Pain Flashcards

0
Q

Pain WHO definition:
An unpleasant sensory and emotional experience associated with actual or potential ___ ___.
-Pain is a ___ ___.

A

Tissue damage

-Protective mechanism

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1
Q

This was originally defined as pain that has lasted 6 months or longer. It is now defined as “the disease of pain” ?

A

Chronic Pain

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2
Q

Pain Management - Applies to the entire discipline of Anesthesiology:
Includes ~
1) ___ = recovering from surgery or with acute medical conditions
2) ___ = diverse group of people in the outpatient setting
3) ___ = short or long term therapy both in and out of the hospital

A

1) Acute
2) Chronic
3) Cancer

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3
Q

With anesthesia ___ is one of our biggest specialties.

A

Pain

airway first, then pain

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4
Q

Any abnormal sensation described as unpleasant by the patient?

A

Dysesthesia

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5
Q

Exaggerated pain response from a normally painful stimulus, usually includes aspects of summation with repeated stimulus of constant intensity and aftersensation?

A

Hyperalgesia

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6
Q

Abnormally painful and exaggerated reaction to a painful stimulus?
*This is related to?

A

Hyperpathia

*Hyperalgesia

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7
Q

Exaggerated perception of touch stimulus?

A

Hyperesthesia (hypesthesia)

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8
Q

Abnormal perception of pain from a normally non-painful mechanical or thermal stimulus; usually has elements of delay in perception?

A

Allodynia

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9
Q

Decreased sensitivity and raised threshold to painful stimuli?

A

Hypoalgesia (hypalgesia)

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10
Q

Reduced perception of all sensation, mainly touch?

A

Anesthesia

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11
Q

Loss of perception of vibration?

A

Pallanesthesia

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12
Q

Reduced perception of pain stimulus?

A

Analgesia

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13
Q

Mainly spontaneous abnormal sensation that is not unpleasant; usually described as “pins and needles”?

A

Paresthesia

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14
Q

Burning pain in the distribution of one or more peripheral nerves?
*Usually what ___ have.

A

Causalgia

*Diabetics

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15
Q

Pain-Receptors:

1) Perception depends on the specialized neurons that function as ___.
2) ___ detect a stimulus (temp, pain, pressure).
3) ___ - very little adaptation, or not at all
4) Stimulus is transduced and conducted to the ___.
5) Sensation is then felt; *____ = noxious (painful)
* ____ = non-noxious, ex: pressure, light touch, temp discrimination

A

1) receptors
2) Neurons
3) Non-adaptive
4) CNS
5) *Protopathic
* Epicritic

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16
Q

Two Types of Pain - each with different pathways & specific qualities:

1) _____ = _________ fibers *Felt about 0.1 sec after stimulus; felt on surface of body (sharp, pricking, electric pain). Very precise, prick finger with needle will know exactly where you pricked it.
2) _____ = _________ fibers *Felt at 1 sec after stimulus; felt in deeper tissue and surface tissue (slow burning, aching, throbbing, chronic). Ex: visceral pain (slower).

A

1) Fast pain
Thinly myelinated Type A delta fibers
2) Slow pain
Unmyelinated Type C pain fibers

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17
Q

1) Both pain pathways fast pain and slow pain are involved with ___ & ___.
2) ____ only has slow pain.

A

1) Mechanical & Thermal

2) Chemical

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18
Q

Painful Stimuli - Chemical (SLOW pain ONLY)

* *___, ___, ___, ___, & ___ - increase permeability to ions
ex: potassium

A
**Bradykinin
Acetylcholine
Prostaglandins 
Substance P
Proteolytic enzymes
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19
Q

Perception that something is painful?

A

Nociception

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20
Q

4 Physiologic processes to Nociceptive Stimuli:

1) ___ = noxious stimuli converted to electric activity at the sensory nerve endings (at the afferent nerve)
2) ___ = propagation of impulses thru the sensory nervous system
3) ___ = process of transmission modified by neural influence
4) ___ = above 3 interact with the psychology of the pt to create what is perceived as pain

A

1) Transduction
2) Transmission
3) Modulation
4) Perception

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21
Q
  • Noxious stimuli causes cell damage with the release of sensitizing chemicals (Prostaglandins, Bradykinin, Serotonin, Substance P, Histamine)?
  • These substances activate ___ and lead to generation of ___.
A

*Transduction
Nociceptors
Action potential

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22
Q

Action potential continues from site of injury to spinal cord > spinal cord to brainstem & thalamus > thalamus to cortex for processing?

A

Transmission

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23
Q

Neurons originating in the brainstem descend to the spinal cord and release substances (ex: endogenous opioids) that inhibit nociceptive impulses (dampening or rampening)?

A

Modulation

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24
Q

Conscious experience of pain?

A

Perception

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25
Q

1) _____ = first order neurons send their axons into the SC via the dorsal (sensory) root, may synapse with interneurons, sympathetic neurons, and ventral horn (motor) neurons
2) _____ = in gray matter of ipsilateral dorsal horn

A

1) Primary afferent neurons

2) Second order neurons

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26
Q

Axons of most second order neurons cross midline and form the ???
^This is the major pain pathway to the thalamus, reticular formation, nucleus raphe magnus & periaqueductal grey.
*Lies ___ in ___ ___ of spinal cord.

A

Spinothalamic tract

*Anterolaterally in white matter of spinal cord

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27
Q

These are located in the thalamus and send fibers to somatosensory areas I & II in the parietal cortex, and the superior wall of the sylvian fissure.
*They are responsible for ?

A

Third order neurons

*Perception & localization of pain

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28
Q

Alternate Pain Pathways: (these are actually stimulated by the ?)
1) Responsible for insomnia due to pain?
2) Activates anti-nociceptive, descending pathways?
(your own opioid system is essentially what gets going here)
3) Activate the hypothalamus and evoke emotional behavior?

A

Slow pain pathway

1) Spinoreticular tract
2) Spinomesencephalic tract
3) Spinohypothalamic & Spinotelencephalic tracts

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29
Q

Pain-Inhibition & Pain-Facilitation in the Dorsal Horn:

Neuronal circuitry within the dorsal horn. Primary afferent neuron axons synapse onto ___ ___ and onto ___ & ____ neurons.

A
  • spinothalamic neurons
  • excitatory
  • inhibitory
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30
Q

~Within the spinal column itself we have ___ that help with modulation of pain.

~Majority of modulation occurs in the ___. However, we have the capacity to also modulate pain to some degree in the ___.

A

~interneurons
~Brain
~Spinal cord

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31
Q

The slow pain pathway is known as? This uses what type of fibers?

A

Paleospinothalamic Pathway

C fibers

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33
Q

Fast Pain Pathway Summary: NEOSPINOTHALAMIC TRACT
1) First order neurons via type ___ fibers-enter lamina ___ & ___ (aka?)
of the dorsal horn of the spinal cord. Synapse with second order neurons.
2) Second order neurons cross the midline through the ___ and pass upwards in the ____.
3) Few of these fibers terminate on the ___.
4) MOST - travel to ___ of the ___.
5) Third order neurons communicate with the ___.

A
1) A delta
lamina I & V 
lamina marginalis 
2) anterior white commissure 
anterolateral columns 
3) reticular formation 
4) Ventrobasal complex (VBC) of the thalamus
5) somatosensory cortex
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34
Q

Fast Pain Pathway - Neospinothalamic tract:

These communicate with the somatosensory cortex so we know where the pain is and can perceive it?

A

Third order neurons

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35
Q

Slow Pain Pathway: PALEOSPINOTHALAMIC PATHWAY:

1) First order neurons via ___ fibers enter lamina ___ & ___ of the dorsal horns (aka?) & synapse with second order neurons.
2) Second order neurons make synaptic connections in ___, can go up ___!!
3) Most second order neurons join fibers from the ___, crossing to the opposite side traveling upwards through the ___.
4) They terminate widely in the ___, with 1/10 of fibers stopping in the ___, and the rest stopping in the ___, ___, ___ of midbrain mesencephalon & _____.

A
1) type C fibers
lamina II & III
substantia gelatinosa 
2) lamina IV-VIII
without crossing
3) fast pathway 
anterolateral pathway (aka spinothalamic tract) 
4) brainstem 
thalamus 
medulla 
pons 
tectum of midbrain mesencephalon 
periaqueductal grey
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36
Q

The second order neurons of this pathway will CROSS the midline through the anterior white commissure and pass upwards in the anterolateral columns?

A

Neospinothalamic tract

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37
Q

The second order neurons of this pathway can make synaptic connections in lamina IV-VIII, can go up without crossing?

A

Paleospinothalamic Pathway

  • **But most second order neurons in the slow pain pathway will join the fibers from the fast pathway, crossing to the opposite side traveling upwards through the anterolateral pathway
  • **Just realize the slow pain pathway can have fibers going up that DO NOT CROSS
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38
Q

____ can either ramp pain up or dampen pain down.

A

Interneurons

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39
Q

Localization of Pain:
1) FAST pain can be localized easily if A delta fibers are ___ ___ with ___ ___.

2) SLOW pain is ?

A

1) stimulated together
tactile receptors
2) poorly localized

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40
Q

The Analgesia System is Mediated by 3 Major Components:

1) ??? (this is located in the ____)
2) ??? (this is located in the ____)
3) ??? (these are located within the ____).

A
1) Periaqueductal grey matter 
midbrain
2) Nucleus raphe magnus 
medulla
3) Nociception (pain) inhibitory neurons
dorsal horns of the spinal cord
41
Q

Brain Analgesia Systems:

This is the biggest one, known as the epicenter of analgesia?

A

Periaqueductal grey matter (in the midbrain)

42
Q

Brain Analgesia Systems:

These act to inhibit nociception (these are the only ones located in the spinal cord)?
*transmitting neurons also located in the ???

A

Nociception (pain) inhibitory neurons

*spinal dorsal horn

43
Q

Periaqueductal Grey Matter:

  • This is located in the ___ ___ within the midbrain.
  • Plays a role in the ___ ___ of pain and in ___ ___.
A

*cerebral aqueduct
*descending modulation
defensive behavior (guarding/not moving affected extremity)

44
Q

Brain Analgesia Systems: Nucleus Raphe Magnus

This is afferently stimulated from ___ in the ___ & ___.

A
  • axons
  • spinal cord
  • cerebellum
45
Q

The main function is mostly pain mediation?

*In fact it sends projections to the dorsal horn of the spinal cord to directly inhibit pain.

A

Nucleus Raphe Magnus

46
Q

This plays a HUGE role in the descending modulation of pain?

A

Periaqueductal grey matter

47
Q

Nucleus raphe magnus projects throughout the ?

A

Cortex

48
Q

Pain Cellular Physiology: Chemical Mediators

1) ____ = released slower, building over few minutes
* Involved in what type of pain?
2) ____ = acts instantly; only lasts a few milliseconds (main excitatory chemical in your brain)
* Involved in what type of pain?
3) ____

A

1) Substance P
* slow chronic pain
2) Glutamate
* fast pain
3) Calcitonin gene-related peptide (CGRP)

49
Q

Pain Cellular Physiology: Modulators

1) Occurs peripherally at the ___, in the ___ ___ or in ___ ___. This modulation can suppress or aggravate pain.
2) One of the biggest modulators we have?

A

1) nociceptors
spinal cord
supraspinal structures (meaning in the brain)
2) NMDA receptor role

50
Q

___ is the only induction agent that we have in anesthesia that is also an analgesic.

A

Ketamine

51
Q

Pain Cellular Physiology-ACUTE: Information about noxious stimuli arrives from the periphery along ___ & ___.

1) ___ & ___ (ex: glutamine) are released.
2) Activation of ___ receptors by Substance P & activation of ___ receptors by EAAs cause ___ ___ of the pain neurons.
3) These are relayed to ?
4) ___ ___ ___ are inoperative as they are chronically ‘plugged’ by ?

A

A delta & C fibers
1) Substance P & Excitatory amino acids (EAAs)
2) neurokinin-1 (NK-1) receptors
AMPA receptors (amino-3-hydroxy-5-methyl-4-isoxazol propionic acid)
-transient depolarization
3) higher brain areas
4) NMDA-linked channels (N-methyl-D-aspartate)
-magnesium ions

52
Q

Newer research shows that administration of ____ can be beneficial for pain management.

A

Magnesium

53
Q

Pain Cellular Physiology: CHRONIC state = In response to intense and/or prolonged barrages of incoming nociceptive information, the neurons become sensitized & ___ to subsequent incoming nociceptive signals.

1) This barrage depolarizes the neurons such that the ___ ___ exit the ?
2) Results in influx of ___ - activates ___, causing conversion of ___ to ___. Because it is a gas, ___ rapidly diffuses out of the neurons.
3) This NO acts presynaptically to cause exaggerated release of ___ & ___.
4) Postsynaptically, NO causes the neurons to become ___ releasing ___, ___ etc.

A
Over-respond 
1) magnesium ions 
NMDA-linked channels 
2) calcium ions
nitric oxide synthase (cNOS) 
L-arginine to nitric oxide (NO) 
NO
3) Substance P & EAAs
4) hyperexcitable 
Substance P & Acetylcholine
54
Q

Need to give adequate medications (narcotics, ketamine) to prevent people from going from acute pain to chronic pain. The 2 most common types of chronic pain are headache and back pain, the third most common chronic pain is ?

*Once it becomes chronic ____ is knocked off.

A

Surgical pain

*magnesium

55
Q

Physiologic Responses to Acute Pain: Neuroendocrine Response

1) Increase secretion of ___ ___
2) ___ response
3) Decrease ___ ___, ___, ___
4) ___ release
5) ___ (if their diabetic, want to really monitor what their blood sugar is doing)

A

1) Catabolic hormones
2) Stress response
3) anabolic metabolism
insulin
testosterone
4) ACTH release
5) Hyperglycemia

56
Q

Physiologic Responses to Acute Pain: Cardiac Responses

1) Increased __, __, __, __
2) ___, ___, ___ (tachyarrhythmias)
3) Decrease ___ ___ secondary to pulmonary dysfunction = ___
4) Coronary artery ___ - high ___ *Release of serotonin may induce ?
5) Increase plasma viscosity = ___ ___ ___

A

1) Increased BP, HR, SVR, CO
2) MI, CHF, dysrhythmias
3) Decrease myocardial oxygenation
atelectasis
4) constriction - high catecholamines
*coronary vasospasm
5) Platelet induced occlusion

57
Q

Physiologic Responses to Acute Pain: Pulmonary Responses

1) Increased total body ___ ___
2) Increased ___ ___
3) Increased ___ ___ (patient compensating)
4) Pulmonary function decreased with ___ or ___ ___.

A

1) Increased total body oxygen consumption
2) Increased CO2 production
3) Increased minute ventilation
4) Abdominal or thoracic incisions (splinting)

58
Q

Physiologic Responses to Acute Pain: Pulmonary Responses

***Increased MINUTE VENTILATION as a result of decreased ___, ___, ___ = most detrimental alteration in post surgical lung volume. As ___ decreases, resting lung volume approaches closing volume, as it continues, ___ results, ___ ___, & ___ ensues.

A
  • decreased TV, FRC, VC
  • FRC
  • atelectasis
  • V/Q mismatch
  • hypoxemia
59
Q

Other Responses to Acute Pain:

1) Vascular system = stress mediated due to ___ & ___ (DVT, Pulmonary edema)
2) Visceral pain is referred to ___ ___ (ex: patient with laparoscopic procedures can have referred shoulder pain)
3) Muscle spasms = ___ & ___ ___ initiates reflex motor response leading to muscle spasm

A

1) platelet adhesion
hyper-coagulability
2) Somatic sites
3) Periosteal & Somatic irritation

60
Q

Other Responses to Acute Pain:
~GI & Urinary Systems = Increased sympathetic tone, increased sphincter tone, decreased gastric motility promoting ___ & ___
*Nausea and vomiting common
*___ ___ can occur = increased gastric juices

A

ileus & urinary retention

*Stress ulcers

61
Q

If lack of pain control ___ & ___ can result.

A

Anxiety & anger

62
Q

Methods to Relieve Pain: Take into Consideration~

1) ___ of pain relief
2) Patient history
3) Goals of management (talk to patient - “You may wake up with some pain”)
* ___ ___ goal is they are not going to have any pain
4) Acute vs Chronic pain (chronic pain patients will have an exaggerated response to acute surgical pain)

A

1) Duration of pain relief

* epidural anesthesia

63
Q

Release of ___ in response to the pain = this may induce coronary vasospasm.

A

Serotonin

64
Q

Methods to Relieve Pain:

1) ___ ___ = BEST POSTOPERATIVE PAIN MANAGEMENT BEGINS PREOPERATIVELY
2) ___ & ___ in General anesthesia
3) Regional blocks
4) ___ ___ at the ___ ___ could be used to control acute pain (hernia repair, tonsilar bed)

A

1) Preemptive Analgesia
2) Opioids & NSAIDs
4) Local infiltration at the surgical site

65
Q

Slow Pain Pathway: Paleospinothalamic Pathway:
Majority of the second order neurons ____, join the fast pain pathway and go up the ____ to the ____ and end there. They can communicate and excite the rest of the brain.

A
  • cross over
  • Spinothalamic tract
  • thalamus
66
Q

Slow Pain Pathway - Paleospinothalamic Pathway:

  • These do not synapse with third order neurons therefore they are poorly localized?
  • One of the areas where the local anesthetics work, very well known area?
A
  • C fibers

* Substantia gelatinosa

67
Q

The fast pain pathway is known as? This uses what type of fibers?

A

Neospinothalamic tract

A delta fibers

68
Q
***\_\_\_ \_\_\_ patients do better overall. 
~less morbidity
~less CV failure
~less infections
~less \_\_\_ \_\_\_ = \_\_\_ significant effect on the neuroendocrine response to surgery 
~lower overall post-op complication rate
A

***Regional Anesthesia patients
~less urinary cortisol
>L1

69
Q

Methods to Relieve Pain: MAXIMUM ANALGESIA
~Opioids ~NSAIDs
1) ___ ___ (___ ___) = inhibits prostaglandin synthesis
2) Two Types of Cox recognized:
*___ = constitutive & widespread through the body
*___ = expressed primarily with inflammation (___ ___ ___ ___ is great for inflammatory states)

A

1) Cyclooxygenase inhibitors (COX inhibitors)
2) *COX 1
*COX 2
(Vioxx - COX 2 inhibitor)

70
Q

_____: Advantages to this are; they are cost effective, higher degree of patient satisfaction. Total drug consumption is less than IM. Harder to overmedicate self.

A

Patient Controlled Analgesia (PCA)

71
Q

Patient Controlled Analgesia (PCA) - Features:

  • Reservoir
  • ___ ___ = pushbutton to be operated BY THE PATIENT ONLY (not family & visitors)
  • Delivers a ___ ___
  • ___ (minimal intervals btw doses)
  • ___ ___ (background infusion)
A
  • Infusion controller
  • Specific dose
  • Lockout
  • Basal infusion
72
Q

PCA prevents the ???

PCA findings = patients consume less drug, males use more than females, shortens hospital stay

A

“Pain no pain cycle”

73
Q

PCA = Prescription - it is crucial that you?

A

relieve the pain before starting PCA

74
Q

PCA:

1) ___ ___ each hit discourages the patient.
2) If the ___ ___ is ___ ___ could cause adverse reactions that also discourage the patient (distrust).

A

1) Too little
2) demand dose
too much

75
Q

PCA - Side Effects:

  • Onset of ___ ___ parallels analgesia and is more rapid with ___ ___.
  • Nausea, vomiting, constipation, pruritis.
  • **Nearly all overdoses have been to errors in the ???
A

Respiratory depression
lipophilic opioids
**
Programming of the Parameters

76
Q

This is 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?

A

Chronic Pain

77
Q

*Chronic Pain has no time limit, often has no apparent cause and serves no apparent biological purpose.
Chronic pain can trigger multiple ___ ___ that confound both patient and health care provider, leading to feelings of helplessness & hopelessness.

A

Psychological problems

78
Q

The most common causes of Chronic Pain include ___ (this is #1), followed very closely by ___, recurrent facial pain, cancer pain & arthritic pain.
*And sometimes chronic pain can have a ___ or ___ cause.

A

1) Low back pain
2) Headaches
* psychosomatic or psychogenic cause

79
Q

Chronic Pain Causes:
~Chronic pathology in somatic or visceral structures
~Psychological mechanisms
~Peripheral mechanisms = Chronic pain syndromes associated with chronic inflammations in the periphery respond to ___ & ___ which prevent synthesis of prostaglandins.

A

~Aspirin & NSAIDs

80
Q

____ = in chronic pain can create excessive muscle tension & tendon stretch. ___ ___ can create local ischemia and persistent disruption of the microcirculation.

A

Reflex role

Sympathetic hyperactivity

81
Q

Chronic Pain - Causes:

1) ____ = Lesions of peripheral nerves, dorsal roots or dorsal ganglion cells. Found in causalgias, and other reflex sympathetic dystrophy, phantom pain.
2) ____ = Suggests that intense stimulation of nerve fibers in the cord activate internuncial neurons creating an abnormal reverberatory activity in a closed loop.
3) ____

A

1) Peripheral-Central Mechanism
2) The Circle Mechanism
3) Chronic Nerve Compression

82
Q

Chronic Pain:

1) ____ = Found in lesions to the thalamus and spinal cord injury as in paraplegia.
2) ____ = Severe stress, usually seen in chronic tension headaches and chronic pain due to muscle spasms in the shoulder, back and chest.
3) ____ = Secondary gain. These patients frequently develop reactive depression and hypochondriasis.

A

1) Central Pain Mechanisms
2) Psychophysiologic Mechanisms
3) Learned Mechanisms

83
Q

Effects of Chronic Pain:
___ & ___ become depleted, so minor injuries become intolerable.
*Very important to do preemptive pain management on these patients!

A

Serotonin & Endorphins

84
Q

Chronic Pain - Psychologic Profiles:
1) The chronic pain patient shows significant differences on the MMPI (Minnesota Multi-phasic Personality Inventory), neuroticism. However, when the pain is relieved the neurotic features dissipate. The longer the duration of the pain, the ???

A

greater the psychological changes

85
Q

Treatment of ??? = must not only remove the pain and the cause of the pain but also rehabilitate the patient and family physically, psychosocially & psychologically

A

Chronic Pain

86
Q

Chronic Pain = Examples of Pain Control include:

1) ___ ___ ___ with or without trigger point injections
2) ___ ___ ___ with neurolytics (cutting off afferent sensory nerves)
3) ___
* **Often require more ?

A

1) Steroid Epidural Injections
2) Peripheral Nerve Blocks
3) Acupuncture
* **analgesics

87
Q

Approximately 19 million people worldwide experience cancer pain every year.
Causes:
*Direct tumor involvement
1) This is the most common cause of cancer pain?
2) The next most common cause?
*Cancer pain can also be due to ___

A

1) Tumor invasion of the bone
2) Tumor compression of peripheral nerves
* Treatment

88
Q

Cancer Pain Effects:

1) ____ = worse than for chronic pain due to loss of sleep, appetite, nausea & vomiting
2) ___ = heightened anxiety, separation & loss, self esteem, life’s goals, effect on the family, disfigurement

A

1) Physical

2) Psychological

89
Q

___ patients with pain had more emotional disturbances and died sooner than those whose pain was controlled.

A

Cancer patients

90
Q

Cancer Pain:

This results from lack of knowledge of Pharmacology of analgesics, fear of addiction and respiratory depression?

A

Poor Pain Treatment

91
Q

Cancer Pain Management:
Start with this (it will not last very long) for mild pain - inhibit prostaglandin synthetase, and some anti-tumor effects in bone metastases?
*Problem - ___ ___ on analgesia

A

Nonopioid analgesic

*Ceiling effect

92
Q

Cancer Pain Management - WHO Recommendations (3 Step):

1) Nonopioid analgesic (mild pain) Name 3???
2) “Weak” oral opioids (moderate pain) Name 2??
3) “Stronger” opioids (severe pain) Name 2??

A

1) Aspirin, acetaminophen, NSAIDs
2) Codeine, oxycodone
3) Morphine, hydromorphone

93
Q

Cancer Pain Management: ADJUNCTS

1) ___ = prevent release of prostaglandins and stimulate appetite
2) ___ = elevate mood, help with sleep, block reuptake of serotonin, potentiate narcotic analgesics

A

1) Corticosteroids

2) Antidepressants

94
Q

Cancer Pain Management:

1) ___ = normal for opioids, especially IV administered. Terminally ill can require ___ of IV morphine.
2) ___ = Rare event in cancer pain patients.
3) ___ = Intensity & duration of pain. Physical, mental & nutritional state. Pharmacology. Route of administration.
* They build tolerance, but are not necessarily addicted

A

1) Tolerance
200 mg/hr
2) Addiction
3) Drug choice

95
Q

Cancer Pain Management:

  • Goal of this is sustained ___ ___ with minimal ___ ___.
  • Cancer patients build tolerance, but are not necessarily addicted to opioids
A

*Pain relief

side effects

96
Q

Other Treatment Modalities for Cancer Pain Management:

1) ___ = local anesthetics, peridural narcotics
* Disadvantage = ?
2) ___ = permanent destruction of the nerve, rare to not get some motor loss as well

A

1) Regional Analgesia
* Short term relief
2) Neurolytics

97
Q

Pain which persists one month longer than expected?

A

Chronic pain

98
Q

This helps with perception?

A

Modulation