Path 1- Integument 3

drraythe's version from 2015-05-02 19:31

Lecture 4

Question Answer
Actinic injury → Caused by what? What happens? Examples?Caused by UV RADIATION (which can lead to solar elastosis, actinic keratosis & neoplasia). Usually affects non-haired & non-pigmented areas of skin. Can induce DNA dmg (formation of thiamine dimers (& mutations) ) & may lead to development of neoplasms such as squamous cell carcinoma
Photosensitization occurs when what happens? How does injury get inflicted from this & what kinda injury is it specifically?Occurs when certain photodynamic compounds are deposited in the skin. These compounds react w/ UV radiation resulting in the production of reactive oxygen species that cause oxidative injury
What is Type 1 Photosensitization?Caused by the ingestion of certain plants (Hypericum perforatum, Fagopyrum esculentum), or the administration of drugs (phenothiazine)
What is Type 2 Photosensitization?Type 2: Caused by inherited defect in pOrPHyrin meTabOlism (spells photo right in it)
What is Type 3 Photosensitization?Aka Hepatogenous Photosensitization (the most common form) associated w/ liver dz & the reduced ability to excrete phylloerythrin, a photodynamic by-product of chlorophyll metabolism
What are Photo-enhanced dermatoses?They are immune-mediated disorders that are aggravated by UV radiation (Lupus Erythematosus, dermatomyositis & photoactivated vasculitis of the horse)
4 Types of chemical injury are?(1) Irritant contact dermatitis
(2) Injection site rxns
(3) Envenomation from snake & spider bites
(4) Selected toxins affecting the skin
Irritant contact dermatitis might be caused by what?Caustic chemicals (drugs, acids, alkalies, soaps, detergents, some plants) & also indirect injury is caused by immune-mediated dmg such as contact hypersensitivity (Type 4) or allergy
Injection site rxns → Explain how & why this is happening? Give examplesAdjuvants are highly immunogenic & can cause rxns. Exaggerated nodular granulomatous inflammation can persist at the injection site. A major example is vaccine related sarcomas in cats
Name 4 selected toxins which affect the skin. Say a little about them(1) Ergot poisoning (from eating the fungus Claviceps purpurea, it causes vasoconstriction+endothelial dmg → ischemic necrosis of extremities)
(2) Tall fescue grass (common pasture plant infected w/ the fungus Neotyphodium coenophialum which also contains ergot alkaloids)
(3) Selenium poisoning (plants w/ high selenium, or over-supplementation → competitive replacement of sulfur in keratin & causes poor hair coat w/ partial alopecia)
(4) Hairy vetch (Vicia villosa Roth - cultivated legume, unknown pathogenesis, possibly immune-mediated, results in dermatitis, conjunctivitis, diarrhea & granulomatous inflammation of many organs)
Acral lick dermatitis is aka? What is happening?Aka lick granuloma, neurodermatitis. PSYCHOGENIC, persistent licking/chewing, usually on extremities
Pyotraumatic dermatitis is aka? What is going on?Aka acute moist dermatitis, “hot spots” (dogs) self-trauma → 2° bacterial infxn. Typically associated w/ underlying cause of pain or pruritus (allergies, parasites, matted hair, etc)
Intertrigo is aka? What is happening w/ this?Aka skin fold dermatitis. Caused by trauma & microbial proliferation at apposed moist skin surfaces. Happens in dogs w/ excessive skin folds around face, tail, vulva, or in cows w/ large pendulous udders
Feline ulcerative dermatitis syndrome → What is going on w/ this?Uncommon disorder of cats caused by self-trauma. Typically develops on dorsal neck & may be associated w/ injections, topical therapy, or hypersensitivity
Callus is what?Caused by chronic trauma at pressure points
How common is frostbite? When might it happen?Rare in healthy animals, may occur in neonates w/ wet fur & hypoglycemia, severe & persistent cold temperature causes vasoconstriction, necrosis of vessels & ↑ blood viscosity → ischemic necrosis & gangrene of extremities
Explain 1st, 2nd & 3rd degree burns(1) 1st degree - epidermis only
(2) 2nd degree - epidermis & part of dermis
(3) 3rd degree - full thickness necrosis of skin (permanent scarring & life threatening due to infxn & fluid loss)
HypOthyroidism → Happens most often in who? What affects are had on the skin? Describe the lesionsDogs, thyroid hormone is necessary for initiation of anagen stage of the hair cycle. Clinical cutaneous lesions include dull, dry, easily epilated (hair pulled out) hair coat that fails to regrow resulting in areas of alopecia w/in areas of frictional wear
HypERadrenocorticism → Who does this occur in? What is the effect of this on the skin? Describe the lesionsMostly dogs, less often cats, rarely in anything else. Occurs w/ adrenal dz or w/ exogenous glucocorticoids (iatrogenic). Glucocorticoids have an inhibitory effect on collagen synthesis & maintenance leading to collagen degeneration w/ manifestations in many tissues including the skin. Clinical cutaneous lesions include thinning of the skin, comedones, ↑ bruising, poor wound healing, dystrophic calcification (calcinosis cutis) & ↑ skin infxns
How does Pituitary Dysfxn affect the skin & in WHOM?Pituitary dysfxn in HORSES (tumors of the pars intermedia) → dysfxn of the hypothalamus &/or neurohypophysis. Cutaneous lesions include ↑ sweating (hyperhidrosis) & excessively long hair coat (hirsutism or hypertrichosis)
Hyperestrogenism → WHO does this occur in? What is causing this? What are some of the lesions?Can happen in MALE OR FEMALE dogs. In FEMALES, it's caused by ovarian cysts or tumors & in MALES it's caused by a fxnal Sertoli cell tumor, both cases cause there to be raised amounts of estrogen → symmetric alopecia, follicular hyperkeratosis & enlarged nipples, prepuce & vulva
Urticaria → What is it? Who is it most common in? What causes them?Hives which happen in horses & dogs most often. There are 2 mechanisms:
(1) Immunological: involves Type I & Type III hypersensitivity rxns caused by pollen, foods, drugs, antisera & insect bites/stings
(2) Non-immunological: from heat, exercise, or stress
What does atopy mean?A genetic predisposition to inflammatory & pruritic allergic skin dz
Atopic dermatitis is most common in who? What is the mechanism behind this? What are the CS? (Histologic lesions?)Common in cats, dogs & horses. Mechanisms involve Type I hypersensitivity w/ IgE antibodies to environmental allergens. Pruritus is the predominant CS of atopic dermatitis w/ frequent excoriations & 2° bacterial & yeast infxns. (Histologic lesions include mild superficial perivascular lymphoplasmacytic & eosinophilic dermatitis)
Insect Bite Hypersensitivity → Which insect bite affects horses & what is this called?Horses affected by Culicoides which is called "sweet itch" (all the hair at the base of the tail rubbed off)
Insect Bite Hypersensitivity → Flea bites cause hypersensitivities in who?Cats & dogs
Insect Bite Hypersensitivity → Mosquito bites cause hypersensitivities in who?Cats
Insect Bite Hypersensitivities are caused by what kind of rxns to what?Caused by Type I & Type IV hypersensitivity rxns to salivary antigens from insect bites
What are some gross lesions caused by insect bite hypersensitivities? (Histologic lesions?)Gross lesions include papular to exudative dermatitis & miliary dermatitis, especially in cats. (Histologic lesions include superficial & deep perivascular eosinophilic dermatitis)
Allergic Contact Dermatitis is which type of hypersensitivity rxn? What are the gross lesions?Type IV hypersensitivity. Causes erythema, papules & exudation in areas of contact to the offending substance. (offending substances might be chemicals in carpet dyes, shampoos, certain plastic food dishes, plant resins, etc.) (histological lesions: superficial perivascular dermatitis w/ lymphocytic exocytosis & spongiosis)
Which type of hypersensitivity has to do w/ drug hypersensitivity? What are the drugs that cause this most commonly?Can be any of the 4 Types of hypersensitivities! Most commonly involved drugs are penicillin & trimethoprim-potentiated sulfonamides, (many others possible). (Histologic lesions are variable & include perivascular dermatitis, interface dermatitis, epidermal necrosis, follicular necrosis, vasculitis & vesiculopustular dermatitis)
Pemphigus foliaceus (PF) → Aka? How severe is this? How common is this? Who does this affect? How does it happen?Aka superficial pemphigus. The milder & more common Pemphigus. Reported in humans, dogs, cats, horses & goats. Usually develops spontaneously; however, may also occur as an adverse rxn to drug therapy
What is the pathogenesis of Pemphigus Foliaceus?Autoantibodies react w/ desmoglein **1** resulting in cytotoxic injury & acantholysis of the superficial epidermis resulting in subcorneal pustules
What are the gross lesions associated w/ Pemphigus foliaceus? What are the histologic lesions?Gross lesions include vesicles that rapidly become pustules which may be localized to the face & feet, or may be more generalized. Histologic lesions include acantholytic keratinocytes & subcorneal pustules
Pemphigus vulgaris (PV) → aka? How severe is this? How common? Who does this usually occur in?Aka Deep Pemphigus & is the MORE severe, less common form in dogs & cats (involves Desmoglein 1 & 3)
How do animals present when they have Pemphigus Vulgaris?Animals may exhibit severe illness w/ pyrexia, depression & anorexia
What is the pathogenesis of Pemphigus Vulgaris?Autoantibodies react w/ desmoglein **1 & 3** resulting in cytotoxic injury & acantholysis of the deep epidermis resulting in suprabasilar vesicles.
What are the gross lesions of Pemphigus Vulgaris?Vesiculo-ulcerative lesions of the oral mucosa, mucocutaneous junctions, or skin
What are the histological lesions of Pemphigus Vulgaris?Histologic lesions include suprabasilar vesicles, pustules, **acantholytic keratinocytes** & “tombstoning” of basal cells
Tombstoning =?Pemphigus Vulgaris
Bullous pemphigoid (BP) → What is this caused by? Who does this affect?BP is caused by autoantibodies directed against hemidesmosomal proteins resulting in separation of basal cells from the basement membrane & subsequent subepidermal vesicle formation. Reported in horses, dogs, cats & Yucatan minipigs
What are the gross lesions of Bullous pemphigoid? What are the histological lesions?Gross lesions include vesicles, erosions, ulcers & crusts w/ variable location & severity. Histologic lesions include subepidermal vesicles & bullae
What are the 6 skin-associated autoimmune disorders?(1) Pemphigus foliaceus (PF)
(2) Pemphigus vulgaris (PV)
(3) Bullous pemphigoid (BP)
(4) Systemic Lupus Erythematosus (SLE)
(5) Discoid Lupus Erythematosus (DLE)
(6) Erythema multiforme (EM)
Systemic Lupus Erythematosus (SLE) → Affects what organ? Who does it affect?SLE is a multi-organ dz of humans & dogs, rarely cats & horses
What is the pathogenesis of Systemic Lupus Erythematosus (SLE)? What is the principal mechanism of injury? What does SLE cause which can be used as a diagnostic aid?Pathogenesis of SLE involves the formation of autoantibodies which are directed against many different cellular & soluble antigens, including nucleic acids. The principal mechanism of injury occurs via immune-complex formation & deposition (Type III hypersensitivity) in a number of tissues, including the skin. SLE results in elevation of antinuclear antibody (ANA) titer which is a frequently used diagnostic aid
What are the gross lesions of Systemic Lupus Erythematosis (SLE)?May be localized or generalized. Erythema, depigmentation, alopecia, scaling, crusting & ulceration. Lesions commonly occur on the face & extend to trunk, pinnae & distal extremities (Lupus DEACUS)
What are the histologic lesions of Systemic Lupus Erythematosis (SLE)?Include lymphohistiocytic interface dermatitis, basal cell apoptosis, pigmentary incontinence, hydropic degeneration, subepidermal vacuolation w/ vesicle formation
Discoid Lupus Erythematosus (DLE) → What is this? What organ is involved?DLE is a mild, localized variant of SLE in which there is only involvement of the skin & no other organ systems (SLE is multi-organ) DLE = SKIN ONLY
Discoid Lupus Erythematosus (DLE) → What are the lesions like? Where do you find them?Lesions are similar to SLE (Erythema, depigmentation, alopecia, scaling, crusting & ulceration (Lupus DEACUS) ) & typically occur nasal planum, dorsal nose, pinnae, lips & periocular areas
Antinuclear antibody (ANA) titer in SLE? In DLE?In SLE the titer is elevated. In DLE the titer is NEGATIVE
How can you tell the difference between mucocutaneous pyoderma & Discoid Lupus Erythematosus (DLE)?Lesions can be indistinguishable from mucocutaneous pyoderma & responsiveness to treatment may be necessary for a Dx
Erythema multiforme (EM) happens in who? What is the pathogenesis?Humans, dogs, horses, cats & cattle. Poorly understood pathogenesis, a proposed mechanism is cell-mediated (Type IV hypersensitivity) immune response to foreign antigens such as drugs or infectious agents expressed on keratinocytes
What are the gross & histological lesions of Erythema Multiforme?Gross lesions may be localized or generalized & include erythema & circular to linear erosions or ulcerations. Histologic lesions include numerous apoptotic keratinocytes w/in multiple layers of the epidermis
What is Toxic Epidermal Necrolysis (TEN)?A much more serious & often life-threatening, form of EM that can result in full thickness epidermal necrosis