Derm Final 2
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- Describe the pathogenesis of atopic dermatitis.
- Atopic dermatitis is “strange disease†and is a familial predisposition to the development of IgE antibodies and clinical allergy to environmental antigens
- Describe the lesions and distribution pattern of atopic dermatitis
- Lesions: -Erythema -Alopecia -Papules -Excoriations -Hypepigmentation -Lichenification Distribution: -Muzzle -Periocular -Axillae -Feet -Flexor surfaces of elbows and tarsus -Extensor surface of carpus -Lesions may become generalized in chronic cases
- What are the advantages and disadvantages of RAST?
- Advantages -Very specific Disadvantages -Poor reproducibility -Poor specificity for IgE -Many false positives -Great seasonal variability
- What are the advantages and disadvantages of IDST?
- Advantages -Gold standard for determining allergens -Shows whether or not an allergen is capable of producing skin lesions in the tested patient -Immediate results Disadvantages -Owners refuse clipping of fur -If skin does not respond to the histamine, it won’t respond to injected allergens -No access to the test
- How do you interpret a negative IDST?
- -Patient not allergic to reaction -SQ injection given -Insufficient antigen -Concurrent drugs blocked the skin test (this is why they must be off drugs before testing) -Prolonged allergy (exhaustion of IgE levels)
- How do you interpret a positive IDST?
- -Patient allergic to antige -Patient allergic to the cross reacting antigen -Irritants -Bacterial or fungal contamination -Antigen contains histamine -Too large volume injected
- What are the advantages and disadvantages of using corticosteroids for the treatment of atopic dermatitis?
- Advantages -Very effective at decreasing skin inflammation and itching Disadvantages -Many side effects (PUPD, panting, weight gain, increased risk of infection, ect.) -Use only if other therapies are not feasible
- What are the advantages and disadvantages of using cyclosporine for the treatment of atopic dermatitis?
- Advantages -Effective in severe allergy cases for decreasing skin inflammation and itching -Suppresses T cells and decreases IgE production -Decreases production of cytokine Disadvantages -Side effects (GI, renal, hepatic, bone marrow) -Costly
- What are the advantages and disadvantages of using hyposensitization (immunotherapy) for the treatment of atopic dermatitis?
- Advantages -Increases T suppressor cell activity, w/ gradual decrease in IgE -Blocks antibodies -Decreases number of mast cells and/or decreases histamine release from mast cells Disadvantages -May req. 9 months or longer to obtain maximal effectiveness -25-50% chance of not working or needed additional treatment
- Discuss client education of the treatment of atopic dermatitis.
- -Must communicate that the animal is a walking dust mite and they must be bathed frequently -Also, if animal is allergic to material in house or what owner wears, significant changes must be made -Owner must be committed to working w/ the disease or the animal will suffer for their entire life
- Describe the MOA of glucocorticoids in treatment of allergy.
- -Glucocorticoids block Cox 1 and 2 as well as phospholipase A (which is needed to make Prostaglandins)
- Describe the benefits of antihistamines in cats and dogs
- -Antihistamines are a good preventative drug, just not great for treatment -Block H1 and H2 receptors -Stabilize mast cells -Few side effects
- Describe the physiological basis of alternate day steroid administration.
- -Alternate day therapy is an attempt to control the animals atopy while giving them less drug. This will decrease the potential for side effects and resistance.
- Are lamb and rice nonallergenic?
- -NO- lamb and rice are not non-allergenic (many animals are, in fact, allergic to lamb)
- Why are lamb and rice chosen for some hypoallergenic diet trials?
- -Lamb and rice are chosen however for some hypoallergenic diets b/c lamb is a novel protein and if the animal has never tried lamb it might be worth a try. Rice is added in as the carbohydrate source
- Devise a restrictive diet trial for a cat or dog for which you have been presented with a list of its past diet.
- HOME COOKED DIETS -Choose a protein source that the animal has never been exposed to (lamb, fish, venison, rabbit, tofu, pinto beans) -Choose a carbohydrate source (brown rice, white rice, potatoe, green peas) -Mix the two as a 1 part protein : 3-4 part carbo STORE DIETS -Again look for a protein source the animal hasn't tried (Hill D/D, Z/D or Purina HA)
- What are the DDX of a cat w/ pruritis on its head and neck.
- -Food allergy -Ear mites -Notoedres -Flea allergy dermatitis
- How can you differentiate allergic contact dermatitis from an irritant contact dermatitis?
- Allergic Contact dermatitis: -An inflammatory skin disease caused by a delayed (cell-mediated) response to an antigen or hapten. Requires repeated or continuous exposure to the substance Irritant Contact Dermatitis: -An inflammatory skin disease which occurs within minutes of contact w/ irritating substance
- Outline measures that can be used to minimize an animals exposure to housedust mites.
- -Remove carpets, blinds, plants, upholstered furniture, cluster -Use plastic encasings for mattresses, boxsprings, pillow -There are some products to kill HDM
- Describe the clinical presentation of erythema multiforme.
- -Erythematous macules and papules that spread -Urticarial plaques that last for many days -Vescilces/bullae -Any combo of these
- Describe the clinical presentation of Toxic Epidermal Necrolysis.
- -Vesicles/bullae -Necrosis -Systemically ill -Entire epidermis of the lesion can be necrotic and slough off
- What are the usual causes of Toxic Epidermal Necrolysis.
- -Drugs*** -Toxins -Infections -Neoplasms
- What are the usual causes of Erythema Multiforme.
- -Drug allergies *** -Trimethoprim/sulfa -Cephalexin
- What are some etiologies for feline miliary dermatitis?
- -Ectoparasites -Dermatophytes -Allergies -Nutritional -Bacterial -Contact -Autoimmune -Idiopathic
- What is a diagnostic plnn for feline miliary dermatitis?
- -Examine for parasites -Woods light -DTM culture
- What is the clinical presentation of an indolent ulcer?
- -Ulcers on upper lip or orally -Female cats (5-6 yrs. Age) -No eosinophils
- What is the clinical presentation of an eosinophilic plaque?
- -Well circumscribed, raised, ulcerative plaque -Abdomen, back, legs, head, neck -Female cats (3yrs) -Eosinophilic and mast cell infiltration
- What is the clinical presentation of a linear granuloma?
- -Linear tract on posterior aspect of hind limbs -Severe cases can be seen in the oral cavity -Either sex (1-5yrs) -+/- Eosinophils
- How would you identify an indolent ulcer?
- -Histopath -Hyperplastic ulcerative dermatitis w/ PMN, plasma cells, mononuclear cell infiltrate -DDX -Squamos cell carcinoma and Fibrosarcoma
- How would you identify an eosinophilic plaque?
- -Histopath -Eosinophilic and Mast cell infiltrate -Workup -Biopsy -Flea control*** -Hypoallergenic diet -IDST
- How would you identify a linear granuloma?
- -Histopath -Necrobiosis of collagen w/ histiocytic and multinuclear giant cell infiltrate +/- eosinophils
- How would you treat an indolent ulcer?
- -Identify and treat underlying cause -Antibiotic trial -Clavamox or Tribissen -Systemic Corticosteriods -Pred -Depo-Medrol REFRACTORY OR RECURRENT: -CO2 laser -Radiation treatment -Cyrosurgery -Immuno-stimulants (Levamisole or Thiabendazole)
- How would you treat an eosinophilic plaque?
- -Identify and treat underlying cause -Elizabethan collar -Antibiotics -Corticosteriods
- How would you treat a linear granuloma?
- -Observation -Identify and treat underlying cause -Antibiotics -Corticosteriods -Immuno-stimulants
- Describe the clinical presentation of feline plasma cell pododermatitis.
- -Non-painful swelling of footpads that may ulcerate Clinical Pathology: -Hypergammaglobuinemia -Lymphocytosis -Neutrophillia
- List the potential side effects of progesterone therapy.
- -Hyperglycemia (leading to DM) -Acromegaly -Mammary hyperplasia (leading to neoplasia) -Pyometra -Infertility -Behavioral changes
- What is cyclosporine? What is its MOA in the treatment of atopy?
- -Cyclosporine is an immuno-suppressive drug. MOA: -Suppresses T helper cells -Decreases IgE production -Decreases production of cytokines -Overall decreases skin inflammation and itching
- How is canine atopic dermatitis diagnosed?
- -Must have at least 3 of the Major Criteria: -Pruritis -Typical morphology and distribution -Involves face, feet, legs -Seasonal or chronic dermatitis -Family or breed predisposition -Must have at least 3 of the Minor Criteria: -Onset of symptoms <3 years of age -Facial erythema and chelilitis (inflammation around lips) -Bilateral conjunctivitis -Superficial staph pyoderma -Increased antigen specific-IgE -Increased antigen-specific IgG4 -Immediate skin test reactivity
- Is it possible to cure an atopic dog?
- -No, just medically manage dog -However, those animals treated w/ hyposensitization 25% may develop complete remission
- What are the major causes of treatment failures in canine atopic dermatitis?
- -Client compliance -Don’t remove all possible environmental contaminants -Don’t dose animals med’s correctly
- What is the “flare factor†relating to atopy?
- -The reaction that occurs in response to certain allergen -Fleas are a big flare factor
- Why is it important for owners to understand the concepts of summation of effects and pruritic threshold.
- Summation of effects: -It is the culmination of all things that can lead to the animals atopy problem -If the owner can understand that there are a whole host of things that play a role in their animals atopy then maybe then can understand why treatment is so difficult and why they must play an active role in the process. Pruritic Threshold: -The level above which the animal will experience atopy -Many factors contribute the animal exceeding the threshold -For example: If fleas are the underlying cause and they are never treated, then the animal can never drop below the pruritic threshold
- What are the causes and pathogenesis of food allergies?
- Causes: -Sudden reaction to a food source (usually one protein) that triggers an immunological response -a lot are not IgE mediated Patho: -Food allergies can be either a Type I, III, IV hypersensitivity reaction
- What is the best way to diagnose a food allergy
- -The best way to diagnose food allergy is to do a restrictive diet trial -Symptoms should subside off food (w/in at least 7 days) -Challenges should be reproducible (onset, duration, clinical features) -Symptoms should be gone after each withdrawal
- What is an allergen? Antigen?
- Allergen: an antigen that stimulates an IgE response (ex. Pollens, dust, animal dander, feathers) Antigen: a substance that elicits an antibody response
- How does contact hypersensitivity manifest in animals?
- -Lesions usually occur in non-haired areas (feet, ears, ventrum, scrotum, chin, neck) -Pruritis may be the only sign -Severe cases: erythema, vesicles, ulcers, crusts, self-trauma
- What are the differences between atopy and contact dermatitis?
- Atopy: -A familial predisposition to the development of IgE antibodies and clinical allergy to environmental allergens. Contact dermatitis: -Can either be allergic or irritant Allergic Contact dermatitis: -An inflammatory skin disease caused by a delayed (cell-mediated) response to an antigen or hepten. Requires repeated or continuous exposure to the substance Irritant Contact Dermatitis: -An inflammatory skin disease which occurs within minutes of contact w/ irritating substance
- What are the common causes of contact hypersensitivity in dogs?
- -Plant or plant pollen -Molds -Meds (neomycin, tetracain, shampoos, insecticides) -Floor wax -Polish or cleaners -Dyes in rugs -Carpets, blankets -Rubber and plastic products
- Will anti-histamine creams lessen inflammation in animals w/ contact hypersensitivity? What other treatments would you recommend?
- -No anti-histamine are good are prevention, not a treatment once the animal is inflamed Other treatments: -Remove offending agent -Bath after exposure -Topical drying agents (Domeboro) -Topical or systemic corticosteroids -Pentoxiphylline -Topical tacrolimus
- What is miliary dermatitis?
- -Variable pruritic papulocrustous eruption occurring over dorsum, head, and neck -Millet seed lesions = hemorrhagic crusts
- What approach would you follow in treating a cat w/ miliary dermatitis?
- 1. Flea control (if they respond, may be the only treatment) 2. Hypoallergenic diets 3. Skin biopsy -Allergic = IDST -Bacterial = C/S and TX -Fungal = DTM and TX -Pemphigus = DFA, TX -Non-specific = Pred -No response = Short term megesterol acetate
- What is erythema multiforme?
- it is an allergy, usually drug associated
- How do you diagnose erythema multiforme?
- -Physical Exam -Clinical signs
- How do you treat erythema multiforme?
- -Removal of drug -Possible corticosteroids??
- What is toxic epidermal necrolysis?
- full thickness coagulation necrosis of epidermis
- How do you diagnose toxic epidermal necrolysis?
- -Histopath -full thickness coagulation necrosis of epidermis
- How do you treat toxic epidermal necrolysis?
- -Correct underlying cause -Supportive care -Pred (be careful there can be a high risk of sepsis)
- What is the mechanism involved with a Type II hypersensitivity reaction?
- IgG, IgM , Complement + target cell = Lysis and phagocytosis of cell
- What is the mechanism involved with a Type III hypersensitivity reaction?
- IgG, IgM , Complement + Ag => complexes trapped and attract PMN’s
- What is the mechanism involved with a Type IV hypersensitivity reaction?
- Cytotoxic action of activated lymphs
- What is the mechanism involved with a Type V hypersensitivity reaction?
- Ab stimulates cellular response
- What are some examples of Type II hypersensitivity reactions?
- -BP -SLE -DLE -Drug
- What are some examples of Type III hypersensitivity reactions?
- -SLE -DLE -Drug -Vasculitis
- What are some examples of Type IV hypersensitivity reactions?
- -Uveodermatologic Syndrome -SLE -Drugs
- What is the pathology of Pemphigus foliaceus?
- Pemphigus Ab => binding to pemphigus antigent (desmosome) on keratinocyte => internalization of pemphigus Ab =>activation and release of prteolytic enzymes (plasminogen activator) =>plasminogen converted into plasmin =>plasmin hydrolyzes cell adhesion molecules (desmosomes) =>Acantholysis (blister)
- What is the pathology of Pemphigus erythematosus?
- Pemphigus Ab => binding to pemphigus antigent (desmosome) on keratinocyte => internalization of pemphigus Ab =>activation and release of prteolytic enzymes (plasminogen activator) =>plasminogen converted into plasmin =>plasmin hydrolyzes cell adhesion molecules (desmosomes) =>Acantholysis (blister)
- What is the pathology of Pemphigus vulgaris?
- Pemphigus Ab => binding to pemphigus antigent (desmosome) on keratinocyte => internalization of pemphigus Ab =>activation and release of prteolytic enzymes (plasminogen activator) =>plasminogen converted into plasmin =>plasmin hydrolyzes cell adhesion molecules (desmosomes) =>Acantholysis (blister)
- What are the lesions associated with pemphigus folliaceus?
- Primary = transient pustule =>crust Secondary = -Alopecia -Scale -Erythema -Erosions -Nasal depigmentation -Hyperkeratosis of pads -+/- Pruritis -Face and ear lesions -Oral lesions are RARE +/- Fever and anorexia CAT: -Crusting around nails -Crusting-Alopecia -Scale -Erythema -Erosions -Nasal depigmentation -Hyperkeratosis of pads -+/- Pruritis -Face and ear lesions -Oral lesions are RARE +/- Fever and anorexia CAT: -Crusting around nails -Crusting around nipples around nipples
- What are the lesions associated with Pemphigus erythematosus?
- Primary lesions: -Pustules to oozing crusts that ocsur on the face (ears, nasal region) -Lesions can also be seen on the paws and genital regions -Erythema -Alopecia -Erosions -Nasal depigmentation -Hyperkeratosis
- What are the lesions associated with Pemphigus vulgaris?
- -Vesiculobullous => erosive to ulcerative skin lesions +/- pruritis -Oral and MC lesions are common -Can also be seen in axillae, groin, clawbed, paw pad, concave pinna -Fever -Anorexia -Depression -Lymphadenopathy -Pain
- What is the histopathology associated with pemphigus folliaceus?
- -Acantholytic cells w/ PMN +/-bacteria -Subcorneal pustules w/ acantholytic cells +/- eosinophils
- What is the histopathology associated with Pemphigus erythematosus?
- -ANA may be positive -Acantholytic cells may be present -Subcorneal pustule +/- cellular infiltrate along the D-E junction
- What is the histopathology associated with Pemphigus vulgaris?
- -Suprabasilar acantholysis resulting in vesicle/cleft -Basal cells appear as a row of tombstones -+/- dermal infiltrates
- What is the pathogenesis of Bullous pemphigoid?
- Autoantibodies directed against self-antigens (hemidesmosomes) resulting in blistering just below the epidermis
- What is the clinical presentation of Bullous pemphigoid?
- -Clinically resemble Pemphigus vulgaris (PV) +/- photoaggrevation -Vesiculobullous (tense) => erosive to ulcerative skin lesions +/- pruritis -Oral MC lesions are common (no oral lesions in pigs) -Axillea, groin, clawbed, paw pad, concave pinna, face -Fever -Anorexia -Depression -Lymphadenopathy -Pain
- What is the histopathology associated with Bullous pemphigoid?
- -Subepidermal clefting + eosinophils in dog -No acantholysis
- What is the pathogenesis of SLE?
- 1.Type II hypersensitivity: -Antibodies directed against self-nuclear antigens (DNA, RNA, histones) 2.Type III hypersensitivity: -Antigen-antibody complexes lodged into vascular epithelium, synovium, muscle, skin BMZ 3.Type IV hypersensitivity: -Cell-mediated activity against self-antigen
- What are some major signs of SLE?
- Skin lesions Polyarthritis Hemolytic anemia Glomerulonephritis Polymyositis Leukopenia Thrombocytopenia
- What are some minor signs of SLE?
- Fever of unknown origin CNS signs Oral ulceration Lymphadenopathy Pericarditis Pleuritis
- What is needed to make a definitive diagnosis of SLE?
- 2 Major and serology + -OR- major/2minor and serology +
- What is needed to make a probable diagnosis of SLE?
- 1 major and serology + -OR- 2 major and serology (-)
- What are some triggers of SLE
- -Genetics (loss of tolerance) -UV light -Hormones -Infectious agents -Drugs -Chemical exposure
- What are some things found in Serology of a patient with SLE?
- ANA (high sensitivity) Ab to nuclear material LE (high specificity) ID opsonized nuclear material in PMN and macrophages
- What are some differentials for nasal depigmentation?
- -Vitilligo (will not loose the normal cobblestone appearance of nose) -Nasal depigmenation (snow nose and Dudley nose) -Nasal solar dermatitis -Contact dermatitis -Uveodermatologic syndrome -PF, PE, PV, BP, DLE, SLE -Drug reaction -Neoplasia
- What are some differentials for oral lesions?
- -DLE, SLE, PV, BP -Erythema multiforme -Vasculitis -Drug reaction -Neoplasia -Candidiasis -Eosinophillic granuloma -Eosinophillic plaque -Indolent ulcer -Plasma cell stomatitis -Gingival hypertrophy -Erosions (chemical, viral, renal) -Vegatative glossitis
- What class of drug is azathioprine (Immuran)?
- Anti-metabolite
- What class of drug is Chlorambucil (Leukeran)?
- Alkylating agent
- What immunosuppressive drug should not be used on cats?
- Azathioprine (Immuran)
- Should Chlorambucil (Leukeran) be used in cats?
- Yes, it is the primary choice for use in cats.
- What is the MOA of Azathioprine?
- Structural analog of natural metabolites that substitute for purines and pyrimidines
- What is the MOA of Chlorambucil (Leukeran)?
- Cross link DNA
- What is the MOA of Cyclophosphamide (Cytoxan)?
- Cross link DNA
- What is the MOA of Cyclosporine (Sandimmune and Neoral)?
- Inhibits Th cells early in the immune response w/ minimal effects on suppressor cells
- What are some side affects of Azathioprine?
- -Myelosuppression -Hepatopathy -GI effects
- What are some side affects of Chlorambucil (Leukeran)?
- -Myelsuppression -GI effects
- What are some side affects of Cyclophasphamide (Cytoxan)?
- -Myelsuppression -GI effects -Sterile hemorrhagic cystitis
- What are some side affects of Cyclosporine (Sandimmune and Neoral)?
- -Myelsuppression -GI effects -Gingival hyperplasia -Papillomatosis -Nephrotoxicosis -Lymphoma like lesions
- What are some side affects of Glucocorticoids?
- -PUPD -Polyphagia -GI ulceration -Steroid hepatopahty -Pancreatitis -DM -Muscle weakness -Hypertension (+/- proteinuria) -PTE (dyspnea)
- What is the general lesion distribution of pemphigus folliaceus?
- -Face, pinna, feet -Perinipple and nails in cats
- What is the general lesion distribution of pemphigus erythematosus?
- -Nose and face
- What is the general lesion distribution of pemphigus vulgaris?
- -ORAL -MC -Nailbed -Axillae -Generalized skin
- What is the general lesion distribution of Bullous pemphigoid?
- -Oral (similar to PV)
- What is the general lesion distribution of DLE?
- -Nose and face
- What is the general lesion distribution of SLE?
- -Oral (localized or generalized) -Footpads -Sub Q nodules
- Are there systemic effects associated with SLE?
- Yes
- Are there systemic effects associated with PE?
- No
- Are there systemic effects associated with DLE?
- No
- Discuss the lesions of color mutant alopecia including the pathogenesis.
- Lesions: -Scaly, dry and brittle hair coat -Papule may be present Patho: -Puppies are usually normal at birth and later the skin becomes diseased -There are defects in the melanization and cortical structures of the affected hair follicles -Melanin clumps in the hair bulbs and shafts and makes it brittle
- Describe your therapeutic plan for color mutant alopecia.
- -There is no cure, just medical management (do not breed these animals) -Use follicle flushing shampoos (benzoyl peroxide or ethyl lactate) -Antibiotics for secondary infections -Topical emollients and humectants -Thyroid therapy if T4 is low
- Describe a diagnostic plan to confirm a diagnosis of dermatomyositis.
- -Skin biopsies (looking for liquefaction necrosis of basal cell layers of epidermis, vesicles) -EMG -Muscle biopsies -ANA -Skin scrapings
- What are some breeds predisposed to dermatomyositis?
- -Collies -Shelties
- What are options for treatment for Dermatomyositis?
- -Avoid trauma -Pred -Vit. E -Pentoxiphylline -Tetracycline and Niacinamide -Spay and Neuter
- Describe the pathogenesis of acral mutilation syndrome.
- -It is a sensory neuropathy w/ decreased numbers of spinal ganglia and dorsal roots -Occurs as a slowly progressive postnatal degeneration
- Describe the pathogenesis of cutaneous asthenia.
- -Cutaneous asthenia (a.k.a. Rubber puppy syndrome) Patho: -Defect in collagen formation -Increased fragility and laxity of skin -In cats the deficiency is of procollagen peptidase
- What breeds are predisposed to lethal acrodermatitis?
- Bull Terriers
- What are some clinical signs of lethal acrodermatitis?
- -Growth retardation -Progressive acrodermatitis -Chronic pyoderma -Chronic paronychia -Diarrhea -Pneumonia -Abnormal behavior -Lighter than normal skin pigmentation
- What are some diagnostic options for lethal acrodermatitis?
- -Breed predisposition -PE findings -Low serum zinc -Low ALKP -Hypercholesterolemia -Decreased lymphocyte blast transformation -Skin biopsy -Parakeratotic hyperkeratosis w/ ulceration and superficial pyoderma
- What is the prognosis for LETHAL acrodermatitis?
- -Poor -Median survival 7 months -Most puppies die of bronchopeumonias
- What are the clinical signs of epidermal dysplasia?
- -Lesions begin in puppyhood -Erythema -Pruritis (feet, ventrum at first and then becomes generalized) -Hyperpigmentation -Seborrhea oleosa -Peripheral lymphadenopathys
- What breeds are predisposed to epidermal dysplasia?
- West highland white terrier
- What is the diagnostic plan to diagnose epidermal dysplasia?
- -Rule out these diseases (atopy, food allergy, sarcoptes, demodex, ichthyosis, endcrinopathies, other seborrheic diseases) -Skin biopsy: epidermal dysplaisa w/ hyperchromasia -Increased mitosis, crowding of basal keratinocytes w/ “ budsâ€, parakeratosis
- What is the treatment for Sebaceous adenitis?
- -No cure -Life long management 1. Keratolytic shampoo (Sialycylic acid) 2.Tetracycline +/- Niacinamide 3.Vit. A 4.Retinoids ($$$) 5.Cyclosporine
- What is the predisposition for Sebaceous adenitis?
- -Vizslas -Akita -Samoyed -Standard poodle (black and apricot)
- What is the prognosis for Sebaceous adenitis?
- -Fair -Trying to minimize symptoms and manage the disease (there is no cure)
- How do you diagnose Sebaceous adenitis?
- -Histopath: -Granulomatous sebaceous adentitis -Chronic cases have complete absence of sebaceous glands
- What is the treatment for ichthyosis?
- -Life long (no cure) -Hydrotherapy -Topical antiseborrheias/keratolytic agants -Emollients -Propylene glycol -Retinoids -Vit. A
- How do you diagnose Ichthyosis?
- -Rule out other causes of seborrhea -Skin biopsy: -Prominent granular layer -Numerous mitotic figures in keratinocytes -Orthokeratotic hyperkeratosis -Follicular keratosis -Plugging
- Which breed of cats is predisposed to primary seborrhea oleosa?
- Persians
- What is follicular dysplasia?
- Schnauzer Comedone Syndrom is associated with this.
- What is pattern baldness?
- ??
- What is Ehlers-Danlos syndrome?
- -It is cutaneous asthenia (a.k.a.Rubber puppy syndrome) -The skin hangs in loose folds
- What is the normal skin extensibility index for dogs and cats?
- Extensibilty index = (vertical height of skin fold)/(body length) * 100 -Normal 9-16% and Affected is 18-24 %
- What is epidermolysis bullosa?
- -Blisters and ulcerations at areas of trauma (footpad, mouth, anus, elbows)
- How do you diagnose epidermolysis bullosa?
- -Histopath: shows dermoepidermal vesicles and bullae -Electron microscopy
- What are the clinical signs of “Schnauzer Comedone Syndrome�
- -Multiple comedones on the back that become a crusted papule
- What is the differential diagnoses need to be ruled out to confirm a diagnosis of Schnauzer Comedone Syndrome?
- -Demodex -Dermatophytes -Staph pyoderma -Cushings
- Papule
- Small solid elevation of skin
- Plaque
- Solid elevation of skin with a flattened top (> 1 cm)
- Macule
- Well circumscribed, flat spot characterized by a change in the color of the skin
- Patch
- A change in skin color > 1-2 cm
- Nodule
- A circumscribed solid elevation that usually extends into the deeper layers of the skin
- Tumor
- Soft or firm, movable or fixed masses of various sizes and shapes
- Wheal
- Sharply circumscribed raised lesion consisting of EDEMA
- Pustule
- Small circumscribed elevation of the skin containing PUS
- Vesicle (bulla)
- Sharply circumscribed elevation of the skin filled with SERUM OR BLOOD
- Scale
- Accumulation of loose fragments of the horny layer of the skin
- Epidermal Collarette
- Peeling edge of epithelium surrounding an erosion or ulcer
- Crust
- Dried exudates on the surface of a lesion
- Furunculosis
- Draining tract (sinus) communicating from an area of suppuration to a body surface, usually indicative of ruptured hair follicles and secondary bacterial infections.
- Abscess
- Accumulation of inflammatory cells and necrotic debris
- Hyperpigmentation
- Increase in skin pigment (melanosis)
- Excoriation
- Superficial (epidermal) abrasion caused by self-trauma
- Fissure
- Linear cleavage into or through the epidermis caused by disease or injury
- Ulcer
- Break in the epidermis with exposure of the dermis
- Scar
- Area of fibrous tissue that has replaced the damaged dermis or SQ tissue
- Lichenification
- Thickening or hardening of the skin with exaggerations of skin markings
- Hyperkeratosis
- Increased thickness of the horny layers of the skin
- Necrosis
- An area of dead cells
- Comedones
- Dilated hair follicles filled with keratin and sebaceous debris
- In regards to flea control, what is the MOA of cholinesterase inhibitors?
- -Inhibit cholinesterase -It is an organophosphate -Potent w/ good residual effects -Carbamates are safer than organophosphates -Toxic to Cats
- In regards to flea control, what is the MOA of Pyrethrins?
- -Oil extract from Chrysanthemum flower -Causes extended membrane depolarization -Inactivated by UV light -Rapidly kill -Low residual effect -Piperonyl butoxide often added -Must be re-applied if animal goes outside
- In regards to flea control, what is the MOA of Permethrins?
- -Synthetic pyrethrin -More UV stable -Fast kill **TOXIC TO CATS** -Found in most OTC flea products
- In regards to flea control, what is the MOA of IGR’s?
- -Juvenile hormone analogs -Ovicida -Larvicidal -Long residual effect
- In regards to flea control, what is the MOA of Lefenuron (Program)?
- -Insect development inhibitor -Inhibits chitin synthesis -Stored in body fat -NOT an adulticide (limits its use in FAD) -All contact animals need to be treated -Slow acting -Oral or injectable
- In regards to flea control, what is the MOA of Fipronyl (Frontline)?
- -Phenylpyrazole -GABA receptor antagonist -Affinity for SQ secretions -Effective against ticks FRONTLINE PLUS: -Fipronyl + Methoprene -Addition of juvenile growth hormone analogs -Prevents emergence of fipronyl resistant flea populations -Can bath animal w/out loosing efficacy -Apply monthly for FAD patients
- In regards to flea control, what is the MOA of Imidacloprid (Advantage)?
- -Chloronicotinyl compound -Binds to post-synaptic nicotinic receptors -NOT effective against ticks -Efficacy may be decreased by bathing -Apply once a month
- In regards to flea control, what is the range of action of Selemectin (Revolution)?
- -Activity against fleas, ticks (only Dermacantor variabilis), dirofilaria, sarcoptes, odectes, hooks, and rounds
- In regards to flea control, what is the MOA of Citrus Oil?
- -Disrupts flea ectoskeleton -Found in many OTC shampoo’s -Skin irritation and adverse side effects
- In regards to flea control, what is the MOA of Nitenpyram (Capstar)?
- -Rapid acting adulticide
- In regards to flea control, what is the MOA of Advantix?
- -Imidacloprdi + Permethrin -Added efficacy against ticks -Use only in dog households -DO NOT USE ON CATS (toxic even if cat rubs on dog)
- What is the basic life-cycle of a flea?
- Egg L1 L2 L3 Pupae Adult
- What are some characteristics of flea eggs?
- -White -Non-sticky -Laid on host and fall into environment to complete life cycle -Hatch in 1-10 days -.5mm in length
- What are some characteristics of flea larvae?
- -Legless, move by a single row of bristles on each segment -Yellow to white in color -Non-parasitic -Geotactic and photophobic so they move deeper into carpets, cracks in wood, soil -Can move over 40cm in carpet -Feed on organic debris and dried blood -3 molts in larval stage -5-11 days is the larval stage if sufficient food and right climate (dryness, extreme heat or cold are detrimental)
- What are some characteristics of flea pupae?
- -Sticky cocoon -Highly resistant to desiccation and parasiticides -Peak emergence is 8-9 days -Emergence depends upon: -Temperature -Physical pressure
- What are some characteristics of adult flea?
- -Small, brown, wingless -Laterally compressed bodies -Attracted to host by: -Movement -Warmth -Carbon dioxide -Live entire life on host (can live on host for up to 100 days) -Female lays eggs 3-4 days after a blood meal -Female can lay 13-35 eggs per day
- How would you diagnose a flea allergy?
- -History -PE -Intradermal skin tests -Serologic tests -Histopathology -Response to therapy
- How would you treat a flea allergy?
- -Flea control -Anti-pruritics -Antibiotics if necessary -Immunotherapy if ineffective
- What are some clinical signs of a flea allergy in a dog?
- -Caudal 1/3 of body -Pruritis -Papules, crusts -Pyotraumatic dermatitis -W/ chronicity can see: -Alopecia -Lichenfication -Hyperpigmentation
- What are some clinical signs of a flea allergy in a cat?
- -Caudal 1/3 of body and neck -Miliary dermatitis -Symmetric alopecia w/ no lesions -Eosinophilic granuloma complex
- Which flea products are toxic to cats?
- -Permethrines, Cholinesterase inhibitors
- What is the most common species of flea found on the dog? Cat?
- -Ctenocephalides felis -Prevelance is greater than 92% in dogs and 97% in cats
- How does intermittent vs. continuous exposure to fleas affect a pet’s reaction to them?
- Intermittent exposure = predisposes animals to FAD (flea atopic dermatitis) Continuous exposure = may lead to tolerance
- What the are signs associated w/ pruritus in cats?
- -Indolent ulcers (lips) -Granulomatous red lesions on ventrum
- What dermatophytes are pathogenic in dogs and cats?
- -Microsporum canis (most common) -M. gypseum -Trichophyton mentagrophytes (seen in rodents) -Sporotrichosis?
- How are Dermatophytes transmitted?
- Dermatophytes are transmitted by contact w/ infected hairs, scales, or fungal elements
- What are typical lesions and distribution patterns of dermatophyte infections in dogs?
- -Classic lesions: annular areas of peripherally expanding alopecia, scale, crust, papules and pustules -Nasal folliculitis and furunculosis -Generalized seborrhea-like infection -Dermatophytic kerion -Onychomycosis (nail infection) M. Canis Head and front limbs M. gypseum Extremities and tail T. mentagrophytes Whole body
- What are typical lesions and distribution patterns of dermatophyte infections in cats?
- -Generalized infections are more common: -Alopecia -Folliculitis, erythema, scale, crust, papule -Generalized seborrhea like eruption -Milliary dermatitis = uncommon to be caused by dermatophytes (usually caused by fleas) -Localized infections: -One or more annular areas of alopecia -May mimic chin acne or “stud tail†-Onychomycosis -Dermatophyte kerion -Dermatophyte pseudomycetoma
- How can you positively identify a fungal agent (genus and species)?
- -Most reliable test fore identification = Fungal culture -Identify the organism through morphologic and microscopic characteristics -DTM (dermatophyte test medium) -Dermatophytes utilized the protein in the media first, leading to alkaline metabolites that cause the media to turn red w/in 10-14 days -Saprophytes utilized carbohydrate first creating acidic metabolites
- Why is it important to make a definitive diagnosis for a dermatophyte infection?
- is important to make a definitive diagnosis in order to properly clear up the problem and prevent re-infection
- What recommendations would you make for a cattery w/ dermatomycosis in each litter of kittens (M canis)?
- -Cessation of breeding program -Identification and isolation of positive animals -Topical and systemic therapy for positive animals -Topical therapy for contact cats -Strict environmental control -Treat all cats until cats are culture negative 3 times -Toothbrush cultures to screen healthy appearing cats for carrier status
- What skin layer do dermatophytes grow in?
- -Keratogenous zone of keratinized tissue (Adamson’s fringe) -Hair, nail, stratum corneum of skin -Don’t affect the hair bulb
- Describe the lesions seen with Cryptococcus.
- -Cutaneous lesions including nodules, ulcers and draining tracts -Nasal discharge and sneezing -Ocular involvement = blindness -Neural involvement = seizures, ataxia, paresis
- What are the risk factors associated with cryptococcus?
- More common in cats Found in pigeon shit
- How is cryptococcus diagnosed?
- -Cytology -Biopsy -Serology
- What are the treatment options for Cryptococcus?
- -Itraconazole -Fluconazole -Flyctosine
- What are the clinical signs of Malassezia dermatitis in a dog?
- -Very pruritic GENERALIZED: -Erythematous, greasy, scaly, crusty, malodorous, lichenification, alopecia, hyperpigmentation LOCALIZED: -Otitis, lips, muzzle, interdigital spaces, ventral neck, medial thigh, groin, axilla, paronychia, intertriginous regions -40% have concurrent bacterial pyoderma
- What are the clinical signs of Malassezia dermatitis in a cat?
- -Not as common as dog GENERALIZED: -Erythematous, scaly to waxy dermatitis LOCALIZED: -Otitis, chin acne, paronychia (base of nail)
- How do you diagnose Malassezia?
- -Cytologic exam: -Impression smear, swab, skin scraping, acetate prep -Look for round to oval budding yeast “peanut shaped†-Skin biopsy w/ histopath -Culture -Look for a response to anti-yeast therapy
- Discuss Treatment for Malassezia.
- -Identify and address the underlying cause: -w/ out correction of the predisposing disease or factors, the disease is likely to reoccur -Treat concurrent Staph pyoderma Topical therapy: -Anti-fungal creams or lotions for localized areas -Anti-fungal shampoos for generalized areas -Dips are not necessary but can be effective Systemic therapy: -Ketoconazole or Itraconazole -**Griseofulvin is NOT effective** -Treat 7-14 days past clinical cure
- What are the predisposing factors for Malassezia?
- -Increased humidity -Immune dysfunction -Genetic (Basset’s or WHWT) -Hypersensitivity -Keratinization disorders -Endocrine or metabolic disorders
- Which of the following are zoonotic? Blastomycosis, Histoplasmosis, Coccidiomycosis, Crytococcus neoformans.
- Cryptococcus neoformans
- What are some clinical signs associated with Blastomycosis?
- -Nodular skin lesions -Draining tracts -Absscesses -Often have concurrent respiratory disease
- What are some clinical signs associated with Histoplasmosis?
- -GIT and respiratory disease -Granuloma and draining tract skin lesions
- What are some clinical signs of Coccidomycosis?
- Dog: -Young, male dogs -Coughing, dyspnea, fever, anorexia, wgt. Loss, lameness, ocular disesase -Papules, nodules, abscesses, draining tract, ulcers -Skin infections often occur over infected bone Cat: -RARE -Anorexia, wgt. Loss, cough, dyspnea, lameness, ocular disease, skin lesions
- What are some clinical signs of Cryptococcus neoformans infection?
- -Cutaneous lesions include nodules, ulcers, draining tracts -Nasal discharge -Ocular involvement = blindness -Neural involvement = seizures, ataxia, paresis
- What are some physical characteristics of Blasto?
- -Broad based budding -Endemic in Mississippi and Ohio river valley -Ingested or inhaled from: soil, bird or bat shit
- What are some physical characteristics of Histo?
- -Tiny organism -Endemic in Eastern US
- What are some physical characteristics of Coccidio?
- -Largest organism w/ spherules that contain endospores -Found in sandy, alkaline soil, high temperature, low rainfall, low elevation -Endemic in SW US, South and Central America
- What are some physical characteristics of Cryptococcus neoformans?
- -Large organism -Relatively common in cats -Found in pigeon shit -Thick candy shell
- Which breed of dog is predisposed to developing cutaneous infections w/ pythium?
- GSD
- What is the usual source of pythium infection?
- Swamps or ponds in southern US
- How is pythium treated?
- Aggressive surgery (amputation) -Itraconazole + Terbenafine -Treat for 2 months and recheck titers at LSU
- What is the prognosis for pythium?
- Poor (“swamp cancer†is invasive and often fatal)
- What is an asymptomatic carrier?
- animal that is carrying and possibly shedding a disease without showing any clinical signs
- How are asymptomatic carriers identified?
- Screening tests
- How are Malassezia infections transmitted?
- Malassezia is part of the normal flora of ears and skin. It is an opportunistic pathogen that proliferates under conditions of increased moisture (i.e. greasy, scaly, inflamed skin)
- Does antibiotic therapy predispose animals to yeast or fungal infections of skin?
- Yes
- What is the most common subcutaneous fungal infection of cats and dogs?
- Microsporum canis
- What are the risk factors for infection with Blasto?
- -Found in the Mississippi and Ohio River valley -Found in nitrogen rich soil and bat and bird shit
- Name some fat sources rich in essential fatty acids.
- -Sunflower oil -Corn oil -Soybean oil
- What are the differences between omega 6 and omega 3 fatty acids?
- OMEGA 6 FA -Predominant in terrestrial plants and animals INCLUDES: -Linoleic acid = maintenance of barrier functions of skin -Gamma-linoleic acid = metabolized into anti-inflammatory PG’s -Arachidonic acid = substrate for inflammatory LT’s and PG’s OMEGA 3 FA -Predominates in marine plants and animals INCLUDES: -Alpha-linoleic acid = it is an eicosapentaneoic acid (EPA) and is metabolized by lipooxygenase and cyclooxygenase to LT’s and PG’s
- Explain why omega 3 fatty acids may be beneficial in decreasing inflammation?
- -EPA metabolized lipooxygenase and cyclooxygenase to LT’s and PG’s (inflammatory mediators)
- Which breed are most commonly affected by vit. A responsive dermatosis?
- Cocker Spaniel
- What are the usual clinical signs for vit. A responsive dermatosis?
- -Thick, inflamed crusty lesions on ventral abdomen and thorax -Frond-like keratinous plugs adhered to their surface
- How do you diagnose vit. A responsive dermatosis?
- -Histopath -Orthokeratotic hyperkeratosis -Follicular keratosis
- What is panniculitis?
- inflammation of SQ fat
- What is pansteatitis?
- inflammation of fat w/ in abdomen
- What are the DDX for panniculitis and pansteatitis?
- -Bacterial or fungal infection -Autoimmune disease -Physiochemical problem -Hereditary
- List 5 diseases which may improve following treatment w/ vit. E.
- 1. DLE 2. SLE 3. Epidermolysis bullosa 4. Acanthosis nigricans 5. Demodecosis
- What breeds are predisoped to zinc responsive dermatosis?
- Syndrome I: -Siberian Huskies, Bull terriers and Alaskan Malamutes (primarily -Has been reported in Doberman Pinschers and Great Danes Syndrome II: -Great Danes, Doberman Pinschers, GSD, German Shorthair pointers, Standard Poodles
- What is the characteristic histopathological finding w/ zinc responsive dermatosis?
- Marked diffuse and follicular parakeratotic hyperplasia (seen w/ Syndrome II)
- What are the causes of Syndrome II zinc responsive dermatosis?
- -Over supplementation w/ calcium which causes decreased zinc absorption
- What are the characteristic histopathological findings of generic dog food dermatosis?
- -Focal epidermal necrosis -Mixed dermal infiltrate -Subacute to chronic dermatitis
- Understand the concepts of “epidermal turnover time†and “disorder of keratinizationâ€.
- Epidermal Turnover Time:| -Number of days from stratum basale to stratum corneum -22 days in normal dog -3-5 days in dog w/ a disorder of keratinization Disorder of Keratinization: -Alterations in basal cell mitotic rate -Alterations in transformation of cytoplasmic proteins into keratin -Alterations in exfoliation (may result from changes in epidermal lipids)
- Outline a diagnostic approach for a dog presenting to your clinic w/ primary complaint of Seborrhea.
- Rule Out: -Parasites -Infections -Allergies -Irritants -Metabolic disorders -Nutritional disorders -Biopsy skin
- Know the principle of topical therapy as they relate to the symptomatic control of Seborrhea.
- -Topical therapy is for its antiseborrheic and keratolytic actions
- List indications of use for systemic retinoids and side effects that must be monitored for.
- -Diseases of sebaceous glands (first generation) -Keratinization disorders (second generation) -Sebaceous adenitis, Mycosis fungoides, Idiopathic seborrhea (third generation)
- Describe the lesions of feline acne including pathogenesis.
- Lesions: -Comedones -Papules -Pustules Patho: -Though to be due to improper cleaning of chin -May also be a seborrheic syndrome +/- secondary infection
- List three breeds w/ an increased incidence of seasonal flank alopecia.
- 1. Airedale terriers 2. English bulldogs 3. Boxers
- List four breeds w/ increased incidence of Alopecia X.
- 1. Pomerarians 2. Chow Chows 3. Keeshound 4. Samoyed
- What treatments would you recommend for acne in a dog?
- -Daily cleansing (Benzoyl peroxide, alcohol, antiseptic shampoos, astringent) -Local antibiotics (erythromycin or mupiracin) -+/-Systemic antibiotics -+/-Topical Retin A ointment/lotion
- What treatments would you recommend for acne in a cat?
- -Observe if non-inflammatory -Clip hair, clean chin (Benzoyl peroxide, alcohol, antiseptic shampoos, astringent) -+/-Local antibiotics and anti-fungals -+/-Systemic antibiotics -+/-Daily cleaning of chin to prevent reoccurence
- List 2 Keratolytic agents.
- 1. Benzoic Acid 2. Vit. A Keratolytic = promotes softening and dissolution of stratum corneum Keratoplastic = normalized epidermal kinetics and keratinization
- List 2 keratoplastic agents.
- 1. Coal Tar 2. Salicylic Acid 3. Sulfur
- List 2 degreasing agents in medicated shampoos.
- 1. Coal Tar 2. Sulfur
- Describe the clinical findings that may be suggestive of Sertoli cell tumor.
- -Hair loss -Bone marrow suppression -Fatal thrombocytopenia or anemia -Oily seborrhea -Pruritis -Comedones -Linear prepucial hyperpigmentation -Nipple enlargement
- List sex hormones produced by the adrenal gland
- -Androgens and Estrogens
- Describe the lesions distribution pattern typical of seasonal flank alopecia.
- -Non-scarring alopecia of thoracolumbar that is bilaterally symmetrical region develops in fall or spring and hair regrows months later
- Describe the lesion distribution pattern typical of Alopecia X.
- -Bilateral symmetrical alopecia -Dry dull hair coat -Primary hairs lost first -Head and front legs spared
- What is the definition of pruritis?
- an unpleasant sensation within the skin which evokes the desire to scratch