Difference between revisions of "Skin Environmental - Pathology"

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===Solar dermatosis and neoplasia===
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===[[Solar Dermatosis and Neoplasia]]===
*Caused by chronic sunlight damage
 
*Damaged tissue generates free radicals than may damage nucleis acids and proteins
 
*If damage repaired prior to mitosis - no lasting effect
 
*If mitosis occurs before repair, post-mitotic repair is prone to faults and DNA mutations may result in neoplasia
 
 
 
 
 
[[Category:Integumentary System - Sunlight Damage]]
 
  
  

Revision as of 16:12, 21 February 2011

Chemical damage

Contact Dermatitis

Ergot Poisoning

Fescue Poisoning

Selenium Poisoning

Physical damage

Acral Lick Dermatitis

Callus

Feline Psychogenic Alopecia

Injection Site Reaction

Intertrigo

Pyotraumatic Dermatitis

Radiation Damage

Low Temperature Damage

=High Temperature Damage

Sunlight damage

  • Transient erythema may develop into sunburn erythema (warmth, swelling, pain)
  • Diffusion of inflammatory mediators (e.g. cytokines) from damaged keratinocytes and endothelial cells
  • Photooxidation of existing melanin -> pigment darkening
  • Melanogenesis
  • Immune responses of skin are reduced by UV light


Solar Dermatosis and Neoplasia

Solar dermatitis

  • Particularly in white animals and where little or no hair is present
  • Grossly:
  • Microscopically:

Photosensitisation

Photoenhanced dermatoses

  • Many immune-mediated cutaneous disease are made worse by sunlight
    • Lupus erythematosus
    • Dermatomyositis
    • Pemphigus erythematosus
  • Vasculitis in extremities, especially white-haired horses
  • Grossly:
    • Erythematous, well circumscribed crusted lesions or hyperkeratotic plaques
  • Microscopically:
    • Vasculitis of superficial dermal vessels
    • Thrombi may be seen