Pain management Flashcards
What is the physiology of processing pain
- Pain sensation STARTS w/ stimulation of nociceptors
- Receptors are in somatic and visceral structures, and help discriminate noxious from innocuous stimuli
- Nociceptors are activated by mechanical, thermal, or chemical stimuli
- Noxious stimuli may activate cytokines or chemokines that activate/sensitize nociceptors
What are the steps in processing pain
- Transduction: stimulation of nociceptors by mechanical, thermal, or physical stimuli
- Conduction: receptor activation causes AP along afferent fibers (large myelinated or small unmyelinated) to spinal cord.
- Transmission: Nociceptive fibers synapse in dorsal horn and release excitatory NT, while spinothalamic tract brings signal to higher brain structures
- Perception: you experience pain when signals reach higher cortical structures
- Modulation: Glutamate, substance P, endogenous opioids, GABA, NE, and serotonin can modulate pain
What is maladaptive pain
Pathophysiologic pain resulting from damage or abn fxn of nerves in CNS or PNS. Pain circuits rewire themselves anatomically and biochemically= chronic pain, hyperalgesia, or allodynia
Examples of maladaptive pain are
postherpetic neuralgia diabetic neuropathy fibromyalgia IBS chronic headaches
Explain Somatic pain
arise from skin, bone, joint, muscle, or connective tissue
Pain presents as throbbing and well localized
Explain visceral pain
arise from internal organs (colon, pancreas, etc.)
Manifests as pain coming from other structures (referred pain) or as a more localized phenomenon
During stimulation of nociceptors, noxious stimuli may lead to release of
Bradykinins H+ and K+ ions Prostaglandins Histamine Interleukins TNF-a Serotonin Substance P
What kind of pain do different size fibers transmit
Large, myelinated A fibers: sharp, localized pain
Small, unmyelinated C fibers: dull, aching, poorly localized pain
What is the endogenous opiate system
consists of NT like enkephalins, dynorphins, and endorphins
Receptors mu, delta, kappa found throughout the CNS
Where are NMDA receptors found
in the dorsal horn
They can increase the receptors responsiveness to opiates
What is the descending system for control of pain transmission in the CNS
a system that originates in the brain and can inhibit synaptic pain transmission at dorsal horn
NT include endogenous opioids, serotonin, NE, and GABA
What cognitive and behavioral functions can decrease pain
Relaxation
Distraction
meditation
guided mental imagery
What can worsen pain
depression and anxiety
What is inflammatory pain
Body shifting from preventing tissue damage to promoting healing
Pain threshold is reduced and the injured area becomes more sensitive
What does adaptive inflammation do
decreases our contact with and movement of injured area, promoting healing
Increased excitability or responsiveness of neurons in CNS (central sensitization)
Central sensitization is a major cause of
hypersensitivity to pain after injury
What is neuropathic vs functional pain
Neuropathic: result of nerve damage (post-herpetic neuralgia, diabetic neuropathy
Functional: abnormal operation of nervous system (fibromyalgia, IBS, HA)
-both are types of maladaptive pain!
How do patients describe neuropathic and functional pain
burning, tingling, shock like, or shooting
hyperalgesia (exaggerated pain response to normal noxious stimuli)
allodynia (pain response to normally non-noxious stimuli)
-Explains why this type of pain manifests long after actual nerve related injury is identified
What are some etiologies of cancer pain
The disease itself: tumor invasion, organ obstruction
Treatment: chemo, radiation, surgical incisions
Dx procedures: biopsy
Non-pharm therapies for acute and chronic pain are
physical manipulation
heat or cold application
massage
exercise
Transcutaneous electrical nerve stimulation (surgical, traumatic, neuropathy, and MSK pain)
Cognitive, behavioral, and social aspects of pain Tx
Pain is…
subjective
best diagnosed based on patient description, H&P
How can you obtain a baseline pain description
PPQRSTl
Palliative (what makes it better)
Provocative factors (what makes it worse)
Quality (describe the pain)
Radiation (and location)
Severity (how does it compare to other pain you’ve felt)
Temporal (intensity change with time)
Describe acute pain
- Not usually dependent or tolerant to medication
- No psych component, depression, or insomnia (usually)
- Tx goal is pain reduction
- Usually has identifiable cause
Describe chronic pain
- Usually dependent or tolerant to meds
- Psych often a major problem (depression common)
- Significant family issues
- Usually no identifiable cause
- Tx goal is functionality
How do infants present with acute pain
change in feeding habits
increased agitation
calling out
Sx of acute distress are
sharp, dull, shock like, tingling, shooting, radiating, fluctuating intensity, varying location
Occur in a timely relationship with obvious noxious stimuli
Signs of acute pain are
HTN tachycardia diaphoresis mydriasis pallor (signs are NOT diagnostic; sometimes there aren't even obvious physical signs of pain)
What must you pay attention to in chronic pain
mental and emotional factors that alter pain threshold; people can appear to have no noticeable suffering
Symptoms of chronic pain are
sharp, dull, shock-like, tingling, shooting, radiating, fluctuating in intensity, and varying in location
occur withOUT a temporal relationship with a noxious stimuli
Over time, pain stimulus may cause Sx to change (sharp to dull, obvious to vague)
Signs of chronic pain are
Most cases, no obvious signs
But they DO have comorbid conditions!
Outcome of Tx is not predictable (where as it IS predictable in acute pain)
What non-opioid analgesics can be used to alleviate pain
ASA: stop 7-10 days before surgery
Choline and mag trisalicylate: no anti-platelet function bc no acetyl group (750 q8hr for old)
Diflusinal: no acetyl group
APAP: 2g max for old, 3g max for gen pop. <50kg, 750mg max single dose
More nonopioid analgesics (used less) are
Anthranilic acid (Mefenamic acid): max 7 days Indolacetic acid (Etodolac)
Non-opioid analgesics approved for adults are
- Phenylacetic acids: Diclofenac potassium, D. epolamine (patch over intact skin), D. sodium (voltaren gel)
- Propionic acid: Ibuprofen (max 3.2g inflamm, 1.2g analgesia/fever), Ketoprofen, Naproxen (OA), Naproxen sodium (acute pain)
What are pyrrolacetic acids
Ketorolac! Max 5 days
parenteral
oral: only use if continuation of parenteral
nasal: old or <50kg, one spray in one nostril q6-8 hrs
What is the selective cox-2 inhibitor
Celecoxib
if cardiac concern, max 200mg x day
(use ASA before Celecoxib)
What do you need to monitor when taking NSAIDs
upper GI bleed: CBC, stool guaiac
acute renal failure: SrCr
What do you need to monitor when taking APAP
Hepatotoxicity: ALT/AST, PT/INR, albumin, APAP serum concentration
NSAIDS, APAP, and ASA are used in
mild to moderate pain
Can be used with opioid agents
NO alcohol with APAP
avoid OD when combining with products that low key include them already