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LECTURE NOTES

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Lecture notes of 5 pages for the course Foundations Of Biomedical, Behavioural And Social Sciences For Medicine 2020/21 at UoS (YR 2 CONTENT)

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  • February 19, 2024
  • 5
  • 2022/2023
  • Class notes
  • Mdl200
  • All classes
  • Unknown
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Tissue repair
Wound-disruption in the integrity of the skin, mucosal surfaces or organ tissue
Causes:
Disease process, accidental, intentional-surgical

4 phases of wound healing:
 Haemostasis
 Inflammation
 Proliferation
 Maturation

Wound repair is similar regardless of the
aetiology

Acute wounds- go through healing process quickly

Soft tissue and bone healing process time scale is different

Abnormal wound repair:
 Increased mobility, morbidity and mortality
 Poor cosmetic outcome
 Health economic outcomes
 Psychological sequelae for the patients

Soft tissue:
Classification of wound closure:
 Primary intention-closing a wound rapidly- edges aligned
 Secondary intention-extensive tissue loss- edges cannot be approximated
 Delated primary healing-contaminated wound-therefore left open-wound closure
days after

Classification of wound contamination:
 Clean- primary closure
 Clean-contaminated- minimal spillage
 Contaminated- gross spillage of GI tract
 Dirty- purulent inflammation

Haemostasis : Bodies immediate response to prevent extreme loss of blood
Damaged arterial vessels rapidly constrict through the contraction of smooth muscle
through high cytoplasmic calcium levels

This leads to tissue hypoxia and acidosis
Production of vasoactive metabolites: NO
=vasodilation and relaxation of arterial vessels

Clot formation- coagulation cascade

,  Intrinsic- endothelial damage-exposure of sub-endothelial tissues to blood=
activation of Hageman factor (factor 12)
 Extrinsic- endothelial damage- exposure of tissue factor
 Platelet activation- thrombin, thromboxane and ADP=platelets under morphological
changes=secrete alpha and sense granules

Histamine release-increases vasodilation and increased vascular permeability=
INFLAMMATION

Inflammation: Prevent infection now that the mechanical barrier is no longer intact
Initial:
Complement activation
Neutrophils:
 Phagocytosis
 NETS- netosis
 Degranulation

Oxygen free radicals are produced as a by-product:
 Bactericidal properties
 Combine with chlorine=steralisation

Once finishes:
 Apoptosis
 Phagocytosed
 Sloughed from the wound surface
Later:
Marcrophages: M1 and M2

Produce TGF-B and EGF=regulation of
inflammation, angiogenesis and formation of granulation tissue

lymphocytes: regulation of wound healing and adaptive responses

Tregs-supress IFN-Y production
Dendritic Epidermal T cells- regulation of keratinocytes by producing keratinocyte growth
factor and IGF-1

Inhibition of T cells=reduced collagen deposition and wound strength

Lipxins and production so arachidonic acid metabolism=anti-inflammatory= dampening of
the immune response= initiation of the next phase

Proliferation:
Simultaneous processes:
 Angiogenesis
 Formation of granulation tissue
 Fibroblast migration

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