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Pathophysiology > Wound Healing > Flashcards

Wound Healing Flashcards

1
Q

Purpose of wound healing

A

To restore normal tissue function

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2
Q

What is the biggest factor that delays wound healing

A

Infection

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3
Q

Healing begins during

A

The acute inflammatory response
Often within 24 hours of injury
Very fast in young healthy people

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4
Q

Healing is promoted by

A

-Clean wound
-Growth factors
-Good nutrition status (water, protein, vit c, copper, zinc, selenium)
-Good apposition of wound edges
-Good blood supply and lymphatic drainage
-Healthy immune system
-Survival of stromal and parenchymal cells for regeneration ( minimal loss of function )

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5
Q

Healing is Delayed by

A

-Chronic inflammation due to continued presence/repeat exposure to causative agent or large area of necrotic tissue
-Growth inhibitors
-Poor nutritional status (dehydration, lack of nutrients
-Poor apposition of wound edges
-Poor blood supply and or poor lymphatic drainage (elderly, CV, resp or lymphatic disorders, tissue hypoxia)
-Immunosuppression (radiation, chemotherapy, drugs; steroids, NSAIDS) diabetes, elderly
-Loss of stromal and parenchymal cells (noticeable loss of function; scarring)

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6
Q

Apposition

A
  • = approximation
    -I.e wound edges are close together; may require stitches or casting
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7
Q

“Repair”

A

Implies healing with scarring
Should use term resolved or healed with client

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8
Q

Debridement

A
  • Process of cleaning up the wound site
  • Includes removal of dead cells, necrotic tissue, and foreign material using physical, surgical, cellular, or chemical means
  • Essential to wound healing
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9
Q

Innate Immune Mechanisms Involved in Debridement

A

-Macrophages (M2)
-Flushing Mechanisms
-Enzymes

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10
Q

Macrophages and Debridement

A

-Macrophages: M2 Macrophages clean up cellular debris/microbes using phagocytosis

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11
Q

Flushing Mechanisms Debridement

A

-Such as tears, urination, stool, mucous, saliva
-Dilute and wash pathogen out/away
-Use copious amounts of fluid to help cleanse mucosal surfaces

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12
Q

Enzymes Mechanisms Debridement

A

-Proteolytic
-Such as lysozyme (tears, saliva)
-Help disrupt pathogens normal protein structure including changing shape and or removing amino acids
-When protein is changed, protein cannot function properly so bacterial/virus protein can’t make you sick

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13
Q

Term used to describe removal of pus laden tissue from wound

A

Aspiration

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14
Q

If wound is not cleaned of debris or is infected …

A

It will not heal properly
Causes chronic inflammation, delayed healing, and probably scarring

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15
Q

Would healing: Resolution

A

-Complete restoration of injured tissues to the original structure and function
-Damaged cells recover
-BEST OUTCOME
-No permanent deficits
-May take as long as 2 years

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16
Q

Examples of Resolution

A

-Mild sunburn (did it blister? = second degree burn)
-Uterus post partum (why doctors suggest waiting 2 years)

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17
Q

Wound Healing: Regeneration

A

-Production of new, healthy stromal and parenchymal body cells to replace those damaged by the injury
-Replacement occurs by mitotic cell division (mitosis)

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18
Q

Regenerative Potential

A

-Based on cells ability to replicate by mitosis
-Varies on specific cell type
-Is that cell capable of mitosis

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19
Q

3 Levels of Regenerative Potential

A

-Labile Cells
-Stable Cells
-Permanent Cells

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20
Q

Parenchymal cells

A

-Functional cells of the organ
-Their survival or ability to reproduce if injured is vital to the ability of the injured tissue to return to normal function

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21
Q

2 Types of cells that do not divide to replace

A

-Neurons
-Cardiac muscle cells

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22
Q

Labile Cells

A

-Capable of mitosis
-Constantly regenerating for normal tissue maintenance and to repair small wounds
-Cause most aggressive cancers (epithelial cancers, blood cell cancers)

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23
Q

Examples Labile Cells

A

-Epithelium
-Areas of wear and tear; epidermis, linings of digestive tracts, resp, urinary, reproductive
-Red bone marrow (all blood cells)

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24
Q

Stable Cells

A

-Do not normally divide but capable of mitosis if stimulated to do so by injury
-Also have ability to undergo cancer

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25
Q

Stable Cell Examples

A

-Endocrine and exocrine glands
-Liver (Hepatocytes)
-Kidney (Glomeruli and Nephron tubules)
-Smooth muscle
-Fibroblasts
-Osteoblasts
-Chrondroblasts
-Vascular endothelium
-Lung alveolar cells
-Neuroglia

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26
Q

Permanent Cells

A

-Have no regenerative potential
-Cannot under mitosis (after very early childhood)
-Even if tissue is injured and cells need replacing
-replaced by SCAR TISSUE

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27
Q

Examples permanent cells

A

-Neurons
-Cardiac Muscle cells
-Skeletal muscle (2+ years of age)

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28
Q

4 Primary Types of Tissue

A

Epithelium, Connective, Muscle, Nervous

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29
Q

Epithelium

A

-Cover surfaces
-Line structures
-Form glandular tissues
-Endocrine glands
-Exocrine glands
-Mucous secreting goblet cells
-Lacrimal glands
-GI glands
-Depending on specific location epithelial cells may be LABILE (at surfaces with lots of wear and tear) or STABLE cells (other areas)

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30
Q

Connective Tissue

A

-Binds (Connects) structures
-Dermis, Adipose, Bones, Cartilage, Tendons, Ligaments, Blood
-Most secrete collagen
-In general CT considered STROMAL TISSUE
-STABLE CELLS

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31
Q

Connective tissue Fibroblasts

A

-Usually considered stromal cells
-In Tendons and Ligaments which are essentially collagen fibroblasts considered parenchymal
-Extremely hardy and survive most tissue injuries

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32
Q

Fibroblasts are responsible for

A

-All collagen secretion including subtypes made during normal wound healing and scar tissue formation

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33
Q

Muscle Tissue

A

-Contracts to provide motility to the organ
-Skeletal, cardiac, smooth
-Skeletal muscle has some limited regenerative potential = considered STABLE until 2 years old then PERMANENT
-Smooth muscle = STABLE
-Cardiac muscle = PERMANENT

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34
Q

Nervous Tissue

A

-Neurons and supportive cells called neuroglia
-In CNS areas of neural atrophy replaced by excess CSF instead of scar tissue
-Decrease in brain tissue noticeable with medical imaging
-Neurons are PERMANENT
-Neuroglial cells are STABLE

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35
Q

Which categories of regenerative potential include stromal cells

A

Labile, Stable, Permanent

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36
Q

Wound Healing: Repair

A

-Replacement of destroyed tissue with SCAR tissue

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37
Q

Scar tissue formation is called

A

Fibrosis
-Made by a subtype of COLLAGEN that is produced by FIBROBLASTS during prolonged wound healing

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38
Q

Functions of Scar Tissue

A

-Weaker “filler” protein within a large wound or area of chronic inflammation
-Replaces dead parenchymal cells but does not restore normal tissue function —> deficits occur

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39
Q

Scar tissue provides damaged tissue with up to __ or original strength

A

80%

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40
Q

Fibrosis

A

-Dual purpose Term
-Used to describe normal collagen production AND scar tissue production

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41
Q

Collagen

A

Major fibre type in all connective tissues except blood

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42
Q

Fibroblasts

A

-Most common type of stromal cell
-Found in all types of connective tissue except blood
-Very hardy/resilient survive in situations that kill parenchymal cells like hypoxia
-

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43
Q

During Wound Healing Fibroblasts Will Become..

A

-Myofibroblasts
-Use their motility to infiltrate the wound site and fill in the site with secreted matrix = proteins and extra cellular fluid
-May simply be framework for new parenchymal cells to repopulate area or remodel to become permanent scar tissue (dependent on specifics of the situation)

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44
Q

Fibrosis: Collagen Production

A

-Production of collagen by CT cells called fibroblasts
-2 meanings depending on its location
-Fibrosis can mean normal collagen production during CT development, maintenance and normal wound healing
-Fibrosis can also mean excessive collagen production that results in scar/fibrotic tissue formation during wound repair

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45
Q

Fibroblasts are

A

Stromal

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46
Q

Fibroblasts can secrete

A

Several types of connective tissue protein fibers
-Main fibre is COLLAGEN

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47
Q

If parenchymal cells are permanently lost..

A

Fibroblasts will fill in the wound with scar tissue (collagen)

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48
Q

Collagen

A

-Most abundant CT fibre type
-Production regulated by gene expression within the fibroblasts (can change with circumstances)
-Normal collagen is healthy tissue and scar collagen are NOT the exact same proteins structurally or functionally

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49
Q

Normal Collagen Vs Scar Collagen

A

-Normal collagen is long, strong, and flexible, providing tensile strength, helps form a framework for parenchymal cells as they reproduce to return damaged tissues to full function
-Scar collagen is short, weak, and has minimal flexibility, very minimal strength to healing tissue, essentially “filler” to replace lost parenchymal cells

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50
Q

Amount of scar tissue and location..

A

Will determine whether normal or close to normal physiological activity is possible
-Cannot take over the normal parenchymal cell job

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51
Q

Other function of collagen..

A

When collagen comes into contact with platelets, it triggers the coagulation cascades =important to keep collagen out of blood stream to prevent intravascular thromboxane

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52
Q

Another name for a scar

A

Cicatrix

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53
Q

Fibrosis means

A

Production of collagen by fibroblasts
-Normal in creation and maintenance of healthy stromal tissues and is required in wound healing

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54
Q

Excessive fibrosis

A

Is scar tissue formation

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55
Q

Dense CT

A

-Collagen is arranged in regular rows, allowing strength and flexibility in the direction of orientation of the fibres (normal tendon)

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56
Q

Dense Irregular CT

A

Collagen arranger in a random pattern, allowing for some strength and flexibility in all directions (pericardium, dermis, sclera)

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57
Q

In scar tissue the subtype of collagen that replaces the normal collagen is..

A

Short, weak and randomly arranged

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58
Q

Dense and Irregular CT

A

Are a vascular

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59
Q

Achilles Tendon

A

Collagen is regularly arranged in long strong flexible bands with a few fibroblasts that produce and secrete collagen
-allows for strength of the tendon along a specific direction
-injury happens when outside forces cause over stretching of the collagen fibers and they break

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60
Q

2 Major Cell Types Involved in Wound Healing

A
  1. Macrophages
  2. Myofibroblasts
61
Q

Macrophages

A

-Phagocytic “clean up” cells
-Typically M2 subtype but M1 tissue residing may still be alive and helping
-Early: Cell debridement
-Promote healing by secreting chemical mediators
-Secrete angiogenic factors and fibroblast growth factor
-Later: Blood clot dissolution

62
Q

Myofibroblasts

A

Early: change gene expression to produce actin —> Myofibroblasts infiltrate damage site and secrete collagen fibers —> form framework for parenchymal cells to re establish in the site
-Later: Wound contraction to shrink size of wound

63
Q

Angiogenic Factor

A

Chemicals that stimulate the production of new arterioles, capillaries, venules, and lymphatic capillaries during wound healing

64
Q

Fibroblast Growth Factor

A

Stimulate the mitotic division of fibroblasts within the wound site

65
Q

What are Myofibroblasts

A

-Fibroblasts in which gene to make protein actin has been turned on
-Called Myofibroblasts due to their ability to migrate into the wound site
-Contract around wound site to reduce edges of wound
-Pulling sensation is Myofibroblasts working
-Can also cause itchy feeling at the irritate nerve endings
-Following wound healing actin secretion ends and cells return to normal tissue fibroblasts
-Parenchymal cells will repopulate the wound using the collagen framework

66
Q

What happens if you scratch a scab off?

A

Restarts at healing stage one if it bleeds

67
Q

Blood Clot Dissolution

A

-Destruction of blood clot happens once the endothelial lining of the vessel has healed

68
Q

Blood Clot Dissolution and Plasmin

A

-Plasmin is made in the liver and circulates in the blood plasma as the inactive precursor plasminogen
-Used to enzymatically digest the fibrin threads =fibrinolysis

69
Q

Fibrinolysis

A

-Process of Plasmin phagocytizing fibrin threads

70
Q

Blood Clot Dissolution Macrophages

A

Will phagocytize any degenerating RBCs or platelets that are trapped in the tissue space
Ie. part of any bruising of the injured tissue

71
Q

What cell makes collagen?

A

Fibroblasts

72
Q

Fibroblasts are part of which basic tissue type

A

Connective tissue (stromal)

73
Q

What determines extent of scar tissue formation within a wound?

A

1) extent of tissue damage
2) complicated healing
3) non regenerative parenchymal cells

74
Q

Does all fibrosis cause permanent scarring,

A

No

75
Q

The ability of a damaged tissue to return to normal physiological activity depends on the relative balance between ____ and ____ function

A

Stromal/fibroblast
Parenchymal

76
Q

The Healing Process Overlapping Phases

A

1) Fill in the wound
2) Seal the wound
3) shrink the wound
Phase 1
Phase 2
Phase 3

77
Q

Healing Process Phase 1

A

-Inflammation
-Begins immediately and lasts 2-3 days
-Epithelialization may continue into phase 2 depending on severity of damage

78
Q

The Healing Process: Fill in the Wound

A

-With inflammatory exudate created during the acute inflammatory response; Debridement occurs; blood clot formed if necessary

79
Q

The Healing Process: Phase 2

A

-Proliferation and Reconstruction (new tissue formation)
-From day 3-14

80
Q

Healing Process: Seal the Wound

A

-Via re-epithelialization at wound surface by myoepithelial cells

81
Q

Healing Process: Phase 3

A

-Remodelling and Maturation
-From several weeks to up to 2 years

82
Q

Overlap in Healing Phases

A

-Overlap in phase 1 and 2 and 2 and 3
-Exact length of each phase depends on severity and location of the wound
-Good blood flow and lymphatic drainage are required, if compromised healing will take longer
-Length of time required for tissue to complete phase 3 is also dependent on the specific tissue type including regenerative potential of each cell type injured

83
Q

3 Types of Wound Healing

A

1) Primary (first) intention healing
2) Secondary (second) intention healing
3) Tertiary (third) intention healing

84
Q

Comorbidities

A

-Individual has more than one risk factor of already has a specific disorder that places individual at higher risk for serious illness

85
Q

Primary Intention Healing

A

-Healing of a wound with minimal tissue loss, no infection
-Clean wound with good apposition of wound edges
-Minimal parenchymal and stromal loss —> resolution and/or regeneration possible
-Original tissue structure and function restored
-Minimal if any visible scarring
-Minimal if any loss of normal function
-Eg. Surgical incision, minor cuts that heal quickly

86
Q

Secondary Intention Healing

A

-Healing of large wound (open wound)
-High risk for infection
-Requires abundance of granulation tissue for wound closure
-Extensive Debridement required; wound edges are separated
-Wounds have significantly more parenchymal and stromal tissue loss —> resolution and regeneration difficult; requires repair processes
-Noticeable scar formation
-Weakness and/or loss of normal tissue function may occur
-Eg. lacerations, burns, ulcers

87
Q

Tertiary Intention Healing

A

-Aka delayed healing (delayed primary intention or delayed closure)
-Healing of a complicated wound that is purposely left open (usually for 3-5 days)
-Infected wound needs lots of debriding, presence of necrotic tissue, crush injuries, poor vascularization, drainage required
-Once healthy granulation tissue is present and wound is clean of debris and infection wound edges are approximated and closed with sutures, staples, or skin graft
-scarring probable

88
Q

Examples Tertiary Intention Healing

A

-Surgical incision left open for drainage due to edema and/or infection
-Slow wound healing due to poor blood flow (decubitus ulcer, diabetic ulcer
-Severe crush injuries with extensive vascular damage (presence of necrotic dead tissue)
-Severely infected wounds requiring extensive Debridement over several days/weeks

89
Q

Common name for decubitus ulcer

A

Bed sore, pressure sore

90
Q

Eschar

A

-Area of necrotic tissue on the skin surface
-Also called slough
-Forms a hard crust or scab of black tissue common in diabetic ulcers and burns
-Is a normal part of wound healing process

91
Q

Phase 1 Key Steps

A

-Hemostasis
-Acute Inflammatory Response
-Physical Debridement

92
Q

Phase 2 Key Steps

A

-Cellular Debridement
-Angiogenesis and Revascularization
-Granulation Tissue Formation
-Fibrosis
-Re-epithelialization
-Clot dissolution
-Wound contraction

93
Q

Phase 3 Key Steps

A

-Resolution, Regeneration, and/or Repair of parenchymal and stromal tissues
-Fibrosis and wound contraction complete

94
Q

Primary also a

A

Bone break the heals good

95
Q

Suture/staples

A

Secondary intention, surgical line is primary intention

96
Q

In phase 2 fibroblasts ..

A

-Establish a collagen framework to help stabilize the tissue and provide new home for parenchymal cells
-Framework will be remodelled many times as healing progresses

97
Q

If Large Amount of Collagen Remains at end of Phase 3

A

Then that fibrous tissue is a scar

98
Q

Re-epithelialization

A

-Secondary
-Epithelial cells at surface are dividing to replace those lost
-Then fibroblasts contract to pull on wound edges =both seal wound to prevent pathogens from entering and decrease size to limit scarring

99
Q

Matrix Metalloproteinases (MMP)

A

-Stimulated by angiogenic factor
-Help with constant remodelling of the wound site as the healing progresses

100
Q

During Organization

A

Histamine levels return to normal, 5 inflammatory signs diminish

101
Q

Healing begins when..

A

Granulation tissue starts to grow into wound site from surrounding healthy tissue including new blood and lymphatic capillaries (angiogenesis), fibroblasts and collagen they make

102
Q

When cells from opposite sides meet..

A

They secrete basement membrane, anchor, and begin to divide in a vertical plane to seal wound

103
Q

Contact Inhibition

A

Once wound is closed contact inhibition between adjacent epithelial cells stops further mitosis that could cause production of excess epithelial cells

104
Q

Myoparenchymal

A

Parenchymal cells use collagen framework as a guide to where they should be, move into area by myoparenchymal movement

105
Q

Fibrosis, angiogenesis and epithelialization are regulated by

A

-Variety of growth factors made by fibroblasts and macrophages

106
Q

Collagen Production Factors

A

-Transforming Growth Factors
-Fibroblast Growth Factor

107
Q

Angiogenesis Factors

A

-Vascular Endothelial Growth Factor
-Fibroblast Growth Factor

108
Q

Extracellular Matrix and Collagen Remodelling Factors

A

-Matrix Metalloproteinase

109
Q

Healthy fibroblasts need

A

Vitamin C and O2

110
Q

Abnormal Gene Expression Of Wound Healing Growth Factors

A

-implicated in cancer pathogenesis

111
Q

Granulation Tissue Is

A

Healing tissue
Composed of Myofibroblasts that migrate from the edges of the wound site and newly formed capillary buds and loops
-New capillaries are fragile and very leaky so Edema will still be present in injury site

112
Q

Myofibroblasts are responsible for

A

Fibrosis
-secrete extracellular matrix including protein procollagen, = precursor to mature stronger collagen fibers during next several weeks or months of wound healing

113
Q

Newly formed collagen is

A

Very weak but does provide a framework for both revascularization and epithelialization to proceed

114
Q

Wound Healing Phase 2 Within 14 Days

A

-Re-epithelialization complete
-Parenchymal cells begin to reestablish function if possible, fill in wound
-Clot dissolution (fibrinolysis) completed by Plasmin
-Scab forms (dried epithelial cells and dried blood clot loosens and falls off, new tissue under scab is pink or red
-Wound contraction may be complete
-Prostaglandins stimulate might be itchy

115
Q

By the end of day 14

A

Uncomplicated wounds should be well underway in the healing process

116
Q

Once wound is sealed by new epithelium…

A

-Scab will loosen and fall off
-Parenchymal cells in the tissue should be re-establishing their functions by this time
-Any living platelets or RBCs that were trapped in the clot can go back to their normal functions
-Old or dead blood cells will be sent to spleen or liver where macrophages will chew them up

117
Q

Wound Contraction

A

-Most noticeable in larger wounds such as surface abrasions
-Helps to decrease dehydration and infection (not so necessary in a paper cut)

118
Q

Clot Dissolution should not begin until

A

-Re-epithelialization is complete
-Since endothelial cells are a type of epithelium, mitotic replacement of endothelial linings of blood or lymphatic vessels is a type of re-epithelialization

119
Q

Removal of blood clot should not occur until

A

Re-epithelialization is complete, otherwise wound site will bleed again

120
Q

Time Course of Cells Infiltrating Wound

A

Platelets: inflammatory (phase 1, 0-1 days)
Neutrophils: inflammatory and proliferation (phase 1 and 2, 0-6 days)
Macrophages: Inflammatory, Proliferation, Remodelling (Phase 1,2,3, 0-13 days
Fibroblasts: Inflammatory, Proliferation, Remodelling (Phase 1,2,3, 0-15 days)
Lymphocytes: Inflammatory, Proliferation (Phase 1,2, 0-10 days)

121
Q

During wound healing, neutrophils are prominent during phase __ whereas macrophages are prominent in phase __

A

Primary, secondary

122
Q

Collagen is made by CT ___ cells called ___

A

Stromal, fibroblasts

123
Q

The ability of damaged tissue to return to normal physiological activity depends on the relative balance between ___ cell and ___ cell activity

A

Stromal, parenchymal

124
Q

What is Fibrosis

A

Production of collagen

125
Q

Is Fibrosis normal or abnormal

A

Normal

126
Q

Does all fibrosis cause permanent scarring?

A

No, part of creation of CT

127
Q

Where does scar tissue form?

A

Forms from CT (Dermis) not on epithelial cells

128
Q

Why is granulation tissue pink?

A

Full of blood vessels

129
Q

Many wounds done by

A

Phase 2

130
Q

What is a scab?

A

Dried epithelial cells, blood clot

131
Q

What do you see if you pick a scab

A

Pink granulation tissue

132
Q

What determines the extent of scar tissue formation within a wound

A

Race/Time amount of collagen deposited in wound site

133
Q

Why are scare white?

A

Collagen is avascular

134
Q

Why does picking a scab increase ur risk of scarring?

A

Increases time of healing, have to go back to phase 1
Promotes fibroblast production of excess collagen

135
Q

Types of Dysfunctional Wound Healing

A

1) Contracture’s
2) Adhesions
3) Keloids
4) Hypertrophic scars
5) Dehiscence
6) Proud flesh

136
Q

Dysfunctional wound healing means

A

Normal tissue function is not restored

137
Q

Contractures

A

-Thick scar tissue and excessive wound contraction
-Severely impedes normal function
-Possible disfigurement
-Eg. Severe burns, prolonged hypertonic spasticity

138
Q

Adhesions

A

-Secretion of excessive Fibrinous (fibrin containing) exudate
-Causes serous membrane to adhere to each other restricting organ movement

139
Q

Serous membranes

A

-Pleural membranes, Pericardial membranes, Peritoneal membranes
-Serous membranes surround the thoracic and abdominopelvic body cavities
-They secrete clear watery lubricating fluid that allows the organs they enclose to move freely without friction

140
Q

Inflammation Pleural Membranes

A

-Surround lungs
-Pleurisy

141
Q

Inflammation Pericardial Membrane

A

-Surround the heart
-Pericarditis

142
Q

Inflammation Peritoneal Membranes

A

-Surround Abdominal and Pelvic Organs
-Peritonitis

143
Q

Keloids

A

-Due to overproduction of collagen
-Overgrow the size of the wound
-Do not decrease over time
-Most common in those with darker skin tones

144
Q

Hypertrophic scars

A

-Are raised but remain within the wound boundary
-May reduce in size over time

145
Q

Risk Factors Keloids/Hypertrophic scars

A

-Familial predisposition to both scar types and location of the lesion

146
Q

Common Locations Keloids/Hypertrophic scars

A

-Neck, Thorax, Shoulders, Upper arms

147
Q

Dishiscence

A

-Breaking open of a poorly healed sutured wound
-Most common in the abdomen due to high intra abdominal pressure

148
Q

Other causes Dehiscence

A

-Infected site, presence of foreign object, obesity, steroid use
-Co-morbiditites Eg diabetes, renal or liver disease, presence of neoplastic tissue

149
Q

Proud Flesh

A

-Overproduction of pink granulation tissue that protrudes out of the wound
-Caused by poor healing due to persistent infection or foreign object
-often problem in horses or cattle legs

Pathophysiology (8 decks)

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