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Unit 11 > W2: Wound healing > Flashcards

W2: Wound healing Flashcards

1
Q

Define wound

A

A disruption of the integrity of the skin, mucosal surfaces or organ tissue.
May be accidental (trauma) or intententional (surgery) or part of a disease process

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2
Q

What is the relationship between a wound an an injury?

A

An injury is an impairement of function.
All wounds could be classified as an injury
But not all injuries are wounds.

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3
Q

What is the consequence of a wound?

A

Triggers a physiologically coordinated sequence of cellular and non-cellular processes to restore tissue integrity.

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4
Q

What are the four stages of wound healing?

A

Homeostasis
Inflammation
Proliferation
Remodelling/scar maturation

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5
Q

What is an acute wound?

A

Wounds affecting soft tissue that usually pass through the healing phases relatively quickly.
Are normally caused by trauma (blunt or penetrating e.g animal bite, gunshot, surgical incision)

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6
Q

What are the different classificiations of acute wounds?

A

Abrasion - superficial shedding of the epithelium
Incision - made by sharp tool, typically clean and close together boundaries but can be deap.
Laceration - deep skin tearing, often through the epidermis and sometimes the dermis or subcutaneous tissue, tend to be larger and more difficult to heal
Puncture - sharp object penetrate into the skin and the tissue beneath, typically narrow and deep
Avulsion - when part of the body has been removed or torn off.
Amputation - removal of distal section of limb or body part wholly from the body.

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7
Q

What is the kinetics of soft tissue wound healing?

A

Homeosatis immediatly on injury
Inflammation lasting from day 1 to day 10
Proliferation from day 3 to day 25
Maturation and remodelling from day 3 over the next months

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8
Q

What are the kinetics of bone healing?

A

Homeostatis happens rapidly initially
Inflammation occurs between 1 to 3 weeks afterwats
Proliferations occurs from 2 to 8 weeks from inury
Maturation/remodelling occuts from 8 months onwards normally till 12 months.

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9
Q

What are the differences in the kinetics of healing of soft tissue compared to bone?

A

Soft tissue - faster, typically healed within months, with end of proliferative phase at 30 days, mautration starts alomst immediatly after proliferation and overlap

Bone - slower, takes months to years, end of proliferative phase at 8 weeks, no overlap between proliferation and maturation.

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10
Q

What are the implications of delayed wound healing?

A

Increased patient morbidity and mortality
Poor cosmetic outcome
Health economic issues - for patient due to ill health and for health system as increased cost of dealing with implications
Psychological damage to patients as appearance of peristant damage and pain.

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11
Q

What are the different categories of soft tissue wound closure?

A

Closure by primary intentions
Closure by seconday intention
Tertiary intention healing

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12
Q

What is meant by closure by primary intention?

A

Delibrate closure of smaller wound
The incision is normally smaller and clear so the edges are easily held together by a suture.
Results in a hairline scar

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13
Q

What is meant by closure by secondary intervention?

A

When there is extensive tissue loss and a gaping irregular wound.
No deliberate closure of the wound
The wound is left to heal on its own, desire the formation of granulation tissue then reepithelisation
This is because an open wound is easier to clean/drain and monitor for signs of infection which is more common in tissue where there is extensive tissue loss.
Normally reepitheliasation grows over the scar.

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14
Q

What is meant by tertiary intention healing?

A

Intentional delay of wound closure
Normally when early risk of infection so allow wound to self heal and form granulation tissue (easier to monitor, clean adn drain for signs of infection)
Wound is closed by sutures later in the process - results in a wide scar

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15
Q

What occurs in the homeostatic phase of wound healing?

A

At time of trauma micro/macrovascular trauma occurs.
Immediatly SNS and locally released vasoconstrictors cause smooth muscle in arteries to contract (vasoconstriction) reduces exsanguination
Vessels up to 5mm and in transverse plan injury can be closed.

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16
Q

What are the local vasoconstrictors released in homeosatis phase of wound healing?

A

Thromboxane A2 - from activated platelets
Endothelin - from endothelial cells.

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17
Q

What happens in the late stage of wound homeostasis?

A

Vasconstriction reduced blood supply causes tissue hypoxia and acidosis
This triggers the release of vasoactive emtabolites (NO and adenosine) which vasodilate and relac arterial vessels
Coagulation is now required for homeostasis.
Hypoxia also activates HIF-1 that acts as a transciption factor for genes essential to cell survival and wound healing such as VEGF expression.

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18
Q

What is the role of NO in late homeostatis in wound healing?

A

During vasoconstriction induced hypoxia can be released from activated endothelial cells or from rbcs undergoing sheer stress.
Stimulates angiogenesis of endothelial cells
Inhibits proliferation of epithelial cells
Causes vascular relaxation
Inhibits platelet aggregation and thrombosis.

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19
Q

What happens in the early inflammatory phase of wound healing?

A

Mast cells are stimulated by PAMPs/DAMPS binding to PRR degranulation releasing histamine.
Histamine causes NO release from endothelial cells, increases vasodilation and increases vascular permeability. This allows the entry of inflammatory cells into the wound. And contributes to edema.
Complement is activated by DAMPs/PAMPs promoting an inflammatory response
Neutrophils infiltrate within an hour from insult, carry out phagocytosis, degranulation and NETosis, contributes to elimination of the microbe.

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20
Q

What happens in the late inflammatory phase?

A

Macrophages are inflammatory in the first days of wound healing - M1 phenotype if dominant
Throughout inflammation dominant phenotype transitions to M2, which promotes wound healing.
This change occurs due to a change in cytokine signalling and shift from Th1 to Th2

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21
Q

What are the effects of classically activated macrophages?

A

Release ROS, NO and lysomsomal enzymes - promote phagocytosis and pathogen killing

Secrete IL-1/12/23 and other chemokines - promotes inflammation

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22
Q

What are the effects of alternatively activated macrophages?

A

Secrete growth factors and TGF beta - to promote tissue repair and fibrosis and appearance on iTreg

Secretes IL-10 and TGFbeta - anti-inflammatory effects.

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23
Q

Describe what the differences are that cause the development of a M1 or M2 phenotype of a macrophage.

A

M1 - Th1 effector cells secretes TNFalpha and INFy

M2- Th2 effector cells secretes IL-13 and IL-4.

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24
Q

In the late stage of inflammation what is the role of a macrophage?

A

M2 macrophage - secretes collagenases the aid scar remodelling
-secrets PDGF to recruit fibroblasts then secretes FGF to stimulate then to proliferate and deposit ECM components
- secrets TGF beta to stimulate fibroblasts, secrete VEGF to activate angiogenesis forming granulation tissue.

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25
Q

What collagenases are produced by M2 macrophages?

A

MMPs 1,8 and 13

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26
Q

What is the role of lymphocytes in the late stage of inflammation in wound healing?

A

Lympocytes regulate wound healing and adaptive response to infection until the wound is healed
Dendritic Epidermal T cells (gamma delta TCR) are a special Y lymphocyte that aids wound healing.
Arachidonic acid metabolism products (lipoxin) can have anti-inflammatory effects and allows transition to the next stage of wound healing.

27
Q

What is the role of Dendritic Epidermal (gamma delta) T Cells?

A

Is an unconventional T cell
Damaged epithelial cells express stress ligands.
Dendritic Epidermal T cells have receptors that detect this and activates the cell.
Have projections to keratonicoytes, use these projections to secrete keratinocyte growth factor (stimulates keratinocye proliferation) and IGF-1 ( differentiation of keratinocytes).
Encourages reepithelisation.

28
Q

What processes occur during proliferation during wound healing?

A

Angiogenesis
Formation of granulation tissue
Fibroblast migration
Collagen depositions
Epithelisation
Wound contraction

29
Q

Why is angiogenesis needed in wound healing?

A

Originally the centre of the wound is hypoxic and relies of diffusion of oxygen from undamaged capillaries at wound boundary.
Angiogenesis forms a rich capillary network to directly supply the nutrients needed for growth and repair.

30
Q

What is the process of angiogenesis?**

A

Increase in pro-angiogenic factors such as VEGF and a decrease in factors that promote quiescence.

Angiopoietin causes pericyte detachement.
ECM components and basement mebrane are degraded by MMPs.
Growth factors, VEGF and Notch signals change the polarity of some endothelial cells, alters cell to cell contact and increases invasive activity. THis forms leading or tip cells.
Grows in EC sprout then vascular stalk follows a VEGF gradient and signals from the matrix.
Tip cells releae PDGFB to recruit pericytes.
Tip cells encounter and adjacent sprouts fuse
Vacuole formation and fusion contribute to lumen formation.
Endothelial cell adhesion is stabilised
Restored blood flow reduces hypoxia and pro-angiogenesis signals are lost.
The vessels mature, cell junction stabilises and matrix deposition occurs.

31
Q

What triggers angiogenesis in wound healing?

A

Homeostatic plug forms causing Hypoxia.
Hypoxia causes VEGF release from macrophages and fibroblasts.
Platelets also release VEGF, TGF-beta, PDGF and FGF
This stimulates endothelial cells to proliferate

32
Q

What is important about the appearance of new capillaries formed by angiogenesis?

A

Are fragile and permeable
Contribute to oedema and appearance of healing granulation tissue.

33
Q

What is the role of fibroblasts in the proliferative phase of wound healing?

A

Growth factors (FGF) stimulates fibroblasts to migrate and proliferate
TGF-beta stimulates deposit of ECM components (collagen, fibronectin and proteoglycans)
Also produces MMPs (collagenase MMP 1,8 and 13) to remodel tissue
Results in increased tissue strength.

34
Q

What makes up the appearance of granulation tissue?

A

Pink, vascular and fibrous
Consists of active fibroblasts, active angiogensis and immature capillaries
Immune cell infiltration.

35
Q

What is the role of myofibroblasts in wound healing?

A

Fibroblasts differentiated into myofibroblasts after they have depositied sufficient matrix
Myofibroblasts a spindle shaped and connect to surrounding cells and ECM proteins by focal adhesions, then contraction of fibres inside mainly actin to pull ECM and cellular componets together, causes wound contraction.

36
Q

How does the degree of collagen deposition relate to the process of wound healing?

A

Maximal collagen deposition by day 5 - closed by primary intentions - often palpated as a wound ridge.
If a wound ridge is not palpable means increased risk of wound reopening

Overproduction of collagen-hypertrophic scar or keloid
Scar appears erthematous

37
Q

What are the risk factors for development of a scar?

A

Wound infections
Excessive tension of the wound
Low proliferative capacity of tissue
Extensive cellular damage of damage to the ECM.

38
Q

What is the process of re-epithelisation in proliferation phase of wound healing?

A

Cytokines/growth factors stimulate basal epithelium cells at the wound edge to migrate and cover the wound bed - this is a epithelial to mesenchymal transition.
Adhere to deposited ECM, then proliferate superficially, differentiate and stratify to repopulation epithelial layer.

39
Q

How is reepithelisation affected by the type of wound healing (by primary or secondary intention etc)?

A

Primary intention - occurs rapidly and may be done within 24 hours
Secondary intention - large area without epithelial cells, wound must contract first, in severe cases skin graft is required to encourage repithelisation.

40
Q

What is the process of wound contraction during the proliferative phase of wound healing?

A

Begins from 7 days after injury
Mediated my myofibroblasts
Purpose is to decrease area of tissue that needs to heal
Shortens scars.
Occurs at a rate of 0.75mm per day.

41
Q

What are the potential consequences if wound contraction goes wrong?

A

Deformity
Contractures

42
Q

What influences wound contraction?

A

Wound shape
Linear wounds contract the fastest and circular wounds contract the slowest.

43
Q

What is meant by tissue remodelling in wound healing?

A

Balance of synthesis and degradation of collagen and ECM proteins
Aims to increase wound tissue strength - although original strength is never fully reached
Results in return of normal epithelium and maturation of scar tissue.
Can take 2 years to complete

44
Q

How effective is tissue remodelling at restoring tissue strength?

A

Never achieves strength of original tissue
One average achieves 50% strength in three months and 80% long term.

45
Q

How does the appearance of a scar change over time?

A

As matures vascularity decreases and scar changes from pink to grey
Scar contracts and becomes smaller

46
Q

What factors influence scarring outcomes?

A

Type/size of the wound
Location of wound
Shape of wound

47
Q

What is a chronic wound?

A

Soft tissue wounds that have not healed within 12 weeks from insult.
Result of prolonged pathological inflammation - as seen in diabetes

48
Q

What happens in the first stage of bone healing after a fracture?

A

Haemostasis:
Hematoma formation from bleeding from bv in bone canals and growth factor released from platelets
Coagulates between and around the ends of the bone
This stabiles the fractures and forms a matrix for infiltrating cells and callus formation.
Will contain signalling molecules to trigger inflammation.

49
Q

What happens in the second stage of bone healing?

A

Inflammation at the fracture site lasts for a few days
Vasodilation and increased vascular permeability
Influx of inflammatory cells and non-cellular factors - this allows the removal of debris and potential pathogens particulary in open wounds. Neutrophils have an important role in phagocytosing dead cells. macrophages drive the resolution of inflammation.
Granulation tissue forms - angiogenesis and fibrobalst activation. Helps connect the bone fracture ends.
Mesenchymal stem cells differentiate into osteoprogenitor cells are recuited to the site

50
Q

What happens in the third stage of bone healing?

A

Soft callus formation gives a stable structure to bone.

Osteoblast from neighbouring perisoteum proliferate and depsoti some bone matrix.
Chondroblasts differentiate into chondrocytes and deposit cartilage.
Fibroblasts deposit collagen
This is a fibrocartilagenous matrix that bridges the fracture ends and forms a scaffold for new bone.
Capillaries and supporting blood vessels invade to the callus.

51
Q

What happens in stage four of bone healing?

A

Three weeks have passed
Soft callus is reabsorbed and osteoblasts produce woven bone by deposting poorly organised collagen.
Cartilage matrix is calcified and reabsorbed and replaced with bone
Bone becomes more mechanically rigid.
The gap between the fracture ends is healed by ossification.
Osteoblasts and osteoclasts are active.
Vasculature matures.
A hard callus has formed

52
Q

What happens in stage 5 of bone healing?

A

Callus is remodelled and cellularity decreases.
Starts after several weeks and may continue over years.
Cutting cones form - Woven bone is reabrobsed by osteoclasts and remodelled into lamellar bone which is deposited by osteoblasts.
Bone marrow is restored
Mechanical stress is important into this phase - encourages collagen to be deposited in an organised manner.
Bone is highly vascular and mineralised.

53
Q

What is meant by a clean wound?

A

An elective, non-emergency, non-truamtic wound that closed by priamry closure.
GI, billary and GU tracts intact - less than 5% risk of infection

54
Q

What is meant by a clean contaminated wound?

A

Urgent or emergency case that is otherwise clean
Elective opening of respiratory, Gi, biliart or GU tract with minimal spillage and not encountering infected urine of bile - 5-10% chance of infection

55
Q

What is meant by a contaminated wound?

A

Gross spillate from GI tract, billlary system or GU tract (infected urine)
Penetrating trauma - less than four hours old
Chronic open wound to be grafted or covered
10-20% chance of infection

56
Q

What is a dirty/high contaminated wound?

A

Preoperative perforation of respiratory, gastrointesinal, billary, or GU tract
Pentrrating trauma more than 4 hours old.

57
Q

How does hypoxia affect wound healing?

A

All wounds are hypoxic to some extend
Some hypoxia encourages healing
However, sufficient oxygen is needed for proper healing, with low oxygen/nutrient supply causing necrosis of bone and soft tissue.
Oxygen is needed for collagen deposition (hydroxylation of proline and lysin residues)
THis means elderly patients with peripheral vascular disease have poor healing.

58
Q

How does smoking effect wound healing?

A

Impaires chemotaxis, migratoy function and oxidative bactericidal mechanisms in the inflammatory phase
Reduce fibroblast migration and proliferation
Dow regulates collagen synthesis and deposition

59
Q

How is risk of infection managed in wound healing?

A

Prophylaxis antibiotics before surgery
Heavily contamined wounds are normally healed by tertiary intention

60
Q

How does immunsuppresion affect wound healing?

A

Delays healing
Anti-inflammatory drugs - impaire healing cascade
Chemotherapy/radiotherapy - reduce VEGF
Radiation injury - tissue ischemia and may cause skin ulcers
Delayed wound healing in HIV, cancer and malnutrition

61
Q

How does chronic disease affect wound healing?

A

Cardio-respiratory disease - affect oxygen and nutrient supply
Diabetes - immunocompromised and high blood glucose impaires cells function, alters MMP function and expression, long term microvascular damage affects oxygen and nutrients supply.

62
Q

How does wound management affect wound healing?

A

Healthy wound environment is a prerequisite for successfull wound healing
Over 250 types of dressing are available to prevent infection, abosrb extra exudate and remain moist.

63
Q

How does age affect wound healing?

A

Eldery - thinner epidemeral layer, slower inflammatory, migratory and proliferation responses due to cell sensecence
Higher risk of wound rupture.

64
Q

What are some key molecular regulators in angiogenesis?

A

VEGF
PDGFB
Notch signalling - increases survival and proliferation signal.
Integrins - signalling from ECM that can be pro-angiogenesis.

Promoted by: VEGFS, FGF and ANGPT1
Inhibited by: Endostatin, Angiostatin, and angiopoietin.

Unit 11 (21 decks)

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