Pain Flashcards
1
Q
What is the definition of pain?
A
- an unpleasant sensory and emotional experience associated with actual or potoential tissue damage.
- pain is a protective mechanism
2
Q
What is dysethesia?
A
any abnormal sensation described as unpleasant by the patient
3
Q
Hyperalgesia
A
- Exaggerated pain response from a normally painful stimulus
- usually additive of repeated stimulus of constant intensity and aftersensation
4
Q
hyperesthesia
A
exaggerated perception of touch stimulus
5
Q
allodynia
A
- abnormal perception of pain from a normally non-painful mechanical or thermal stimulus
- usually has elements of delay in perception
6
Q
hypoalgesia
A
decreased sensitivity and raised threshold to painful stimuli
7
Q
anesthesia
A
reduced perception of all sensation, mainly touch
8
Q
analgesia
A
Reduced perception of pain stimulus
*warn pts to expect some pain after surgery, analgesia can only reduce it, not fully eliminate it
9
Q
paresthesia
A
- spontaneous abnormal sensation that is not necessarily unpleasant
- usually described as “pins and needles”
- ex. diabetic patients
10
Q
Causalgia
A
- burning pain in the distribution of one or more peripheral nerves (wherever the affected nerve(s) innervates)
- ex: shingles
11
Q
What is the overview of how pain perception works?
A
- perception depends on the specialized neurons that function as receptors
- neurons detect a stimulus
- stimulus is transduced and conducted to the CNS
- sensation is then felt
12
Q
Are neurons adaptive?
What are the two types of sensation?
A
- Neurons are non-adaptive- you never “get used” to pain like you might get used to a noxious smell
- Two types of sensations
- protopathic- noxious
- epicritic- non-noxious
- pressure, light touch, temperature discrimination
13
Q
What are the two types of pain?
A
- Fast pain
- myelinated A delta fibers
- felt 0.1 sec after stimulus
- felt on surface of body (sharp, pricking, electric pain)
- easy to localize
- slow pain
- unmyelinated type C pain fibers
- felt 1 sec after stimulus
- felt in deeper tissue and surface tissue (slow burning, aching, throbbing, chronic)
14
Q
What are the different types of painful stimuli?
A
- mechanical
- fast and slow pain
- thermal
- fast and slow pain
- chemical- uses bradykinin, Ach, prostaglandins, substance P, and proteolytic enzymes to increase permeability to ions like potassium
- slow pain only
15
Q
What are the four steps of nociception?
A
- Transduction- the noxious stimuli is converted to electric activity at the sensory nerve endings
- transmission- propagation of impulses through the sensory nervous system
- Modulation- process of transmission modified by neural influence
- may be up-regulated or down-regulated
- perception- the signal interacts with the psychology of the pt to create what is perceived as pain
16
Q
What is the transduction process?
list the chemicals (5)
A
- Mechanical, thermal, and chemical receptors convert to electrical action potential by opening and closing Na and K ion channels
- A noxious stimuli that causes cell damage which release sensitizing chemicals
- prostaglandins
- bradykinin
- serotonin
- substance P
- histamine
17
Q
What is the route of action potential transmission?
A
- site of injury to spinal cord
- spinal cord to brainstem and thalamus
- thalamus to cortex for processing
18
Q
What is the pathway for most pain sensation?
A
-
First order neuron- from site of problem to spinal cord via dorsal (sensory) root
- may synapse with interneurons, sympathetic neurons, and ventral horn (motor) neurons
-
second order neuron- in gray matter of ipsilateral dorsal horn
- most cross midline and go up the spinothalamic tract to the thalamus, reticuar formation, nucleus raphe magnus, and periaqueductal grey
-
third order neuron- send message from thalamus to somatosensory areas I and II in the parietal cortex and the superior wall of the sulvian fissure
- where pain is localized
19
Q
Where does the spinothalamic tract lie?
A
anterolaterally in white matter of the spinal cord
20
Q
What are the three (four) alternate pain pathways?
A
- Spinoreticular tract-Causes insomnia due to pain
- spinomesencephalic tract- activates anti-nociceptive descending pathways
- spinohypothalamic and spinotelencephalic tracts- activate the hypothalamus and evoke emotional behaviour
21
Q
Details about the neospinothalamic tract (fast pain):
Where do first order neurons enter?
Where do second order neurons cross midline?
Where do most travel to?
A
- First order neurons (via A delta fiber) enter lamina I and V (lamina marginalis) of the dorsal horn of SC.
- Second order neurons cross the midline through the anterior white commissure and pass upwards in the spinothalamic tract
- Few terminate in reticular formation (affecting sleep cycle)
- MOST travel to Ventrobasal Complex of Thalamus
- Third order neurons comminicate to somatosensory cortex
22
Q
What is the other name for the Spinothalamic tract?
A
anterolateral column
23
Q
Details of the Paleospinothalamic pathway (slow pain):
Where to first order neurons enter lamina?
Where do second order neurons connect?
Where do the third order neurons terminate?
A
- First order neurons (C fibers) enter via laminae II and III of the dorsal horns (aka substantia gelatinosa)
- Second order neurons connect in laminae IV-VIII and go up without crossing over
- most join fibers from the fast pathway, crossing to the other side and saking the STT
- 1/10th of fibers stop in thalamus
- the rest terminate in the medulla, pons, and tectum of midbrain mesencephalon periadueductal grey
- B/C these fibers do not go beyond the thalamus to the somatosensory cortex, these sensations are not localized
24
Q
When can fast pain be easily localized?
A
If the A delta fibers are stimulated together with tactile receptors
25
What three components mediate the analgesia system?
* the periaquaductal grey matter (in the midbrain)
* the nucleus raphe magnus (in the medulla)
* the nociception inhibitory neurons within the dorsal horns of the spinal cord
26
What is the periaquaductal grey matter?
* the epicenter of analgesia
* it plays a role in the descending modulation of pain and in defensive behavior
* has enkephalin producing cells
27
What is the Nucleus Raphe Magnus?
* afferently stimulated from axons in the spinal cord and cerebellum
* main function: **pain mediation**
* sends projections to the dorsal horn of the spinal cord to directly inhibit pain
28
What are the chemical mediators of pain?
Which one is released slowly?
Which one is released instantly?
* Substance P- slow release, builds over a few minutes for slow, chronic pain
* Glutamate- acts instantly; only lasts a few milliseconds- fast pain
* CGRP- calcitonin gene related peptide
29
Where can pain moculation happen?
* peripherally at the nociceptors
* in the spinal cord
* in supraspinal structures
* \*modulation can suppress or aggravate pain
30
What is the cellular physiology of acute pain?
Mechanism?
fibers?
* **Peripheral mechanism**
* Information about noxious stimuli arrives from the periphery along A-delta and C fibers
* Substance P and excitatory amino acids (EAA) i.e. glutamate are released
* **Substance P**- activates neurokinin-1 (NK-1) receptors
* EEAs activate amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors
31
What is the cellular physiology of pain in the chronic state?
(not chronic pain, but chronic barrage of signals)
mechanism?
* **Central mechanism**- the information is relayed to higher brain areas
* normally the NMDA-linked channels are inoperative b/c they always have the Mg ion "plug"
* the Mg gets bumped off due to intense and prolonged barrages of nociceptive info
* the neurons become sensitized and over respond to subsequent incoming nociceptive signals
* The loss of Mg results in Ca ions influxing in and activating nitric oxide synthase (cNOS), converting L-arginine to nitric oxide
* This NO acts **presynaptically** to cause exaggerated release of substance P and EAAs
* **Postsynaptically** NO causes the neurons to become hyperexcitable and releasing Substance P, ACh, etc
32
What is the neuroendocrine responses to acute pain?
* Neuroendocrine response
* increased secretion of catabolic hormones
* stress response
* decrease anabolic metabolism
* insulin, testosterone
* ACTH release
* hyperglycemia
33
What are the cardiac responses to acute pain?
* Increased HR, BP, SVR, CO
* MI, CHF, dysrhythmias
* decrease myocardial oxygenation- d/t pulmonary dysfunction/atelectasis
* Coronary artery constriction d/t high catecholamines
* release of serotonin may induce coronary vasospasm
* increased plasma viscosity
* platelet induced occlusion
34
What are the pulmonary responses to acute pain?
* Increased total body O2 consumption
* increased CO2 production
* increased MV
* decreased TV, VC
* decreased FRC- most detrimental change in post surgical lung volume. As FRC decreases, resting lung volume approaches closing volume, continues on to atelectasis, V/Q mismatch, and hypoxemia ensues
* Pulmonary function decreases with abdominal or throacic incision (splinting)
35
What are the other physiologic responses to acute pain?
* Vascular system- stress mediated due to platelet adhesion and hyper-coagulability
* DVT, pulmonary edema
* Visceral pain is referred to somatic sites
* GI and urinary systems have increased sympathetic done (sphinctor); decreased gastric motility
* promoting N/V, ileus, urinary retention
* Muscle spasms- periosteal and somatic irritation initiates reflex motor response leading to muscle spasm
* Anxiety and anger
36
What should you consider regardings the different methods of pain relief?
* Duration of pain relief
* patient history
* goals of management
* acute vs chronic pain
37
What is the BEST postoperative pain management?
* Preemptive analgsia!
* opioids and NSAIDS in GA
* regional blocks
* local infiltration at the surgical site
38
What are the benefits of regional anesthesia?
Where does a block need to be to have a significant effect on the neuroendocrine response to surgery?
* Pts do better overall
* less morbidity
* less CV ailure
* less infections
* less urinary cortisol- means less of a stress response
* lower overall post-op complication rate
* \*\*higher than L1 has a significant effect on the neuroendocrine response to surgery
39
What is the current COX concept?
* COX 1- Constitutive
* homeostatic funtions- GI tract, renal, platelet function, macrophage differentiation
* **Inhibition undesirable**
* COX 2- Induced
* Inflammation
* **Inhibition desireable**
40
What are the advantages of patient controlled analgesia?
Features?
* Advantages?
* Cost effective
* higher degree of pt satisfaction
* total drug consumption is less than IM
* harder to overmedicate self
* Features
* Reservoir
* infusion controller- pushbutton to be controlled **by the patient only**
* delivers a specific dose
* lockout
* basal infusion
41
What do PCAs prevent?
What are the findings regarding PCAs?
* prevents the "pain no pain cycle"
* findings
* patients consume less drug
* male use more than females
* shortens hospital stays
42
What are nearly all PCA overdoses attributed to?
Other side effects?
* errors in the programming of the parameters
* N/V, constipation, pruritis
43
What is the definition of chronic pain?
* pain which persists **one month** longer than expected
* Originally defined as pain that lasted 6 months or longer
* Now it is the "disease of pain"
* What is chronic pain often associated with?
* musculoskeletal disorders
* chronic visceral disorders
* lesions of peripheral nerves
* nerve roots
* dorsal root ganglia (including causalgia, phantom limb pain)
* lesion of the CNS and cancers invading the nervous system
44
What are the most common forms of chronic pain?
What can chronic pain trigger?
* low back pain
* HA
* recurrent pacial pain
* cancer pain
* arthritic pain
* can have a psychosomatic or psychogenic cause
* Chronic pain can trigger multiple psychological problems that confound both patient and health care provider, leading to feelings of helplessness and hopelessness
45
What are some causes of chronic pain?
(7)
\*there is another card with 3 others.....sorry
\*hint: physical
* C**hronic pathology** in somatic or visceral structures
* **peripheral mechanisms**
* chronic pain syndromes associated with chronic inflammation--respond to aspirin and NSAIDS which prevent synthesis of prostaglandins
* **reflex role**- chronic pain can create excessive muscle tension and tendon stretch
* sympathetic hyperactivity can create local ischemia and persistent disruption of the microcirculation
* **Lesions** of peripheral nerves, dorsal roots or dorsal ganglion cells
* found in causalgias and other reflex sympathetic dystrophy, phantom pain
* **The circle mechanism**- intense stimulation of nerve fibers in the cord activate internuncial neurons creating an abnormal reverberatory activity in a closed loop
* **chronic nerve compression**
* **Central pain mechanisms**- lesions to the thalamus and spinal cord injury, such as paraplegia
46
Whart are some other causes of chronic pain?
(3)
\*hint: psych (kinda)
* **Psychological mechanisms**
* **psychophysiologic mechanisms-**
* severe stress- chronic tension HA, muscle spasms in the shoulder, back and chest
* **Learned mechanisms-** Secondary gain
* these patients frequently develop reactive depression and hypochondriasis
47
What are the effects of chronic pain?
* Serotonin and endorphins become depleted, so minor injuries become intolerable
* psychologic profiles
* chronic pain pt shows significant differences on the MMPI, neuroticism
* When the pain is relieved, the neurotic features dissipate
* the longer the pain, the greater the psychological changes
48
Chronic pain treatment
goal
examples
* Must remove pain and the cause of pain
* also rehabilitate the pt and family psysically, psychosocially and psychologically
* Examples:
* steroid epidural injection (with or without trigger point injections)
* peripheral nerve blocks with neurolytics, acupuncture
* Note: chronic pain patients often require more analgesics
