skin anatomy 3 parts
3 parts:
-epidermis
-dermis
-subcutis (mostly adipose tissue)
epidermis structure 4 layers
-top to bottom
Stratum Corneum
Stratum Granulosum
Stratum Spinosum
Stratum Basale
Stratum Lucidum (nonhaired skin only)
rete pegs/ rete ridges
the basement membrane is the scaffold of wound healing
-hold the epidermis to the subcutis, strengthens connection.
-calluses are thickening of epidermis with more rete pegs.
nerves in the skin
-motor nerves for hair follicle movement and skin contraction
-sensory: itchy, pain. touch, pressure, temperature
hair growth cycle
-humans and poodles anagen is the growing phase
-most mid hair dogs 20% in anagen
-large hair breeds Husky 9% in anagen takes along time for hair to grow back.
-anagen: growing
-catagen: transitional
-telogen: resting
-early anagen
-exogen
follicular growth anagen phase
Anagen = growth stage
Stimulated by:
Thyroid and growth hormone
Melatonin
Suppressed by:
Estrogen and glucocorticoids
-hair Needs protein, starving leads to weak, not growing hair.
functions of hair
-hair follicles: protection, thermal insulation, social communication, sensory perception
-tactile hairs: specialized mechanoreceptors
stratum corneaum function
-insoluable and impermeable, protection
-melanin protects from UV rays
-basement mambrane zone helps with achoring of skin and filering of chemicals
-collagen and elastin: resilience strength support
functions of skin
Adnexal glandular secretions:
Sebaceous = sebum (oil)
Apocrine = sweat to protect skin
surface
Eccrine = foot sweat
Panniculus (subcutis):
Padding and anchoring
Facilitates movement
Store fat, etc.
Claws, hooves:
Thick cornification for traction and
protection
alterations in epidermal growth in response to injury
-hyperkeratosis: increase in thickness of the stratum corneum. normal in some locations (paw pads, nasal planum). parakaratosis are cells with nucli present.
-hyperplasia: increase # of cells in the epidermis, common with inflammation
-Acanthosis: hyperplasia of the stratum spinosum
-hypoplasia: decrease in # of cells/ size (hyperadrenocorticism)
-aplasia: failure to develop (epitheliogenesis importfecta
-apoptosis: cell death, programed kertitination or pathological (Immune disease)
alterations in fluid balance and cell adhesion of the epidermis
-edema: spongiosis is inflammatory change, swelling with some viruses
-acantholysis and vesicles: loss of cohesion between epidermal cells. (pemphigus), pyoderma
-alterations in epidermal growth: atrophy (thin skin in cushing dogs)
inflammatory lesions of the epidermis in response to injury
-exocytosis of leukocytes into the epidermis, vesicles with inflammatory cells and crusts of dried ecaudate on epidermal surface.
epidermal pigmentation in response to epidermal injury
-leukoderma: hyperpigmetation
-lentigo (common) older orange cats, where they rub skin (anus, face, ears) dark pigments, normal.
response to injury dermis
follicular atrophy in response to injury
PHYSIOLOGIC ATROPHY
Growth of hair is seasonal* and it
is controlled by environmental*
and genetic factors
PATHOLOGIC ATROPHY
Hormonal abnormality*
Inadequacy of vascular supply
Inflammation*
Systemic illness & Stress
panniculitis
-inflammation of SUBQ fat
causes:
primary: vit E deficiency, vaccination
secondary: bacterial foliculitis
folliculitis
-inflammation of the hairfollicle
-causes: parasites (demodex), bacteria (staph), dermatophytes
-furnucolosis: perforating folliculitis, has edema, hair follicle fully ruptures and invades tissue around it
-the progression of folliculitis is: perivascular, mural, luminal , rupture, drain
congenital or hereditary skin disorders
epitheliogenesis imperfecta:
1 complete failure of epithelium and adenxa to develop
2 small lesions animal will be fine
-bacteria can get in and lead to septicemia (e.coli)
ichthyosis fetalis:
1 FATAL, congenital and inherited disorder (calves, puppies)
-usually on feet and muzzle, on charlae cattle entire body. not common.
Temperature injuries cold
frostbite:
Freezing of water in and around cells -> ice crystals pull water from cells -> increased osmotic pressure
-leads to vasoconstriction-> tissue anoxia
-endothelial damage-> decreased BP
-coagulation necrosis from blood clots
temperature injuries heat
burns
Dry heat (hair dryer) -> desiccation + carbonization
Moist heat (hot water) >coagulation of tissue
different degrees of burns
Partial thickness = 1 st (epidermis) and 2nd degree burns:
Accelerated cellular metabolism
Inactivation of enzymes
Vascular injury
Scarring, but adnexa are preserved, regeneration
Full thickness = 3rd degree burns
Coagulation of the epidermis and dermis
4 th degree burns extend into the fascia and SQ
Sloughing
temperature solar injury
-called Actinic dermatosis
UVB is most damaging
Acute = sunburn
Chronic = solar dermatosis or neoplasia
-lesions develop in poorly haired or lighty pigmented sites (exp abdomen)
photosensitization
Pathogenesis:
UV light absorbed by photodynamic chemical in skin tissue -> reactive oxygen
(free radicals) -> mast cell degranulation
-erythema and edema–>blisters, excudation, necrosis, sloughing
photosensitization types
Primary photosensitization
type 1
Ingestion of preformed photodynamic substances
Administration of drugs (tetracycline, sulfonamides…)
type 2
Abnormal porphyrin metabolism
(NB: Triple “I”: ingestion, injection and inheritance)
Secondary photosensitization
-type III Hepatic diseases