Week 3 Flashcards

1
Q

What is the definition of pain?

A

an unpleasant sensory & emotional experience associated with or resembling that associated with actual or potential tissue damage

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2
Q

What is nociceptive pain?

A

arising from an identifiable tissue causing damage (thermal, mechanical, chemical (infection))

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3
Q

What is somatic pain?

A

within the skin or deeper (bones/joints or muscle); pain stimulus detected by the somatosensory nerves

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4
Q

What is visceral pain?

A
  • within or around the organs
  • sympathetic nervous system fibers detect the pain stimulus
  • poorly localized; can present as referred pain
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5
Q

What is neuropathic pain?

A

caused by dysfunction of nervous system. Often no identifiable tissue damage
- can be present in many different ways
- poorly or well-localized

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6
Q

Describe some of the characteristics of acute pain

A
  • fast, localized
  • stimulated by injury (mechanical, thermal)
  • pathway of fast A-delta myelinated fibers
  • sudden, short term
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7
Q

Describe some of the characteristics of chronic pain

A
  • slow, diffuse, prolonged
  • simulated by something existing (chemical)
  • pathway of slow unmyelinated C fibers
  • long-term, disabling
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8
Q

What is chronic pain?

A
  • lasting more than 3 months
  • not usually an extension acute pain (different underlying mechanisms)
  • may become on issue of nerve hypersensitivity
  • may be localized within the CNS
  • may be a mix of excitatory & inhibitory systems
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9
Q

What is the current research saying about chronic inflammation? What is the ideal combo treatment?

A
  • inflammation of the nervous system due to malfunctioning glial cells) as a cause of chronic pain
  • ideal treatment combo = exercise, fish oil, neuromodulation
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10
Q

What are the pharmcological treatments for pain management?

A

analgesic and anesthetics

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11
Q

How do analgesic drugs work?

A

reduce the ability to perceive pain

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12
Q

How do anesthetic drugs work?

A

block the ability to sense pain

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13
Q

What are some non pharmacological treatment for pain management?

A
  • prevention (sleep management, nutrition, education, goal-setting)
  • psychological (mindfullness)
  • physical (safe exercise, level of pain, learn your body)
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14
Q

What is neuromodulation work?

A
  • use an electromagnetic coil to deliver a magnetic pulse that stimulates nerve cells in specific regions of the brain
  • shown to be an effective treatment for chronic depression & chronic neuropathic pain
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15
Q

What is inflammation?

A
  • an important defense mechanism of the body; immunovascular response to some form or insult
  • caused by a stimulus
  • can be acute (hours, days, weeks) or chronic (weeks, months, years)
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16
Q

What are the 5 cardinal signs or acute inflammation?

A
  1. pain
  2. heat
  3. redness
  4. swelling
  5. loss of function
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17
Q

What causes pain from inflammation?

A
  • chemical mediators increase nociceptors
  • pressure on nerves
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18
Q

What causes heat and redness from inflammation?

A

increased blood flow

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19
Q

What causes swelling from inflammation?

A

edema from increased capillary permeability

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20
Q

What is the initiation and amplification phase of acute inflammation?

A

chemical mediators are released into the blood & at site of injury by resident immune cells; more immune cells are recruited to the area

21
Q

What is the destruction phase of an acute inflammation response?

A

neutralization of the injury & debris removal by chemical mediators & immune cells

22
Q

What is the termination phase of an acute inflammation response?

A

cytokines & chemokines end the inflammatory process

23
Q

What are cytokines?

A
  • proteins coordinate the immune response
  • some are pro-inflammatory and some are anti-inflammatory
24
Q

In a typical sequence of events during an acute inflammatory response, where are chemical mediators released?

A

into the blood and at the side of injury (or infection) by resident immune cells

25
What are the local action of chemical mediators?
pain response: bind to nearby that nociceptors vascular response: vasodilation & increased capillary permeability cellular response: attract immune cells to the site of injury (chemotaxis)
26
What cells are involved in the inflammatory response?
platelets, mast cells, neutrophils, macrophages
27
What do platelets do?
release blood-clotting proteins at the wound site (if needed); platelet activating factor → platelet aggregation (increased blood clotting and blood vessel repair)
28
What do mast cells do?
secrete chemical mediators
29
What do neutrophils do?
migrate to the site and secrete factors that kill pathogens, phagocytosis to remove pathogens and debris
30
What do macrophages do?
secrete cytokines, phagocytosis to remove pathogens and debris, fever, chemotaxis, leukocytosis
31
What are the 3 mast cells to know?
histamine, prostaglandins, leukotrienes
32
What does histamine do?
vasodilation & increased capillary permability
33
What do prostaglandins do?
vasodilation & increased capillary permeability, pain, fear
34
What do leukotrienes do?
vasodilation, increased capillary permeability, chemotaxis
35
What are the different types of plasma proteins?
Bradykinin, complement system, C-reactive protein, prothrombin & fibrinogen
36
What does bradykinin do?
vasodilation & increased capillary permeability
37
What does complement system do?
vasodilation & increased capillary permability, chemotaxis
38
What do C-reactive proteins do?
secretion of more cytokines, activates complement system, chemotaxis
39
What do prothrombin & fibrinogen do?
blood clotting
40
What is exudate?
interstitial fluid collected in area of inflammation
41
Describe serous exudate
- classic 'edema' during inflammation - watery, fluid + small amounts of protein & white blood cells
42
Describe fibrinous exudate
- thick & sticky, higher cell & fibrin content
43
Describe purulent exudate
thick & yellow-green colour, higher white blood cells & cell debris; may also contain microorganisms, suggests a bacterial infection
44
Describe hemorrhagic exudate
blood vessels damaged
45
What are non-pharmaceutical treatments for inflammation?
compression, cold, hot, elevation, rest/avoid further trauma in acute phase
46
What are the potential fates of healing from inflammation?
resolution: damaged cells recover regeneration: damaged cells are a cell type that can divide by mitosis (eg. epithelial cells) and can therefore be replaced by identical cell types replacement: damaged cells replaced by connective (scar) tissue; loss of function in area
47
chronic inflammation can result from...
- acute inflammation that is unable to resolve - low level exposure to an irritant or foreign material - autoimmune disorders - inflammatory & biochem inducers causing oxidative stress & mitochondrial dysfunction (free radicals, advanced glycation end products, oxidized lipoproteins, other
48
What are some non-pharmacological treatments of chronic inflammation
- nutrition (anti-inflam vs inflam foods) - aerobic & resistance exercise (promotes metabolic healthy tissue & anti-inflammatory reponse) - sleep quality & quantity - stress reduction