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196 Cards in this Set

  • Front
  • Back
Primary Lesion
: Initial eruption that develops spontaneously as a direct result of the underlying disease.
• When present, these are the most significant type of lesions, should be included in your problem list and may significantly limit the initial differential diagnosis
• Primary lesions develop quickly and then disappear rapidly. However they may leave behind secondary lesions (such as focal alopecia, epidermal collarettes, scales, hyperpigmentation, crusts) which may be more chronic and give clues about the presence of previous primary lesions.
• Not all diseases have primary lesions: ex: atopy (aka “air-borne” allergy)
Define Pustule
1. Pustule: A small circumscribed elevation of the skin containing purulent material. May be intraepidermal, subepidermal or follicular. Neutrophils usually predominate. Most often infectious but can be sterile. (Lay term: “pimple)
NOTE: Pustules may start as papules, then develop into pustules. Pustules are VERY transient in animals, i.e., they rupture  crusts, erosions or epidermal collarettes.
Define Papule
2. Papule: A small, solid elevation of the skin up to 1 cm in diameter; can be palpated as a solid mass. Often are pink or red swellings produced by tissue infiltration of inflammatory cells in the dermis, intraepidermal and subepidermal edema, or epidermal hypertrophy. (Lay term: “rash”)
Define Plaque
3. Plaque: A larger solid elevation of the skin with a flattened top (> 1 cm). (Lay term: “rash”)
Define Nodule
4. Nodule: A circumscribed, solid elevation > 1 cm in diameter that extends into deeper layers of the skin. Usually result from massive infiltration of inflammatory or neoplastic cells into the dermis or subcutis. (Lay term: “lump” or “bump”)
Define Tumor
5. Tumor: A large mass that may involve any structure of the skin or SQ tissue. Lay term: “lump” or “bump”)
Define Cyst
6. Cyst: An epithelium-lined cavity containing fluid or a solid material. Usually smooth, well-circumscribed, fluctuant to solid mass. Usually lined by adnexal epithelium (hair follicle, sebaceous or epitrichial) and filled with cornified cellular debris or sebaceous or epitrichial secretions. (Lay term: “lump” or “bump”)
Define Vesicle
7. Vesicle: A small, sharply circumscribed elevation of the skin filled with clear fluid. Can be intraepidermal or subepidermal. Very fragile in animals, rupture ® crusts, erosions or ulcer. (Lay term: “blister”)
Define bulla
8. Bulla: A large (> 1 cm) vesicle.
Define hemorrhagic bulla
9. Hemorrhagic bulla: bulla whose contents includes blood.
Define Wheal
10. Wheal = Urticaria: A sharply circumscribed, raised lesion consisting of edema that usually appears and disappears within minute or hours; usually do not cause change in the overlying skin and hair. (Lay term: “hives”)
Define Urticaria
10. Wheal = Urticaria: A sharply circumscribed, raised lesion consisting of edema that usually appears and disappears within minute or hours; usually do not cause change in the overlying skin and hair. (Lay term: “hives”)
define angioedema
11. Angioedema: A huge wheal in a region that is distensible. (Lay term: “swelling”)
define macule
12. Macule: A circumscribed, nonpalpable area characterized by a change in the color of the skin; < 1 cm in diameter. (Lay term: “freckle” or “splotch”)
define macule
13. Patch: A macule which is > 1 cm.
define nevus
14. Nevus: a circumscribed developmental defect in the skin; may arise from any skin component(s). Ex: pigmented nevus = “mole”
define secondary lesion
B. Secondary lesions: Evolve from primary lesions or are artifacts induced by the patient or by external factors such as trauma (usually self-induced trauma from pruritus) or medications. • These are much less specific in origin but are useful hints as to the presence of previous primary lesions.
Define epidermal collarettes
1. Epidermal collarettes: A special type of scale arranged in a circular rim of loose keratin flakes or peeling keratin. It represents the remnants of the roof of a vesicle, bulla, pustule or papule.
define crusts
2. Crusts: Dried exudate, serum, blood, medications or excessive scale on the skin surface; often sequel to a pustule. (Lay term: “scab”)
define excoriation
3. Excoriation: Superficial (epidermal) erosions or ulcers caused by self-trauma. May have a linear pattern.
define lichenification
4. Lichenification: Thickening of the epidermis and/or dermis with exaggeration of the superficial skin markings.
define erosion
5. Erosion: A shallow epidermal defect that does not penetrate the epidermal basal cell layer. Usually results from epidermal diseases or self-inflicted trauma.
define ulcer
6. Ulcer: A break in the epidermis with exposure of the dermis. Result of a deep pathologic process.
define scar
7. Scar: An area of fibrous tissue that has replaced the damaged dermis or subcutaneous tissue. Most are alopecic, atrophic and depigmented or hyperpigmented.
define fissure
8. Fissure: A linear cleavage into the epidermis or through the epidermis into the dermis. They occur when the skin is thick and inelastic and then subjected to sudden swelling from inflammation or trauma.
define callus
9. Callus: A thickened, rough, hyperkeratosis, alopecic, often lichenified plaque. Most occur over bony prominences and result from chronic, low-grade pressure.
define alopecia
1. Alopecia: partial or complete loss of hair
1˚ alopecia: abnormal hair growth (endocrine related or congenital alopecia)
2˚ alopecia: self-trauma induced by pruritus
define scale
Scale: Accumulation of loose fragments of the stratum corneum. (Lay term: “dandruff”)
1˚ scale: genetic keratinization defects such as primary seborrhea
2˚ scale: common with any inflammatory or pruritic disease
define comedones
3. Comedones: Dilated hair follicle filled with cornified cells and sebaceous debris. (Lay term: “black head”)
1˚ comedones: feline acne, Schnauzer comedo syndrome
2˚ comedones: secondary to hair follicle infections (Demodex, dermatophytes)
define follicular cyst
4. Follicular cast: Accumulation of keratin and follicular material that adheres to the hair shaft extending above the surface of the follicular ostia
1˚ casts: many primary keratinization disorders
2˚ casts: secondary to hair follicle infections (Demodex, dermatophytes)
define hypopigmentation
5. Hypopigmentation: Reduction or total loss of pigment in the skin or hair in areas that should be pigmented
1˚ hypopigmentation: congenital albinism, vitiligo, DLE
2˚ hypopigmentation: post-inflammatory
define hyperpigmentation
6. Hyperpigmentation: Increase in the amount pigment of the skin or hair
1˚ hyperpigmentation: lentigo simplex, feline acromelanism
2˚ hyperpigmentation: post-inflammatory
Which lesions are primary lesions?
pustule, papule, plaque, nodule, tumor, cyst, vesicle, bulla, hemorhagic bulla, wheal, urticaria, angioedema, macule, patch, nevus
which lesions are secondary lesions?
epidermal collarettes, crusts, excoriation, lichenifcation, erosion, ulcer, scar, fissure, callus,
which lesions can be primary or secondary depending on the disease process
alopecia, scale, comendones, follicular cast, hypopigmentation, hyperpigmentation
pruritis
1.Pruritus: An unpleasant sensation within the skin that produces the desire to scratch
seborrhea
2. Seborrhea: Excessive scaling; adjectives often used with seborrhea include:
Seborrhea sicca: dry scales and dull hair coat.
Seborrhea oleosa: greasy/ sticky scales and hair coat
fistula
1. Fistula: Sinus or abnormal passage leading from an abscess to the surface
abscess
4. Abscess: A circumscribed SQ collection of pus
actinic
5. Actinic: Relating to the chemically active rays of the electromagnetic spectrum
erythema
6. Erythema: Redness of the skin associated with inflammation
furunculosis
7. Furunculosis: Inflammation secondary to rupture of a hair follicle; usually pyogranulomatous
pyotraumatic dermatitis
1.  Pyotraumatic dermatitis: superficial, ulcerative inflammatory process caused by trauma; also referred to as acute moist dermatitis. (Lay term: “hot spots”)
pyotraumatic foliculitis
1.  Pyotraumatic folliculitis: deep suppruative folliculitis usually a manifestation of deep pyoderma.
intertrigo
1.  Intertrigo: surface irritation and inflammation caused by frictional trauma of skin rubbing against skin; also referred to as “skin fold dermatitis”
types of regional distribution
1. Regional distribution: Generalized, truncal, extremities, nasal planum, footpads, etc.
types of configuration of lesions
2. Configuration of lesions: Single, grouped, linear, annular, serpiginous, central healing
eval for parasites
skin scrapings, acetate tape impressions, flea comb. Part of a dermatological minimum data base
trichogram
hair exam - pluck hairs, lay in mineral oil on glass slide. Exam under low power. Use to confirm presence of broken hairs, distorted hair, pigmentary disorders of hair follicles, dermatoohytosis, demodicosis
eval for dermatophytosis
woods light microscope, direct exam, culture. Part of a dermatologoic minimum data base
cytology
part of a dermatologic minimum data base. Perform on anything you can get to stick to a slide
bacterial and fungal c/s
dermal or subcut infections; superficla infections that are not responding to rational antimicrobial therapy. Collection of samples: prep skin surface gently first
flea allergy dermatitis
pruritic dermatitis resulting rrom an allergic reaction to flea salivary antigens. Very common. The most common of the four types of allergic skin dz in both dogs and cats. Familial and genetic predisposition
pathoophys of FAD
type 1 and or tyoe IV hypersens (delayed, cell mediated hypersens)
histopath for FAD
non specific, epidermal hyperplasia and spongiosis, perivascular infallmation, eosinophils may predominate
FAD signalment
more common in dogs and cats with atopy. Age of onset usually between 1-3 years or within several months of first flea exposure
FAD clinical signs
pruritis assoc with fleas / flea exretea. More common in warm weather
FAD in dogs- primary and secondary leasions
primary- papules and crusted papules. Secondary - due to excoration are common, pyotraumatic dermatitis.
pyotraumatic dermatitis
acute onset, trigered by excoriations, surface infection, caused by an puritic dz, but FAD is the most common. D
dogs FAD distribution
tail bse, rump, perineum, inner thighs
is secondary superficial pyoderma common in dogs with FAD?
no
FAD distribuion in cats
generalized, often bigns at head and neck.
what can FAD in cats cause
eosinophilic plaques
DDX for FAD
other papular plaque diseases, esp scabies. Pruritic diseases which do not present with primary lesions
diagnosing FAD
tentative: clinical signs (Esp distribution in dogs) and presence of fleas, flea excreta or dipylidium caninum segments. Note: many allergic cats efficiently remove the fleas and ecreta thru grooming. . Definitive: response to flea eradication, positive immediate ID reactions to salivary antigens at 30 minutes or a delayed reaction at 24-48 hours
FAD management
elim the fleas (topical vs oral), temp symptomatic relief with short acting glucocorticoids. Antihistamines. Omega 3 or omega 6 fatty acids, topical shampoo/rinse. Only effetive TX is to elim fleas!
tx of pyotraumatic dermatitis
clip, clean BID with chlorhex until resolution. O not apply occlusive topicals. Can use drying agents and or topcal non occlusive steroids. The infection does not inviade the viable epidermis and does not require systemic Abs
in dogs, assume that pyotramatic dermatitise is caused by ____ until proven otherwise
FAD
in cats, assume milliary dermatitis is caused by ___ until proven otherwise
FAD
insect hypersns in horses
pruritic dermatits resulting from an allergic rxn to Culicoides, Stimulum (black flies) > stomoxys calcitrans and possible haematobie irritans. Most common allergic skin dz in horses. Familial and enetic predisposition. Ost react to >2 kinds of flies
pathophys of nsect hypersens
type 1 or type IV hypersensitivty
when do most cases of insect hypersens manifest?
3-4 years of age
clinial signs of insect hypersens
gnat/fly season pruritis. Primary lesions - papules and crusted palules. Secondary lesions - common and are due t the extreme pruritis- crusts, alopecia, excoriations, lichenification, post inflamm hyper or hypopigmentation.
insect hypersens distribituoin
dorsal or ventral or both depending on insect inolved.
insect hypersens is the most common cause of
tail and mane alopecia
ddx for insect hypersens
other excoparasites, atopy, food allergy
dx insect hypersens
clinical signs, history, response to insect avoidance,
mgmt of insect hypersens
insect control, protective housing, topical insectisides or repellants. Temp symptomatic relief with oral prednisolone. Antihistamines, omega 3/6 FA, topical shampoo/rins, hyposensitization
scabies in dogs
contagious, severely pruritic dermatitis caused y sarcopties scabies var canis
pathogenesisis of scabies
tunnels within the stratum corneum, most likley causes such severe prurutis in individuals who are allergic to the parasite
scabies incubation period
pruritis may be dalyed until several weeks after exposure (esp wth the first exposure)
histopath of scabies
non specific epidermal hyperplasia and spongiosis, perivascular inflammation, eosinophils predominate. Rarely see mites in s. corneum
scabies clinical signs (primary and secondary lesions, distribution)
1- papules that may coalesce into plaques, this lesions are quickly excoriated. 2- thick crusts and scales may predominate. Severe pruritis leads to excoriations and alopecia. Distribution- usually ventral (axillae, groin, elbows) and pinnae, but may generalize with time. can occur in any season
DDX for scabies
FAD, pruritic deiseases that do not have primary lesions
scabies DX
clinical signs, deistribion, skin scrapings (but may have to rely on response to a treatment)
treatment options for scabies
miticidal therapy, weekly systemic ivermectin for 2-4 weeks, weekly milbemycin, selemectin, temp relief with anti inflamm doses of pred. do not nead to treat enviornment. Antipruritic shampoo.rinse.
zoonosis of scabies
may transiently infect humans resulting in a self limited papular, prritc eruption in areas of exposure
notoedres in cats
contagious, severely pruritic dermatitis caused by n. cati.
clinical signs of notoedres in cats
may see papules early in the dz. Secondary lesions predominate- lichenifcations, wrinkled skin surface, sense tightly adherent yellow to gray sales, pruritis leads to excoriations and alopecia. Distribution begins on tops of pinnae and head, progresses to trunk
DDX for notoedres
otodectes, cheyletiellosis, pruritic ds which do not have primary lesions,
ddx of notoedres
usually found in large numbers in SS
mgmt of notoedres
topicals (lime sulfuer, amitraz). Treat all incontact cats. Ivermec for 6-8 weeks.
zoonosis of notoedres
transient lesions in humans
hookwork dermatitis in dogs
pruritic dermatitis caused by penetration of the skin by the 3rd stage larvae of hookworms. Uncommon except in puppies kept in unclean conditions
pelodera dermatits in dogs
erythematous pruritic dermatits caused by the llarval stage of a free liviing nematode - Pelodera strongyloides. Uncommin except where puppies are kept in very unclean conditions
list four other causes of papules
acne, schnauzer comedone syndrome, calcinosis cutis (initial lesions). Eosinophilic plaques
what is important to remember about pustules
that they are fragile and easily ruptured, therefore patients often presnt with crusts or epidermal as the only clinical signs
superficial pyoderma in dogs
bacterial infection confined to the stratum corneum and or hair follicles
organisms that cause superficial pyoderma
coag positive staph: s. pseudintermedius >> s aureus >>hyicus
most common skin dz in dogs
superficual pyoderma
pathophys of superficial pyoderma
a secondary infection that results from changes in the micrclimate of the skin that then leads to the overgrowth of S. pseudintermedius.
histopath of superficial pyoderma
neutrophilic pustules withbacteria within the stratum corneum or hair folicular epithelium
clinical signs of superficial pyoderma
primary lesions - pustules, papules. Secondary - crusts, epidermal collarettes, post inflamm hyperpigmentation, lichenifcation
changes associated with pruritis
alopecia, excoriations, erythema
what distribuion of superficial pyoderma is common in short coated breeds
primarily follicular distribution
horses can develop bacterial folliculitis secondary to
atopy, food allergy, insect hypersensitivity
what is important to remember about superficual pyoderma
that it is a secondary skin infection and that the underlying dz must be recognized and txed
most common cause of papules/pustles in dogs
superficual pyoderma
definitive diagnosis of superficial pyoderma
cytology of intact pustule, scale from a collarette or crust bed: neutrophiles, bacteria, macrophages. Bacterial c/s- coag pos staph (usually not necc to culture). Histopath findings.
treatment trial for bacterial folliculitis (no pustules present)
topical- chlorhex or benzoyl peroxide shampoos, local Abs system Ab's (1st gen ceph, clavamox, TMS, etc). TX 1 week past resolution of signs. AVOID steroids.
impetigo
puppy pyoderma. Superficial pyoderma limited to the stratum corneum in the glabrous skin of young dogs. Usually s. pseudintermedius
histopath of impetigo
subcorneal neutrophilic pustules with bacteria
clinical signs of impetigo
primary -- non follicular pustules and papules n the ventral abdomen (glabrous skin). Secondary- epidermal collarettes, crusts. NOT pruritic.
mgmt of impetigo
may resolve spontaneously. Topical Ab ointment/cream, chlorhex shampoo. Systemic Ab if widespred, pruritic or persistent lesions
pemphigus foliaceus in dogs, cats, horses, goats
autoimmune pustular dermatoses.
pemphigus
pustular diseases in which autoAb are directed against desmosomal proteins of the viable epidermis
pathophys of pemphigus foliaceus
type II hypersens. Antibodies are specific for the exact protein involed. For PF, ab directed against esmosomal proteins present in the upper layers of the epidermis --> in subcorneal pustules
histopath of pemphigus foliaceus
subcorneal pustules which contain neutrophils, acantholytic keratinocytes and NO bacteria. May have eosinophils
clinical signs of PF
primary - pustules. Secondary lesions predominate - crusts, epidermal collarettes, erosions, erythema, scale, alopecia. Distribution - begins head and ears --> generalized. Pruritis variable. May have hyperkeratotic footpads with peeling of the pads. cats may have paronychia. may have systemic signs - fever, anorex, wt loss, lethargy. OFten photoaggravated
PF in horses
lesions often begin on face or legs. May have exfoliative dermatitis, may have coronary band dermatitis, may have edema of the distal limbs and ventral abdomen due to concurrent vasculitis
DX PF
suggestive - pustular dermatitis that has not respodned to treatment for superficial pyoderma. Tent: cytology of pustule of crust bed: neutrophils, acanthocytes, NO bacteria. Definitive: histpath, immunohistochemistriy
immunosuppressive therapy for PF
corticosteroids
when should PF be suspected?
when a pustular or crusting dermatitis does not respond to treatment for SP
dermatophilosis in large animals
common infectious, superficial pustular and crusting dermattis of horses, cattle, sheep and goats caused by dermatophilus congolensis.
d. congolensis
gram pos facultative anaerobic actinomycete
favorable climatic conditions for growth of d congolensis
skin damage (mechanimal vectors, fomites), moisture (heavy rainfall), stress may predispose.
d. congolensis incubation
~2 weeks
histopath of dermatophilosis
folliculitis, epidermal pustular dermatitis, perivascular dermattis, crusts are alternating layers of hyperkeratosis and leukocytic debris. May see organisms in crusts
clinical signs of dermatophilosis
primary lesions: pustules (rare), papules. Secondary lesions predominate - exudaitve, thick crusts are oftne predominant sign, circular coalescing crusted lesions in which hairs become matted (paint brush lesions) and leave eroded/ulcerated purulent skin surface when removed; alopecia from folliculitis or pruritis. often painful but rarely pruritic
dx dermatophilosis
cytology of crust bed or saline soaked crust: fine branching hyphae or railroad track organism. Histopath is diagnostic if organism is present in the keratinous surface or follicular debris
mgmt of dermatophilosis
topicals (iodophors, lime sulfur, chlorhex), systemic ab, vector control, correct poor hygeine, potential fomites, etc
zoonosis of dermatophilosis
pitted erythematous, pruritic or painful pustural lesions which resolve in 2-8 weeks without treatment
juve cellulitis in dogs
granulomatous dermatitis of puppies affecting the skin of the face, pinnae, submandibular and prescapular lymph nodes
pathogenesis of juve cellulitis
unknown - sterile granulomas that respond to steroids suggests immune dysfunction. Evidence of genetic involvement
histopath of juve cellulitis
multiple discreet or confluent granulomas or pyogranulomas within the epidermis or dermis. No infectious agents present!
signalment of juve cellulitis
3-16 wk old puppies. Goldens, dachshunds, labs, lhasas, gordon setters
clinical signs of juve cellulitis
primary- acute swelling and surface pustules of the muzzle, lips, eyelids, inner pinnae. Secondary - small ulcers, crusts, draining tracts. Lesions may be painful. Enlarged submandibular / prescap LNs (may rupture and drain pus). Systemic signs- fever, anorexia, depression, joint pain. Rapid onset
DDX juve cellulitis
other pustular dz, angioedema, demodicosis
diagnosing juve cellulitis
cytology (neutrophiles, macrophages but no bacteria), SS and c/s negative
mgmt juve cellulitis
systemic steroids, supportive care (warm soaks). Systemic Ab if secondary infection suspected
what should be done prior to starting steroid therapy for juve cellulitis?
rule out demodicosis and pyoderma
atopic dermatitis
a genetic predisposition to form IgE antibodies to innocuous environmental substances leading to pruritis. V common.
pathophys of atopy
type I hypersens. Starts with percutaneously abosrobed proteins -> production of IgE by sensitized B cells -> igE binds to dermal MC via Fc rc -> when MC again encounters the allergen -> allergen binds to the Fab portion of IgE and causes cross linking of the IgE molecules -< MC membrane disruption -> stimultes the MC to 1) release stored mediators and 2) immediate production of newly generated mediators
histopath of atopy
non specific epidermal hyperplasia and perivascular dermatitis
atopy signalment
young dogs (1-2 yrs), horses (<4 yrs),cats (young to midle ate). Terriers, dalmations, setters, labs, goldens, GSDs, bocers, english bulldogs, beagles, mini shnauzers, shar peis
clinical signs of atopy
seasonal pruritis. NO PRIMARY LESIONS. Secondary lesions form pruritis and excoriations.
what is the most common cause of otitis externa, recurrent pyoderma and malassezia dermatitis in dogs
atopy
atopy distribution in dogs, cats, horses
dogs - feet, face, ears and ventrum. Can generalize. Cats- generalized pruritis and crusted papules (milliary dermatitis). May have non inflammatory alopecia. Horses- face, ears, ventrum, legs, chronic pruritic urticaria
diagnosing atopy
history, clinical signs, exclusion of other differentials (pruritic ectoparasites, food allergy, other pruritic dz).
atopy TX
treat secondary infections. Balance clinical signs with side effects of treatment - NOT curable. Three levels of therapy - innocuous/symptomatic, systemic steroids/cyclosporine, hyposensitization therapy based on ID of relevant allergens
atopy level 1 therapy
for mild cases; as an adjunct. 1) antihistamines 2) essential Fas 3) topical antipruritics
atopy level 2a vs 2b therapy
leval 2a - steroids. Level 2b- cyclosporin for patients for which steroids are contraindicated.
MOA cyclosprine therapy
down regulates IL2 from TH2 cells, this leads to a decrease in infallmatory mediators =
pros and cons of cyclosporine
pros - relatively fewer side effects. Cons- cost, takes several weeks to become effective. Not effective in all patients. Some owners have difficulty with admin. Only approved for dogs
IDST pros and cons
pros- measures skin reactivity which mimcs the pathophysiological process. Can tailor a panel to specific region. Cons- many drugs interfere with IDST rxns, expensive to stock allergens. Must develop expertise in procedure/ interpretation
in vetro serum test (pros/cons)
pros- easy to collect sample, don’t need special equipment (allergens), can be on systemic or topical antihistamines. Cons- need to stop steroids before testing, many false positives. Only 60% pts will respond to allergens when therapy based on serum testing
Food allergy dermatitise / adverse rxn to food
non seasonal pruritic skin dz assoc with the ingestion of a certain substance in the diet. Not common in general population but up to 20% of atopic pts have food allergy
pathophys of ARF
evidence of involvement of type I, III, IV hypersns rxns. Some may not be a true allergy. Rxn may take place at the mcuosa or may be a rxn to an absorbed allergen. A long sensitization period is required
ARF histopath
variable due to pleomorphine gross lesions, not specific, epidermal hyperplasia, perivascular dermatitis
ARF signalment
any age but more common in young. No sex/breed predispostion in dogs. Siamese cats may be predisposed. Atopic dogs >> non atopic dogs
clinical signs ARF
no primary lesions. Secondary lesions result from pruritis. May cause GI signs - inc defecation, loose stools, thin body condition. Dog distribution - variable but often includes otitis externa, axillae, groin. Cat distrubtion - variable but usually head, neck, may be generalized, crusting is prominent.
ARF dx
feeding trial. (one protein/one carb, both novel). Hydrolyzed protein. Trial needs to be at least 8 weeks.
factors that may help distinguish food allergy from atopy
perennial pruritis from the initial onset, may not respond to steroids, can occur at any age, may have GI signs, may present with otitis externa as only clinical sign
ARF in horses
rare, similar to dogs/cats EXCEPT - clinical signs may be seasonal or non seasonal depending on feeding practices. Urticaria is more common in horses.
eosinophilic granulaoma complex (EGC) in cats
reaction pattern, often allergy mediated. Pruritis is variable, often have primary lesions. Four syndroms with some common features. May see all four lesion types in an individual.
four syndroms of EGC
1) eosinophilic plaque 2) linear granuloma 3) indolent ulcer 4) mosquito bite hypersensitivity
eosinophilic plaque
predominating. May see flame figures (Area of altered collagen surronded by eosinophils). Often inguinal, ventral abdomen, intensly pruritic, moist plaques, secondary infections common.
linear granuloma (eosinohilic granuloma)
etiology - may be genetic predisposition (Cats >1yr of age, spontaneously regress). Histopath - granulomatous dermatitis, collagen degeneration. Linear, usually non pruritic, cd thighs, face, oral caivty of young cats, may cause lower lip and chin swelling. If pruritic tx with short tern synth steroids
indolent ulcer (rodent ulcer, eosinphilic ulcer)
some cases are allergy mediated. Histopath - non specific ulcer and perivascular dermatitis. Upper lips, oral cavity, non pruritic, usually non painful well circumscribed, red brown, alopecic ulcer. Oral lesions may be painful. TX- ID/tx specific allergy or steroids. sx removal if oral lesions refractory to medical treatment
mosquito bite hypersensitivity
probably type 1 and/or IV hypersensitivty. Face, ears, margins of pads, eruptive moist lesions.
feline demodicosis
two distinct mites - demodex cati, demodex gatoi
demodex cati
infests hair follicles, possibly contagious, may have asymptomatic carriers. Histopath- folliculitis, perifolliculitis, mites within hair follicles. Clinical signs - localzied ds most common (head, neck, +/- ceruminous otitis). NO primary lesions. secondary lesions - pruritis, erythema, scales, alopecia, crusts, non inflmmatory alopecia. if gernelized ds, may have underlying immunosuppression
demodex gatoi
short stubby demodectic mite. Burrows in stratum corneum, true pathogen. Prob contagious, may have asymp carriers. Cats with severe pruritis probably have allergic component. Histopath - minimal inflamm, acanthosis, may find mites in s. corneum. NO primary lesions. secondary lesions - moderate to severe pruritis -> erythema, scales, alopecia, crusts. distribution - head/neck, ventral abdomen, rear legs
which demodex has a better prognosis?
gatoi, because not dependent on underlying dz
low environmental humidity
dry skin, scales, mild pruritis
poor nutrition
diets low in FA - dry skin, scales, mild pruritis
feline psychogenic alopecia
alopecia which results form repeated local or multifocal self trauma that is a manifestation of an OCD. Alopecia secondary to self trauma. Pathogen -excessive grooming due to anxiety. Behavior may induce endorphine release. Clinical signs- alopecia with broken hairs remaining. skin is NORMAL but excoriations may be present. distribution - ventral abdomen, inner thighs, dorsal midline.
how to dx feline psychogenic alopecia
trichogram - to distinguise traumatic alopecia from primary alopecia: pluck hairs, examine under 4x. DX of exclusion, dule out other pruritic diseases
mgmt of feline psychogenic alopecia
address environmental factors, behavior modification drugs
acral lick dermatitis
psychodermatosis resulting from repeated self trauma to a specific area caused by OCD. Lesions grossly look like nodules.
acral lick dermatitis pathogenesisis
1) lifestyle factors (boredome, personality, change in life style), 2) underlying dz- chronic localized pain, pruritic dermatoses, localized trama, neoplasia. 3) secondary bacterial involvement common (folliculitis, furunculosis). 4) OCD (itch/scratch cycle)
acral lick dermatitis histopath
irregular epidermal hyperplasia, perviascular dermatitis, fibroplasia of the dermis. Folliculitis/furunculosis may be present
acral lick derm signalment
dobermans, GSD, retrievers, great danes, st bernards, irish setters. M>F
acral lick derm clinical signs
primary - well circumscribed, alopecic plaque or dermal nodule on the dorsal aspect of a distal limb. Secondary - surface may be hyperpigmented or eroded. May have surface exudate.
other psychogenic dermatoses in dogs
tail biting, flank sucking (dobes), anal licking (poodles)
treating OCD behavior
tricyclic antridepressants, anxiolytics, endorphine blockers, endorphin substitution
diseases where the primary lesions can be obsucred by excoriations
FAD and culicoides hypersens, sarcoptesa, cheyletiella, malassezia derm, notoedres mange, cutaneous t-cell lymphoma
review normal hair physiolgoy
review normal hair physiology
mechanisms of alopecia
1) self induced alopecia from pruritic dermatoses 2) hair follicle inflamm (folliculitis) 3) arrested hair cycle 4) congenital / hereditary 5) poor nutrition 6) systemic illness or stress 7) alopecia as a result from ischemia
self induced alopecia from pruritc dermatosse
very common. Ex: allergic, parasitic, infectious, autoimmune. Alopecia is a secondary lesion and distribution is a result of the underlying dz. Will have other lessions assoc with pruritis (Excoriation,s lichenification, etc) except cats with non inflamm pruritic alopecia
folliculitis
very common cause of non pruritc alopecia in all species. Common causes - bacterual folliculitiis, demodicosis, dermatophytosis. Usually causes pathy alopecia or moth eaten apperance
arrested hair cycle
telogen arrest: hypothyroid, cushings; catagen arrest: sex hormone abnormalities, post clipping alopecia. Usually leads to discreet areas of compelte alopecia on the lateral trunk and tail
congenital alopecia
generlized alopecia is normal for certain breeds. Follicular dysplasia, color dilute dysplasia. Pattern baldness "normal" for some breeds (dach, chi)
alopecia from poor nutrition
poor quality hairs, generlzed thinning
systemic illness / stress alopecia
telogen / anagen defluxion. Large areas of truncal hair may be lost precipitously.
alopeca as a result of ischemia
very discreet areas of complete alopecia. Underlying skin may be inflamed (Dermatomyosisitis, ear margin vasculitis) or normal (rabies injection site alopecia)