Pain Management Flashcards
Define Algesia
Increased sensitivity to pain
Define Alogenic
Pain producing
Define Allodynia
A normally non-harmful stimulus is perceived as painful
Define Analgesia
The absence of pain in the presence of a normally painful stimulus
Define Dysethesia
An unpleasant painful abnormal sensation, whether evoked or spontaneous
Define Hyperalgesia
A heightened response to a normally painful stimulus
Define Neuralgia
Pain in the distribution of peripheral nerves
Define Neuropathy
An abnormal disturbance in the function of nerves
Define Paresthesia
An abnormal sensation, whether spontaneous or evoked
What is acute pain?
- unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
- <1 month
What is chronic pain?
- Persistent pain associated with a distinct period of uninterrupted pain f 3 months or more, that includes negative sensory and emotional experiences
- > 3 months
What is considered nociceptive pain?
Stimulus of specific nociceptors
- somatic
- visceral
What is considered non-nociceptive pain?
- neuropathic
- inflammatory
What occurs with somatic pain?
- identifiable focus
- tissue damage
- chemical release modulates pain
- Well localized area, sharp, hurts at area
What occurs with visceral pain?
- diffuse, referred
- dull, cramping, squeezing
- Example: distention of organ capsule, obstruction of hollow viscous
- associated with autonomic reflexes such as N/V, diarrhea
What occurs with neuropathic pain?
- Damage to peripheral or central neural structures resulting in abnormal processing of painful stimuli
- dysfunction of CNS
- Burning, tingling shock-like
What occurs with inflammatory pain?
- sensitization of the nociceptive pathway from multiple mediators
What is transduction?
The transformation of noxious stimulus (chemical, mechanical, thermal) into an action potential
Explain the A-delta fibers
Fast, sharp pain
6-30m/sec
Reflex alert
Explain the C-fibers
Slow
0.6-2m/sec
Dull, burning, throbbing, aching
What are the chemicals released during transduction?
- substance P
- glutamate
- bradykinin
- histamine
- serotonin
- prostaglandins
- cytokines
- calcitonin gene
What happens with the release of Substance P?
- C fibers (slow chronic pain)
- G protein linked neurokinin-1 receptor
- vasodilation, extravasation of plasma proteins, degranulation of mast cells, sensitization of stimulated sensory nerve
- *inflammation and algesia
What happens with the release of Glutamate?
- CNS, A-delta and C fibers
- instantaneous effect, fast sharp pain
What happens with the release of Bradykinin?
- peptic algesic
- Direct stimulating effect on peripheral nociceptors via bradykinin receptors
What happens with the release of Histamine?
- Amine released from mast cells, basophils and platelets—> via Substance P
- edema and vasodilation
What happens with the release of Serotonin (5-hydroxytryptamine) [5-HT]?
- Amine stored and released from platelets after tissue injury
- Algesic
What happens with the release of Prostaglandins, thromboxanes and leukotrienes?
- made from COX-1 and COX-2
- Hyperalgesia
What happens with the release of Cytokines?
- released in response to tissue injury
* * increase production of prostaglandins—> HYPERalgesia
What happens with the release of Calcitonin gene-related peptide (CGRP)?
- peptide released from C fibers (afferent)
- causes local cutaneous vasodilation, plasma extravasation and sensitization
What happens during transmission?
- Action potential is conducted from periphery to CNS
- multiple pathways ( ex: spinothalmic (anterolateral) tract)
What happens during perception?
- occurs once signal is recognized by various areas of the brain
- amygdala, somatosensory areas of cortex, hypothalamus, anterior cingulate cortex
What happens during modulation?
- altering neural afferent activity along pathway:
Can either: - suppress (inhibitory)
- enhance (excitatory)- mostly excitatory via substance P
What are the inhibitatory neurotransmitters and which receptors do they work on?
- Glycine —> Chloride linked (GlyR)
- GABA—> GABAa, GABAb, GABAc
- Enkaphalin—> mu, delta, kappa
- Serotonin—> 5-HT
- Norepinephrine—> alpha 2
What do NSAIDs do?
Treat mild to moderate post-op pain
- anti-infammatory, antipyretic, and analgesic properties
- inhibit COX —> thereby stop conversion of arachidonic acid to prostaglandin
What does Ketorolac (Toradol) do?
- Non-selective COX inhibitor
- 30mg IM equivalent to 12 mg morphine IM
- do NOT give longer than 5 days
What are contraindications for Toradol?
- coagulopathies
- renal failure
- active P.U.D./GIB
- history of asthma
- hypersensitivity to NSAIDS
- surgery with high potential for post-op bleeding
What does Acetaminophen do?
- decreases prostaglandin synthesis
- analgesic, anti-pyretic, and minimally anti-inflammatory
- contraindication—> liver failure
What do NMDA antagonists do?
Ketamine:
- prevents activation of NMDA receptor
- NMDA is associated with “wind up”
What do alpha 2 agonists do?
Clonidine and Precedex:
- interact with G protein coupled and 2 receptors, centrally and peripherally
- inhibit adenyl Cyclades and decrease cAMP
- activate post-synaptic K+ channels and inhibit presynaptice Ca+ channels which decrease neurotransmitter release
What do opioids do?
Bind to and activate G protein coupled receptors in periphery and CNS
- CNS: opioid receptors in dorsal horn, specifically REXED LAMINA II (substantiated gelatinosa), periaqueductal grey, medial thalamus, amygdala, lambic system
- Peripheral: afferent sensory fibers, GI tract, lungs, joints
What medications are used for acute pain in chronic pain patients?
- anti-convulsants
- anti-depressants
- corticosteroids
- methadone
What do anti-convulsants do?
Gabapentin (neurontin) and pregabalin (Lyrica):
- neuropathic pain syndromes
- inhibit neuronal excitation and stabilize nerve membranes
- should continue on the day of surgery
What do anti-depressants do?
- block re-uptake of serotonin and norepinephrine, thus increasing availability
- should continue
What do corticosteroids do?
- anti-inflammatory:
Decrease cytokines and prostaglandin release - continue, possible stress dose
What does methadone do?
- synthetic opioid, NMDA, opioid receptor action
- continue * does have opioid effect
When the source of pain cannot be identified we call it ________________.
Fibromyalgia
What are the 3 heuristic subdivisions of painful stimuli?
- ) painful stimulation without tissue damage
- withdrawal from stimulation, stop damage
- local event - ) tissue damage without nerve damage
- pain persists after withdrawal, intensified response to tactile stimulation, sensation of pain will spread, release of response mediators - ) nerve damage
- direct damage to nerve
- can be demyelinating, or axonal
What are the 3 anatomic regions associated with pain?
- peripheral
- spinal
- cerebral
What are the goals in treating chronic pain?
- must address the source
- the dysfunctional inhibitory mechanism in the peripheral or spinal nervous system
- address the dysfunctional pain perception in the cerebrum
What are the 3 types of chronic pain?
- psychogenic
- inflammatory
- neuropathic
What is psychogenic chronic pain?
Term falling out of favor
Unable to validate or find source
What is inflammatory pain?
- tissue damage resulting in pain and release of inflammatory mediators
- produce capillary vasodilation, smooth muscle contraction and promote synaptic transmission of pain implement to CNS (histamine, bradykinin, substance P)
T/F Substance P and substance P receptors are specifically associated with inflammatory pain and are diminished or absence in neuropathic and cancer pain
TRUE
What is neuropathic pain?
- nerves damaged, pain radiates along dermatome
- commonly leads to allodynia (painful stimuli that is normally not painful)
- differs from inflammatory pain—> persistent allydonia is not managed well with NSAIDS
What is wind up?
- cyclic response to pain that leads to abnormal pain response
- pts often labeled as drug seekers
