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111 Cards in this Set
- Front
- Back
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Describe type A delta fibers
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fast, mylenated
2-5 (size) 5-30 m/sec pricking pain, somatic, acute, runs dermatomes, immediate |
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Describe type C fibers
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Slow, non-mylenated, bidirectional
0.3-3 (size) 0.5-2m/sec chronic, slow, visceral, aching, burning, hard to localize |
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are type C fibers afferent or efferent
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They are afferent but can have an efferent componet to begin the inflammatory and sensitization process
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Describe AB fibers
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fast, myelinated
6-20 (size) 33-75 m/sec perceive pressure and touch type sensations |
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are AB fibers nociceptive
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usually not but can take over if C fibers are damaged
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What is converting one form of energy to another
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Transduction
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Is pain perception the same for everyone
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no but the pain threshold is
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What types of sensations do pain receptors sense
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Mechanical
Thermal <8 or >43 degrees C Chemical (acid, ischemia, infection, inflammation) |
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Mechanical and Thermal run on what type of fibers
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type A delta
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Chemicals run on what type of fibers
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type C fibers
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what are some other endogenous chemicals that can stimulate pain receptors
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bradykinin
acetylcholine histamine prostaglandins potassium |
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Pain receptors are usually what...
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Vanilloid Receptor (VR1)-capsacin pepper
or Acid sensing ion channels ASIC |
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When the phospholipid bilayer of the cell is interrupted what happens
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we get the arachidonic acid cascade.
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Most of the chemicals from cell damage that stimulate pain receptors come from what
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the metabolic breakdown products of arachidonic acid (local mediators).
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Can damaged pain pathways spontaneously fire
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yes
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What do activated nerve endings release that causes increase capillary permeability
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Substance P
Calcitonin (CGRP) |
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What inflammatory factors do the capillaries release that increase the firing of teh nerve and pain sensation
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neutrophils
lymphocytes bradykinin nerve growth factor |
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What can be given preop to diminish or prevent activation of substance P
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NSAIDs
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All paths of pain sensations lead to where
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the thalamus
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We can try to interrupt the ligand in the tissue periphery at the ligand channels with what
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NSAIDs
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Once the pain sensation has started it is transmitted how
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Voltage channels
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How do we stop pain transmission after it has started
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with a local block
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Where do primary afferent synapses enter in the transmission of pain
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laminae 1,2,5,10
Cranial nerves 5,7,9,10 |
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Substance P stimulates what receptors
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NK 1 &2
Neurokinins |
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Glutamate stimulates what receptors
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NMDA
AMPA |
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Glutamate is not very successful at which receptor at first
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NMDA because of a Mg on the receptor, but with repeated pain stimulation it will be able to remove the Mg to open the receptor
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Where is the first place we get modulation of the pain impulse
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at the second order neuron when glutamateand substance P is released
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What is the primary excitatory neurotransmitter for pain in the spinal cord
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Substance P
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What are some neurotransmitters that modulate substance P
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Norepi
Serotonin (5-HT) Endorphins Enkephalins Opiods (exogenous) |
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What does substance P cause in the periphery
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Sensitization of nocireceptors
Degranulates histamine from mast cells Degranulates 5-HT from platlets Chemo reactant for leucocytes Potent vasodilator Capillary permeability |
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What are some spinal cord receptors that modulate release of substance P
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5-HT
GABA Alpha 2 Mu 2 |
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How do we get spinal mediated analgesia with activation of alpha 2 receptors
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cause a decrease release of substance P, Neurokinins, and glutamate in the spinal cord so the signal is stopped and pain perception decreases
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What gives you fine perception of pain
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cortex
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which pathway gives us temp, touch pain perception
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Spinothalamic
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What pathway gives us fear, memory, behavior, autonomic action, addiction,
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Spinolimbic
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What pathway is packed with Mu receptors wher our chemicals affct the behavioral and sensory response
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Spinolimbic
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what pathway modulates the reflex withdrawl response
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Spinoreticular
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What pathway begins in the periaquaductal gray- we interrupt with the tens unit
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Spinomesencephalic
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What pathway stays ipsilateral and deals with chronic pain
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Spinocervical-thalamic
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What pathway is ipsilater but has to do with pelvic visceral pain
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Postsynaptic Dorsal Column Pathway
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What is the root for all supra spinal modulation
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Periaquaductal gray
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Can secondary afferents become hypersensitized in chronic pain patients
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yes
the receptor changes and some can send impulses without the stimuli being present |
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What happens when you give opiods right in the spinal cord
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can give 1/10 of the dose and get drastic results
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Explain the gate control theory
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Stimulation from larger fibers can block the stimulus from smaller fibers- we can override the stimulus
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What do we use to activate the gate control theory
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TENS
counter irritants accupuncture bengay |
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What is epicritic senstation
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fine localization of touch and temperature to pain
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What is protopathic sensation
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affective component of pain
Sensiblity to curde stimulations such as pain, temp and touch which acts as a defensive agency |
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What is pain senstation coming from skin and muscles
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somatic pain
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What is interrupting the pain transmission before the pain sensation starts
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preemptive analgesia
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What is a good example of preemptive analgesia
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giving a spinal to a pt before amputation to decrease occurance of phantom limb pain
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What is a non pain stimulus that is now eliciting pain
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allodynia
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Who usually experiences allodynia
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chronic pain sufferers. There is damage to type C fibers and AB fibers are taking over for them
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Locations that do not have pain receptors
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Parenchyma of liver, lung, brain
visceral pleura |
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How do we decrease the multiple pathways that pain can travel
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giving combinations of meds
ex. Toradol with opiod |
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What does pain cost the CV system
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HTN, Tachycardia
Myocardial irritability Increased SVR CO increases in normal person aggravates Myocardial ischemia |
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What is the #1 common denominator for perioperative MI
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tachycardia
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What does pain cost the resp system
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Increases O2 consumption, Co2 production, minute ventilation, work of breathing
Can worsen ischemia by making the pt not breath adequately |
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What does pain cost the GI and GU system
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Decreases motility
Increase sphincter tone, gastric acid secretion causes ileus and urinary retention (also can be caused by the narcotics) |
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What does pain cost the endocrine system
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Increases catabolic hormones (pt starts to consume himself)
catecholamines, cortisol, Glucagon Decreases anabolic hormones Insulin, and testosterone |
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What does pain do to water and sodium retention
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increase it by angio II, aldosterone, and ADH
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What does pain cost the hematologic system
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Increases platelet adhesiveness (DVT)
reducesd fibrinolysis |
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What does pain cost the immune system
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Causes leukocytosis and leukopenia
Depresses the reticuloendothelial system which predisposes the patient to infection |
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What will completely stop the SNS response to pain
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Adequate regional anesthesia not general anesthesia or opiates
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Are there Mu receptors in the periphery
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not until the inflammatory response has started
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Pain is modified where
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brain
spinal cord periphery |
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Peripheral pain nerves that are inflammed produce what
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opiod receptors
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What are acids that interrupt the arachadonic cascade
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NSAIDs
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What is neuraxial analgesia
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put analgesic into or around nerves to interrupt pain transmission down the cord
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What is non opiod analgesia esp helpful with
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musculoskeletal pain
post traumatic pain inflammatory pain dysmenorrhea renal colic biliary obstruction |
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what is the only IV nsaid
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toradol
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Enogenous opiods are derived from where
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3 pro hormones
proenkephalin prodynorphin pro-opiomelanocortin (POMC) |
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Where are proenkephalins located
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brain
spinal cord peripheral sites, particulary the adrenal medulla Mu and delta receptors |
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Where are prodynorphins located
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throughout the brain and spinal cord and in peripheral sites
dynorphin and kappa receptors |
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What is the major site of synthesis for POMC
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pituitary
but also in pancreas and placenta |
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POMC is a precursor for
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Beta-endorphins (mu and delta)
ACTH Melanocyte-stimulating hormone |
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initial classifications of opiod receptors
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mu
kappa sigma delta- added later |
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what is the primary function of mu
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presynaptic decreasing of neurotransmitter release
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what is the most common site of action of all opiods
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Mu receptors
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how do mu receptors exert their effects
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through a second messenger
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what decreases the efficacy of all Mu receptors
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estrogen
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Mu receptors in the higher brain usually respond by
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postsynaptic
increasing K conductance |
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Where is primary location for Kappa and delta receptors
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spinal cord and periphery
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how does kappa work
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presynaptically increases ca conductance
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How does delta work
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increases K and Ca conductance
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How do mu receptors work
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increase K conductance
or decrease Ca conductance inhibits NT release and hyperpolarizes the membrane |
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What type of opiods are receptor specific
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synthetic opiods
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What isomer is more potent? antitussive?
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L-potent
D-antitussive racemic |
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What is the main modulator of pain in the dorsal grey horn that we are shooting for
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Mu 2
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What receptor does this describe....
Euphoria, miosis, bradycardia, hypothermia, urinary retention |
Mu 1
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What receptor does this describe....
Depression of ventilation constipation |
Mu 2
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What receptor does this describe....
Dysphoria, sedation, Miosis, Diuresis |
Kappa
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What receptor does this describe...
Depression of ventilation, constipation, urinary retention |
Delta
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How are opiods eliminated
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biotransformation
oxidation and reduction conjugation Ester hydrolysis (remifentanyl) Excretion primarily renal bile and intestinal |
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What opiods have active metabolites
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morphine
meperidine |
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opiods must be reversible by what
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narcan (naloxone)
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What can we use to decrease some post op resp depression without reversing all pain control
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partial agonist
Nalbuphine Butorphanol (Stadol) |
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What are some uses for opiods
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pain releif during monitored anesthesia
Attentuate the response to laryngoscopy reduce MAC of inhaled and IV anesthetics |
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What opiods are not CV stable
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Morphine
demerol |
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Do opiods provide muscle relaxation? amnesia? hypnosis??
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no
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Where is pain perception centrally mediated
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higher brain centers
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What area of brain has mu and delta receptors adn is responsible for mood, euphoria, tranquility, and rewarding properties
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Nucleus accumbens
part of the limbic system |
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Do opiods cause burst suppression
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no
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What does opiods do to CMRO2, ICP
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CMRO2 decreases in a coupled fashion, doesnt change ICP unless have hypoxia or hypercarbia
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are opiods neuroprotective
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no
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what is unique about pupil reaction to opiods
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Mu receptor stimulation causes miosis but the reaction is never altered with tolerance
exception is demerol (atropine like that will block the pupil response) |
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Explain wood chest or muscle rigidity seen with opiods
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usually seen with high doses
increase CVP, PAP, PVR decrease compliance, FRC, ventilation Increase O2 consumption and ICP vocal cord closure This is a central Mu receptor effect |
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treatment and prevention of "wood chest"
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Finish induction
pre-medicate with non-depolarizing NMB Treat with induction dose of thiopental or sedation dose of valium or versed Rapid NMB is needed if glottis is closed |
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what do opiods do to the thermoregulatory threshold
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decrease the threshold to stop shivering
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Drugs used to stop shivering
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Meperidine-12.5 mg
Tramadol-opiod derivative Dexmedetomidine |
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What causes pruritus with opiods
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not histamine release
Mu receptor mediated- that increases with neuroaxial placement |
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Treatment of pruritus from opiods
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Naloxone
zofran time |
