Pain pathways - test 2 Flashcards
Nerve/electrical impulses/signals start at the nerve endings:
Transduction
Travel of nerve/electrical impulses to the nerve body connecting to the dorsal horn of the spinal cord:
Transmission
Process of altering (inhibitory/excitatory) pain transmission mechanisms at the dorsal horn to the PNS and CNS:
Modulation
Thalamus acting as the relay station for incoming pain signals and the primary somatosensory cortex serving for discrimination of specific sensory stimuli:
Perception
Location of nociceptors:
Skin, muscles, joints, viscera, vasculature
Unmyelinated fibers:
C fibers - burning pain from heat and pressure from sustained pressure
Myelinated fibers:
A fibers -
Type 1 (Aβ & Aδ) = heat, mechanical, chemical
Type 2 (Aδ) = heat
What chemical mediators are peptides?
Substance P, calcitonin, bradykinin, CGRP
What chemical modulators are lipids?
Prostaglandins, thromboxanes, leukotrienes, endocannaboids
What are the different chemical mediators?
- Peptides
- Eicosanoids
- Lipids
- Neutrophins
- Cytokines
- Chemokines
- Extracellular proteases and protons
This type of hyperalgesia results from the presence of enhanced pain from heat AND mechanical injury.
Primary hyperalgesia
What are the characteristics of primary hyperalgesia?
- Decreased pain control
- increased response to suprathreshold stimuli
- Spontaneous pain
- Expansion of receptive field
This type is characterized by the uninjured skin surrounding the injury and sensitization of central neuronal circuits? (mechanical only)
Secondary hyperalgesia
- sensitization of central neuronal circuits
When pain enters the spinal cord and travels to the brain is changes from peripheral pain to _______ _____
Central pain
The increased responsiveness of peripheral neurons responsible for pain transmission to heat, cold, mechanical or chemical stimulation is called ____?
Sensitization
(Slide 18, pg. 370 Stoeltings)
The release of _________ mediators and adaptation of signaling pathways in primary sensory neurons induced by noxious stimuli causes sensitization.
This process usually resolves as tissues heal and the peripheral sensitization diminishes. ________ pain occurs when this does NOT happen.
inflammatory; chronic
Increased pain sensations to normally painful stimuli is called ______?
Hyperalgesia
Perception to pain sensations in response to normally non-painful stimuli is called _______?
Allodynia
This type of hyperalgesia results from the presence of enhanced pain from heat AND mechanical injury.
Primary hyperalgesia (Heat & Mechanical)
This type of hyperalgesia is characterized by the uninjured skin surrounding the injury and sensitization of central neuronal circuits?
Secondary hyperalgesia (only mechanical)
What is the relay center in the spinal cord for nociceptive & other sensory activity?
The Spinal Dorsal Horn
Pain signals use ________ pathways to reach the brainstem and forebrain (SI and SII).
What does SI and SII stand for and what does this structure do?
afferent
SI (primary somatosensory)
SII (secondary somatosensory)
Accounts for the perception of pain location and intensity (the discrimination of pain stimuli)
Is the dorsal root ganglia peripheral or central?
Which fibers are myelinated?
Unmyelinated?
DRG = peripheral (the dorsal root is central)
Mylelinated = A beta, A delta
Unmyelinated = C fibers
Lamina I (marginal layer) and lamina II (substantia gelatinosa) are innervated by _____ fibers.
C fibers
(slide 21)
What are the laminae and area that become desensitized/affected with spinal/subarachnoid or epidural agents?
Laminae I, II, III, IV, VII and NKI receptor
Which lamina do opioids work on specifically?
Lamina II (substantia gelatinosa)
The ventral horn and laminae ___, ___, ___ are innervated by _____ fibers that innervate the muscles and viscera, so this means they are also affected from our anesthetic agents
Both the dorsal and anterior section will be affected
I, IV, VII
Myelinated fibers
Laminae III and IV, where the NKI is with substance P can be affected by spinals and epidurals, too. T/F?
True!
What are the 5 excitatory Neuromodulators in the CNS?
Glutamate, Calcitonin, Neuropeptide Y, Aspartate, Substance P
What are the 5 inhibitory Neuromodulators in the CNS?
GABA, Glycine, Enkephalins, Norepinephrine, Dopamine
What specific inhibitory Neuromodulator in the CNS is most specific to Midazolam?
GABAa
In the CNS, what are the 4 Ascending pathways of nociceptive information?
Spinothalamic, Spinomedullary, Spinobulbar, Spinohypothalamic
What type of impulses and laminae are associated with the Spinothalamic tract (STT)?
Pain, temperature, and itch (Laminae I, VII, & VIII: All afferent fibers)
(direct projections to the thalamus) (slide 29)
What type of impulses are associated with the Spinomedullary tract?
direct projections to homeostatic control regions in the medulla and brainstem
What type of impulses and laminae are associated with the Spinobulbar (the hindbrain) tract?
Behavior component toward pain (Laminae I, V, & VII)
(direct projections to homeostatic control regions in the medulla and brainstem)
What type of impulses and laminae are associated with the Spinohypothalamic tract (SHT)?
Autonomic, neuroendocrine, and emotional aspects of pain (Laminae I, V, VII, & X)
(direct projections to the hypothalamus and ventral forebrain)
What are the 6 most commonly activated supra-spinal Modulations of the nociception?
Forebrain S I & S II (somatosensory), Anterior cingulate cortex (ACC), Insular cortex (IC), Prefrontal cortex, Thalamus, Cerebellum
The Supra-spinal modulator: Forebrain S I & S II (somatosensory) receives input from where?
And is responsible for the perception of what?
Input from the Thalamus
For the location and intensity of pain
The Supra-spinal modulator: Insular cortex (IC) receives input from where?
And is responsible for the perception of what?
Input from the Thalamus
Responsible for emotional and motivational aspects of pain. (goes through the amygdala)
The Supra-spinal modulator: Thalamus receives input from where?
Input from the dorsal horn
Once pain had been interpreted, it also must be acted upon. Which tract is responsible for this action?
Descending Inhibitory Tract
What are the 3 supra-spinal modulation Descending Inhibitory Tracts/pathways that promote and suppress nociceptive transmission through the dorsal horn of the CNS?
- Originate Periaqueductal gray (PAG),
- Neurotransmitters,
- Hyperpolarize A-delta and C fibers
How does the Originate Periaqueductal gray (PAG) of the supra-spinal modulation Descending Inhibitory Tract, inhibit activity of nocireceptors?
- Through rostral ventromedial medulla (RVM),
- Dorsolateral funiculus,
- Synapse in dorsal horn
Which 3 Neurotransmitters of the supra-spinal modulation Descending Inhibitory Tract, inhibit activity of nocireceptors?
Endorphins, enkephalins, serotonin
How does Hyperpolarized A-delta and C fibers of the supra-spinal modulation Descending Inhibitory Tract, inhibit activity of nocireceptors?
- Decrease release of substance P,
- Opening of K+ channels/inhibition of Ca++ channels
The Descending Pathways of pain modulation in the CNS can either be Inhibitory (DI) or Faciliatory (FD) based on what factors?
- Other somatic stimuli,
- Psychological factors (arousal, attention, and expectation)
The PAG-RVM system contains what 3 opioid receptors and contributes to what 2 physiological pain sensations?
- µ, κ, δ opioid receptors,
- hyperalgesia & Allodynia
Where does the pain impulse originate if it is pertaining to the descending inhibitory tract?
PAG-RVM
What two components does the pain include?
Sensory- discriminative, Motivational- effective
(pain can be affected by physical, emotional, spiritual, or psychological)
Is sensory-discriminative ascending or descending?
Its ascending pathway
Describe the pathway of sensory-discriminative.
Nerve impulse at the site (Skin, muscles, or organs) –>spinothalamic and trigemino-thalamic tracts –> cerebral cortex(somatosensory cortex) –> perception of pain
What does motivational-affective response to painful stimuli include?
Attention and arousal, somatic and autonomic reflexes, Endocrine responses, Emotional changes
Why is attention and arousal important in the context of pain management?
Lack of sleep makes us more irritable and susceptible to pain.
(Use a holistic approach of pain management like how your patient is sleeping, eating, or exercising. All of this affects the management of pain.)
What is Nociception?
It is part of the nervous system that protects from the response of harmful or potentially harmful stimuli.
What Kind of stimuli do specialized nerve endings like nociceptors detect?
mechanical, chemical, thermal
Besides nociception what other factor can influence the pain?
Biological factors
(It amplifies nociception signal to the brain–> nerve fibers are activated repeatedly –> brain decides that the body needs more stress sensors –>body becomes so sensitive to pain that with light touch body feels intense pain)
Patient who has _____pain are more susceptible to pain related to ________.
Chronic pain, Biologic factors
What defines chronic pain?
Pain lasting more than 3 months.
(Chronic pain outlasts the physical pain and is difficult to reverse if this continues to go.)
According to the experiment, who experienced more pain? Children who believe that they had no control over pain or children who had some control?
Children who believed that they had no control over pain.
(psychological factor)
What are the location of Nociceptors we talked about in class?
Skin, muscles, joints, viscera, & vasculature.
If you get stabbed in the leg, what would be the pathway the pain impulse would travel? (start with stimulus)
Stimulus -> Nociceptor: Resting Threshold -> Transmission -> Modulation (where you rate your pain) -> Interpretation
In an experiment, volunteers with the cold rod (with the same temperature) placed back on their hands experienced ___ pain when they were shown red light than volunteers who were shown blue light.
More pain
(Features of the environmental factor on pain)
What would be an example of modulation when discussing pain?
- You get stabbed in the leg before Schmidt’s test and decide it is not that bad because you really have to take that test!
- You get stabbed in the leg and decide that you have to go to the hospital because your in-laws are visiting.
______factor like availability of family and support matters in the perception of pain.
Social factor
Define pain
Pain emphasizes the complex nature of pain as a physical, emotional, and psychological condition.
What are the two types of afferent fibers that deal with pain?
C fibers and A fibers.
Define nociception.
The experience of pain with a series of complex neurophysiologic processes.
What fiber is unmyelinated and deals with burning pain from heat and pressure from sustained pressure?
C-fibers.
What are the targets of medication on the action of pain?
Transduction, transmission, interpretation, and modulation in both PNS and CNS.
Slide 5.
________ deal with acute pain ________ deal with chronic pain
A fiber, C fiber.
All sensory fibers are ________.
Afferent.
What are 7 chemical mediators of pain?
- Peptides (Substance P, Calcitonin, Bradykinin, CGRP),
- Eicosanoids,
- Lipids (Prostaglandins, Thromboxanes, Leukotrienes, Endocannabinoids),
- Neutrophins,
- Cytokines,
- Chemokines,
- Extracellular proteases and protons.
What chemical mediators do we target when we are giving spinal anesthetics or epidural anesthetics?
Peptides (Substance P, Calcitonin, Bradykinin, CGRP).
What chemical mediators are first released when it comes to pain?
Peptides such as Substance P, Calcitonin, & Bradykinin.
What is the treatment for the following lipid chemical mediators? Prostaglandins: Thromboxanes: Endocannabinoids:
- Prostaglandins: NSAIDS,
- Thromboxanes: NSAIDS,
- Endocannabinoids: Cannabis. When cannabis binds to the endocannabinoid receptor there is no experience of pain.
Pain that is limited to the short-term, lasts days to weeks after injury.
Acute pain.
Pain that lasts for more than 3-6 months; persists beyond tissue healing.
Chronic Pain.
Per lecture, what are some unpleasant emotional experiences that follow the same pathways as those for painful sensory transmission?
Anxiety, depression, cognitive deficits, emotional distress.
Pain that persists after tissue injury characterized by reduced sensory and nociceptive thresholds (Allodynia and Hyperalgesia).
Neuropathic Pain.
What type of patients are more susceptible to neuropathic pain?
Cancer patients due to chemo and radiation therapy.
Slide 37.
Treatments for patients with neuropathic pain usually treat symptoms and include…
Opioids, gabapentin, amitryptiline, cannabis.
Pain that is diffuse and poorly localized - Referred to somatic sites like muscle and skin.
Visceral Pain.
Ischemia, stretching of ligamentous attachments, spasms, and distention are all causes of what type of pain?
Visceral pain.
A variety of painful conditions following injury in a region with impairment of sensory, motor, and autonomic systems.
Complex Regional Pain Syndromes.
CRPS (Complex Regional Pain Syndrome) is a neurological disease including:
Autonomic, sensory, and motor systems as well as cortical areas involved in the processing of cognitive and affective information.
Involves: Spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, active and passive movement disorders, and trophic changes of skin and SQ tissues.
Complex Regional Pain Syndromes.
Pain in the neonate and infant leads to ________ pain threshold and ____________ pain responses.
Lower, Exaggerated.
The human fetus develops pain perception by __________ of gestation.
23 weeks.
Slide 38.
True or False: Toddlers and adolescents exhibit long-lasting hypersensitivity to painful stimuli after painful experiences as neonates.
True.
The process by which a noxious stimulus (e.g., heat, cold, mechanical distortion) is converted to an electrical impulse in sensory nerve endings, is known as?
Where does it occur?
Transduction.
Peripheral nociceptors
____________ is the conduction of (pain-related) nerve/electrical impulses to the ___ with the major connections for these nerves being in the ______ horn of the spinal cord and ________ with projections to the cingulate, insular, and somatosensory cortices.
Transmission; CNS; Dorsal; Thalamus.
Define Modulation:
Where does it occur in the CNS?
Modulation of pain is the process of altering (inhibitory/excitatory) pain transmission mechanisms. Occurs in the Dorsal Horn of the spinal cord.
At what level on the pain perception pathway do our injectable local anesthetics (LA) become active at?
Will Modulation still occur once LA have been injected properly?
Between the Transduction and Transmission levels.
No: “Hence, there will be NO modulation because there would be no pain transmission to the dorsal horn…”.
Name the cardiovascular responses to pain mentioned in lecture.
Hypertension, Tachycardia, Myocardial irritability (demand), Increased SVR, Decreased CO, Myocardial Ischemia.
When is it important to monitor pain in our patients?
At all times because it can impact their hemodynamics.
Thalamus acts as the _______ _____ _______ for incoming pain signals.
The _____________ ______ serves as the site for discrimination of specific sensory stimuli.
Both of these neurobiological sites determine our __________.
central relay station. Somatosensory cortex. Perception.
Name the possible pulmonary responses from pain mentioned in lecture.
- Increased total body oxygen consumption/CO2 production,
- Increased minute volume and work of breathing,
- Decreased movement of chest wall,
- Atelectasis,
- Intrapulmonary shunting (VQ mismatch), - Impaired coughing.
What is the gate control theory of pain?
Made in 1965. “Gates” exist along the pain signaling pathway. Gates along the pathway may open or close to allow the pain signal to continue to the CNS or stop its progress.
According to the gate control theory of pain, “gates” can be found where?
In the spinal dorsal horn.
According to the gate control theory of pain, if a gate is “open” then the pain signal will reach supraspinal regions of the brain. The supraspinal regions consist of what 4 areas of the brain?
Thalamus, medulla oblongata, hindbrain, somatosensory cortex.
Name the possible GI responses from pain mentioned in lecture.
Enhanced sympathetic tone, Increased sphincter tone, Decreased motility (Ileus), N/V, Abdominal distention, Hypersecretion of acid (stress ulcer, aspiration risk).
How many ml’s of stomach content is considered an increased risk for aspiration?
25ml’s
You bump your elbow and it hurts. You massage the area and now it doesn’t hurt. Using the gate control theory of pain, explain how your elbow stopped hurting.
Elbow gets bumped and it hurts. Pain signal travels along ‘open’ gate through A delta + C fibers. A delta = small diameter, myelinated nerve. C = unmyelinated.
Open gate becomes ‘closed’ when sensory input is received through larger, faster, myelinated A beta fiber. Rubbing at the elbow to relieve pain is sending info to brain about pressure and touch. Because pressure/touch travels along faster nerve, it ends up suppressing the pain signal from the slower nerve, thus ‘closing’ the gate from the original pain signal.
Is the patient at risk of aspiration if the stomach is empty?
Yes. Contents from the small intestine can make their way back into the stomach and be aspirated.
Name the GU responses from pain mentioned in lecture.
Urinary retention
Name the catabolic hormones that are increased as a response to pain.
Catecholamines, Cortisol, Glucagon
Name the anabolic hormones that are decreased as a response to pain.
Insulin, Testosterone
What is the purpose of the PAG - RVM system in supraspinal regions?
The periaqueductal gray - rostral ventromedial medulla system is where a pain signal will first travel through in the supraspinal brain regions.
This usually suppresses a lot of pain signals, but a small portion may travel through this area for further processing in the brain.
Name the endocrine responses from pain mentioned in lecture.
Increased catabolic hormones, Decreased anabolic hormones, Negative nitrogen balance, Carbohydrate intolerance, Increases renin, aldosterone, angiotensin system (RAAS)
Which are some alpha-2 agonist medication examples mentioned specifically in lecture?
dexmedetomidine and clonidine
Name the stress related hematologic responses from pain mentioned in lecture.
Platelet adhesiveness, Reduced fibrinolysis, Hypercoagulability
SCDs: Maybe some prophylactic blood thinning going on
Name the emotional responses from pain mentioned in lecture.
Anxiety, Sleep disturbance, Depression
What is the purpose of the thalamus and somatosensory cortex in the pain pathway?
These areas of the supraspinal brain regions are where perception of pain occurs. Here a pain signal is fully processed, and the brain attempts to sort where the pain is coming from, what type of pain it is, and what sort of response should occur.
What is the purpose of the limbic cortex in the pain pathway?
This part of the brain is where we deal with the motivational - affective pain components.
Name the immune responses from pain mentioned in lecture.
Stress related Leukocytosis, Depressed Reticuloendothelial system (increased chance of infection)
Name the meds in their respective sites of action according to the picture.
- Perception: Opioids, alpha-2 agonists, GA;
- Modulation: LA, opioids, ketamine, alpha-2 agonists;
- Transmission: LA;
- Transduction: LA, and NSAIDS
What would happen if the amygdala was ‘clipped’?
Some pain signals travel through the amygdala before being processed/perceived by the cortex. If the amygdala were ‘clipped’, then the pain signal would not travel to the cortex. This means you would not feel that you are in pain, even if something painful was happening to you.
What are the 7 neuromodulators that propagate a pain signal?
Substance P, Glutamate, CGRP, NMDA, AMPA, BDNF, Cytokines
Which of the 7 neuromodulators that propagate pain can be targeted by ketamine?
NMDA receptors
Which of the 7 neuromodulators that propagate pain can be targeted by opioids?
AMPA, BDNF, Cytokines
Nociceptors release ____ and ____ in response to tissue injury.
Substance P, Glutamate
What 6 mediators are released by damaged cells, mast cells, and platelets to activate nociceptors and start a pain response? What meds can target these mediators to stop them?
Bradykinin, histamine, prostaglandins, serotonin, H+, lactic acid. NSAIDs and Opioids can inhibit these.
Which one is an excitatory pain impulse mediator: GABA, glycine, Glutamate, or Norepinephrine?
Glutamate
Is sensory-discriminative ascending or descending path?
Its ascending pathway
