Wound Healing Flashcards

1
Q

What is a wound?

A

Disruption in the integrity of the structure of a tissue usually from injury induced by various agent.
This could be minor, moderate or severe
Severe injury leading to necrosis or death

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2
Q

What is an acute and chronic wound?

A

Acute wound – these are wounds that occur with in 0-4 weeks

Chronic wounds are present for more that 4-6 weeks
Arterial ulcers, presure ulcers, diabetic foot ulcers and venous ulcers, mixed vascular ulcers

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2
Q

What are the types of wounds?

A

Close or open wounds
Contusion/bruise: sub epithelia damage. Damage is below the surface- subcutaneous, submucosa,
Open wounds
A-abrassion- loss of the superfical layer of the epithelium, not a full thickness injury
B-incision a clean linear wound usually made by a sharp object
C-larceration: a non linear ragged wound with widely separated edges
Penetrating wound: wound enters a body cavity e.G stab wound to the abdomen, thigh, chest
Perforating wound it is a through and through wound, it enters and leaves at the other end. There is and entery and exit wound
Avulsion: open wound that results from a pull or shearing force,
Partial or complete
Degloving

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2
Q

Etiology of wounds

A

Mechanical:- truama, accidents, fall, industrial injury
Chemical:- acid and bases, venoms and stings
Radiation: x-rays, beta and alpha radiation
Microorganism: viruses, bateria, fungus

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2
Q

What are the steps to managing a wound?

A

History
Examination
Abcd: airway, breathing, circulation, disability
Golden hours for wound care-6-8hrs
Primary closure or delayed closure

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2
Q

Means of treating a wound

A

Debridement: removing dead and dying tissue as well as foreign material.
Copious wound irrigation and washing
Wound closure: suturing, skin grafts, or flaps, avoid dead spaces for fluid collections
Primary closure, delayed closure, secondary wound healing
Healing strategies involve keeping the wound moist, platelet-derived wound healing techniques,
biological skin equivalents, topical growth factors, stem cells, scaffolds, and the application of
biophysical forces.

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2
Q

What is wound healing?

A

the repair or reconstitution of a DAMAGE OR DEFECT in an organ or tissue, commonly the skin. However, it is clear that the process of wounding activates systemic processes that alter the physiology far beyond the confines of the defect itself
Wound healing may be best understood as an organism’s global response to injury, regardless of whether the location is in the skin, liver, or heart. Seen from this perspective, it is certainly not an exaggeration to regard the response to injury as one of the most complex physiologic processes occurring during adult life.

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3
Q

What are the types of wound healing?

A

Regeneration
Perfect-hydra, earth worm
Inperfect-not complete, accompanying scaring
Fetal wound healing
Resolution-minimal damage recovery without scaring e.G boil
Epithelialization and fibrous tissue formation
Essential the type of healing that takes place in surgical wounds

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3
Q

Discuss healing by primary and secondary intention

A

Healing by primary intention-
Healing takes place rapidly with epithelization an minimal scar tissue formation
Wound edges are very close, like a sutured wound

Healing by secondary intention:
Wounds left to be filled with granulation tissue, to contract and eipthelised or closed by other intervention

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3
Q

What occurs in wound healing?

A

Epithelialization

Fibrous tissue formation

Wound contraction

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3
Q

What are the Phases of wound healing?

A

These phases are distinct and overlapping
Hemostasis
Inflamation
Proliferative phase
Remodelling

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3
Q

Discuss Hemostasis

A

Fibrillar collagen and tissue factor, act to activate the clotting cascade and prevent ongoing hemorrhage.
Disrupted blood vessels allow circulating elements into the wound while platelets clump and form an aggregate to plug the disrupted vessels.
Platelets degranulate to release growth factors such as platelet-derived growth factor (pdgf) and transforming growth factor p (tgf-b).

The end result of the coagulation cascade is the conversion of fibrinogen to fibrin and subsequent polymerization into a mesh.
This provisional matrix provides the scaffolding for cell recruitment and attachment required during the subsequent phases of wound healing

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3
Q
A

Next inflamatory cells are attracted
Neutrophil : day 1-2
Phagocytosis, o2 or non o2 dependent
Proteases
Monocytes/macrophages - day 2-3
Phagocytosis, gf, regulation of wound healing
Attracted by monocyte chemotatic factor 1
Lymphocytes : day 5-7

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4
Q

Discuss the inflammatory stage

A

Wound healing begins immediately following tissue injury.
The functional priorities
Hemostasis,
Removal of devitalized tissues,
And prevention of colonization and invasive infection
Bacteria.

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5
Q

Discuss the Demolition phase

A

Next inflamatory cells are attracted
Neutrophil : day 1-2
Phagocytosis, o2 or non o2 dependent
Proteases
Monocytes/macrophages - day 2-3
Phagocytosis, gf, regulation of wound healing
Attracted by monocyte chemotatic factor 1
Lymphocytes : day 5-7

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6
Q

Discuss the Proliferative phase

A

Occurs day 4-21 but overlaps
Reepitheliliazation: day 1
Keratinocyte migration, loses connection and migrates across the wound
Granulation tissue formation: day 4
Cell: macrophages, fibroblast and endothelia cell
Forms ecm and new blood vessels
Macrophages continue to produce
Growth factors
Pdgf and tgf-beta1 >
Fibroblasts to proliferate, migrate, and deposit ecm,
As stimulate endothelial cells to form new vessels.
Endothelium
Proliferates to form new blood vessels
From marrow derived progenitor cells
Proangiogenic factors
Vascular endothelial growth factor,
Fibroblast growth factor 2,
Angiopoietin 1, and thrombospondin.
At a certain point all of these processes need to be turned off and the .Formation of granulation tissue/ecm halted stabilization

7
Q

Discuss Remodelling

A

The least understood phase
Longested component: day 21-1 year
Remodeling : two processes
The processes of wound contraction
wound myofibroblasts,
Which are fibroblasts with intracellular actin microfilaments capable of force generation and matrix contraction
Collagen remodeling

8
Q

Discuss Collagen remodelling

A

Type iii collagen is initially laid down by fibroblasts during the proliferative phase, but over the next few weeks to months this will be replaced by type i collagen.
Mediated by a class of enzymes known as matrix metalloproteinases that are secreted in large part by m.Acrophages, fibroblasts, and endothelial cells
The beginning of the remodeling phase, wounds have only about
20% of the strength of unwounded skin and will ultimately only
Possess 70% to 80% of the breaking strength of unwounded skin
At 1 year.

9
Q

Abnormal response to injury and abnormal wound healing

A

Inadequate regeneration underlying an abnormal response to injury
Cns injury, nonunion, corneal ulcer
Inadequate scar formation underlying an abnormal response to injury
Diabetic foot ulcers, decubitus ulcers
Excessive regeneration underlying anabnormal response to injury
Neuroma, precancers, keratosis, psoariasis
Excessive scar formation underlying anabnormal response to injury
Keloid and hypertophic scars
Keloid grow beyond their margin, and rarely regress

10
Q

What are the Factors affecting wound healing?

A

Age :because of comorbid conditions
Severe constitutuional diseases
Radiotherapy/irradiation
Connective tissue disease
Metabolic diseases/obesity
Nutritional factors –protein def,trace elementseg zinc
Hormones inbalances
Local factors-blood supply,residual infection, inadequate immmobilzation,foreign bodies, surgical technique, radiation, cytotoxic agents

11
Q

What are the Strategies for wound healing?

A

Biological therapy
Skin grafts, xenografts, collagen scafolds, hyperbaric oxygen growth hormones, stem cells
Biophysical strategies
Extracorporal shock waves therapy
Negative pressure wound therapy
Remove excess fluids and aid granulation tissue

12
Q

What are the Complications of wounds?

A

Infection
Keloids an hypertrophic scars
Hyperpigmentation
Implantation cyst
Atrophic scars
Wound dehiscience
Pyogenic granuloma