Pain Flashcards
1
Q
What is WHO’s definition of pain?
A
an unpleasant sensory and emotional experience associated with actual or potential tissue damage
pain is a protective mechanism
2
Q
What is dyesthesia?
A
any abnormal sensation described as unpleasant by the patient
3
Q
What is hyperalgesia?
A
- Exaggerated pain response from a nromally painful stimulus
- usually includes aspects of summaiton with repeated stimulus of constant intensity and aftersensation
- people on chronic opioids can develop hyperalgesia
- theory- with nerve propagation, can’t stack signalts (or response isn’t as great)but in these patients, propagation is continuous and there’s no dampening of pain signals
4
Q
What is hyperesthesia (hypesthesia)
A
exaggerated pereception of touch stimulus
5
Q
What is allodynia?
A
abnormal perception of pain from a normally non-painful mechanical or thermal stimulus; usually has elemtents of delay in perception
6
Q
What is hypoalgesia
A
decreased sensitiivty and raised threshold to painful stimuli
(patient with no pain sensation in OR)
7
Q
What is anesthesia?
A
reduced perception of all sensation, mainly touch
8
Q
What is analgesia?
A
reduced perception of pain stimulus
9
Q
What is paresthesia?
A
mainly spontaneous abnormal sensation that is not necessarily unpleasant; usually described as pins and needles
10
Q
What is causalgia
A
burning pain in the distribution of one or more peripheral nerves
11
Q
How is pain transferred to brain (in general)
A
- Perception depends on the specialized neurons that function as receptors
- neurons detect a stimulus
- stimulus is non-adaptive: very little adaptation, or not at all
- stimulus is transduced and conducted to the CNS
- sensation is then felt
- protopathic- noxious
- epicritic- non-noxious ie pressure, light touch, temperature discrimination
12
Q
What are the types of pain?
A
Two types, each with different pathways and specific qualities
-
1) fast pain- thinly myelinated type Adelta fibers
- felt about 0.1 sec after stimulus- protective
- felt on surface of body: sharp, prickling, electric pain
-
2) slow pain- unmyelinated type C pain fibers
- felt 1 sec after stimulus
- felt in deeper tissue and surface tissue: slow burning, aching, throbbing, chornic
- ex- chronic pain, visceral pain ie pancreatitis
13
Q
Pain fibers invovled in various painful stimuli?
A
- Mechanical
- fast and slow fibers
- Thermal
- fast and slow
- Chemical
- increase permeability to ions ie potassium
- bradykinin
- ach
- prostaglandins
- substance P
- proteolytic enzymes
- slow pain only! (c-fibers)
- increase permeability to ions ie potassium
14
Q
What are the 4 physiological processes to nociceptive stimuli?
A
-
Transduction- noxious stimuli
- converted to electric activity at the sensory nerve endings
- Transmission- propagation of impulses through the sensory nervous systme
- Modulation- process of transmission modified by neural influenced
- Perception- above 3 interact with the psychology of the pt ot create what is perceived as pain
15
Q
What happens during transduction of pain?
A
- Noxious stimuli causes cell damage with the release of sensitizing chemicals
- prostaglandins
- bradykinin
- serotonin
- substance P
- histamine
- These substances activate nociceptors and lead to generation of action potential
16
Q
What happens during transmission of pain?
A
- Action potential continues from
- site of injury to spinal cord
- spinal cord to brainstem and thalamus
- thalamus to cortex for processing
17
Q
What happens at perception of pain?
A
conscous experience of pain
18
Q
What happens durign modulation of pain?
A
- Neurons originating in the brainstem descend to the spinal cord and release substances (eg endogenous opioids) that inhibit nociceptive impulses
19
Q
What is the primary afferent neuron involved in pain pathway?
A
- first order neurons- send their axons into the spinal cord via the dorsal (sensory) root
- may synapse with inter-neurons, sympathetic neurons and ventral horn (motor) neurons
- primary neurons synapse with interneurons or directly with second order neurons
20
Q
What is the second order neuron in pain pathway?
A
- in gray matter of ipsilateral dorsal horn
21
Q
What is the interneuron in pain pathway?
A
- r/t sympathetic ganglion and involved in modulation
- ability to modulate pain in SC (either up or down modulation)
- Interneuron have opioid receptors– with chronic pain, can upregulate pain at interneuron, more release bradykinin, histamine, substance P
- bodies ability to interpret pain can happen right at spinal cord
22
Q
What is the spinothalamic tract?
A
- axons of most second order neurons cross midline and form the spinothalamic tract
- major pain pathway to the thalamus, RF (reticular formation), nucleus raphe magnus and periaqueductal gray
- lies anterolaterally in white matter of spinal cord
23
Q
What are third order neurons?
A
- located in the thalamus and send fibers to somatosensory areas I and II in the parietal cortex and the superior wall of the sylvian fissure
- responsbile for perception and localization of the pain
- what makes you say ouch
- A delta fibers are very precise, go to the somatosensory areas. C fibers are not so precise
24
Q
What is the spinoretricular tract?
A
alternate pain pathways
insomnia due to pain
25
What is spinomesencephalic tract?
Activates antinociceptive, descending pathways
26
What are the spinohypothalamic and spinotelencephalic tracts?
* activate the hypothalamus and evoke **emotional** behavior
27
What is the neospinothalamic tract?
* First order neurons
* via **type A-delta** fibers enter **lamina I and V (lamina marginalis)** of the dorsal horn of the spinal cord
* synapses with 2nd order neurons
* Second order neurons
* cross midline throught he anterior white commissure *(same as STT- spinothalamic tract)* and pass upwards in the anterolateral columns
* few of these fibers terminate on the reticular formation
* MOST travel up to ventrobasal complex (VBC) of the thalamus
* Third order neurons
* communicate with somatosensory cortex
## Footnote
*Neospinothalamic tract was named becaues this system was devleoped later compared to type C fibers, which are part of paleospinothalamic pathway*
28
What is the paleospinothalamic pathway?
* First order neurons
* via type C fibers, enter laminae (II and III) of the dorsal horns (substantia gelatinosa) synapses with 2nd order neuron
* Second order neurons
* make synaptic connections in lam IV-VIII, can go up without crossing
* Most 2nd order neurons join fibers from the fast pathway, crossing to the opposite side, traveling upwards through the anterolateral pathway (*with STT)*
* They terminate widely in the brain stem, with one tenth of fibers stopping in the thalamus, and the rest stopping in the medulla, pons and tectum of midbrain mesencephalon periaqueductal grey
## Footnote
*these fibers don't reach the somatosensory area of the brain, so they're not as well localized*
29
Which pain is more localized, slow or fast?
Fast pain can be localized easily if A-delta fibers are stimulated together with tactile receptors
slow pain is poorly localized
30
What is the CNS analgesia system?
* The analgesia system is mediated by 3 major components
* the periaquaductal grey matter (in the midbrain)
* the nucelus raphe magnus (in the medulla)
* and the nociception inhibitory neurons within the dorsal horns of the spinal cord (*aka interneurons)*
## Footnote
*all interneurons have own endogeous opioids*
31
What is periaquaductal grey matter?
* the epicenter of analgesia
* it plays a role in the descending modulation of pain and in defensive behavior
* *defensive behavior is avoid using arm, getting near things, guarding the pain, etc*
* *can be genetic how well it manages pain*
* *varies from person to person*
* *difference more liver enzymes but feeling pain can be different too*
(*from picture later, this area is found in midbrain)*
32
What is the nucleus raphe magnus?
* Afferently stimulated from axons in the spinal cord and cerebellum
* the main function of magnus- pain mediation
* sends projections to the dorsal horn of the spinal cord to directly inhibit pain
* *just like periaquaductal gray in terms of ramping down pain*
* *if tumor impeding on these area, will have hyperalgesia-- overly painful because no modulators regulating*
* *has serotonin containing nephrons that interact with interneurons in spinal cord. nucleus raphe magnus will release serotonin onto interneuron, triggering enkephalin (endogenous opioid) release from the interneuron onto opiate receptors in the SC*
## Footnote
*from picture later, this area is found in the medulla*
33
What is the locus ceruleus?
* in pons, has norepinephrine containing neurons that will release NE onto interneurons, which contain enkephalins
34
What happens at cellular level in pain?
* Chemical mediators
* subs P- released slower, building over few minutes- slow chronic pain
* glutamate- acts instantly; only lasts a few milliseconds- fast pain
* CGRP- calcitonin gene-related peptides
* *combo of fast/slow*
* *lots of research into developing drugs- new migraine drug antagonizes CGRP*
* Modulators
* occurs peripherally at the nociceptors, in the spinal cord, or in supraspinal structures.
* This modulation can suppress or aggravate pain
* NMDA receptor role
35
What is the peripheral mechanism involved in acute pain physiology?
* Information about noxious stimuli arrives from periphery along A-delta and C fibers
* Substance P and excitatory amino acids (EAAs) ie glutamate are released
* activation of neurokinin-1 (NK-1) receptors by substance P and activation of amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors by EAAs cause transient depolarization of pain neurons
36
What is central mechanism to pain cellular physiology (chronic)
* The information is relayed to higher brain areas
* **N-methyl-d-aspartate (NMDA)** linked channels are **inoperative** as they are chronically plugged by **magnesium** ions
* in response t**o intense and/or prolonged barrages** of incoming nociceptive information, the neurons become **sensitized** and over-respond to subsequent incoming nociceptive signals
* this barrage **depolarizes** the neuron such that the **magnesium ions exist the NMDA-linked channel**
* results in **influx** of **calcium** ions- **acitvates nitric oxide synthas (cNOS**), causing conversion of **L-arginine to nitric oxide (NO)**
* because it is a gas, **NO** rapidly diffused out of the nneurons
* this **NO** acts **presynpatically** to cause exaggerated **release** of **substance P and EAAs**
* postynaptically, **NO** causes the neurons to become **hyperexcitable**, releasing substance P, ACh, etc
EAAs= excitatory amino acids, ie glutamate
37
What are pysiologic responses to acute pain?
Neuroendocrine resposne
* increase secretion of catabolic hormones
* stress response
* decrease anabolic metabolism
* decrease anabolic metabolism, insulin, testosterone
* ACTH release
* Hyperglycemia
38
What is cardiac resposne to pain?
* Increase HR, BP, SVR, CO
* MI, CHF, Dysrrhythmias
* decrease myocardial oxygenation- secondary pulmonary dysfunction-atelectasis
* coronary artery constriciton- high catecholamines
* release of serotonin may induce coronary vasopasm
* increase plama viscosity- platelet induced occlusion
39
What is pulmonary response to pain?
* increase in total body o2 consumption
* increase CO2 production
* increase minute ventilation
* decrease in TV, VC, FRC- most detrimental alteration in post surgical lung volume
* *FEV1, also decrease*
* as FRC decreases, resting lung volume approaches closing volume, as it continues, atelectasis results, V/Q mismatch, and hypoxemia ensues
* *most detrimental alteration in post surgical lung volume*
* Increase in RR
* pulmonary function decreases with abdominal or thoracic incisions (splinting)
40
Other responses from vascular system with pain?
* Stress mediated due to platlet adhesion and hyper-coagulability
* dvt, pulmonary edema
41
Other response from GI and urinary systems in response to pain?
* visceral pain is referred to somatic sites
* GI and urinary systmes increase sympathetic tone, increase sphincter tone, decrease gastric motility, promoting ileus and urinary retention
* nausea and vomiting common
* stress ulcers can occur-- increase gastric juices
42
What response do muscles have to pain?
* muscle spasms- periosteal and somatic irritation initiates reflex motor resposne, leading to muscle spasm
* anxiety and anger- if lack of pain control
43
What is chronic pain?
* **pain which persists one month longer than expected**
* chronic pain was originally defined as pain that has lasted 6 months or longer. It is now defined as the disease of pain
* associated with musculoskeletal disorders, chronic visceral disorders, lesions of peripheral nerves, nerve roots, dorsal root ganglia (including **causalgia**, phantom limb pain), lesions of the CNS and cancers invading the nervous system
* may be due to nociception, neuropathic pain, but in which psychological and behavioral factors often play a major role
* **acute pain is a symptom of disease, but chronic pain is itself a disease**
* *no protective mechanism for chronic pain*
* chronic pain has no time limits, often has no apparent cause and serves **no apparent biological purpose**
* chronic pain can trigger multiple psychological problems that confound both patient and HCP, leading to feeling **sof helplessness and hopelessness**
* the most common causes of chronic pain **include low-back pain, HA,** recurrent facial pain, CA pain, arthritic pain. sometiems chronic pain can have psychosomatic or psychogenic cause
44
All main causes/theories of chronic pain?
1. Psychological mechanism
2. peripherla mechanism
3. reflex role
4. peripheral- central mechanism
5. circle mechanism
6. chronic nerve compression
7. central pain mechanism
8. psychophysiologic mechanism
9. learned mechanism
45
What role does psychological mechanis, peripheral mechanism and reflex role play in causing chronic pain?
Chronic pathology in somatic or visceral structures
1. **psychological mechanisms**
* *anxiety, depression, something releases glutamate, substance P and start to feel pain*
* *poorly localized, can't describe well. sometimes the pain move etc*
2. **peripheral mechanisms:** chronic pain syndromes associated with **chronic inflammation** in the periphery respond to ASA and NSAIDS, which prevent synthesis of prostaglandin
* *ie arthritic pain*
3. **reflex role-** in chronic pain, can create excessive muscle tension and tendon stretch
* sympathetic hyperactivity can create local ischemia and persistent disruption of the microcirculation
* *big in low back pain*
46
What role does peripheral-central mechanism, circle mechanism, chornic nerve compression and central pain mechanism have in chronic pain?
* **peripheral-central mechanism-** lesions of peripheral nerves, dorsal roots or dorsal ganglion cells
* found in causalgia, and other reflex sympathetic dystrophy, phantom pain
* **Circle Mechanism-** suggests that intense stimulation of nerve fibers in the cord activate internuncial neurons creating an abnormal reverberatory activity in a closed loop
* *interneurons firing when they shouldn't*
* **chronic nerve compression-** nerve being compressed, causign chronic pain
* **central pain mechanism-** found in lesions to the thalamus and spinal cord injury as in paraplegia
* *supratentorially in brain*
47
What role does psychophysiologic mechanisms and learned mechanisms have in causing chronic pain?
* **Psychophysioligc mechnism-** severe stress, usually seen in chronic tension headaches and chronic pain d/t muscle spasm in the shoulder, back and chest
* **learned mechanism-** secondary gian. these patients frequently develop reactive depression and hypochondriasis
48
What are effects of chronic pain?
* serotonin and endorphins become depleted so minor injuries become intolerable
* psychological profiles- the chronic pain patient shows significant differences on the MMPI, neuroticism. however, when the pain is relieved, the neurotic features dissipate
* the longer the duration of the pain, the greater the psychological changes
49
What is treatment for chronic pain?
* must not only remove the pain and the cause of the pain, but also rehabilitate the patient and family physicallyh and psychosocially and psychologically
* examples of pain contorl include
* steroid epidural injection with or without trigger point injections
* peripheral nerve blocks with neurolytics
* acupuncture
* note- often require more analgesics
