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PHTH 7111 Summer 2014 > Exam 2: pain inflamaiton medication > Flashcards

Exam 2: pain inflamaiton medication Flashcards

1
Q

3 phases of Healing

A
  1. Inflammation
  2. Proliferation
  3. Maturation
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2
Q

Inflammation Phase (general)

A

Prepares for healing

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3
Q

Proliferation phase (general)

A

rebuilds and

strengthens damaged tissue

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4
Q

Maturation phase (general)

A

modifies tissue to mature form

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5
Q

Inflammation phase (specific)

A
  • 1-6 days
  • Induced by disease/trauma
  • Cardinal signs of inflammation present
  • hyperemia
  • swelling
  • pain from pressure
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6
Q

Inflammation phase time

A

1-6 days

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7
Q

Cardinal signs of inflammation (5)

A
  1. Calor
  2. Rubor
  3. Tumor
  4. Dolor
  5. Functio laessa
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8
Q

Hyperemia

A

Increased blood flow (redness, erythema)

occurs with inflammation

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9
Q

erythema

A

reddening of skin

occurs with inflamation

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10
Q

Calor

A

heat.

one of the 5 cardinal signs of inflammation

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11
Q

Rubor

A

Redness.

one of the 5 cardinal signs of inflammation

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12
Q

Tumor (in regards to inflammation)

A

swelling.

one of the 5 cardinal signs of inflammation

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13
Q

Dolor

A

pain.

(In inflammation: caused by chemical mediators released during inflammation and from pressure from swelling)

one of the 5 cardinal signs of inflammation

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14
Q

Functio laessa

A

decrease in function.

one of the 5 cardinal signs of inflammation (this one was recently added)

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15
Q

Swelling (in inflammation)

A

also known as tumor

increased permeability of cells and vasodilation

often accompanied by ecchymosis

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16
Q

Ecchymosis

A

a discoloration of the skin resulting from bleeding underneath, typically caused by bruising.

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17
Q

Injuries causing inflammation: (8)

A
  1. sprains, strains, & contusions
  2. Fractures
  3. Foreign bodies (sutures)
  4. Autoimmune diseases (RA)
  5. Microbial agents
  6. chemical agents
  7. thermal agents (burns/frostbite)
  8. Irradiation (UV or radiation)
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18
Q

Sprain

A

ligament tear

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19
Q

strain

A

tendon tear

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20
Q

contusion

A

bruise:

bone or soft tissue

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21
Q

How is inflammatory process triggered?

A

mast cells, the most important activator (NOT the trigger)

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22
Q

How do mast cells induce inflammation (2 ways)

A
  1. Degranulation
    • release of contents of mast cell granules
    • Acute
  2. Synthesis
    • new production and release of mediators in response to stimuli
    • Long term
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23
Q

Mast cell degranulation

A

Acute: release of contents of mast cell granules within seconds:

  • Histamines
  • Chemotactic Factors
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24
Q

Mast cell synthesis (what it is and 3 things synthesized)

A

Activated mast cells begin new synthesis of inflammatory mediators to be released later:

  • Leukotrienes
  • Prostaglandins
  • platelet-activating factors

Long term response (takes over from histamine response)

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25
Q

What do mast cells release during degranulation? (2 things)

A

Histamines

Chemotactic Factors

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26
Q

Histamines cause: (in inflammation)

A
  • temporary rapid constriction of smooth muscle + dilation of veinules (increases blood flow)

  • Increases vascular permeability
  • Improves adherence of leukocytes to endothelium

VERY QUICK

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27
Q

Chemotactic Factors, (what they do and 2 types)

A

form gradient that cause chemotaxis of cells towards inflammation

  1. neutrophil chemoactic factor (attracts neutrophils)
  2. Eosinophil chemotactic factor of anaphylaxis (attracts eosinophils)

TNF-a (tumor necrosis factor-alpha) is also a chemotactic factor

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28
Q

Leukotrienes

A

synthesized by mast cells

effects similar to histamine except slower and longer response

Important later in stages of inflammation

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29
Q

Prostaglandins

A
  • synthesized by mast cells
  • cause increased vascular permeability, neutrophil chemotaxis, & pain
  • (NSAIDs inhibit prostaglandins and are non-selective)
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30
Q

NSAIDs

A

Non-Steroidal Anti-Inflammatory Drug

non-selective

inhibit prostaglandins

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31
Q

Platelet-activating factor

A

synthesized by mast cells

cause

  1. endothelial retraction to increase vascular permeability,
  2. leukocyte adhesion to endothelial cells, and
  3. platelet activation
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32
Q

What causes leukocyte adhesion to endothelial cells (one for long term and one for short term)

A

Short term: Histamines released by degranulation of mast cells (early part of inflammatory response)

Long term: Platelet-activating factor synthesized by mast cells after histamines are spent during longer inflammatory response

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33
Q

Vascular response to inflammation

A

Initial (5-10 min after injury): vasoconstriction (chemically induced –> norepinephrine)

Later (1 hour after injury): Vasodilation (chemically induced–> histamine, Hageman factor, bradykinin, prostaglandins, and complement fractions)

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34
Q

bradykinin

A

a compound released in the blood during later stages of inflammation that causes vasodilation. It is a peptide comprising nine amino-acid residues.

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35
Q

Hageman factor

A

plasma protein that causes later vasodilation during inflammation

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36
Q

Vasoconstriction (clot formation)

A

Blood vessel linings adhere

Neutrophils migrate to injury area - extravasion

Leukocytes line vessel wall - margination

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37
Q

Extravasion

A

Neutrophils migrate to injury area

part of vasoconstriction (clot formation)

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38
Q

Margination

A

Leukocytes line vessel wall

part of vasoconstriction (clot formation)

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39
Q

Neutrophils

A

Short term: predominant phagocytes in early inflammatory process (Arrive 6-13 hrs after injury)

not capable of cell division

become puss (short life)

Primary role: Sterile lesions: remove debris and dead cells Non-sterile lesions: phagocytosis of bacteria

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40
Q

Phagocytosis

A

cell eating (bacteria is more solid)

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41
Q

Pinocytosis

A

cell drinking (bacteria is more liquid)

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42
Q

Leukocytes (general, not specific types)

A

Long term.

Many forms: Monocytes immature form that becomes macrophage after inflammatory site entry. (Eosinophils & Basophils are leukocytes too)

Arrive 24 hrs post injury

Largest normal blood cell

produced in bone marrow

Seen in higher proportions in chronic inflammation

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43
Q

Leukocytes (3 types)

A

Monocytes –> become macrophages after entry into inflamed site

Eosinophils

Basophils

Long term

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44
Q

Eosinophils

A
  • type of leukocyte
  • mildly phagocytic
  • primary defense against parasites
  • help regulate vascular mediators from mast cells
  • Help limits inflammation
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45
Q

Basophils

A

type of leukocyte

Mobile mast cells which release similar inflammatory agents

46
Q

Edema

A

Swelling; accumulation of fluid in extravascular space/interstitial tissues

Diapedesis = leukocytes squeeae through vessel wall

emigration: chemotactic agents attract leukocytes to interstitial tissues

47
Q

Diapedesis in Edema

A

Leukocytes squeeze through vessel wall

48
Q

Emigration in Edema

A

Chemoactic agents attract leukocytes to interstitial tissues

49
Q

Effusion: definition and 4 types

A

swelling contained in cavity.

  1. joint effusion
  2. Pleural effusion
  3. ascites
  4. peritoneal effusion
50
Q

Difference between edema and effusion

A

Edema is more likely in interstitial tissue

Effusion is more likely in joint cavity (or I assume other body cavities??)

51
Q

4 Forms of Edema/Effusion

A
  1. Transudate
  2. Exudate
  3. Pus
  4. Blood
52
Q

Transudate

A

Dissolved electrolytes and H2O (clear)

can be found in effusions/edema

53
Q

Exudate

A

plasma proteins, lipids, cellular debris (cloudy)

can be found in effusions/edema

54
Q

Pus

A

neutrophils, digested tissue, fluid, bacteria

can be found in effusions/edema

55
Q

Aspiration of a joint

A

stick a needle in in a joint cavity and remove fluid.

Used to determine contents of effusion

56
Q

Increased vascular permeability (4 stages?)

A
  1. Endothelial cell contraction- 15-30 minutes – Opens spaces between cells
  2. Endothelial injury- altered substance release – Contents of vessel spill into interstitium
  3. Leukocyte bind to injured area – Release chemicals and enzymes creating injury
  4. Regenerating capillaries- – In later stages of healing tight junctions yet to form
57
Q

Hemostatic Response

A

Platelets bind to collagen, release fibrin

Fibrin and fibronectin limit fluid drainage and hemorrhaging

clot formed

58
Q

Cellular Response

A
  • — Hematoma- erythrocytes (RBC’s) present in injured tissue ( hemarthrosis )- usually severe —
  • Leukocytes (WBC’s)- present in different concentrations in different healing phases —
    • Neutrophils, eosinophils , basophils, monocytes, lymphocytes, macrophages —
  • Phagocytosis- enzymes
59
Q

Immune response

A
  • * Lymphocyte and phagocyte leukocytes (WBC’s) —
  • *Complement system —
    • —20 Enzymatic plasma proteins (just know it released a bunch of protein - most important are C3 & C5)
60
Q

Compliment System

A

Consists of large number of proteins (20) that are activated.

Most important are C3 & C5:

  • result in following subunits:
    • Opsonins
    • Chemotactic factors
    • Anaphlatoxins
61
Q

Proliferative Phase (general and length of time)

A

3-20 days

Prepared for by inflammation phase

Main tissues:

  • Epithelial cells & connective tissue
  • Cover and strengthen injury site
  • Epitheliazation, collagen production, wound contracture, & neovascularization
62
Q

When do we start to see callous formation on a broken bone in an x-ray?

A

The proliferation phase

63
Q

Epithelialization

A

Healing:

Primary intention: close approximation of tissues (with sutures)

Secondary intention: indirect union (without sutures)

64
Q

Fibroplastia/Collagen Production

A
  • Granulation tissue
  • Type III collagen
  • Formation of scar
  • Type I collagen day 12
65
Q

Type III collagen

A

Initial type of collagen in proliferative phase collagen production

weak and thin

66
Q

Type I collagen

A

type of collegen produced by day 12 (proliferatave phase) - I think it can be converted from type III colagen

more mature and stronger than type III collagen

67
Q

Scar formed from (2 things) during proliferation.

A

Glycosaminoglycan (GAG)

and

Collagen

68
Q

Wound Contraction

A

myofibroblasts help pull edges together through creation of smooth muscle cells

not the same as a wound CONTRACTURE (which is pathological)

69
Q

Neovascularization

A

development of new blood supply (angiogenesis)

70
Q

Maturation phase

A

day 9 on (may take 1-2 years from injury)

Goal: return function (depends on what kind of structure is healing:

  • Type I collagen: bone, skin, tendon, and mature scars
  • Type II collagen: replaces former fibrocartilage & articular
  • Type III collagen: GI tract, uterus, and blood vessels
71
Q

Hypertrophic scars

A

synthesis greater than lysis

treatment: pressure garments

kind of looks like keloid but not

72
Q

Keloid

A

scar beyond boundaries of injury

treatment: surgical, poor outcomes

73
Q

Importance of scar management techniques during scar maturation phase

A

If not moved, tissue underneath can bind to scar

74
Q

scar management techniques

A

after scab falls off:

  • scar massage
  • lotion with vitamin E
  • Cross-friction massage

Ideally for one year

TKR a good example of when to use

75
Q

cross-friction massage

A
  • if scar is vertical go across it
  • usually done daily for 3-5 min
  • usually can begin about 3 weeks post surgery
76
Q

Determination of final collagen structure (6)

A
  1. muscle tension
  2. joint movement
  3. soft tissue loading/unloading
  4. facial gliding
  5. temperature changes
  6. mobilization
77
Q

Chronic Inflammation

A
  1. progression of active inflammation
  2. tissue destruction
  3. healing
78
Q

Tendonitis

A

acute

79
Q

tendonosis

A

chronic and weaker than tendonitis

80
Q

Inflammation (define acute, sub-acute, and chronic normal expected time periods)

A
  • acute: 0-2 weeks
  • sub-acute: > 4weeks
  • chronic: several months or years

(this is not consistently defined, but this is a good normal expectation)

81
Q

Two types of factors affecting healing process

A
  • Local factors
  • Systemic factors
82
Q

Local factors affecting healing process (4)

A
  1. injury type, size & location
  2. infection
  3. vascular supply external forces (modalities affect here)
  4. movement
83
Q

Systemic factors affecting healing process (6)

A
  1. age
  2. disease
  3. medications
  4. nutrition
  5. smoking status
  6. fitness level
84
Q

Tendonitis pain (sharp or dull)

A

sharp

85
Q

Tendonosis pain (sharp or dull)

A

dull

86
Q

Specific healing: Cartilage - both types

A

poor blood supply

poor healing

87
Q

Specific Tissue Healing: Tendons/ligaments

A
  • 72 hr inflammation
  • collegen synthesis - 1 wk
  • Tendons no AROM x 3 wks
  • PROM indicated for both tissues within limits
88
Q

Specific Tissue Healing: muscle

A

no proliferation

myocitis ossificans risk

89
Q

myocitis ossificans

A

calcium build up in the muscle

Typically occurs when a muscle is bruised or from muscle contusion

A reason it is really important to use ice, not heat, on muscle right away

90
Q

Specific Tissue Healing: bone

A
  1. Inflammation
  2. soft callus
  3. hard callus (3 wks - 4 months)
  4. Remodeling (months to years)

can see callus on x-ray around 3 weeks

6-8 wks before you can put stress on bone after fracture

91
Q

3 phases of Tissue healing

A
  1. Inflammation
  2. Proliferation
  3. maturation
92
Q

Timeline for three phases of tissue healing

A
  1. Inflammation: 1-6 days
  2. Proliferation: 3-20 days
  3. Maturation: day 9 on (can be as many as 1-2 years)
93
Q

What is the fifth vital sign?

A

pain

94
Q

What is the most common symptom prompting patients to seek medical attention including rehabilitation?

A

Pain

95
Q

What are the five vital signs?

A
  1. HR
  2. RR
  3. BP
  4. Body Temp
  5. Pain
96
Q

Three goals of treating pain

A
  1. Resolving the cause (find belt & fix)
  2. modify patient’s perception
  3. maximize function within pain limits
97
Q

4 main Types of pain

A
  1. Nociceptive (Somatic & Visceral)
  2. Neuropathic (Central & Peripheral)
  3. Psychogenic (non-organic)
  4. Carcinogenic (cancerous)
98
Q

Somatic pain

A

A type of nociceptive pain all tissues except neural tissues:

Acute:
Chronic: persists beyond normal tissue healing time

99
Q

Visceral pain:

A

A type of nociceptive pain

organs

often referred

100
Q

2 types of nociceptive pain

A

Somatic

Visceral

101
Q

2 types of Somatic pain

A

(nociceptive pain)

Acute:
Chronic: beyond normal tissue healing time

102
Q

Visceral pain:

A

(nociceptive pain)

organs

referred

103
Q

acute pain

A

SNS response: increased muscle tone, HR, BP and skin conductance.

Sudden onset
Lasts days to weeks
normal pain behavior
good response to treatment
localized

104
Q

chronic pain

A
  1. persists beyond normal tissue healing time
  2. Caused from acute pain,
  3. several failed treatments
  4. medication tried & failed but continues to take unbearable or incapacitating alterations in SNS
  5. Gradual/diffuse and/or reffered lasts months-years (much more gradual onset)
  6. often abnormal pain behavior
  7. poor treatment response
105
Q

Neuropathic pain (2 types)

A

Peripheral

Central

106
Q

some treatments for Acute pain

A

Cryotherapy, cold laser, pulsed US

Stop aggravating activity to allow healing (if it hurts don’t do it)

107
Q

Is acute or chronic pain easier to treat?

A

Acute

108
Q

Will we likely see acute or chronic pain most often?

A

chronic pain

109
Q

What are the most common pain types we will see? (2)

A

Somatic pain

peripheral nervous system pain

110
Q

What is a test that can be used to detect psychogenic sources of pain?

A

Waddell signs and symptoms for back pain

111
Q

Referred Pain

A
  • hip to knee
  • L5-S1 nerve root to lateral leg
  • MI or angina to LA, Jaw
  • Diaphragm to lateral tip of either shoulder
  • spleen to left shoulder gall bladder to R shoulder or inferior angle of R
  • scapula

Referred pain is dull

112
Q

Wound Contrature (not contraction)

A
  • Contractures: pathological wound contraction that causes adhesions, muscle shortening, and tissue damage.
  • This is different than the normal wound contraction that is part of healing.
  • I think it is when the normal process gets out of control

PHTH 7111 Summer 2014 (2 decks)

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