Module 3 - Post op Pain Flashcards by Unknown Unknown

Pain description

unpleasant sensory/emotional experience assoc with actual or potential tissue damage

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Pain transmission stages

Transduction
Transmission
Perception
Modulation

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Transduction

somatic & visceral receptors are stimulated by external stimuli –> convert stimulus into an electrochemical signal

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Transmission

a-delta & c-fibers generate action potentials that are transmitted towards the CNS

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Perception

cortex, limbic system, hypothalamus, reticular system involved in processing & sensation of pain

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Modulation

descending pathway

release of neurotransmitters at the dorsal horn to modulate pain sensation

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Complications of pain

PSR
shallow breathing, atelectasis, pneumonia
chronic pain
sleep disturbance
decreased appetite
impaired mobility & ADLs –> increased risk of pressure ulcers, DVT, PE

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Acute pain

<3-6 months
resolves with healing/removal of stimuli
protective purpose
activates SNS

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Chronic pain

> 3-6 months
pain lasts longer than recovery period
pathological
no SNS activation. psychosocial damages

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Types of pain

nociceptive

neuropathic

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Chemical mediators causing pain

prostaglandins
kinins
intracellular contents (potassium & hydrogen)

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Substance P

neuropeptide released by C-fibers

sensitize pain receptors –> decrease pain threshold

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Hyperalgesia

increased sensitivity to pain

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Neurogenic inflammation

substance p released by C-fibers
activates mast cells to rls histamine
histamine –> vasodilation increasing inflammation

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Allodynia

pain perceived in response to a non-painful stimulus

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Excitatory neurotransmitters

glutamate
substance P
norepinephrine
dopamine

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Inhibitory interneurons

loc near the dorsal horn

release GABA to inhibit 2nd order neurons

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Gate control theory

the dorsal horn acts as pain gate where incoming nerve impulses COMPETE to get through
increasing non-painful sensation can decrease pain by activating inhibitory interneurons

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Gate control pathway

nociceptors stimulated –> pain sensation
glutamate & substance P are released from axon terminal of nociceptors
2nd order neurons @ the dorsal horn excited & generate AP
pain gate is opened –> impulse proceeds to thalamus

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A-beta fibers

another type of sensory fiber that responds to non-painful stimuli

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Gate control modulation

A-beta fibers stimulate inhibitory interneurons at the dorsal horn –> release GABA –> hyperpolarizes 2nd order neuron (takes longer for 2nd order neuron to depolarize)
A-beta fibers travel via the MCL pathway. A-delta ascends the spinothalamic tract

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Serotonergic pathways

descending neurons rls serotonin

serotonin activate opioid-releasing interneurons

Endogenous opioids

enkephalins
endorphins
dynorphin

Modulation phsyiology

rls of serotonin activates opioid interneurons loc near the dorsal horn
opioids bind to receptors on the 2nd order neuron hyperpolarizing them & bind to nociceptors inhibiting rls of glutamate & substance p (excitatory neurotransmitters)

Where are opioid receptors most concentrated?

brainstem | regulate descending pathways

Opioids MOA

act at all steps of pain pathway | transmission, transduction, perception, modulation

Local anesthesia MOA

block Na+ channels --> inhibit production of APs blocking pain sensation (transduction & transmission)

NSAID MOA

inhibit production of PGs that sensitize nociceptors (transduction)

4 P's of pain management

Prevention Psychological Physical Pharmaceutical

Breakthrough pain

transient increase in pain

Multi-modal analgesia

combines analgesics from 2+ drug classes to act on different parts of the pain pathway increased therapeutic fx, decreased risk

Non-opioid analgesia

NSAIDs acetaminophen adjuvants (antidepressants, anticonvulsants)

Mild opioids

codeine | tramadol

Where are opioid receptors located

brain spinal cord GI tract plexus periphery

Therapeutic fx of opioids

analgesia sedation euphoria

Types of opioid receptors

mu (main) kappa delta

PK of opioids

``` IV = most reliable IM/SC = variable absorption metabolized by liver excreted by kidneys/bile teratogenic ```

Common adverse fx of opioids

``` nausea/vomiting sedation (happens before respiratory depression) constipation pruritus urinary retention respiratory depression hypotension (vasodilation) ```

PCA assessments

``` drug concentration dose (loading, bolus) delay interval 4-hr dose limit attempts successful attempts total injections ```

Epidural assessment

sensory dermatome | motor score

Withdrawal

body develops a physical dependence on a drug --> withdrawal symptoms occur when drug is stopped/decreased

Tolerance

body develops increased tolerance for drug requiring higher amounts for same therapeutic fx

Addiction

physiologic compulsion to take a drug for its euphoric/psychic fx

S/S of overdose

``` choking cyanosis dizziness/disorientation cold/clammy skin slow/absent breathing somnolence pinpoint pupils ```

Adverse fx of opioid antagonists

headache tachycardia hypertension +w/drawal symptoms

S/S of withdrawal

``` increased HR & BP vomiting diarrhea anxiety shivering tremors yawning body aches sweating sneezing/runny nose abdominal cramps ```

Inhibitory neurotransmitters

serotonin gaba dopamine

Opioid neurons

release endogenous opioids that act on presynaptic and postsynaptic neurons

Opioids & presynaptic neuron

binds to receptors inhibiting the opening of calcium channel gates --> inhibits release of neurotransmitters

Opioids & postsynaptic neuron

hyperpolarizes postsynaptic neuron --> decreased nerve transmission

What # on the pain scale are pts comfortable at

0-3

Location of opioid receptors

brainstem spinal cord peripheral nerves GI tract

Methadone

opioid agonist long acting higher risk of overdose similar adverse fx as opioids

Suboxone

buprenorphine + naloxone partial opioid agonist less likely to cause overdose (d/t naloxone) preferred agonist