L7: Path of the Integumentary System (Ginn) Flashcards
fxs of skin
- temp/BP regulation
- fluid regulation
- protection
- sensation
- nutrient metabolism
- immune functions: SALT
layers of skin
panniculus (deep fat layer)
adnexa (sebaceous, apocrine glands, hair follicles)
dermis (prod. by fibroblasts)
basement membranes
epidermis (surface of skin; composed of s. basal/s. spinosum/s.granulosum/s.corneum)
stages of hair follicle
anagen (growth)
catagen (cessation)
telogen (resting)
acanthosis***
hyperplasia of the epidermis
-can be regular (ie. drug rxn), irregular, paillated (ie. seborrhea, viral infection) or pseudocarcinomatosis
hyperkeratosis
increased width of stratum corneum
-2 types: ORTHOKERATOTIC (cells of stratum corneum develop normally but lose nuclei too quickly; ie. chronic insult to skin) or PARAKERATOTIC (cells haven’t matured normally and haven’t lost nuclei normally; signals epi not returning normally, underlying dz such as chronic liver dz, diabetes, pancreatic tumor)
ichthyosis
congenital hyperkeratosis
seborrhea
condition in which flakes of dead skin are shed from the epidermis and hair follicles
dyskeratosis
- premature keratinization of cells in the epidermis
- often seen in parakeratosis**
- often due to sun damage
- cells taking first steps to neoplasm
apoptosis
individual cell necrosis
- programmed cell death
- most common cause = drug rxn
- causes erythema multiforme
2 types of epidermal necrosis
- apoptosis
- full thickness epidermal necrosis (also usually drug rxn; ex- toxic epidermal necrolysis)
cutaneous atrophy
- not getting enough blood, hormones (most common), etc.
- can affect epidermis, hair follicles, and dermis
- telogen hair follicles –> alopecia
- acantholysis: loss of intercellular connections, such as desmosomes, resulting in loss of cohesion b/w keratinocytes
- epidermis becomes very thin
spongiosis
intercellular edema
-type I hypersensitivity rxns
hydropic degeneration
fluid accum. in basal epidermis
- type of intracellular edema
- can form blisters
ballooning degeneration
keratinocytes w/n epidermis balloon up and can burst
- type of intracellular edema
- often a viral cytopathic effect
- mech. of vesicle formation
Acantholysis
loss of intercellular connections, such as desmosomes, resulting in loss of cohesion b/w keratinocytes
- enzymatic destruction (caused by neuts), type II hypersensitivity (ie. pemphigus foliaceus)
- main differentials: bacterial or fungal rxn, true cytotoxic rxn**
most common autoimmune disease
pemphigus foliaceus
3 locations of vesicles/bullae**
1) subepidermal (worst, ulcerative; bolus phemphigoid, burns, toxic epidermal necrosis, EB or lupus can cause)
2) subcorneal (pemphigus foliaceous)
3) suprabasal (pemphigus vulgaris can cause)
path. of vesicles or pustules
- marked spongiosis, hydropic or ballooning degen.
- enzymatic/immune/mechanical or destruction
- genetic structural defects
Pautrier’s microabscesses
- collection of lymphocytes in the epidermis –> pustule
- indicative of epitheliotrophic lymphoma aka mycosis fungoides (neoplastic dz. of lymphocytes)**
3 possible fillings of pustules
neuts
eos
Pautrier’s microabscesses
what causes hypopigmentation?
damage to melanocytes or BM, defects in form. of melanin or lack of melanocytes
3 causes of folliculitis***
demodex
dermatophytes
bacteria (staph)
urticaria
hives
-compressible, fluid-filled
mucinosis
- excess mucin (mucin = glycosaminoglycan substance b/w collagen bundles)
- Sharpeis
- can be caused by hormonal imbalance like hypothyroid or feline eosinophilic plaques
infiltrate of eos or mast cells –> collagen
degeneration/collagenolysis
2 categories of collagen mineralization
1) dystrophic (hyper?adrenocorticism, chronic renal failure)
2) metastatic
elastosis
added compliance/elasticity of skin by inc. elastin
calcinosis cutis
deposition of Ca salts
- hyperadrenocorticism
- eventually ulcerates
things that cause vasculitis
thrombosis ischemia edema hemorrhage atrophy
presence of mononuclear phagocytes indicates:
persistent Ag in tissue
perivascular dermatitis
- most common type of dermatitis
- generic response of skin to injury
- suggests hypersensitivity*
- aggregates of inflamm. cells around vessels
- acute or chronic
- often eos present**
Culicoides hypersensitivity
- insect bite hypersensitivity
- pruritis, alopecia, acanthosis, hyperpigmentation
interface dermatitis
-hydropic degen/apoptosis in basal layer
-leuks at interface b/w dermis and epidermis
-usually immune-mediated
-pigmentary incontinence
+/- vesicles
-most common path = T cell attack on keratinocytes or melanocytes or BM components
-Discoid Lupus in GSD –> erosions, depig, crusting
Uveodermatologic Syndrome
- Akitas
- depig, uveitis
Vasculitis
- leuks WITHIN walls of capillaries and venules
- edema, hemorrhage, necrosis
- type III hypersensitivity (immune complex deposition in vessels)
- primary bacterial skin dz, bacterial septicemia (ie. Diamond Pig Skin Dz) or systemic infection w/ endotheliotropic orgs. such as Rickettsia
- lesions usually on extremities
Nodular to Diffuse Dermatitis
- difuse infiltrates of leukocytes in dermis
- path: persistence of Ag in tissue stimulate a cell mediated immune response
- grossly: multiple papules, nodules +/- ulceration
- causes: fungi, acid fast bacteria, parasites, protozoans, oomycetes, algae, idiopathic, FB, neoplasm
Vesicular or Pustular Dermatitis
- vesicles of pustules are w/n or below epidermis(subcorneal, suprabasilar, or subepidermal)
- marked spongiosis, hydropic or ballooning degen.
- enzymatic/immune/mechanical destruction
panniculitis
- SC fat is focus of inflamm.
- gross: papules, nodules
- histo: inflamm. of subcutis; nodular to diffuse
- causes (same as nodular to diffuse): fungi, acid fast bacteria, parasites, protozoans, oomycetes, algae, idiopathic, FB, neoplasm, + pancreatitis
Atrophic dermatoses
- symmetric hypotrichosis, thin skin
- comedones, telangiectasia, hyperpigmentation
- focal atrophic dermatosis - partical ischemia
- hormonal imbalance: hyperadrenocorticism, hypothyroidism, sex hormone imbalance
- ischemia if focal
