Wound Healing Flashcards

1
Q

Key events in healing

Specifics in each?

A

Haemostasis–>inflammation–>proliferation–>remodeling

Haemostasis- platelets, fibrin, proteogylcans
Inflammation- neutrophils, macrophages, lymphocytes
Proliferation- fibroblasts, collagen, epithelial cells, endothelial cells
Remodeling- scar maturation, collagen fibril cross linking

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2
Q

Difference between repair and regeneration

A

Regeneration- proliferation of cells and tissue with replacement of lost tissue (regeneration of liver/superifical abrasions of skin)
Repair- combination of scar formation and regeneration by the deposition of collagen (healing by second intention)

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3
Q

Problems with wound healing and repair- def and impairments

What stages are affected?

A

Deficiency- inadequate blood supply, poor nutrition, clotting deficiency
Impairment- infection, foreign body, movement, mediation (corticosteroids), radiation, defective collagen synthesis

Poor perfusion affects ability to get to inflammatory stage
Infection affects inflammatory stage and ability to transition to proliferative stage
Hypertrophic scars, keloids, contractures affect remodeling stage
Impair collagen synthesis with corticosteroids or congenital diseases in proliferation phase

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4
Q

Healing impairments in different phases of time/wound healing

A

0-3 hours phase- impaired clotting, poor nutrition, infection
24-48 hours- poor perfusion, reduced influx of inflammatory cells needed to remove foreign material and secrete signal for repair, movement
Day 5-21- if early phase was poor formation of collagen by fibroblasts will be decreased, abnormal collagen synthesis

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5
Q

Common bacteria that infect wounds

A
S. Aureus
P. Aeruginosa
E. Coli
Kiebsiella spp
Often polymicrobial
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6
Q

Pilonidal sinus

A

Hair as foreign body- sinus tract from skin to deep subcutaneous tissue–>abscess formation
Hair breaks off and bacteria can penetrate the skin

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7
Q

Dehiscence

A

Wound splitting open- most frequent after abdominal surgery

Increased mechanical stresses

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8
Q

How wounds become chronic risk factors

A

Usually halted in inflammatory phase*

Poor nutritional status- chronic disease states like diabetes: hyperglycemia inhibits fibroblasts
Poor oxygenation- smoker/PAD
Chronic edema- congestive heart failure from CAD

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9
Q

Cellular events at the chronic wound

A
Increased chances of infection
Poor granulation tissue formation
Degradation of needed components
Increased inflammatory cytokine present
Stalled in inflammatory phase
Elevated tissue matrix metalloproteinases 
Prolonged inflammatory phase
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10
Q

Chronic leg ulcers are defined as

A

In the skin below the level of knee persisting for more than 6 weeks and shows no tendency to heal after 3+ months
Many causes*

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11
Q

Most common type of chronic wound in adults

A

Venous ulcers- venous insufficiency incompetence leads to leg discomfort, edema, elevated venous pressure resulting in decreased skin perfusion.
Usually ulcer is anteriolateral leg- hyperpigmentation is common due to RBC deposition and breakdown in interstitium. Brown colors because low pressure ulcer and hemosiderin

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12
Q

Arterial insufficiency ulcers

A

Combination of mural thickening or accretion and intramural restriction
Most acute forms of vasculitis and some sub-acute and chronic forms are likely to cause leg ulceration due to tissue hypoxia and exudation of fibrin-like substances

Toes, heels, bony prominences of foot
Punched out appearance with well demarcated edges and a pale, non-granulating and necrotic base. Has gangrene (neutrophils)

Associated with atherosclerotic obstruction of large arteries supplying lower limbs- can extend into deeper structures to expose tendon or bone

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13
Q

Vasculitic leg ulcers

A

Infectious, immunologically mediated- immune complex formation (leg prone due to increased hydrostatic pressure because of gravity) with vascular wall damage leading to activation of complement system

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14
Q

Necrobiosis Lipoidica

A

More common in diabetics
Rare granulomatous skin disorder of unknown cause that can affect the shin of insulin dependent diabetics and others
Tender, yellowish brown patches on shin over several months persisting for years
Center of the patch becomes shiny, pale, thinned, with prominent blood vessels
Minor injury can cause it to ulcerate

Septal panniculitis with chronic inflammation, macrophages with destruction of collagen and fat*

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15
Q

Marjolin’s ulcer

A

Exuberant vegetations on sacral region that appear warty- lesion has infiltration patterns areas with presence of ‘keratin pearls’
Squamous cell carcinoma complication

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16
Q

Treatment options for venous ulcer types

A

Leg elevation, compression therapy, aspirin/pentoxifyline, surgical, management

17
Q

Treatment options for arterial ucler types

A

Revascularization
Antiplatelet meds
Management of risk factors

18
Q

Neuropathic ulcer treatments

A

Off loading of pressure
Topical growth factors
Tissue-engineered skin

19
Q

Treatment of pressure ulcers

A

Off loading of pressure, reduction of excessive moisture, sheer and friction
Adequate nutrition

20
Q

When compared to normal fibroblasts, keloid fibroblasts show increased numbers of:

A

Growth factors like PDGF and TGF-beta, which may upregulate these abnormal cells from beginning of wound healing

Dysfunction of underlying regulatory mechanisms may lead to persistent inflammation, excessive collagen synthesis or deficient matrix degradation and remodeling

21
Q

Keloids and hypertrophic scar treatments

A

Prophylaxis- silicone gel, pressure therapy
Current therapy- corticosteroids, cryotherapy, scar revision, laser therapy, radiotherapy (all delay collagen synthesis)
Emergent therapies- interferon injections, 5FU injections

22
Q

Volkmann ischemic contracture

A

End result of an unrecognized or untreated compartment syndrome of forearm. Results in permanent flexion contracture of the hand at the wrist, resulting in claw-like deformity