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A Cut Above the Rest (ABSITE) > Wound healing > Flashcards

Wound healing Flashcards

1
Q

Role of PMNs in would healing

A
  • PMNs release proteases that degrade ground substance within the wound site
  • Neutrophils use fibrin clot generated at the wound site as scaffolding for migration into the wound
  • Neutrophil migraton is stimulated by local prostaglandins, complemet factors, IL-1, TNF-a, TGF-B, platelet factor 4, or bacterial products
  • PMNSa re the first cells to infiltrate the wound peaking at 24-48 hours
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2
Q

The proliferative phase of wound healing occurs how long after the injury?

A

7 days

Wound healing

  • hemostasis and inflammation
  • proliferation
    • 4-12
  • maturation and remodeling
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3
Q

strongest chemotactic factor for fibroblasts

A

PDGF

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4
Q

fibroblastic phase of wound healing

A
  • Even though the tensile strength of a wound reaches a plateau after several weeks, the sensile strength will increase over 6-12 months dur to fibril formation and cross linking
  • Maturation and Remodelling
  • MMPs
  • MAtrix deposition
    1. fibronectin and collagen type III
    2. glycosaminoglycans and proteoglycans
    3. collagen type I
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5
Q

Commonly seen in Ehlers Danlos Syndrome

A
  • Direcent or recurrent hernias in children
  • group of 10 disorders
  • defect in collagen formation
    • alpha chain of type V
  • fribale skin, easy bruising, poor wound healing
  • atrophic scar formation, hyperextensible joints
  • bleeding, hiatal hernia, intestinal diverticula, rectal prolapse
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6
Q

Patients with Marfan syndrome are assoicated with what genetic defect?

A

FBN-1 gene mutation

  • Fibrillin
  • tall stature, arachnodactyly, lax ligaments, myopia, scoliosis, pectus excavatum
  • aneurysm of the ascneding aorta
  • no delay in wound healing
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7
Q

When a long bone facture is repaired by internal fixation with plates and screws.

A

Direct bone to bone healing occurs without soft callus formation and endochondral ossification

  • internal reduction does not prevent delayed union
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8
Q

Healing of Full thickness injuries of GI tract

A
  • Serosal healing is essentail to form a water tight barrier to the lumen of the bowel
  • Extraperitoneal segments of the bowel that lack serosa have higher rates of anatomotic failure
  • there is an early decrease in marginal strength due to an imbalance of greater collagenolysis versus collagen sysnthesis
  • collagen syntheis is done by fibrolast and smooth muscle cells
  • The submucosa is the layer that imparts the greatest tensile strength and greatest suture holding capacity
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9
Q

Steroids impair wound healing by __________

A
  • Decreasing angiogenesis and macrophage migration
  • Steroid used after the first 3 to 4 days do not affect
  • also inhibitss epithelialization and contraction and contribute to increase rates of wound infection.
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10
Q

Steroid-delayed helaing of cutaneous wounds can be stimulated to epithelialize by __________

A

topical vitamin A

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11
Q

What type of nerve injury involves disruption of axonal ontinuity with preserved schwann cell basal lamina

A

Axonotemesis

3 type of nerve injuries

  • Neurapraxia - focal demyelination
  • Axontomesis
  • neurotmesis - complete trasection

pattern of changes

  1. survival of axonal cell body
  2. regeneration of axons that grow across the transected nerve to reach the distal stump
  3. migration and connection of the regenerating nerve ends or organ targets
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12
Q

Phagocytes remove the degenrating axons and myelin sheath from the distal stump

A

Wallerian degenration

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13
Q

The major cause of impaired wound healing

A

Local tissue infection

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14
Q

How does diabetes mellitus impair wound healing?

A

Local hypoxemia, reduced angiogenesis, and inflammation due to vascular disease

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15
Q

Supplementation of this microtnutrients improves wound healing in patients without micronutrient deficiency

A

Vitamin A

  • increases the inflamamtion response
  • increase influx of macrophages
  • increase collagen synthesis
  • increase epidermal growth factor
  • supplemental dose : 25 000 to 100 000 IU/day
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16
Q

Which type of collagen is most important in wound healing?

A

Type III

  • Type I : major component of extracellular matrix in skin
17
Q

Cartilage healing

A
  • Cartilage is avascular and depends on diffusion of nutrients
    • hypervascular perichondrium
  • Depends on depth of injury
    • Superficial cartilage wounds are not associated with an inflammatory response
  • cartilage injuries often heal slowly and result in permanent structural defects
18
Q

Signs of Malignant transformation in chronic wound

A
  • Overturned wound edges
  • malignant transformation of chronic ulcers can occur in any long standing wound (marjolin ulcer)
  • Squamous or basal cell carcinoma
19
Q

DIfferene between hypertrophic scarsand keloids

A
  • Hypertrophic scars often regress over time, whereas keloids rarely regress
  • HTS rise above the skin level but stay within the confines of the original wound
  • Keloids rise above the skin as well but extend beyond the the border of the original wound and rarely regress
  • Keloids are more common in darker pigmented ethnicities
20
Q

Treatment of choice for keloid

A

Excision with adjuvant therapy (Radiation)

  • Excision alone is subject to high recurrence rates
  • silicone application is relatively painless and should be maintained for 24 hours a day for about 3 months ro prevent rebound hypertrophy
    • MOA: increased hydration of the skin, which decreases capilalry activity, inflammation, hyperemia and collagen deposition may be involved
21
Q

Peritoneal adhesions

A
  • Most peritoneal adhesions are a result of intrabdominal surgery
  • intra-abdominal adhesions are the most ommon cause of small bowel obstruction especially in the ileum
  • Adhesions are a leading cause of secondary infertility in women

Fibrous bands

22
Q

Growth factor formulated and approved for treatment of diabetic foot ulcers

A

PDGF

(platelet derived growth factor BB)

A Cut Above the Rest (ABSITE) (48 decks)

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