications are emphasized. Long acting opiods may be required in some, and short acting opioids may be required for breakthrough pain
General mechanisms for managing chronic pain
Enhancement of Descending Inhibitory pathway, Decrease in Central Sensitization and Decrease in Peripheral Sensitization
Drugs used for Enhancement of Descending Inhibitory pathway in chronic pain
Activation of opioid receptors: opioid analgesics, tramadol. Block of NE-5HT reuptake: antidepressants-TCAD-SNRI-SSRI
Drugs used for Decrease in Central Sensitization in chronic pain
Block of VSCC: decrease excess NT release: anticonvulsants- gabapentin, pregabalin (a2d ligands). Block of NMDA-Glu receptors: ketamine. Block of Cyclooxygenase-2: NSAID, celecoxib, acetaminophen
drugs used to Decrease Peripheral Sensitization in chronic pain
Block of Voltage sensitive sodium channel: inhibit excess neurotransmission: local anesthetics- lidoacaine, anticonvulsants- carbamazepine, oxcarbazepine.
Common syndromes causing neuropathic pain
Diabetic nephropathy, Postherpetic neuralgia, Trigeminal neuralgia, Low back pain, Fibromyalgia, Irritable bowel syndrome
List adjuvant medications for chronic pain and syndromes they are used for
• TCADs (nortriptyline, desipramine): Diabetic neuropathy, migraine, low back pain, postherpetic neuralgia • SNRIs (duloxetine, venlafaxine, milnacipran): Fibromyalgia • Anticonvulsants (pregabalin): Spinal cord injury, trigeminal neuralgia, diabetic neuropathy • Local Anesthetic (topical): Post herpetic neuralgia, allodynia if pain localized
List non-opiod analgesics for chronic pain and syndromes they are used for
traditional NSAIDs, acetaminophen, COX-2 selective. Indicated for mild to moderate pain, particularly of somatic origin (soft tissue injury, strains, sprains, headaches, osteoarthritis, arthritis). For pain localized to specific joints, can try topical NSAIDs
Use of opioids in chronic pain
may be used for patients with acute neuropathic pain, neuropathic cancer pain, or episodic exacerbations of severe pain
management of mild (1-3) acute pain
Non-opioid (e.g., NSAID or acetaminophen) ± Adjuvant analgesics (useful, not classified as analgesics)
management of moderate (4-6) acute pain
Immediate-release, short-acting opioids with slow titration + Non-opioid (NSAIDs more effective) ± adjuvant analgesics
management of severe (7-10) acute pain
Immediate-release, short-acting opioids with rapid titration + Non-opioid ± adjuvant analgesics (most commonly LAs) Commonly managed with multimodal analgesia approach
Describe the mechanistic approach to multimodal management of acute pain.
Use of different classes of analgesics that act through different pathways. Opioid monotherapy is useful in postoperative pain and side effects limit practical efficacy. Benefits of combinding opioids with other agents: Greater analgesic efficacy from synergistic actions of agents with different mechanisms and Synergism between agents allows use of lower doses (“opioid-sparing”) limiting dose-related side effects
What are the available targets in multimodal analgesia
transduction: local anesthetics, anticonvulsants,
NSAIDs-COX-2 inhibitors. Transmission: local anesthetics, opioids. enhance descnding Modulation: opioids, NMDA antagonists, a2-agonists. Perception reaction: : opioids acetaminophen-NSAIDs-COX-2 inhibitors, anticonvulsants, α2-agonists, NMDA antagonists,transduction: local anesthetics, anticonvulsants,
NSAIDs-COX-2 inhibitors. Transmission: local anesthetics, opioids. enhance descnding Modulation: opioids, NMDA antagonists, a2-agonists. Perception reaction: : opioids acetaminophen-NSAIDs-COX-2 inhibitors, anticonvulsants, α2-agonists, NMDA antagonists,
Opioids -use in acute pain
Agonists at m-opioid receptors - modulate both transmission of pain (dorsal horn) and the perception - reaction to pain (cortex -limbic system). Opioids ar mainstay for moderate to severe acute pain
Opioids route of administration
For any given route, the more lipid-soluble opioids will have the more rapid onset of analgesia. IV is fastest, > neuraxial > transmucosal > IM > oral > transdermal
opioids onset/duration
Immediate release: most last 2-4hrs. Fentanyl – 0.5-1 hrs. Methadone – 6-8 hrs. Sustained release: Morphine (MS Contin®) to 8-24 hrs and oxycodone (OxyContin®) to 12 hours. Transdermal: Fentanyl (Duragesic®) to 48-72 hrs
Opioids nausea management
Nausea/vomiting- managed with antagonists( 5HT3: ondansetron, D2: metoclopramide-prochlorperazine, Muscarinic: scopolamine, decreased PG: dexamethasone, GABA: propofol)
Most serious acute side effect of opioids and management
respiratory dpression (Mu)- decrease in sensitivity of respiratory centers to CO2 that leads to a fall in the respiratory rate. Sedation precedes significant depression. Reverse with naloxone
sedation scale
5 = Wide awake, 4 = Drowsy, 3 = Sleeping but arousable, 2 = Difficult to arouse, 1 = Not able to arouse
opioid induced constipation management
Managed with stool softeners (docusate), stimulant laxatives (bisacodyl, senna), osmotic laxatives (Miralax®, milk of magnesia)
opioid induced pruritis management
Mast cells release histamine-H1 receptors. Managed with antihistamines (diphenhydramine) for systemic admin, or opioid partial agonist (nalbuphine) for neuraxial admin.
Mast cells release histamine-H1 receptors. Managed with antihistamines (diphenhydramine) for systemic admin, or opioid partial agonist (nalbuphine) for neuraxial admin.
How do local anesthetics work
Block voltage-sensitive sodium channels (VSSC) to interfere with nociceptive transmission
local anesthetic benefits, routes and side effects
Intense, prolonged analgesia: opioid sparing action with reduced potential for opioid-related side effects. Allows earlier ambulation:decreased potential for DVTs. Mobilizes secretions: better cough. Earlier return of bowel function. Routes: Neuraxial (epidural or spinal) infusion or peripheral nerve block. Side effects: Neurotoxicity, hypotension, dizziness, drowsiness
Differential nerve block- which fibers are affected first
Small fibers affected before larger fibers, If same size (diameter), myelinated fibers affected before unmyelinated. Sensory pain and postganglionic sympathetic neurons smallest. The faster the neuronal firing rate, greater the blocking effect (use dependent)
Describe which nerve functions are lost first to last with differential nerve block
Autonomic (SNS postganglionic [C fiber] to vessels)
Pain [C fiber > Aδ]
Note: Any dose of LA that causes loss of pain will cause loss of SNS vasoconstriction vasodilation
Cold > warmth > touch
Pressure > vibration > proprioception > motor. recovery happens in revers order
ketamine- action, benefits, routes, side effects
Block glutamate binding at NMDA receptors in the ascending pain pathway. Ketamine administration can reduce the development of tolerance to long-term opioid use. Routes: Administered as IV infusion and intranasal spray. Side effects: Suboptimal tolerability profile limits usefulness. Side effects include hypertension, diplopia, dizziness, arrhythmias, nausea-vomiting, psychotomimetic reactions
memantine- MOA
low-affinity non-competitive antagonist at Mg++ site in open NMDA channel and can block effects of tonic excessive glutamate in Alzheimer’s disease. However, a phasic burst of glutamate and depolarization will remove the low-affinity memantine and allow normal neurotransmission
alpha2- adrenergic agonists- MOA, examples, route, side effects
Action at postsynaptic α2 adrenergic receptors on dorsal horn neurons and in LC cells to modulate pain transmission. May decrease opioid requirements - generally reserved for severe intractable pain as adjunct to neuraxial opioids. Route: Epidural infusion
Side effects: Analgesic efficacy limited by potential for:
Hypotension, Bradycardia, Excessive sedation, Rebound hypertension upon withdrawal
NSAIDs and acetaminophen MOA in acute pain
COX-2 blockers
NSAIDs and acetaminophen side effects
NSAIDS: GI upset, bleeding, decreased renal function, decreased labor. Acetaminophen: hepatotoxicity only main concer, b/c it doesn’t act at COX-2 in periphery
caution with acetaminophen in opoiod combo
tolerance develops to analgesic effect but not to hepatotoxicity
