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Theories and Procedures > Lecture 2: Inflammation & Tissue Repair > Flashcards

Lecture 2: Inflammation & Tissue Repair Flashcards

1
Q

What is an INJURY?

A

Impaired structure and function

Cells of tissues unable to carry out normal function

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2
Q

Causes of injury:

A 
Physical agents (burns, radiation)
Metabolic processes (ischemic tissue)
Biological processes (bacteria, viruses, parasites)
Chemical agents (acids, gases)
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3
Q

What is trauma?

A

Injury that results from physical force, not the actual force

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4
Q

Physical trauma types

A

Macrotrauma & Microtrauma

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5
Q

Macrotrauma

A

acute injury affecting multiple tissues

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6
Q

Microtrauma

A

overuse injuries, like chronic repetition; low grade stress that doesn’t allow tissues to heal properly

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7
Q

Secondary injury

A

May result from a trauma; an injury that may affect other tissues

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8
Q

What factors affect the healing process?

A

Health of pt
Severity of injury
Site of injury
Acute vs chronic injury

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9
Q

What is the PT goal in the Healing process?

A

Affect the healing process; how well the healing process occurs
Eliminate the cause of the injury
Promote regeneration of normal tissue

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10
Q

Phases of Tissue Healing Continuum

A

Inflammation, Proliferation, and Maturation

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11
Q

General Purpose of Inflammation Phase

A

prepares wound for healing

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12
Q

General Purpose of Proliferation Phase

A

rebuilds damaged tissue & strengthen the wound

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13
Q

General Purpose of Maturation Phase

A

modifies scar tissue into its mature form

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14
Q

Goals of Inflammatory phases

A

Defend the body against foreign substances

To dispose of dead and dying tissue to allow for repair

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15
Q

How can Inflammation phase be harmful?

A

it can become chronic or is directed at wrong tissue

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16
Q

Cardinal Signs of the Inflammation Phase

A 
Heat 
Redness
Swelling 
Pain 
Loss of function
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17
Q

Inflammatory phase events

A 
Injury 
Ultrastructural changes 
Chemical mediation 
Hemodynamic/Vascular changes 
Metabolic changes 
Permeability changes 
Leukocyte migration 
Phagocytosis
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18
Q

Vasoconstriction

A

Immediate response to stop bleeding

Lasts 5-10 min post-injury

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19
Q

Vasodilation

A

Lasts about 1 hour post injury
Increased capillary permeability
Goal: to allow chemical mediators to get to site of injury

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20
Q

Chemical Mediators

A

Histamine, Bradykinin, Hageman Factor, Prostaglandins, Complement System

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21
Q

Histamine

A

released by mast cells, platelets, basophils

contributes to swelling & chemotaxis (attraction of leukocytes to dead tissue)

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22
Q

Bradykinin

A

Biologically active peptides derived from plasma

↑ capillary permeability

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23
Q

Hageman Factor

A

Coagulation
Plasma protein → plasmin kallikrein
Activates complement system

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24
Q

Prostagladins

A

PGE1: ↑ vascular permeability
PGE2: attracts leukocytes & synergy with mediators
responsible for febrile states

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25
Q

Complement System

A

anaphylatoxins C3a, C4a, C5a
Induce mast cell and basophil degranulation → release histamine, further increase in vascular permeability
Main responsibility of complement system: increase permeability, stimulate phagocytosis, &
Chemotactic stimuli for leukocytes

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26
Q

Antihistamine

A

decreases histamine release to reduce inflammatory response

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27
Q

NSAIDs

A

Inhibit synthesis of prostaglandins, which can inhibit the inflammation phase

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28
Q

Role of Neutrophils

A

Short-lived leukocyte (7 hours) that is the first line of defense against bacteria via extravasation

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29
Q

Extravasation

A

Margination
Pavementing
Diapedesis
Emigration

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30
Q

Margination

A

Where the neutrophil move to the sides of capillaries

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31
Q

Pavementing

A

When the neutrophil is stuck to the side of the capillary vessel

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32
Q

Diapedesis

A

The neutrophil finds a gap in the capillary and squeezes through

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33
Q

Emigration

A

Neutrophils gets through capillary and is in perivascular space

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34
Q

Types of edema fluid

A

Transudate: thin, clear serum
Exudate: Cloudy, serum highly concentrated with protein WBCS, lipids cellular debris
Pus (Suppurative exudate): opaque, exudate highly concentrated in leukocytes, tissue debris, microorganisms; can result in abscess

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35
Q

Cells responsible for clot formation

A

Platelets

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36
Q

What do platelets do to form a clot?

A 
Bind to collagen, releasing fibrin→ stimulates clotting 
Released PDGF (platelet derived growth factor)→ stimulates cell growth and division
37
Q

When does clot formation begin?

A

around 12 hours and completed by 48 hours

38
Q

Macrophages

A

Most important cell in inflammatory phase

Produce chemicals and enzymes → removal of tissue and bacteria

39
Q

Immune Response Order

A

Macrophages → T-lymphocytes → B cells → Plasma cells → antibodies bind to antigens → Complement system
*Macrophages present foreign antigens to T lymphocytes to activate them which activate B cells, causing them to evolve into plasma cells, which make antibodies that specifically bind foreign antigens

40
Q

Types of activation of the Complement system

A

Classical activation: antibody-antigen association

Alternative activation: cellular or microbial substances

41
Q

Inflammation Phase occurs during what days of injury healing process

A

Days 1-6

42
Q

Proliferation Phase occurs during what days of injury healing process

A

Days 3-20

43
Q

Goal of Proliferative Phase

A

Cover and strengthen the wound

44
Q

Phases of Proliferation

A

Epithelialization
Collagen production
Wound contraction
Neovascularization

45
Q

Epithelialization

A

Reestablishment of the epidermis (if injury is external)
Superficial vs deep wounds (superficial will occur faster)
Protective barrier
↓ fluid and electrolyte loss
↓ infection
Insufficient strength

46
Q

Signs & Symptoms of Proliferation Phase

A

Scars are red and swollen (increased vascularity)
Tenderness to tension or pressure
decreasing signs & symptoms from inflammation phase

47
Q

Collagen Production Stage

A

Fibroblasts make collagen and produce hyaluronic acid
Collagen: Connective tissue protein
provides increased strength (still poor overall) and facilitates movement of other cells

48
Q

Granulation Tissue contents:

A

Newly formed capillaries
Fibroblasts/myofibroblasts
Collagen
*Decreases fibrin cloth and is mediated by chemotatic factors to increase fibroblast activity

49
Q

Type III Collagen

A

thin, weak-structured collagen, inconsistent organization

50
Q

Type I Collagen

A

mature and stronger than type III (replaces it ~day 12)
By day 21: collagen production maximal but strength ~20%
By 6 weeks: 80% of its long-term strength is present

51
Q

Excessive Collagen production can lead to…

A

excessive scar tissue

52
Q

Role of Hyaluronic Acid

A

Glycosaminoglycan (GAG) produced by fibroblasts
Draws H2O into area, inc amount of intracellular matrix and facilitates cellular migration
collagen + hyaluronic acid = scar architecture

53
Q

Myofibroblasts

A

cells similar to fibroblasts that have contractile properties of smooth muscles

54
Q

Wound Contraction

A

Pulls the edges of the injured sit together

begins about day 5 and peaks about 2 weeks

55
Q

“Picture frame” theory

A

the ring of myofibroblasts moves inward from the wound margin
linear wounds with one narrow dimension heal rapidly; square/rectangular wounds progress at moderate pace and circular wounds contract most slowly

56
Q

Contractures

A

permanent shortening of scar tissue resulting in deformity

57
Q

Wound healing categories:

A

Primary Intention
Secondary Intention
Delayed Primary Intention

58
Q

Primary intention (primary union):

A

Sutures

Minimal loss of tissue and minimal bacteria

59
Q

Secondary intention (indirect union)

A

Significant loss of tissue or bacterial contamination

Wound edges are not approximated

60
Q

Delayed primary intension

A

Delayed approximation with sutures or skin grafts

61
Q

Neovascularization

A

Angiogenesis
Supply O2 and nutrients to injured and healing tissue
Signaled by macrophages
Immobilization helps protect vessels

62
Q

Angiogenesis

A

*growth of new blood vessels
New vascular network
Anastomosis of preexisting vessels
Coupling of vessels in injured area

63
Q

Goals of Maturation Phase

A

Restore prior function of injured tissue
Long term process
Scar whiter in appearance (because less blood flow)

64
Q

Time line for Maturation Phase

A

Day 9+

65
Q

Maturation Phase Features

A

↓ fibroblasts, macrophages, myofibroblasts, and capillaries; ↓ water content
Collagen matures, vascularity decreases
Realignment/remodeling of collagen fibers
Rate of maturation and scar characteristics

66
Q

Collagen Synthesis/Lysis

A 
Type 1 (bone, skin, tendon, scars)
Tensile strength ↑ faster than mass 
Keloid/hypertrophic scar (too much scar tissue)
May last 12-24 months post injury 
Redness= remodeling 
Scars are inelastic
67
Q

Induction Theory

A

scar attempts to mimic the characteristics of tissue its healing
*Dense tissue has preferential status

68
Q

Tension Theory

A

internal and external stresses placed on the injured area during maturation phase determine final tissue structure

  • Phase of repair
  • Nature of applied force
  • Low-load, long duration stretch in correct phase for permanent changes to occur
69
Q

Chronic Inflammation

A

Inflammatory response unable to eliminate cause of injury and restore normal function
Simultaneous progression of active inflammation, tissue destruction and healing
Macrophages accumulate, less stress or overuse keeps process going

70
Q

Causes of chronic inflammation

A

Following acute inflammation due to persistence of injury or interference in healing process
Immune response or autoimmune disease

71
Q

Acute inflammation phase

A

no longer than 2 weeks

72
Q

Subacute inflammation phase

A

4 weeks +

73
Q

chronic inflammation phase

A

months to years

74
Q

cellular components in chronic inflammation

A

Lymphocytes, macrophages, monocytes, eosinophils
Increased fibroblast proliferation → collagen production → increased scar tissue and adhesion formation → loss of function

75
Q

Local factors affecting healing process

A

Type, size, location
Infection
Vascular supply

76
Q

External factors affecting healing process

A

Physical agents used to modify the healing process; thermal, mechanical, electromagnetic
Movement: immobilization vs CPM

77
Q

Systemic factors affecting the healing process

A

Age
Disease
Medications
Nutrition

78
Q

Cartilage healing

A

Lacks lymphatics, blood vessels, and nerves
Results in bad healing
Cartilage and subchondral tissue

79
Q

Tendon healing

A

1st 3-4 days: inflammation; day 7-8: collagen synthesis, day 14: fibroblasts
Fibroplasia: intrinsic and extrinsic
Cell and collagen orientation
Synovial sheath injury may affect rehab by creating adhesions
Mobilization: active after 3 weeks

80
Q

Ligament healing

A

Type, size of defect, amount of applied load
Intracapsular (less vascularity) < extracapsular/capsular
Stabilization vs early controlled loading
Mature repair still 30-50% weaker

81
Q

Skeletal muscle healing

A

CANNOT proliferate
Satellite cells proliferate and differentiate to form new skeletal muscle cells
Myositis ossificans: calcified hematoma

82
Q

Bone healing

A

Heals itself with like tissue

83
Q

Primary vs secondary healing in Bone

A

Primary: bone has to be approximated with hardware
Secondary: bone is not displaced so it doesn’t need to be realigned

84
Q

Stages in Bone healing

A 
Impaction
Induction
Inflammation
Soft Callus
Hard Callus
Remodeling
85
Q

Impaction

A

dissipation of energy from an insult; proportional to energy applied; inversely to volume of the bone: small fx: force is large or bone is small

86
Q

Induction

A

osteogneic cells are activated

87
Q

Soft callus

A

begins when pain and swelling decrease

88
Q

Factors the impeded Healing

A 
Extent of injury 
Edema
Hemorrhage
Poor vascularity 
Separation of tissue
Muscle spasm
Atrophy
Corticosteroids
Keloids
Infection 
Humidity, climate, oxygen tension 
Health, age, nutrition

Theories and Procedures (5 decks)

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