Dermatology Flashcards
0
Q
Describe the epidermis.
A
The outer epidermis is a tough waterproof barrier. basal epidermal cells continually divide, migrate outwards and are shed from the surface. The thickness varies with breed and anatomical site. It is usually 3-4 cells deep in haired skin in dogs and cats but thicker over the nose and footpads. The skin is thicker in farm species and horses. The basal epidermis also contains melanocytes that are important in pigmentation and langerhans cells that are important in immunity and inflammation. There are no blood vessels in the epidermis.
1
Q
What are the functions of the skin?
A
Tough outer barrier, immune system protects against infection, protection against UV radiation, temperature regulation, sensations of touch, pressure, itch pain and heat, produces vitamin D.
2
Q
What are the different layers of the epidermis?
A
Stratum corneum - tough waterproof barrier formed by keratinised squames and intercellular sebum.
Granular layer - keratin granules form and nuclei are lost
Spinous layer - cells begin to migrate
Basal layer - actively dividing cells
Basement membrane - adheres the basal layer to the dermis.
3
Q
Describe the dermis
A
A network of collagen and elastin fibres in a gel like proteoglycan matrix that makes the skin tough, flexible and elastic. The dermis also contains blood vessels, lymphatics and nerves to the skin. Fibroblasts, mast cells, dendritic cells and other cells important in inflammation and repair. It also has hair follicles and associated structures.
4
Q
Describe hair follicles found in cats and dogs
A
hair follicles are found everywhere except the nose and footpads. They are denser along the back and sparsar on the underside of the boyd. hairs are produced by division of epidermal cells at the base of the follicle. An invagination of the dermis - the dermal papilla - rich in blood vessels and hormone receptors governs hair growht. Hair growth follows: exogen (Active expulsion of the hair), anagen (growth), catagen (involution) and telogen (resting). Most animals moult and grow a new coat. Exceptions to this are breeds with anagen type coats such as poodles etc that dont shed hair but need haircuts.
5
Q
how is hair growth controlled?
A
Multiple influences including genotype, photoperiod and temperature, thyroid, adrenocortico and sex steroid hormones and nutrition. Basic type of coat has coarse primary guard hairs and a dense undercoat of fine secondary hairs. This is also known as a double coat. Short and long single coats have a more uniform collection of hairs. The hairs can be straight (smooth) or curly (wooly or wire haired). dogs and cats tend to have compound follicles whereas other species have simple folicles. The hair follicles lie at an angle within the skin allowing the coat to lie naturally from head to tail. Arrector pili muscles can pull them upright, raising the hairs for insulation and social signals. Whiskers are specialised touch sensitive hairs, longer and thicker than ordinary hairs, found on the muzzle and face. Smaller whisker like hairs also sensitive to touch are scattered throuughout the coat.
6
Q
Describe different coat and skin colours
A
There are two t ypes of melanins - blackbrown and yellow red. The final colour depends on the distbution of micromelanosomes in the keratinocytes and hairs. Agouti hairs have a brown base gradually darkening towards the tip. Other coats are a single colouur, have piebald distribution or lack pigment 9white). Blue and fawn coats are dilutions of black and red, caused by clumping of melanin granules into macromelanosomes. These are associated with colour dilution alopecia in some breeds. Many colours do not breed true.
7
Q
Describe sebum and sweat
A
Sebum is secreted by sebaceous glands that secreete into hair follicles. Sebum provides nutrients, antibodiies, protects against infection and prevents drying. Atrichial sweat glands secret onto the skin surface, on the nose and footpads, and epitrichhial glands secrete into hair follicles. Sweat is used to thermoregulate in humans, cattle and horses but not in dogs and cats.
8
Q
Where is the specialised skin of the body found
A
the nose and footpads are different from the rest of the skin, it is hairless, very thick and tightly attached to underlying tissues making these sites very tough ad resilient. Claws and hooves are also tightly adherent to underlying tissues. The specialised epidermis of the corium or nailbed produces a thick and highly keratinised stratum corneum with a low lipid content, making it very strong and rigid.
9
Q
Describe how age/breed may affect your ddx for skin cases
A
75% of allergic diseases start between 6 months and 3 years old. very young: congenital problems and parasites.
Young adult: immune mediated and follicular dysplasias.
Elderly: neoplastic and metabolic.
Many conditions have a breed/sex predisposition.
10
Q
Describe how onset and duration may affect your ddx for skin cases.
A
Insidious: hypersensitivity, metabolic, endocrine, neoplasia
Acute: parasite, infectious, immune mediated
WAxing and waning: hypersensitivity, immune mediated
Progressive: metabolic, endocrine, neoplastic
Intermittent: parasites, infections.
Seasonality: allergies and some parasites.
11
Q
How is clinical exam of the skin done?
A
Skin easily examined - carefully observe and evaluate skin lesions and other findings e.g fleas, lice trombicula. you should be able to recognise and understand common skin lesions type and distribution. The common causes of skin disease: dogs- parasitic, infections - staphylococcal, malassezia, dermatophytes, allergic, endocrine, neoplastic.
12
Q
What are the common parasitic causes of pruritis?
A
Flea infestation, otodectes cyanotis, cheyletiella species, neotrombicula autumnalis, sarcoptees scabiei, demodex, lice, notoedres, endoparasites
13
Q
What are the most common types of hypersensitivty reaction which cause pruritis?
A
Flea allergic dermatitis, atopic dermatitis, adverse food reactions, allergic or contact dermatitis.
14
Q
What are the most common infectious causes of pruritis?
A
Bacteria/malassezia, cowpox, feline herpesvirus, dermatophytosis, FIV and FeLV.
15
Q
What are fleas?
A
Small red brown laterally compressed and fast moving insects. most commonly infest the tailhead, rump, dorsum, ventral abdomen and flanks but cats may show clinical signs elsewhere. They cause mild irritation to severe pruritis and inflammation; anaemia is possible in young animals. they are the vector for dipylidium caninum and cat scratch fever. Fleas will affect dogs, cats, rabbits ferrets and humans.
16
Q
How can fleas be controlled?
A
For immediate control treat all inc ontact animals with an efefctive on animal adulticide and the environment with a combined larvidcide/insect growth regulator. Vacuuming will stimulate the pupae to hatch and improve the efficacy of environmental treatment. Monthly on animal treatment is enough for long term control in most cases but some animals will benefit from concurrent long term environmental treatment. IGRs are very safe but only break the life cycle and prevent environmental build up - adult fleas can stil be acquired. Wide range of flea control products available with combined insecticidal, acaricidal, anti tick and anti endoparasite actibity. They come in a variety of forms including oral, sprays, spot ons and collars. Neer use permethrin in homes with cats.
17
Q
What are the clinical signs of sarcoptes scabiei and notedres cati?
A
papules, scaling, crusting, excoriation and alopecia. on the ears, face, elbows, hocks and ventral chest in sarcoptes scabiei and in notedres cati - head and neck.
18
Q
What are the clinical signs of cheyletiella in cats and dogs?
A
Variable pruritis and scaling - walking dandruff, truncal
19
Q
What are the clinical signs of otodectes cyanotis in dogs and cats?
A
Otitis, dark brown waxy discharge, zoonotic, on ears head cranial body
20
Q
What is the treatment for mites and lice?
A
Treat all in contact animals with an effective acaricide for 4-6 weeks to kill newly hatched larvae. Adults can live in the environment for short periods - clean bedding equipment etc. Environmental treatment may be necessary.
21
Q
describe non contagious parasites that may cause pruritis?
A
Neotrombicula adults live in thick vegetation. the larvae infest animals in the late summer and autumn. the bright orange mites can be seen in the ear, axillae, ventral body, interdigital skin and tail. Vulerable to most acaricides but animals will be re infested from environment. A long acting product such as fipronil spray applied to feet and ventral body every 7-14 days can be effective. Demodicosis is usually associated with erythema, papules, alopecia, scaling and comedones. Free living pelodera nemotodes or hookworm larvae can occasionally cause severe dermatitis of the feet and ventral body in kenneled dogs where hygiene is poor.
22
Q
Describe malassezia in dogs
A
Malassezia are part of normal flora, in the ears, feet and mucocutaneous junctions and infections are usually secondary to an underlying cause. In dogs malassezia otitis and dermatitis are common. (odour erythema, hyperpigmentation, lichenification, seborrhoea and alopecia) its less comomn in cats but can be associated with otitis externa, paronychia, felie acne, facial dermatitis and underlying systemic diseases. Treatment with chlorhexidine/micoonazole shampoo and topical clotrimazole/miconazole and nystatin containing products is usually effective but some cases may need systemic treatment with itraconazole.
23
Q
Describe the most common hypersensitivity diseases which may cause pruritis
A
Allergic skin diseases are complex familial conditions that involve abnormalities in skin barrier function and skin inflammation in addition to an alergy. Animals can exhibit multiple overlapping patterns. Most cases of atopic dermatitis are associated with allergies to environmental allergens such as house dust mites, epidermals, insects, pollens and moulds. boxers, labradors, gsds, whwts and other terriers predisposed. Animals with pollen allergies may have seasonal clinical signs but most start or eventually become perennial. OTher fare flactors include stress or anxiety, change in temperature and humidity, ectoparasites and infections.
24
What are the clinical signs of atopic dermatitis and adverse food reactions?
pruritis, no skin lesions, mild to moderate erythema, saliva stains, muzzle ventral pinnaae neck axillae abdomen groin perineum and feet. Chronic inflamation with hair loss, excoriatioin, papules, scaling and crusting, hyperpigmentation and lichenifiation. Skin may be dry, moist or greasy. Chronic or recurrent otitis externa, occasionally unilateral with or without other skin lesions. Recurrent staphylococcal pyoderma and malassezia dermatitis.
25
How are alergic skin dieases diagnosed?
By eliminating other causes of pruritis, controlling infection and determining the pattern of allergies for each patient. A 6-8 week food trial with a home cooked or commercial nvoel single protein diet and water only should be used to see whether food is a trigger for the pruritis. hydrolysed diets may help in cases where it is difficult to fiind novel ingredients but these are expensive and some animals may still react to the ingredients. Clear written instructions, follow up and good communication are important in maintaing compliance. They wax and wane so relapse after challenge with the usual diet is necessary to confirm diagnosis.
26
What is allergy testing?
Can be used to identify environmental allergens for avoidance or allergic specific immunotherapy. Most dermatologists prefer intradermal allergen tests as these directly test the capacity of the skin to react to the allergens. Most first opiinion practices use serology tests although there are some concerns over the reliability of these. allergy tests must not be used to confirm the diagnosis of atopic dermatitis - positive tests can be seen in healthy animals or other pruritic skin diseases.
27
What is allergic and irritant contact dermatitis?
Only affect skin in direct contact - usually sparsely haired ventral skin, the feet or the site of application of topical medication. REactions can be seen to topical drugs, cleaning fluids, plastics or metal bowls, carpet dyes, concrete etc. It usually resolves within a week of removing the suspect substances. Patch tests with suspect substances applied to the skin can confirm the diagnosis but these are difficult to perform.
28
What is acral lick dermatitis?
Caused by chronic self trauma to the cranial and lateral aspects of the distal limbs and other sites. Most involve a long standing deep bacterial folliculitis, lichenification and scarring. these are numerous potential cases including behavioural problems, musculoskeletal problems, neurlogical disorders and other pruritic skin diseases. Take good history. Long term control may require behavioral therapy and mood modifying drugs. It is important to note that stress and anxiety can worsen allergic skin disease.
29
What is epitheliotropic cutaneous T cell lymphoma?
Usually seen in older dogs and rarely cats. the clinical signs can be very varied with diffuse or localised erythema and scaling, plaques, ulcers or nodules an variable, often severe pruritis.
30
What is demodex?
Demdex mites are commensal, although the short bodies D gatio can be contagious in cats. Dogs and cats have at least three species of mites with different morphology that are found in hair follicles associated with sebaceous glands and on the skin surface. Localised juvenile onset demodicosis occurs during adolescence and presents with multifocal alopecia, scaling, comedones and follicular casts. It isnt pruritic unless there is secndary infection. Generalised demodicosis is more severe alopecia, scaling, hyperpigmentation, comedones and follicular casts. Clinical signs may b e limited to feet. Secondary bacterial infection common. May be peripheral lymphadenopathy with pyrexia. Juvenile form often resolves with maturity. Generalised form is more serious, probably wont resolve and requires treatment. True adult onset demodicosis usually secondary to underlying disease.
31
What is the treatment of demodex?
Amitraz (aludex) dip once weekly. Wash with keratolytic and degreasing shampoo to remove debris and clip longhaired animals. Adverse effects include vomiting, sedation, bradycardia, pruritis, exfoliative erythroderma and hyperglycaemia. It is toxic to chihuahuas and cats and can cause side efects in humans. Lime sulphur dip used in mild cases. Imidacloprid spot once weekly in milder cases. Ivermectin or moxidectin. not licensed. Milbemycin oxime once daily effective and well tolerated even in MDR positive dogs. Should be treated until 2-3 skins crapes negative at 7-14 days intervals.
32
what is dermatophytosis?
Dermatophytes are fungi that metabolise keratinised tissues. Common species include microsporum canis, microsporum gypseum and trichophyton mentagrophytes. Dermatophytosis is usually associated with multifocal alopecia and scaling. Less common problems include paronychia and kerions, miliary dermatitis and fungal granulomas in persian cats. Trichophyton species in rodents and rabbits are more inflammatory causing alopecia, erythema scaling crusting and secondary infection. Persian cats and Yorkshire terriers are predisposed. Most cases seen in young animals but cases also occur secondary to underlying immunosuppresive diseases. Highly contagious and zoonotic.
33
What is the treatment of dermatophytosis?
localised dermatophytosis in young animals usually spontaneously resolves but all cases should be treated to reduce contamination of environment, contagion and zoonosis. Clipping long haired animals may help, but can also worsen clinical signs. Itraconazole licensed in cats, well tolerated, should be treated until they have had at least two consecutive negative cultures at least 7 days apart. Topical treatment can be used on very local lesions, but usually use d to decrease time to clinical cure and decrease environmental contamination. Suitable products include chlorhexidine/miconazole malaseb shampoo or enilconazole dip. Environmental decontamination very important especially in multicat households and shelters. This includes thorough cleaning and vaccuming, careful disposal of contaminated items and use of antifungal agents.
34
What is leishmania?
Should be suspected in animals that have travelled to endemic areas. Owners should use anti sandfly products in endemic areas e..g delttamethrin colalrs. Cutaneous - focal alopecia with fine silvery white scaling, depigmentation, nodules, ulcers and crusting of the face nose pinnae and feet. Systemic - lymphadenopathy,hepatomegaly, splenomegaly, anaemia, ocular signs, kidney failure, lameness, muscle atrophy and pyrexia. Serology PCR and identifying the organism in biopsies from affected skin used as diagnosis. treatment options include meglumine antimoniate, allopurinol and miltefosine but a complete cure is difficult.
35
How many immune mediated diseases cause alopecia?
Clinical signs of dermatomyositis and vasculitis include alopecia, erythema, crusting and scaling f the extremities, periocular skin and bony rominences, although mild vasculitis may present with alopecia only. Dermatopmyositis may show muscle atrophy, weakness, stiff gait and facial palsy. Inflammation usually not apparent in alopecia areata which can be restricted to pigmented hairs. lymphocytic mural folliculitis is uncommon that causes variable patterns of alpecia and erythema.
36
How many endocrinopathies cause alopecia?
Perturbations in hormone lvels at the follicular level tend to have similar effects so endocrine dermatology have similar clinical effects. common features include; symmetrical non inflammatory alopecia, dull dry faded coat that is easily epilated, coat fails to regrow after clipping, mild to moderate scaling, easily bruised skin and poor wound healing, increased susceptibility to infections.
37
How is hyperadrenocorticism characterised?
Bilaterally symmetrical truncal hair loss, comedones, atrophic and inelastic skin, prominent blood vessels and calcinosis cutis, fragile skin and tearing is more common in cats.
38
How does hypothyroidism affect the skin?
Can be very variable with any combination of systemic and cutaneous signs. Truncal alopecia with thickened hyperpigmented and cool skin is classical but most dogs show partial alopecia with a faded coat. In others it may be restricted to the tail and dorsal nose.
39
How do sex hormone alterations cause alopecia?
They tend to initially affect the caudal ventrum and genitalia spreading to the limbs, flanks and neck. hyperoestrogenism is asssociated with gynectomastia, vulval swelling and signs of oestrus. Sertoli cell tumours are most common ni cryptorchid testes and cause attraction to male dogs, gynectomastia, pendulous prepuce and linear preputial erythema. Hyperandrogenism associated with neoplasia or functional abnormalities in older dogs causes caudal and perianal gland hyperplasia and patchy anogenital hyperpigmentation.
40
What is telogen effluvium and anagen defluxion?
Associated with synchronous hair cycle arrest and subsequent hair loss. In telogen effluvium events such as pregnancy lactation systemic illness etc cause the hairs to enter telogen. Alopecia arises some time later when the resting hairs are pushed out by new anagen growth or removed by grooming. anagen defluxation is similar but caused by more severe insults that interupt anagen. the weakened hair shaft is easily fractured causing apparent hair loss. causes include systemic illness, bacteriaemia, malignancies, chemotherapy and drug reactions. uncommon but may be seen in anagen breeds such as poodles.
41
What is feline paraneoplastic alopecia
usually associated with pancreatic and bile duct carcinomas. Cutaneous signs are highly specific and usually noted before systemic illness. Ventral truncal alopecia with strikingly smooth, shining thin and translucent skin. If diagnosed early the clinical signs are reversible with surgical exciision of the tumour - although metastasis are common and prognosis generally poor.
42
Describe congenital alopecias?
Rare sporadic problem in many breeds although considered normal in hairless breeds. The clinical sign depend on the genetic abnormality whiich may be dominant recessive or sex linked. the adnexae, skin claws and teeth may also be affected.
43
What is pattern baldness?
these syndromes are caused by follicle miniaturisation resulting in focal alopecia. the skin may be hyper pigmented but is otherwise normal. pattern baldness seen in Yorkshire terriers, daschunds and greyhounds.
44
What are follicular dysplasias?
Inherited diseases causing abnormal growth and development of the hair follicles in irish water spaniels, water dogs and other breeds. the puppy coat is initially normal but becomes dull brittle and is lost predominantly from the trunk and wear oints. There is often scaling and secondary infection, which can be pruritic. hair regrowth is irregular and abnormal. Black hair follicle dysplasias affect black areas in black and white dogs. Colour dilute alopecia affects dilute colour coats such as blue or fawn dobermans.
45
What are the treatments for congenital and hereditary alopecias?
Avoid further damage to coat, gentle anti scaling and moisturising shamppos, control secondary infections, high quality diets and essential fatty acids, sun protection, melatonin, vitamin A or retinoids.
46
What is sebaceous adenitis?
A comon problem in standard poodles, vizlas, akitas, samoyeds and ocasionally other breds - associated with inflammation and destruction of sebaceous glands. CLinical signs include dry skin, tightly adherent frond like scales, hair loss and secondary infections. Treatment: anti scaling shampoos, vitamin A or retinoids, high quality diet and fatty acids, ciclosporin, antibiotics and anti bacterial shampoos to counter secondary infections
47
What is seasonal or cyclical flank alopecia?
Seasonal hair loss on back and flanks in dogs - underlying skin is darker but normal. hair loss and regrowth can vary from year to year. possibly linked to changes in day length. some dogs respond to melatonin.
48
What is alopecia X?
Chows, pomeranians, keeshonds, poodles and other breeds suffer an unusual pattern of hair loss, which starts in adolescence or young adulthood with loss of primary hairs leaving a wooly puppy like coat, eventually there is a complete alopecia and hyperpigmentation sparing head and limbs. some dogs have abnormal adrenal sex hormone production and respond to trilostane. other treatments include general skin and coat care, melatonin, neutering, deslorelin or sex hormones. regrowth and relapse, regrowth at biopsy, skin scrape sites also seen.
49
What is the diagnostic approach to focal or multifocal alopecia?
Cytology to rule out stpahyloccal pyoderma. deep skin scrapes, hair pluck, tape strips or impression smears to rule out demodex. dermatophytosis - dermatophyte endospores and hyphae can be visible on microscopy of affected hair shafts. Dermatophytes produce a red colour change that coincides with early fungal growht on dermatophyte test mediium. skin biopsy.
50
What is the diagnostic approach to symmetrical and diffuse alopecia?
Routine haematology, biochemistry and urinalysis are indicated in symmetrical and diffuse alopecia or where previous skin biopsies are comatible with endocrine alopecia. These do not confirm a diagnosis and further tests reqiuired to confirm diagnosis.
Hyperadrenocorticism - acth stimulation test, low dose dexamethasone suppression test, urinary cortisol:creatinine ratio.
Hypothyroidism - total t4, free t4, TSH.
Serrtoli cell tumour, hyperoestrogenism, praneoplastic alopecia - abdominal imaging.
Alopecia X - sex hormones pre and post ACTH.
51
What are the common presentations in cats with allergic and parasitic skin deases?
Self induced alopecia, head and neck pruritis, eosinophilic skin diseases - miliary dermatitis, eosinophilic plaque, eosinophilic granuloma, indolent ulcer.
52
What is miliary dermatitis?
An erythematous papular and crusting dermatitis, commonly seen over the dorsal body, flanks, neck and head. most commonly associated with flea allergic dermatitis.
53
What are eosinophilic plaques?
Well circumscribed, raised, erythematous and alopecic erosions. They vary in size from small focal lesions to large confluent plaques. They are most common on the ventral abdomen, hind limbs, ventral neck and interdigital skin.
54
What are eosinophlic granulomas?
Classically seen in young cats with thickened, linear, non ulcerated lesions on the caudal thighs or elsewhere. These are often asymptomatic and can spontaneously regress. These is also an ulcerative and proliferative oral form that may cause halitosis and dysphagia. eosinophilic granulomas have also been associated with firm swelling of the chin. Another form associated with hypersensitivity to mosquito bites causes erythematous erosive and crusting nodules of the nose, pinnae and footpads.
55
What are indolent ulcers?
erythematous, non healing ulcers of the lips, nasal planum, tongue and hard palate. They are usually small and shallow but can be large and destructive.
56
What are the Ddx for parasites causing feline pruritis?
Flea allergic dermatitis, otodectes cyanotis, trombicula autumnalis, demodex gatoi, mosquito, sarcoptes scabeiei, notoedres species, cheyletiella, lice.
57
What are the ddx for infectious causes of pruritis?
Bacterial folliculitis, malassezia, cowpox, feline herpes virus, dermatophytosis.
58
What are flea control trials?
It is vitally important to eliminate flea allergic dermatitis in cats. all cases should be thoroughly exminaed using a flea comb to look for evidence of fleas and flea faeces. Flea faeces will leave red stains on damp cotton wool. Microscopic examination of skin debris collected using adhesive tape strips can be used to detect tiny fragments of flea faeces. Flea allergen tests are very specific for flea allergic dermatitis but will miss many cases. Pruritis cats also groom away evidence of fleas and trial therapy is therefore necessary in all pruritic cats. aLl in contact animals should be intensively treated over a6-8week period with an on animal adulticide. the environment should be treated with a combined larvicide insect growth regulator. prednisolone can be used for 3-5 days to break the itch scratch cycle.
59
Describe food trials in cats
Food trials are more difficult to perform in cats. they are selective feeders and tend to like more variety than dogs. they usually wont eat carbohydrate and home cooked trials normally use protens onl. these are deficient in taurine and other nutrients, although this shouldnt cause problems in healthy adult cats over a 6-8 week food trial. outdoor cats will have access to other foods but keeping these cats indoors can increase stress that could exacerbate their skin disease. dogs can be starved if they wont eat the trial food, but this cant be done in cats because of the risk of hepatic lipidosis. many food trials stopped early.
60
How may psychological triggers affect skin disease?
Purely behavioural or psychological skin disease is uncommon but these triggers can be important exacerbating factors in allergic and other inflammatory skin diseases. potential problems can be seen with oriental breeds, cats with a nervous or shy nature, addition or loss of a human family member, another cat, territorial competition and home environment changes. cats are solitary animals and it is very important to determine how many social units there are in multi cat households - esentially, cats that engage in relaxed physical contact can be regarded as one social unit. there should be at least one feeding station, litter tray and rest point per social unit in different parts of the house.
61
Describe allergy testing in cats.
Th diagnosis of atopic dermatitis is uncertain in cats, as unlike dogs, suitable clinical and diagnositic criteria have not been established. positive tests may also be seen in healthy cats and cats with other skin diseases and many cats with presumed allergic skin disease have negative tests. nevertheless, allergy testing to identify reactive allergens for avoidance and immunotherapy is warranted in cats with pruritus and or eoosinophilic skin diseases where other potential triggers have been ruled out.
62
What is exfoliative dermatitis and thymoma?
A rare paraneoplastic syndrome seen in older cats with focal to generalised erythema, exfoliation and malassezia and or pyoderma. systemic clinical signs include anorexia, malaise, coughing and dyspnoea. the thymoma can be demonstrated on thoracic radiography. thoracotomy and excision of the thymoma is curative. similar syndromes with erythema, alopecia,e xudation, scaling, pruritis and malassezia dermatitis can be seen with underlying systemic diseases including hepatopathy, lymphoma, pulmonary tumour, chronic renal failure. Pulmonary tumours can also metastasise to the digits, infiltrating p3 causing lung digit syndrome.
63
What is feline ulcerative dermatitis?
Associated with well defined ulcerative and crusting lesions over the dorsal neck or shoulders. pruritis is variable. some lesions have been associated with injection site or spot on reactions but not consistent. diagnosis based on the clinical signs and biopsy. the prognosis is guarded as these lesions can be difficult to manage. treatment options include prevention of self trauma using collars or bandages, avoiding injections and spot on treatments, surgical excision, aggressive steroid therapy and ciclosporin.
64
What is oro facial pain syndrome?
An uncommon problem mostly seen i burmese and related cats. the cats present with violent and frenzied self trauma of the mouth face and neck. the problems seem to arise in the oral cavity and there is a poor response to anti inflammatory agents. it is probably a neurological problem as there is a better response to gabapentin, phenobarbital and benzodiazepines. some cases have associated with herpes virus neuritis and may respond to famciclovir.
65
What is feline cowpox?
Feline cowpox infections superficially resemble Miliary dermatitis but the papules are fewer in number and larger with a depressed centre that is covered with a small crust. Careful examination will distinguish these from miliary lesions. there should also be a primary bite wound or scratch. affected cats have a 7-10day viraemic phase before the generalised skin lesions develop. Although clinical signs such as malaise and pyrexia may not be evident. some cats especially if treated with steroids develop systemic disease with pulmonary lesions and vasculitis.
66
what is feline chin acne?
associated with mild to severe furunculosis of the modified sebaceous glands of the chin. Affected cats present with swelling of the chin, seborrhoea, exudates and crusts. the lesions may be paiinful. there is usually a secondary a bacterial infection. There are a variety of potential triggers but this is most commonly associated with behavioural triggers causing hyperplasia of the glands and increased rubbing. treatment involves cleaning the lesions, treating any secondary infection and behavioural modification.
67
What is facial seborrhea?
Facial seborrhea is almost always seen in persian cats. Affected cats present with thick, black, greasy and tightly adherent scales overlying erosions around the eyes and nose. there may be secondary malassezia infection. severe lesions may be extensive and painful in severely affected cats. the cause is unknown. prognosis is guarded as there is variable response to bathing, anti malassezia treatment, steroids and ciclosporin.
68
What is fragile skin syndrome?
Fragile skin syndrome is an uncommon condition associated with cutaneous atrophy, tearing of the skin and poor wound healing. this can be idiopathic but has also been associated with long term steroid treatment, hyperadrenocorticism and diabetes mellitus. the prognosis is variable - some cases resolve following correction of the underlying cause but in others the cutaneous atrophy is permanent. these cats should be kept indoors and protected from injury.
69
What are the flare factors for atopic dermatitis?
Atopic dermatitis is multifactorial involving skin barrier defects, allergic sensitisation, inflammation, microbial infections and other flare factors. Including ectoparasites such as fleas and trombicula autumnalis, staphyloccal and malassezia skin and ear infections, stress, behavioural therapy and perhomones. Excesses of temperatures and humidity, irritants or cleaning solutions etc.
70
What diet should be used in atopic dermatitis?
Animals with partial cutaneous adverse food reaction or food induced ad should avoid the offending items. many atopic animals benefit from foods supplemented with omega 3 fatty acids (important in epidermal lipid barrier formation, eicosanoid poduction and inflammation), omega 6 FAs and other nutrients.
71
Which topical therapies should be used in atopic dermatitis?
shampoo and leave on conditioner spray. percutaneous exposure to allergens - so physical washinig and removal of allergens likely to be helpful. Use emollients to counter driving. virbacs allermyl shampoo reduce pruritis used in whirlpool bath. contains linoelic acid, vitaminE and mono and oligosaccharides and piroctone olamine. Antimicrobial shampoos containing chlorhexidine, allerderm spot on contains ceramids and fatty acids that help restore the epidermal lipid layer structure. Dermoscent essential 6 is a st on mix of plant derived oils.
72
Which essential fatty acids should be used in atopic dermatitis?
polyunsaturated essential fatty acids particularly the n3 eicosapentanoic acid and n6 EFA gama linolenic acd.
73
How should atopic dogs avoid allergens?
Ideal way to manage an allergy is to avoid the alergen. unfortunately most cases of AD are associated with allergies to ubiquitous environemntal allergens such as house dust mites and pollens. these are difficult to completely avoid. house dust mite avoidance measures including avoiding bedrooms and bedding, vacuuming with a HEPA filtered cleaner, using hard floors, washing dog beds and using environmental flea sprays in the home. animals can be kept indoors during high pollen counts and washed off after being outside.
74
What is allergen specific immunotherapy?
ASIT is b eneficial in canine AD and in some cases of feline AD. should be specific and based on results of allergy testing trying to ensure that the allergens are clinically relevant. dose and freq need to be adjusted according to the individual patient. ASIT is not anti inflammatory treatment. It prevents flares associated with future exposure to the allergen. AD is also a complex disease with other abnormalities in addition to the allergy.
75
What is ciclosporin?
Treats canine and feline AD. Potent inhibitor of fT cells which have been imlicated in pathogenes of canine AD. Profound affects on immune system including antigen presentation ige production, mononuclear cell activity and development of inflammatory lesions. Metabolism is via cytochrome p450 system with subsequent biliary excretion. Withdraw treatment for up to two weeks either side of vaccination.
76
What is hydrocortisone aceponate?
A topical non halogenated diester glucocorticoid. Esters at the c17 and c21 ensure rapid absorption potent anti inflammatory action and metabolism within the derims into less active compounds minimising cutaneous and adverse systemic affects. HCA well tolerated, no changes to skin thickness, haematology, biochemistry or ACTH.
77
Describe the use of traditional glucocorticoids in atopic dermatitis?
Halogenated glucocorticoids are widely used in AD. they are cheap easy to administer systemically or topically and highly efficacious but have many side effects. Prednisolone, hydrocortisone, cortisone, dexamethasone, betamethasone. Used for genuine seasonal AD that requires 3-4 months short treatment. short courses can be used to treat flares. Topical treatments avoid the need for systemic therapy and can be used where inflammation is localised to hairless skin or the ears and eyes. systemic therapy iis necessary with more severe or widespread lesions. there are various ways to reduce the dose. only suitable for alternate day dosing is prediisolone. Long acting preparations should not be used unless absolutely necessary as the drug cannot be withdrawn.
78
describe the use of antihistamines in atopic dermatitis management?
Have synergistic activity with EFAs and flucocortioids. adverse effects of first generation drugs are uncommon. adverse effects to second generations include git upsets. medium efficacy for first generation antihistamines and second generation non sedating drug oxatomide.
79
What is oclacitinib?
Targeted JAK1 inhibitor that inhibits expression of IL-31 controlling pruritis in dogs with allergic dermatiits. Used in apoquel. oclacitinib appears to be highly effective with rapid onset of action.
80
What does the international committe for allergic diseases in animals position paper state that the aproach to AD should be?
acute flares treated with non irritating baths and topical glucocorticoids. attempts to identify and remove cause of flare. oral glucocorticoids and antimicrobial therapy must be added. in dogs with chronic AD combination of interventions should be considered. Avoid flare triggers -food, flea, environmental allergens and staph and malassezia. Skin and coat hygiene improved by bathing and dietary supplementation with essential fAs. Severity of pruritis reduced with combination of anti inflammatory drugs. DASIT should be offered whenever feasible.
81
What is the structure of the external ear?
The earflap or the pinnae and the ear canal which form an L shaped tube. They consist of cartilage lined by skin, which is sparsely haired but contains lots of wax or ceruminous glands. the earflap can be pendulous, semi erect or erect. The ear canal ends at the eardrum or tympanic membrane separating it from the middle ear.
82
Describe the structure of the middle ear
An air filled bony cavity that consists of the ventral tympanic bulla, which communicates with the pharynx via the auditory or Eustachian tube, the middle ear cavity that borders the cochlea and the dorsal epitympanic recess housing the auditory ossicles. The sympathetic trunk runs through and the facial nerve runs just ventral to the tympanic bulla. the tympanic bulla is continuous with the rest of the middle ear in dogs but is separated by a bony shelf from the middle ear and epitympanic recess in cats. The middle ear is lined by a mucus secreting periosteum and drains through the auditory tube into the pharynx.
83
Describe the inner ear
lies in the petrous temporal bone. the spiral cochlea communicates with the middle ear through the round window and mediates hearing. the semi circular canals communicate with the middle ear through the oval window and mediates balance.
84
How should ear cleaning be done when approaching otitis?
healthy ears shouldnt need cleaning as cerumen and debris are naturally removed. however cleaning is important in treating and controlling ear infections and in excessively hairy waxy or narrow ears. use appropriate ear cleaner e.g dry wax - ceruminolytic agnts, moist ears - surfactant and drying agents. Infected - antimicrobial agents. Clipping hair from around the ear can help ventilation and cleaning but routinely don't pluck hairs. If necessary sedate or anaesthetise dogs to thoroughly remove all the hair from ear canals and then use a short course of topical or systemic steroids to reduce inflammation.
85
What are the causes of ear infections?
Most dogs have occasional ear infections that respond to eardrops. Recurrent ear infections suggest there is an underlying skin disease, which will need diagnosis and treatment. Causes of otitis can be broken down into three groups. Primary causes - the trigger factor. Predisposing causes - make otitis more likely to develop or be more svere in an individual. Perpetuating causes - prevent resolution and or trigger recurrence. Secondary infections.
86
What are primary causes of otitis?
Foreign bodies e.g grass seeds - in the summer and autumn. Ear mites - otodectes cyanotis are commonest cause of otitis in cats and common in young dogs. Dry dark brown waxy discharge. Juvenile cellulitis causes severe otitis externa in young dogs. Atopic dermatitis and/or adverse food reactions - most common cause of recurrent infections. Other skin diseases - including hormonal problems, keratinisation disorders and immune mediated diseases. Allergic contact dermatitis - to ear cleaners and ear drops can cause on going inflammation. Ceruminous gland tumours are common in older cats and dogs - often obstruct ear canal and cause otitis before tumour is visble. Most are benign and are surgically excised. Inflammatory polyps - can arise in middle ear or nasopharynx. Primary secretory otitis media - common in cavalier KCS - tympanic bulla fails to drain properly resulting in a build up of mucous.
87
What are predisposing factors in otitis?
Conformation - pendulous narrow or hairy ears. Environment - warm, humid climates. Iatrogenic - over cleaning, wetting and maceration, traumatic cleaning especially with cotton buds, plucking. Swimming - wetting and maceration of the ear canals may be a primary cause in some dogs, especially in dirty stagnant water which is often contaminated by pseudomonas.
88
What are perpetuating factors of otitis?
chronic pathological changes include hyperplasia and fibrosis, leading to thickened and narrowed ear canals and ceruminous gland hyperplasia and excess secretion. This both encourages infection and impedes treatment, leading to a vicious circle of repeated infections and inflammation. Otitis media can cause depression, pain, head tilt and difficulty in eating, but most cases are clinically indistinguishable from otitis externa alone. most cases of otitis media in dogs arise from chronic otitis externa and rupture of the tympanic membrane. the tympanic membrane can heal and trap infection and inflammation of the middle ear.
89
Describe secondary infections of the ear
Primary ear infections are rare but secondary infections are veery common. the most common organisms in erythroceruminous otitis are staphylococci and malassezia, whereas suppurative otitis is usually associated with pseudomonas.
90
Describe the approach to diagnosis of chronic or recurrent otitis?
Thoroughly clean and inspect the ear canals, check integrity of tympanic membrane, look for ceruuminous hyperplaasia, chronic pathological changes, stenosis of ear canal and changes to tympanic membrane. Deep ear cleaning and flushing will require anaesthesia. Myringotomy - deliberate rupture of tympanic memmbrane may be required to inspect ad sampple the tympanic bulla. Ct scans are very sensitive and specific for identifying middle ear disease and chronic inflammatory changes. LEft and right lateral oblique, DV skull and open mouth rostro caudal radiographs.
91
Describe how ear flushing and cleaning should be performed?
remove all the debris from the ear canals and middle ear cavity. allows proper inspection and removes focus for irritation and infection. Gentle cleaning can be performed conscious or under light sedation. apply a ceruminolytic to break up wax then use cleansing and drying agents to remove debris. bulb syringes are very effective but must be used with care not to seal the ear canal and rupture the tympanic membrane. /More thorough cleaning requires general anaesthesia. saline should be used to flush debris out of ear canals and tympanic bulla. antimicrobial compounds can retard microbial proliferation in ear cleaners eg cleaners with isopropyl alcohol, chlorhexiine and a low ph seem to be most effective.
92
Which antimicrobial treatments should be used in otitis?
systemic antibiotic therapy may be less effective in erythematocerminous otitis externa as micro organisms are present only in the external ear canal and cerumen. there is no inflammatory discharge and antimicrobial penetration can be poor. systemic treatment may be more useful in suppurative otitis externa and otitis media where there is an active inflammatory discharge with concurrent infections in the deep ear canal tissues (pyoderma of ear canal lining) and middle ear. Topical therapy can achieve local concentrations much higher than systemic. Topican antimicrobial treatment may therefore be effective against apparently intermediate or resistant organisms. another potential advantage of topical therapy is that total body exposure may be lower than with systemic.
93
Which topical antibiotic treatments may be used in otitis?
Topical products containing polymixin B, fusidic acid, gentamicin, enrofloxacin and marbofloxacin are suitable for most bacterial infections. Polymixin B and miconazole have synergistic activity against pseudomonas and framycetin and fucidic acid show synergistic activity against staphylococci and streptococci. Fluoroquinolones, gentamicin and polymixin B are usually effective against pseudomonas.use of fluoroquinolones - associated with selection for drug resistant bacteria. Removal of debris and purulent material greatly improves efficacy of topical antibiotics especially aminoglycosides and polymixin B.
94
Describe the use of systemic antimicrobial agents
Systemic treatment is indicated when the ear canal cannot be treated topically e.g with stenosis or compliance probblems. in some cases of otitis media. cefadroxil, cefalexin and clavulanate potentiated amoxicillin are good first line drugs for staphylococcal infections. Clindamycin and lincomycin are also good first line antibiotics although resistance may limit their efficacy.
95
Describe pseudomonas otitis
Pseudomonas are resistant to may antibiotics. They readily develop further resistance if treatment is ineffective. multi drug resistance is therefore common. Once fluoquinolone resistance is established other anti pseudomonas antibiotics are indicated. Marbofloxacin, enrofloxacin, ticarcillin, gentamicin, others include carbenicillin, pieracilin, ceftazidime.
96
What can be used as anti malassezia treatment?
topical preparations containing clotrimazole, miconazole or nystatin are appropriate. Clotrimazole and miconazole appear to be very safe and non ototoxic when used in the middle ear. Itraconazole once daily can be used if topical treatment isnt effective. long term pulse therapy can also be used to control recurrent malassezia otitis.
97
What is the treatment of otitis media?
may need up to 4-8 weeks systemic antibiotcs. pseudomonas infections usually clear quickly once efefctive cleaning, antimicrobial treatment and control of the primary cause are estbalished. antibiotics can be directly instilled into the middle ear every 3-10 days.
98
Describe the potential toxicities of some antimicrobials?
Ticarcillin, polymyxin B, neomycin, tobramycin, amikacin - potentially ototoxic and should be used with care if the tympanic membrane is ruptured. enrofloxacin, marbofloxacin soluble gentamicin, cefazidime and silver sulfadizzine appear to be safe in the middle ear. systemic aminoglycosides can be nephrotoxic and renal function should be monitored. fluoroquinolones can cause cartilage damage in dogs <12 months, neurlogical signs and blindness in cats.
99
How can you treat chronic pathological changes seen with otitis?
Glucocorticoids will help reverse pathological changes but are not alangesic. Mild acute inflammation might only require topical treatment. PRogressively more severe and chronic changes will need 1-2mg/kg pred for 1-3 weeks. chronic fibrosis can be treated with intralesional triamcinolone. Ciclosporin can also be effective in some severely inflamed ears.Severe cases can be painful and appropriate analgesia may be required.
100
What is lateral wall resection/vertical canal ablation
outer wall or complete vertical portion of the ear canal is removed to improve access to the horizontal portion of the ear canal. appropriate where ear disease is limited to the vertical canal.
101
What is total ear canal ablation and lateral bulla osteotomy?
Where the whole of the ear canal and middle ear cavity is removed. more radical but necessary in most cases of long standingg ear disease affecting the whole ear canal and middle ear.
102
How can cytology be used in the diagnosis of bacterial skin infections
Techniques include adhesive tape strips, indirect and direct impression smears, fine needle aspirates, modified wright giemsa stains such as diff quik are quick and easy to use and reliably identify inflammatory cells and micro organisms. Neutrophils predominate in most cases. macrophages and multiucleate giant cells are often seen in chronic and deep pyoderma. large numbers of these cells could be consistent with mycobacterial or fungal infections. low to moderate numbers of lymphocytes, plasma cells and eosinophils are seen in most inflammatory reactions. All bacteria that take up modified wright giemsa stains stain blue purple whether they are gram positive or gram negative. full identification requires further tests and cultures. bacterial overgrowth syndrome is characterised by large numbers of bacteria with few inflammatory cells. Bacteria are readily seen with surface and superficial infections, but may be more difficult to detect in deep pyodermas. Mycobacteria do not take up wright giemsa stains.
103
When is empirical antibacterial treatment appropriatE?
Where there is a non life threatning infeection, a first episode of infection, surface or superficial pyodermas, cytology is consistent with staphylococci and antibiotic resistance is unlikely.
104
When is culture and sensitivity necessary?
Life threatening infection, a deep pyoderma, inconsistent clinical signs and cytology, rod shaped b acteria, if empirical treatment fils, if resistance more likely (e.g after multiple antibiotic courses, non healing wounds, post operative and other nosocomial infections)
105
What are kirby bauer discs?
Diffusion tests use antibiotic impregnated paper discs. the zone of inhibition around the disc determines whether the bacteria are susceptible or resistant to the antibitiioc. Samples with intermediate sensitivity are best regarded as resistant. these tests may be misleading for example cefoxitin and amoxicillin nclavulanate susceptibility or resistance iis poorly predictive of MecA positive staphylococci.
106
What is the MIC?
The minimum inhibitory concentration - the lowest concentration of an antibiotic that completely inhibits growth, can be determined in broth culture or using E strips. if the isolate is susceptible then it is likely that systemic treatment will exceed the MIC in target tissue but antibiotics with susceptibilities close to the break point therapeutic concentrations int he target tissue. using topical therapy which delivers mg/ml antibiotic concentrations can overcome resistance.
107
Which bacteria are most skin infections associated with?
Coagulase positive staphylococci, staphylococcus pseudintermedius the most common in dogs. Antibiotic resistant isolates have become more prevalent but susceptibility patterns vary between countries.
108
Describe the use of first line, second line and third line antibiotics
First line antibiotics are no less potent than higher tier drugs in the correct circumstances and are appropriate for empirical treatment. second line antibiotics should only be used when there is culture evidence that first line drugs will not be effective. Third line antibiotics must only be used when there is culture evidence of sensitivity, no first or second line antibiotics are effective and topical antimicrobial therapy is not feasible or effective. Veterinarians should never use drugs deemed citically important to human health e.g vancomycin, teicoplanin, linezolid etc. First line 1. cefadroxil, cefalexin, clavulanate amoxicililn, clindamycin, lincomycin. 2. cefovecin.
Second line - difloxacin, enrofloxacin, marbofloxacin, orbifloxacin,
Third line - aminoglycosides, azithromycin, chloramphenicol, clarithromycin, imipnem, piperacillin, rifampicin, ticarcillin.
109
How do pharmacokinetics relate to efficacy?
The efficacy of concentration dependent drugs with post antibitioc effects depends on the peak concentration in the target tissue exceeding the MIc. the larger the peak concentration/ic ratio the better the efficacy- this ratio is therefore an important predictor of efficacy. these drugs should be administered at the full dose every 24 hours. the efficacy of time dependent antibiotics without post antibiotic effects depends on maximising the duration of exposure i.e the concentration should exceed the MIC for at least 70% of the dosing interval. Type 3 antibiotics eg tetracyclines have mixed properties showing time dependent killing with moderate post antibiotic effects. the ideal dosing regimen for these maximises the amount of drug received. depending on the organism, tissue and dose, administration every 12 or 24 hours can be appropriate.
110
Describe the dose and duration of antibiotics when treating bacterial skin infections?
Antibiotics should be used at the upper end of their dose range in pyoderma. animals should be weighed to allow accurate dosing. superficial pyodermas typically need 2-3 weeks of treatment. Deep pyodermas can be greatly improved after two weeks but full resolution often takes 4-6 weeks or longed.
111
Which hygiene routines should be implemented in bacterial skin infections?
Alcoholb ased hand disinfection highly effective but hand washing with warm water and detergent neccessary if hands are soiled. Frequently touched surfaces should be cleaned and disinfected regularly. Extra measures should be undertaken with patients with antibiotic resistant infections. Contact with staff and other animals should be minimised and rooms and equipment thoroughly cleaned and disinfected before the next patient. The risks to human health from colonised animals should be assessed and owners given appropriate advice on hygiene.
112
What is orthokeratotic hyperkeratosis?
An increase in normal keratinocytes, common i inflammatory diseases and keratinisation disorders.
113
What is parakeratotic hyperkeratosis (parakeratosis)?
Thickened stratum corneum with nucleated keratinocytes; malassezia dermatitis, zinc responsive dermatisosi, superficial necrolytic dermatitis.
114
What are the primary scaling diseases?
Nasodigital hyperkeratosis, idiopathic keratinisation disorders, sebaceous adenitis, schnauzer comedo syndrome, ear margin dermatosis, itchyosis, lethal acrodermatitis.
115
What is superficial necrolytic dermatitis?
A rare skin disease associated with end stage liver disease and pancreatic atrophy or glucagonomas. Some cases also present with diabetes mellitus. clinical sgns include erythematous plaques and erosions overlain by thick yellowish adherent scales. lesions usually occur at the mucocutaneous junctions, pressure points, ventrum, genitalia and feed with severe hyperkeratosis and fissuring of the footpads. Treatment often unrewarding. hepatic support diets with zinc, essential fatty acids and high quality protein supplements and amino acid solutions can help.
116
What is zinc responsive dermatosis?
Diets low in zinc - rare unless home cooked, where it can be seen with diets high in soya and cereals (bind zinc) and supplemented with calcium or iron. (competes for uptake). Zinc malabsorption - mot common in arctic breeds - probably hereditary. clinical signs include bilaterally symmetrical scaling and alopecia of the face, pinnae, elbows, hocks, paws, genitalia and fissuring of footpads. Change diet and supplement with zinc sulphate or zinc methionine.
117
What is pemphigus foliaceus?
Caused by auto antibody destruction of cell membrane adhesion molecules, resulting in loss of cohesion of superficial epidermal cells. Triggers include bacterial and viral infections, chronic inflammatory dermatitis, drugs and neoplasia, but most are idiopathic. Akitas are predisposed. The primary clinical lesions are pustules which quickly rupture leaving epidermal collareettes, scaling and erosions. can be generalised or limited to the dorsal nose face pinnae nipples feet footpads and in cats the claw sheat. Mucocutaneous lesions are rare. Cytology of pustules or crusts reveals neutrophils, acanthocytes andno bacteria. culture should be sterile. a definitive diagnosis requires biopsy and histopathology.
118
What is naso digital hyperkeratosis?
this causes hyperkeratosis, fissuring and secondary infection of the nose and footpads, which may be painful. its commonly seen in dogues de bordeaux, cocker and english springer spaniel dogs, but may be an ageing change or a feature of hypothyroidism, pemphigus foliaceus, lupus erthematous, SND, zinc responsive dermatosis and distemper. ear margins dermatosis is a similar but rare condition with frond like tightly adherent scales on the ear margins. it may cause fissuring and leave erosions. treatment options include warm water soaks and vaseline or topical salicylic acid propylene glycol, 0.5% tretinoin and lactic acid.
119
What is a callus?
these form on bony prominences in large dogs that lie on hard surfaces. they are a protection mechanism so take care in treatment and do not try to surgically remove they may get fissured and infected so control infection provide padding and treat as for naso digital hyperkratosis.
120
What are idiopathic keratinisation disorders?
Hereditary defects of keratinisation with decreased epidermal transit time and increased turnover. common in cocker and english springer spaniels, irish setters, dobermans and ocasionally in other breeds. also seen in persian cats. secondary pyoderma and malassezia are common. the clinical signs include generalised scaling, erythema and seborrhea of the lips, periocular skin, ventral neck, ventral body, tail, feet and ears. Milder dry scaling of the trunk is seen in other dogs. treat secondary infections and give topical keratolytic and keratoplastic followed by moisturising shampoos or rinses. Give essential fatty acids, retinoids, vitamin A.
121
What is itchyosis?
A rare group of hereditary and congenital diseases with severe accumulation of tightly adherent scales and alopecia. secondary malassezia infections are common. golden retrievers commonly have a milder form with the large dry scales and hyperpigmentation of the skin. genetic test for the disease. treatment is for other scaling disorders but prognosis very poor.
122
What is lethal acrodermatitis?
A rare hereditary condition of english bull terriers causing stunted growht with scaling, crusting erosions of extremities and pressure points, fissured footpads, onychodystrophy and concave hard palate. pyoderma, malssezia, pneumonia and diarrhoea common. the diagnosis is based on history, clinical signs and biopsy. Manage secondary infections, zinc and EFA supplements and topical therapy.
123
Which diagnostic tests are used in skin disease?
Rule out parasites - coat brushing, skin scrapes, tape strips, sarcoptes serology, trial therapy. Malassezia and pyoderma - tape strips, impression smears, response to treatment. Dermatophytosis - woods lamp, trichogram, fungal culture. If still pruritic - pursue pruritic skin diseases. If not pruritic - screening tests for haematology, biochemistry, urinalysis, total or free T4, TLI, folate, B12. Endocrine tests, absorption tests/endoscopy, biopsy and histopathology - ensure any secondary infection is treated first.
124
What is the difference between erosions and ulcers?
Erosions - loss of epidermis leaving basement membrane, heal by re epithelisation. Ulcers - loss of epidermis and basement membrane to expose dermis; heals with scarring.
125
What is an immune mediated drug eruption?
Result from immune mechanisms or non immune pharmacological damage. a very wide range of drugs have been implicated including vaccines with a particular association with sulphonamide use in dobermans. the clinical signs are very variable and can include urticaria and anaphylactic shock, widespread pruritis erythema, exfoliation, erosions, crusting.
126
What is cutaneous lupus erythematosus?
CLE is one of the most common immune mediated diseases. It most commonly affects the nasal planum causing loss of the cobblestone appearance, swelling, depigmentation, erosions, ulcers and crusting. Lesions may also be found on the scrotum and involve the claws. More generalised lesions and muco cutaneous involvement is rare. Ulcerative CLE is a specific form seen in sheptland sheepdogs and rough collies with severe ulceration of the ventral body. Exfoliative CLE is a form seen in german short hairedpointers with generalised scaling and erosions.
127
What are nasal depigmenting diseases?
Seasonal nasal depigmentation - collie nose, snow nose, relatively common benign disease with depigmentation of the nasal planum but preserving the cobblestone appearance with no erosions or crusting. May seasonally wax and wane. Uveodermatological syndrome - rare immune mediated disease with prominent panuveitis also causes nasal and neurological signs. Akitas are predisoposed.
128
What is vasculitis?
An uncommon clinical syndrome that can be spontaeous drug induced or associated with other immune mediated diseases and infections. The clinical signs include; extremities - most commonly affected, well dermarcated or wedge shaped ulceration, crusting and necrosis, punched out ulcers. Claws - onychodystrophy, fracture and claw loss, panniculitis, vasculopathies - etechiae, ecchymoses, purpura. Cold agglutinin disease - necrosis of exttremities, associated with RBC agglutinating antibodies that react below normal body temperature.
129
What is systemic lupus erythematosus and what affects does it have on the skin?
SLE is a rare immune mediated disease with a wide variety of clinical signs. many cases are idiopathic but SLE can be associated with drug reactions, infections and neoplasia. Cutaneous lesions - erosions, ulcers, scaling and crusting, depigmentation, alopecia, vasculitis or panniculitis. Lesions are usually symmetrical and can affect the extremities or be generalised. systemic - anaemia, thrombocytopenia, polyarthritis, protein losing nephropathy.
130
What is pemphigus vulgaris and sub epidermal blistering diseases?
These comprise a range of similar and rare diseases. the initial lesion is a bulla that rapidly ruptures leaving an ulcer. PV disrupts junction between the basal cells and the basement membrane whereas other conditions affect the basement membrane itself. Great Danes are predisposed. The clinical signs include ulceration and crusting of mucocutaneous junctions, nasal planum, ventral body, footpads and sloughing of claws. the lesions are painful and affected animals are often depressed. The diagnosis is based on history and clinical signs with biopsy of an intact vesicle.
131
What is erythema multiforme and toxic epidermal necrolysis (TEN)?
A spectrum of uncommon diseases divided into EM minor, EM major, Stevens-Johnson syndrome, SJS TEN overlap syndrome and TEN. EM is more likely to be idiopathic, whereas SJS and TEN are more likely to be associated with adverse drug reactions. EM - necrosis of individual cells - causes erythema, exfoliation, circular, acring or target like plaques, erosions and crusts. SJS/TEN - widespread full thickness necrosis of epidermis and ulceration.
132
What is Ehlers Danlos Syndrome?
A rare group of diseases seen in dogs, cats, rabbits horses and farm animals caused by defect in dermal collagens and basement membrane proteins. there is abnormal elasticity of skin, which may be fragile and tear easily. There may also be joint abnormalities and oesteoarthritis. there are a number of variants depending on exact abnormalitiy and spectrum of clinical signs.
133
How can Immune mediated skin diseases be diagnosed?
Cytology is usually non specific but can identify candida, staphylococci and other bacteria and acanthocytes, /hair plucks and scrapes are necessary if demodex is suspected. histopathology is required to confirm the diagnosis in most cases. Try to biopsy early, non ulcerated and infected lesions. wait for lesion to develop or take several biopsies from a range of lesions. Blood tests and other tests may be indicated - haematology and biochemistry - systemic illness and a baseline for monitoring treatment, coombs test - anaemia, cold agglutinin titres lesions on extremities, urinalysis - protein losing nephropathy, ANA titres - can be difficult to interpret as positive results are also seen with a variety of other inflammatory diseases.
134
How can immune mediated skin diseases be treated?
Glucocorticoids - prednisolone, deexamethasone, triamcinolone, topical glucocorticoids. Tetracycline and niacinamide. Pentoxifylline - promotes peripheral blood flow and oxygenation and is imunomodulating useful in vasulitis.
Azathiporine and chlorambucil - do not use in cats. Ciclosporin and tacrolimus - ciclosporin good in cell mediated auto immune diseases and less so in neutrophil antibody mediated diseases.
Maintenance taper to lowest and most infrequent dose possible. broad spectrum bactericidal antibiotics to treat secondary infections. UV light may exacerbate DLE, SLE and dermatomyositis. Monitor clinical response and adverse effects and adjust if necessary.
135
What are tick bite reactions?
nodular granulomatous inflammatory reactions can develop to tick bites. Ticks transmit babesia, erhlichia, Borrelia and Bartonella and regular treatment with monthly Fipronil spray or permethrin products is advised in tick areas.
136
What are abscesses?
Pus filled cavities caused by penetrating injuries, bites and foreign bodies. They may be associated with cellulitis (diffuse infection and inflammation dissecting along tissue planes). Commonly implicated organisms include staphylococcus pseudintermedius and in cats, pasteurella multocida, streptococci and anaerobes. Treatment involves lancing to establish drainage and flushing to remove pus, debris and any foreign bodies.
137
What is a deep pyoderma?
Deep pyoderma is associated with rupture of hair follicles and extension of bacterial infection into the dermis. It can be secondary to demodex, dermatophytosis, immunosuppressive conditions or idiopathic. The clinical signs are more severe than for surface or superficial infections and inlcude haemorrhagic bulla, nodules with purulent discharge, swelling, ulcers, draining tracts and scarring. These can be localised to the feet causing severe paronychia and interdigital furunculosis or the muzzle. The diagnosis is based on the clinical signs, cytology and bacterial culture. These cases need at least 4-6 weeks of antibiotics.
138
What are filamentous bacteria?
Infections with atiinomyces and nocardia are rare and usually inoculated by penetrating injury or foreign body. The clinical signs include abscesses, ulceration and draining sinus tracts, panniculitis, nodules which may ulcerate and drain red brown to yellow grey fluid with tissue grains and systemic illness. The diagnosis is based on the clinical signs cytology and histopathology. Lesions should be drained and foreign bodies removed if possible. Appropriate antibiotics should be given for at least one month beyond clinical cure.
139
What are mycobacterial infections?
Rare, mostly seen in cats and potentially zoonotic. there are four basic types: true tuberculosis - M tuberculosis or M bovis; granulomatous diseases, lymphadenopathy, discharging sinuses and systemic involvement. Feline leprosy - M lepraemurium from rodents causes multiifocal crusting papules. Atypical mycobacteria - M microti from voles - granulomas, non healing wounds, panniculitis, lymphadenopathy. Opportunistic mycobacteria - soil organisms implanted with penetrating wounds, non healing wounds and ulcers, granulomas, panniculitis, discharging sinuses.
140
Describe fungal infections that can cause Skin diseases.
Rare in the Uk more Common in warm humid climates. Soil organisms can be inoculated by penetrating wounds and foreign bodeies, especially in immune suppressed animals. subcutaneous M canis infections can be seen in persian cats and occasionally other breeds. Cryptococcus, blastomyces, histoplasma, sporothrix, la gendium and pythium seen in the US and elsewhere. Usually see nodules, draining sinus tracts and discharge with tissue grains. May also see systemic signs from disseminated disease. Diagnosis is based on cytology, histopathology and culture. treatment is based on radical surgical excision and systemic antifungal therapy using itraconazole, terbinafine or other drugs.
141
What is juvenile cellulitis?
common in young puppies - also known as big head disease or lymphadenitis. the cause is unknown and there is no firm link to vaccination. there is acute onset facial swelling, serous to mucopurulent discharge, otitis externa, enlarged lymph nodes and pyrexia. Bacterial infection is uncommon and secondary despite the name. histopathology consistent with sterile pyogranulomatous inflammation and lymphadenitis. Treatment based on prednisolone. Pain relief necessary.
142
What is sterile panniculitis?
Inflammation of the subcutaneous fat, resulting in nodules with a haemorrhagic and fatty discharge, ulceration and non healing wounds. Most cases are idiopathic, but potential triggers are subcutaneous infection - bacteria, mycobacteria, fungi Immune mediated diseases - vasculitis, sle. Miscellaneous - pancreatitis, poor quality diet, excess of fish.
143
What is sterile pyogranuloma/cutaneous histiocytosis?
Cases develop focal to multifocal nodules that may be erythematous and alopecic. May be swelling of nasal planum. Diagnosis is based on cytology and biopsy with special stains and cultures to rule out infectious organisms. Treatment is for immune mediated diseases, with ciclosporin effective and well tolerated. Systemic histiocytosis is also a sterile reactive proliferation of histiocytes. There is involvement of the mucocutaneous junctions, mucosa, sclera and internal organs. this tends to be slowly progressive with a much poorer prognosis.
144
How should Approach to diagnosis be made?
Most important to differentiate whether the lesion is caused by infection, sterile immune mediated disease or neoplasia. Cytology - fine needle aspirates or impression smears can be used to identify the type of inflammatory cells, potentially neoplastic cells and organisms. Tissue grains can be crushed to look for inflamatory cells and organisms. Biopsy early lesion, avoid old ucers and secondary infection. Histopathology lab should do special stains for filamentous bacteria. Culture - best to send discharge with tissue grains and fresh biopsy material. Serology - possible to do serology for aspergillus and cryptococcus. PCR for some mycobacteria, leishmania, borrelia, bartonella.
145
Describe the nail diseases which may occur in isolation or as part of a more generalised skin condition?
Onychodystrophy - abnormal nail growth
Onychomadesis - sloughing of nails
Onychorrhexis - splitting of claws
Paronhycia - inflammation of claw folds and nail bed
146
Describe the normal structure of the nail?
Nail - a specialised thick, very strong and rigid keratinised structure tightly adherent to underlying PII. Produced by corium (dermis) of proximal PII - nail bed. Grows out and adapts to shape of PII. Constant growth - need clipping of not worn down naturally. Claw fold - normal skin that overlies proximal claw but not involved in claw growth. Pads - thick hairless stratum corneum and dermis overlying fibrous cushion.
147
What are the common causes of nail and claw fold problems.
Dogs on poor diets or with serious metabolic or hormonal illnesses can develop dry brittle and deformed nails. Scars and poor foot conformation can cause deformed nails Which can grow into the pads. overweight dogs can have nail and pad problems due to excessive weight bearing, weight bearing on haired skin, in growing hairs, infection, scarring and altered conformation. Caustic or irritant substances can cause nail bed inflammation and infection. Demodex, dermatophytosis and hookworms can cause paronychia but bacteria and malssezia are usually secondary invaders. Immune mediated diseases can cause discolouration, softening fracture and sloughing of nails.
148
What is lupoid onychitis?
Symmetrical lupoid onchyodystrophy is an immune mediated disease specific to the nail bed that only affects the nails.
149
What is idiopathic onychodystrophy?
The development of soft and brittle nails or nail loss in the absence of other problems. The cause is not known.
150
How can diagnosis of nail problems be made?
Cytology samples can be expressed from around the nail and broken nails and sent for bacterial and fungal culture. biopsies of the claw fold just reveal non specific secondary inflammation. Biopsies of the claw fold just reveal non specific secondary inflammation. Accurate diagnosis requires a pIII amputation - ideally a dewclaw, but amputation of weight bearing digits causes few long term problems.
151
How can nail diseases be treated?
All losses and disease nails should be gently removed and the nail beds kept clean. Secondary infection should be treated appropriately. Keeping the nails short can help avoid further trauma and fracture. nail clippers may split the nails so using electric sanding discs ca be better. the most appropriate treatment depends on the final diagnosis. bear in mind that nail growth is slow so resolution on any treatment takes several weeks. Treatments useful in idiopathic nail disease include high quality diets, mineral and vitamin supplements, biotin, nicotinamide and tetracycline and essential fatty acids. more severe cases may require topical glucocorticods, systemic glucocorticoids, systemic ciclosporin or other immunosuppressive agents. P3 amputation of all digits has also been successful in intractable nail disease.
152
What post inflammatory changes in pigmentation may be seen?
Hyperpigmentation - infections, parasites, pruritis, diffuse to complete hyperpigmentation, usually with lichenification, scaling etc.
Hypopigmentation - scars, immune mediated disease, burns, trauma, Vulnerable to UV damage.
153
What is lentigo?
A normal ageing change especially in ginger cats. develop black foci on mucous membranes and mucocutaenous junctions. benign lesions.
154
What is acanthosis nigricans?
seen in dachshunds and other breeds that develop raised hyperpigmented plaques especially in the axillae and ventral abdomen. May be associated with malassezia and endocrinopathies.
155
What are naevi?
Benign skin masses caused by local deveopmental defect
156
What is albinism?
Hereditary lack of pigment with white skin hair and red eyes. rare in dogs and cats. common in rabbits and rodents. very vulnerable to uv damage.
157
what is vitiligo?
A rare immune mediated disease that destroys melanocytes causing multifocal depigmentation. may wax and wane or spontaneously regress.
158
What is idiopathic leucotrichia?
Loss of pigment in groups or individual hairs. May wax and wane. regional leucotrichia is a common ageing change (eg muzzle).
159
How do you differentiate haemorrhage from erythema?
erythema - diffuse usually symmetrical, blanches with pressure.
Haemorrhage - petechiae, ecchymosses, usually non symmetrical, does not blanch.
160
What are the clinical signs of anal sac disease?
Distended inflamed and painful anal sacs, anal sac abscesses, chewing or dragging the rear end along the ground, difficulty in passing stools, pyotraumatic dermatitis around the base of the tail.
161
What is the treatment for anal sac disease?
Manually emptying the sacs. uncomplicated anal sac impaction does not require antibiotics. severely impacted sacs or abscesses need flushing and antibiotics. Long term management - weight loss, change of diets, adding fibre, surgical removal (risks incontinence).
162
What are the most common skin tumours in dogs?
Mast cell tumours, perianal adenomas, lipomas, sebaceous adneoma/hyperplasia, histioccytoma, squamous cell carcinoma, melanoma, fibrosarcoma, basal cell tumour, heamngiopericytoma.
163
What are the top 5 skin tumours in cats?
Basal cell tumours, mast cell tumours, fibrosarcoma, squamous cell carcinoma, sebaceous adenoma.
164
What are the common clinical findings with cutaneous neoplasms?
Owners usually discover growth, benign tumours usually present for a long period of time, usually painless, slow growing and moveable. malignant tumours may have history of rapid growth and may be fixed to underlying structures. both malignant and benign tumours may b e ulcerated. appearance of growth varies depending on type of tumour and location.
165
What are the general treatment options for skin tumours?
complete surgical excision, cytoreductive surgery for palliation of large tumours, amputation for large tumours on extremities, radiation therapy for incompletely excised tumours, other treatment modalities may include photodynamic therapy, cryosurgery, laser ablation and hyperthermia.
166
What is a papilloma?
Common in the dog, rare in cats, associated with DNA papilomavirus, more common in young dogs where a spontaneous resolution is common, occurring over about 3 months. If treatment is necessary, surgery or cryotherapy can be used.
167
What is a squamous cell carcinoma?
Accounts for 15% of feline and 5% of canine cutaneous tumours. often associated with poorly pigmented skin and UV exosure. in dogs - most common area for SCC development is in the nail bed. it can also be found on the nasal planum. in cats most common areas are the nasal planum, eyelids and pinnae. May be productive or erosive. Multifocal distribution of superficial lesions has been reported in cats.
168
What is a basal cell tumour?
Considered benign tumours. common in the cat, rarer in the dog, surgery is treatment of choice, which is often curative. rare cases of metastases have been reported.
169
What is a sebaceous gland tuour?
Include sebaceous hyperplasia, sebaceous epithelioma, sebaceous adenoma, sebaceous adenocarcinoma. surgery is the treatment of choice.
170
What is a sweat gland tumour?
Apocrine gland adenoma or adenocarcinoma. Malignant tumours tend to be invasive but with low metastatic potential. Wide surgical excision is the treatment of choice.
171
What is a keratocanthoma?
An intracutaneous cornifying epithelioma. Considered a benign lesion, can b e solitary or multile. Solitary lesions are treated with surgery. multiple lesions have been treated with cryosurgery but would recommend referral to a specialist oncologist.
172
What are tumours of the hair follicles?
Include trichoblastomas, trichoepithelioomas and pilomatrixomas. Generally considered benign, good prognosis following surgical excision.
173
Describe mesenchymal tumours of the skin - soft tissue sarcomas?
mesencgymal origin that develop in the subcut tissue. irrespective of tissue type. vary in degree of malignancy. more common in dog. most common in dog are peripheral nerve sheath tumours and hemangiopericytoma. in cat fibrosarcoma most common. Usually develop in older animals. Distribution is wide sread. They have an infiltrative pattern of growht. may appear to be encapsulated due to the formation of a pseudocapsule composed of compressed cancer cells. the tumour invariably extends beyond this structure. regional lymph node is uncommon. histopathological grade is predictive of metastasis.
174
What is a haemangiosarcoma?
A tumor of mesenchymal origin that can affect the skin. its biologic behaviour is distinctive from that of the tumours collectively referred to as soft tissue sarcomas. haemangiosarcomas are a particularly malignant tumour that may arise at any site and metastatic rates as high as 90% documented. cutaneous form - haemangiosarcoma tumours that invade into subcutis or deeper are associated with a worse prognosis due to a higher probability of metastasis than tumours confined to dermis.
175
What are injection site sarcomas in cats?
Disease associated with post vaccination inflammation through both rabies and feLV vaccinations. also been seen after methyl prednisolone and certain antibiotics. tumours are typically mesenchymal in origin and fibrosarcoma is the most common. Other histologies include osteosarcoma chondrosarcoma, malignant fibrous histocytoma.
176
What can be done to limit vaccination site sarcomas?
Avoid administering vaccinations in the interscapular space, subcutaneous rather than intramuscular vaccination is preferred as tumor development can be detected more easily. FELV/rabies vaccines on the distal aspect of the right (rabies) and left (felv) pelvic limbs. other vaccines should be administered in the right distal shoulder. Administration of any vaccine should proceed only after consideration of risk.
177
What can be done once an injection site sarcoma is found?
Pre surgical tissue biopsy. Cytology unreliable. complete staging: blood count & chemistry, urinalysis, thoracic radiopgrahy, MRI. Treatment aimed at achieving local tumour control. Invasive nature - single surgical excision rarely curative. Local recurrence common. Amputate on limbs. Radiotherapy improves outcome over surgery aalone. Pre operative and post operative theray. Surgical excision following radiation.
178
What are melanocytic tumours.
Melanomas arise from melanocytes situated in the basal layer of the epidermis, the epithelium of the gingiva or in the nai bed. Cutaneous and digital melanomas are less common than oral. Cutaeous melnomas arising from haired skin are usually benign. Mitotic rate highly predictive of malignant behaviour. Digital melanomas also have a higher risk of metastasis. malignant melanomas may be pigmented but amelanotic forms are recognised. ulceration and secondary infection are common features. regional lymph node metastasis and widespread distant metastases frequently occur early in the course of disease in association with malignant melanoma.
179
What is the therapy for melanocytic tumours?
For benign cutaneous lesions, surgery is curative. therapy for primary malignant tumours requires radical surgical excision. surgical margins of up to 3cm ar necessary to ensure complete resection. Therapeutic melanoma vaccines have been used with varying degrees of sucess. Altnerative therapies include radiation, photodynamic therapy, local hyperthermia, and intra lesional platinum based cahemotherapeutic agents.
180
What are mast cell tumours?
Most common skin tumour of dogs. Primary MCTS can occur in other tissues: conjunctiva, connective tissue or GI tract. the non cutaneous MCTS are rare with a diferent biological behaviour. Cutaneous MCTS occur in middle aged dogs. No sex predilection. OVer represented breeds include: boxer, staffie, lab, golden retriever, beagle, schauzer, boston terrier, shar pei.
181
Describe the pathology and behaviour of Mast cell tumours?
All MCTS are locally infiltrating to varying degrees. approx 30% are aggerssive, rapidly metastasising to adjacent skin, the drainage lymph node and distant organs. Mast cells have intracytoplasmic granules containing biologically active molecules, important in mast cells noral role of mediating inflammation. These intracytoplasmic granules stain metachromatically. Tumour cells may degranulate releasing these vasoactive amines spontaneously or following trauma. some MCTS present with local oedema, pruritis and haemorrhage. simple palpation of a mct may induce erythema and wheal formation.
182
what is the common clinical presentation of MCTS?
They can mimic any other skin lesion, may develop anywhere on the body, well differeentiated cutaneous MCTS tend to be slow growing hairless solitary lesions and may be present for months. poorly differentiated mcts tend to be rapidly growing ulcerated and pruritic with small satellite lesions close by. a significant minority of MCTS look and feel like lipomas.
183
How can mast cell tumours be distinguished cytologically?
The cells can be distingushed from other round cells by their metachromatically staining granules and the spotty fried egg appearance of the cells usually makes diagnosis easy. poorly differentiated mcts may l ack these granules necessitating more specialised staining.
184
Describe surgery treatment for mast cell tumours
Pre treated with an H1 and H2 blocker. 2times diameter of tumour up to 2cm resection in each direction. include a deep fascial plane in all cases. almost certainly curative for well differentiated MCTS and majority of ntermediates. submit tumour for histopathological grading. For poorly differentiated MCTS surgery may alleviate the signs associated with the primary lesion but these tumours are very infiltrative and are prone to wound break down so should be approached with care.
185
Describe Feline mast cell disease?
Two major anatomical forms; cutaneous and visceral - intestinal only, diffuse splenic with mastocytosis, generalised visceral. Cutaneous feline MCTS relatively common. There are three cutaneous presentations. the more common is the mastocytic - subdivided into compact mastocytic, diffuse mastocytic. The rarer histiocytic form of mct typically seen in cats under 4yo & presents as multiple lesions.
186
What is the most common clinical presentation of cats with mast cell disease?
Cutaneous MCTs of cats reportedly more common on the head and neck. Can be single or multiple, nodular or plaque like (not dissimilar to eosinophilic granuloma complex) but typically appear as round, hairless lesions. The vasoactive granules within the mast cell can cause the lesion to appear erythematous causing paraneoplastic GI signs and cause the lesion to be pruritic, leading to self trauma, ulceration and bleeding.
187
What diagnostic investigations and staging should be done for feline mast cell disease?
Excisional biopsy is preferred to FNA. Feline MCTS frequently have poorly staining intracytoplasmic granules. Mast cells are often seen associated with eosinophils in both eosinophlic granuloma complex or MCCT and therefore a biopsy rather than FNA may be more useful to distinguish the two.
188
What are the treatment options for feline mast cell disease?
Surgery - compact tumours have limited local iinfiltration and a low metastatic rate therefore narrow margin usually sucessful. diffuse tumours have a higher incidence of recurrence and need a wider margin of excision. Cats with mastocytosis and diffuse splenic involvement can achieve duration remission following splenectomy. Anecdotally external beam rt has been used for incompletely resected tumours. strontium 90 plesiotherapy has been used to control cutaneous mast cell tumours. Chemmotherapy for MCT yet unproven but with metastatic or intestinal disease could benefit. prednisolone for unresectible tumours but with little effect.
189
What is a splenic mast cell tumours?
a MCT primary to the spleen in cats is most common in older non purebreed cats. signs include nonspecific ilness or chronic vomiting due to histamine release causing gastroduodenal ulceration. liver lymph nodes and bone marrow commonly affected . staging includes a CBC biochemical profile, urinalysis, feLV, FIV thoracic radiographs, abdominal ultrasonography and bone marrow aspirate. FnA cytology or biopsy of spleen indicated. Splenectomy normaliszes other disease within 5 weeks.
190
What are histiocytic disorders?
histiocytic proliferative disorders represent a range of disorders with different pathologies; iincluding canine cutaneous histiocytoma (benign - fast growing hairless lesions), reactive histiocytosis cutaneous and systemic, histiocytic sarcoma localized and disseminated, haemophagocytic histiocytic sarcoma.
191
What would be your diagnostic approach to a dog presenting with multiple skin masses? what would be the common ddx and include a discussion of the techniques you could use to help you achieve a definitive diagnosis.
FNA - least invasive, gives you many cells from multiple approached, preserves future biopsy site, does not give architecture of cell, cannot give full details of what type of mass it is. Skin punch biopsy - take a piece of skin and dermal tissue not too invasive of a procedure, get architecture of mass and cells. Incisional biopsy - tae out a piece of the mass, architecture and cells, maybe useful for cytoreductive surgery in a neoplastic case, not curative if needed to remove all of lump, could affect a future biopsy site, may grow back. excisional biopsy- can be curative if non metastatic, architecture, cells, full histopathology report.
192
Describe the cytological appearance of the three major groups of skin tumours
epithelial: Scc, papilloma. SCC found on poorly pigmented skin cells and tends to look aplastic, abnormal, high mitotic rate, not well encapsulated, nuclei look abnormal. Mesenchymal - Soft tissue sarcoma - varies, most are slow growing, well encapsulated, well differenttiated, normal mitosis rate and nuclei, metastatic grow fast. Melanomas: coloured/pigmented melanocytes with predictable appearance of metastatic vs benign tumours.
193
Name two diseases that are associated with abnormalities of the pituitary gland in the dog
Pituitary dwarfism and acromegaly. Measure IGF-1 serum concentration and whether it is below or higher than normal. Acromegaly would also have raised liver enzymes ALT and AP and hyperglycaemia. could also look at history and clinical signs to help make a diagnosis as well.
