Wound healing Flashcards

1
Q

What is Primary Intention - Wound healing ?

A

Primary intention - edges of injury / wound in contact with each other - e.g incision made with scalpel/ knife etc.
0 Rapid vs secondary intention
0 easier

( IVI ) - cut will look like this - the - just need to bring top edges together - so the do edges will heal into each other.

( IVI ——— ( T)
T - represent edges closed up - brought together & held there ( by suture , super glue) - medical intervention - simple injuries - suture

0 Would not use P intention - if infection , foreign body etc ——- close it will promote spread of infection , chronic inflammation , pus , abscess formation – as no where for infection to go
especially aerobic respiration - no longer exposed to surface oxygen - WOULD USE SECONDARY INSTEAD.

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2
Q

Types of wound healing ?

A

0 Primary intention

0 Secondary intention

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3
Q

What is secondary intention ?

A

Extensive tissue loss - so edges cant be brought together

Haemostasis
Inflammation
Ploliferative phase.

Wound left open to heal by :
0 granulation -

0 Contraction

0 epithelialization -

0 Maturation

in practice
- if you have certain would shap - sinus (vase with narrow neck ) - wound is packed to ensure the top of neck does not heal first ( bacteria would get trapped ) - packing helps healing to start from bottom up.

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4
Q

Stages of Primary intention & secondary intention.

A

FIRST FEW DAYS

  1. Haemostasis - prevention of bleeding
    o clot formation - platelets , fibrin - easy as dermal edge of wound are close. - formation of platelet plug ( addition of fibrin strands ) ———————-> scab formation

o vasoconstriction

AFTER FIRST FEW DAYS

  1. inflammation - WBC ( e.g neutrophils ) migrate to wound - removes cell debris , pathogens from wound.

( SECONDARY - inflammation phase more intense - infection , cell debris more likely present.

  1. Proliferation - wound rebuilt e.g
    o granulation
    tissue - new- connective tissue ( red in
    colour ) & microscopic BV forms on
    wound surface - grow from base of
    and fill it. (temporary filling )
  • ( SECONDARY - MORE GRANULATION TISSUE NEEDED )
 * Fibroblast  -  which 
      produces 
      collagen ---> 
      hold wound 
      together. 
     ( old collagen 
       is degraded 
       and replaced 
       by new - Extracellular matrix (collagen , elastin etc )broken down by macrophages & promote angiogenesis)
     * new BV form 
      - to bring 
      oxygen & 
      nutrients to new cells.
  • Macrophages relsease cytokines :
    Tissue necrosis factor (TNF )
    Interleukin (IL -1 )

o contraction - reduce size of tissue defect - myofibroblast ( specialised smooth muscle cells - contain actin & myosin) - grip edge of wound - decrease space btw dermal edges.
o can deposit collagen - for scar tissue formation as well.

o epithelisation - epithelial cells rise from wound bed & replicate & cover the surface of would - closing it to the environment.

CAN LAST AS LONG AS 2 YEARS

0 Maturation
cells & capillaries no longer need thin out.

  • original collagen replaced by a stronger type of collagen - better arranged
  • wound continues to contract
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5
Q

What affects speed of wound healing ?

A

Wound

- Depth 
- Size
- Type 
- Location 

0 Infection

0 Health
- chronic diseases e.g renal failure

  • Diabetes - micro vascular pathology
  • poor nutrition - deficiency Vitamin C , Zn , Cu

0 Age

0 Anti - inflammatory drugs

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6
Q

Complication of would healing ?

A

Keloid scars - excessive collagen production causing extensive scarring.

more common in darker skin.

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