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Repair

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Repair Dr. Gehan Mohamed Dr. Abdelaty Shawky – PowerPoint PPT presentation

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Title: Repair


1
Repair
  • Dr. Gehan Mohamed Dr. Abdelaty Shawky

2
Intended Learning outcomes
  • Understanding the classification of human cells
    according to their ability for proliferation.
  • Identifying the types of repair.
  • Discussing the mechanism of wound healing.
  • Recognizing the complications of wound healing.
  • Understanding the process of healing of bone
    fracture.
  • Being oriented with the factors affecting the
    process of repair.

3
Types of cells according to the ability of cell
proliferation
  • 1. Labile cells are Conteniously dividing cells
    and renew themselves e.g skin epithelium
    ,mucosal lining of the GIT, haematopoietic cells
    (blood cells ).
  • 2. Quiescent cells (Stable) cells divide when
    there is a need e.g hepatic, kidney and pancreas
    .
  • 3. Permanent cells Non-dividing cells so when
    injured heal by fibrous tissue e.g nerve cells
    and skeletal, cardiac muscle cells

4
Repair (Healing)
  • Definition Replacement of damaged tissue with
    new healthy living tissue.
  • Types
  • A. Regeneration
  • healing by the same type of tissue cells from
    surrounding healthy living cells, this occurs
    with small damages of labile cells and stable
    cells for examples liver cirrhosis and bone
    fractures
  • B. Fibrosis (scar tissue)
  • healing by granulation tissue (fibroblast with
    new capillaries) which mature to hypovascular
    fibrous tissue (scar), this occurs in the healing
    process of permanent cells or in stable cells
    with high damage. for example myocardial
    infraction and wounds

5
Wound Healing
  • Cutaneous wound healing is generally divided into
    four phases
  • Homeostasis.
  • Inflammation.
  • Granulation tissue formation and
    Re-epithelialization
  • Remodeling.
  • - Wound healing is a fibroproliferative response
    that is mediated through growth factors and
    cytokines.

6
1. Homeostasis
  • Immediately after injury the cut vessels bleed
    inside the wound defect to form a blood clot that
    unit the two cut ends temporarily.
  • Vasoconstriction of the injured vessels at the
    edges of the wound followed by platelets
    aggregation and adherence to the damaged
    endothelium.
  • Stimulation of coagulation system will form
    fibrin.
  • Fibrin network is formed over the aggregated
    platelets to form a 1ry homeostatic plug that
    stops bleeding inside the wound.

7
  • 2. Inflammation
  • Mediated by polymorphs and macrophages.
  • Within the first 6-8 hours, the
    polymorphonuclear leukocytes (PMNs) kill any
    organism in the wound and liquefy any necrotic
    debris.
  • As the process continues, monocytes also exude
    from the blood vessels. These are termed
    macrophages. The macrophages continue and engulf
    the necrotic debris and also manufacture various
    growth factors during days 3-4.

8
  • 3. Granulation tissue formation and
    re-epithelization
  • In days 5-7, fibroblasts migrate into the wound,
    laying down new collagen of the subtypes I and
    III
  • Angiogenesis is the formation of new capillaries
    from the healthy blood vessels at the edge of the
    wound. These new capillaries fill the wound
    defect and surrounded by fibroblasts.
  • The newly formed capillaries fibroblasts
    granulation tissue.
  • Re-epithelization occurs by proliferation and
    migration of the healthy epidermal cells from the
    edges of the wound inwards.

9
Granulation tissue
10
Granulation tissue
Epithelization
capillary
fibroblast
11
  • 4. Remodeling
  • - After the third week, the wound undergoes
    constant alterations, known as remodeling.
  • Collagen is deposited from fibroblasts and
    degraded by collagenase enzyme which secreted
    from macrophages in a controlled manner.
  • Wound contraction is a process occurs by the
    action of myofibroblasts (modified fibrobalsts),
    which resemble contractile smooth muscle cells.
    This occurs to give the healing wound more
    strength.

12
Types of wound healing
  • 1. Healing by primary union (first intention)
  • - Occurs with clean, non-gaping wounds (stitched
    surgical incision).
  • 2. Healing by secondary union (secondary
    intention)
  • - Occurs with extensive tissue loss as in large
    wounds, infected wounds, abscess, ulcers.etc.

13
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14
Complications of the healing process
  • A. Complications from deficient granulation
    tissue formation
  • 1. Ulcers discontinuity of the covering
    epithelium or mucous membrane .
  • 2. Sinus is blind end track of septic
    granulation tissue connecting a cavity to the
    outside e.g. pilonidal sinus
  • 3. Fistula is a tract of septic granulation
    tissue connecting 2 epithelial surfaces e.g.
    perianal fistula.
  • 4. Weak atrophic scar this may lead to hernia .

15
  • B. Complications due to excessive granulation
    tissue formation
  • 1. Hypertrophied scar.
  • 2. Keloid formation if the formed scar
    exceeded the original size of the wound.

16
Keloid
Hypertrophic scar
17
Keloid
B
A
18
  • C. Other complications
  • Infection leading to delayed healing
  • Squamous cell carcinoma rarely scars may develop
  • Cicatrisation contracture of the size of the
    scar
  • Implantation epidermiod cyst is a cyst formed
    secondary to entrapment of part of the epithelium
    inside dermis.
  • Stump neuroma following amputation causing a
    painful coiled mass of nerves

19
Bone Fracture
  • TYPES
  • Simple.
  • Compound .
  • Comminuted fracture into pieces.
  • Greenstick is a partial fracture involve only
    one side of bone , common in children.

20
Types of Fracture
21
Mechanism of healing of bone fracture
22
Complications of bone fracture
  • 1. Delayed union (healing) due to old age,
    anaemia, calcium or vitamin D deficiency
  • 2. Non union due to soft tissue interposition
    between the two fracture ends.
  • 4. Mal union of healed bones due to improper
    reduction.
  • 5. Bone necrosis due to injury to nutrient
    artery.

23
Factors affecting Repair
  • I. Local factors
  • The type of the damaged cells ( labile, stable or
    permanent).
  • Severity of the damage.
  • Presence of foreign body.
  • Presence of necrotic tissue.
  • Infection.
  • Irradiation.
  • Blood supply.

24
  • II. General factors
  • Age of patient.
  • Nutrition status.
  • Diseases Diabetes, malignancy, anaemia.
  • Drugs Corticosteroid therapy, chemotherapy..
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