Scaling disease Flashcards
What is scale? What does it result from?
Presence of flakes of keratinized skin in the hair coat and on the skin
Results from
- Normal skin function ( a little scale (dandruff) is normal in many situations)
* Abnormal desquamation (shedding of corneocytes)
* Abnormal cornification (creation of the outer epidermal layers)
* Inflammation (inflammation influences cell turnover and structures)
* Bacterial and fungal enzymatic action
What primary and secondary diseases cause scale?
Primary
* Primary keratinization disorders
◦ Particularly ichthyosis
◦ Several breeds
* Primary seborrhoea
◦ A poorly defined group of conditions with scale and sometimes greasiness
* Zinc–responsive dermatosis
* Ichthyosis of the golden retriever
* Ear margin seborrhoea
* Nasodigital hyperkeratosis
Secondary
* Callus (compact adherent scale)
* Hypothyroidism
* Allergy
* Parasites
* Bacterial infection
* Dermatophytosis
* Sebaceous adenitis
* Almost any resolving inflammatory dermatosis
* Exfoliative dermatitis in cats (2˚ to thymoma)
* Leishmaniasis
What should be your diagnostic plan when investigating scale?
- Check for parasites
◦ Clinical examination
◦ Coat brushings, hair plucks, skin scrapes
◦ Consider parasite treatment trial - Check for infection
◦ Clinical examination
◦ Skin surface cytology - In older dogs perform general health screening (e.g. urinalysis, haematology & biochemistry)
- Biopsy
- Genetic testing if indicated
◦ Ichthyosis of the Golden retriever, Great Dane and American Bulldog
◦ Pedal hyperkeratosis of the Dogue de Bordeaux
◦ Nasal parakeratosis of Labrador Retrievers (NPLR)
What is zinc responsive dermatosis? What do you see clinically? How is it treated?
- Genetically predisposed breeds eg Husky (type I)
- Genetic poor Zn absorption, often young adult onset in the winter
- Dull coat and specific hard plaques with marked scale and crusting
- seen in areas where there is trauma, eg head (if push through doors), elbows)
- Beware concurrent hypothyroidism (older animals – later onset)
- In nutritional restriction seen in young rapidly growing large breeds (type II)
- Clinically
- Crusted hyperkeratosis (bacterial infection common)
- Bacterial infection
- Variable pruritus
- Histologically
- Parakeratosis is key finding
- Zinc is required for normal keratinisation – disease most common at areas of trauma
- Treatment
- Zinc supplementation, correct diet (consider steroids in type 1 if poor response as will increase zinc uptake)
- Zinc sulphate traditionally used – may cause vomiting
What history and clinical signs are associated with ichthyosis of the golden retriever? How is it managed?
History and clinical signs
* Seen from a few weeks of age, scale is variable over life, but can be severe
* Barrier function is not compromised so 2˚ infection is uncommon, but can get 2˚ otitis
* Symptomatic treatment only
* Recently retinoids used with some success
Genetic disease
* An insertion-deletion mutation in exon 8 of PNPLA1-gene (patatin-like phospholipase domain-containing protein 1) was identified that leads to a premature stop codon
- 2 genetic tests needed
What is canine ear margin seborrhoea? How does it present?
- Relatively uncommon - marked breed predilection in Dachshunds
- Can be a feature of hypothyroidism
- Adherent keratin on both medial and lateral sides of the pinna
- Follicular casts and plugs may trap hair
- Rubbing produces erosions and ulceration
- Pruritus is variable
- Fissuring and secondary infection can be problematic
How is canine ear margin seborrhoea diagnosed? How is it treated?
Diagnosis
* When restricted to the ear margins alone in the Dachshund: diagnosis on clinical signs
* Rule out other causes
* particularly early sarcoptic mange and other ectoparasites
* Biopsy
* Use edge resection rather than wedge for best cosmetic effect (but may not get many sebaceous glands) and to avoid vascular compromise
* Retract skin before resection to ensure adequate closure
Treatment
* incurable condition
* topical anti-seborrhoeic shampoos, combined with moisturisers.
* Fissures should be treated with surgery if steroids (e.g. hydrocortisone aceponate) are not useful.
What is nasodigital hyperkeratosis? What history is associated? WHat clinical signs are seen?
A broad term for dogs with non-inflamed, quiescent and tightly adherent hyperkeratosis affecting the nose and sometimes the feet.
History
* Long list of differential diagnoses, but most affect other areas
* Usually older dogs
* No sex or breed predisposition
* Probably a senile change
* Associated with Distemper virus
Nasal lesions can be variable
* frond-like projections to a hard pavement-like surface
* the nose is dry.
* cracks and fissures can occur leading to irritation.
Pad lesions
* all the pads
* most prominent at the edges - weight bearing.
* lack of flexibility, cracking and the formation of corns lead to lameness
How is nasodigital hyperkeratosis diagnosed? How is it treated?
**Diagnosis **
* Clinical signs in the older dog with no other skin problems
- Slowly developing
- Bilaterally symmetrical
* Not appropriate if
- Generalised or systemic disease
- Ulceration
- Depigmentation
- Pain on localised palpation
* If in doubt biopsy
- Difficult – ensure stitches in living epithelium
Treatments
* cutting off prominent fronds with scissors or a scalpel blade
* hydrating the keratin using shampoos and soaks as described elsewhere
* Essential fatty acids
What history is associated with nasal parakeratosis of LB? What clinical signs are associated? How is it diagnosed? How is it treated?
History
* First observed between 6 & 12 months
* Affects all colours
* Often several members of the family affected.
Clinical signs
* Roughening of the nasal skin
* Moderate hyperkeratosis
* Some (often diffuse) hypopigmentation
* Clear demarcation on bridge of the nose (sometimes affected by previous topical agents)
Treatment is for life and affected dogs should not be bred from.
Differential diagnoses
* Discoid lupus erythematosus and mucocutaneous pyoderma
Diagnosis
* Biopsy
* Genetic testing
Treatment
* Zinc supplementation, steroids and retinoids give a poor response
* Topical vitamin E, petroleum jelly and propylene glycol have been advocated.
* Urea based humectants and petroleum jelly chronically after good antimicrobial treatment useful
Trying to soften the nose: Will get some iatrogenic alopecia around the nose due to fact that products are used, try and keep treatment just to the nose
What history is associated with footpad hyperkeratosis of the DdB? What clinical signs are associated? How is it diagnosed? How is it treated?
History
* Present in the UK
* First signs start at 4-6 months of age
* Larger animals (males) appear to start signs earlier suggesting a mechanical component to the disease
Clinical signs
* Foot pads only, with severe thickening with deep cracks appearing centrally
* conical to flap like projections appearing at the edges of the pads.
* Lameness on rough ground
* Often signs of bacterial infection (cytological or pedal swelling and peripheral lymph node enlargement)
Diagnosis
* history and clinical signs
* biopsy
- a deep wedge from the middle of the pad and crossing the hyperkeratotic edge
- close using deep and widely placed vertical mattress sutures to hold the opposing sides of the pad in position so that simple interrupted sutures along the incision are not pulled.
* Genetic testing (keratin 16 abnormality)
Treatment
* 50% propylene glycol soaks (requires an obedient dog and willing owner)
- Problems occur when dog aggressive
* Retinoids – very expensive in 60-80 kg dog
* Antibiotics for secondary infection
* Affected dogs should not be bred.
What history is associated with calluses? How is it diagnosed? How is it distinguishable on histopath? How is it treated?
History
* round or oval hyperkeratotic plaque that develops on the skin at points of trauma.
* Often hocks, elbows, sternum and ischium
* Other areas involved when orthopaedic problems or hypothyroidism.
* Callus is the normal response to pressure induced ischemia and inflammation.
* Secondary infection is common.
Diagnosis
* typical clinical signs and position, combined
* Biopsy especially if needed for tissue culture
- could be helpful for Histology ± tissue culture if there is infection
- risk that won’t heal due to the pressure on the area after biopsy
* Skin surface and exudate cytology and bacterial culture should be employed
Histopathology
* epidermal hyperplasia
* moderate to severe acanthosis
* variable epidermal hyperkeratosis sometimes parakeratotic.
* Follicles are often cystic with keratin and hair fragments leading to furunculosis).
Treatment
* treatment of the secondary infection
- Deep pyoderma is a common complication
- Extended therapy makes Meticillin-resistant & MRD bacteria likely
* removal of the trauma / pressure
* Bandaging and padding?
* Surgery is possible
- often curative for sternal lesions
- limb lesions often breakdown post surgery as the factors that led to the callus cannot be removed.
- Even risk for extensive biopsy
What signalment is associated with thymoma induced exfoliative dermatitis? What clinical signs are associated? How is it diagnosed? How is it treated?
Signalment
* Rare paraneoplastic syndrome
* Middle to older age
Clinical signs
* Diffuse, non-pruritic erythema and exfoliation (large 1+ cm flakes if skin)
+/- alopecia
* Concurrent signs from respiratory compromise
Note: exfoliative dermatitis reported in rare cases of FASS
Diagnosis
* Biopsy
* Chest radiography / CT
Treatment
* Immunomodulatory drugs (e.g. prednisolone & ciclosporin) have been used with some success
* Surgery is reported to be curative, but some have reported needing immunosuppression after thymoma removal
What causes idiopathic canine sebaceous adenitis? What clinical signs are associated? How is it diagnosed? How is it treated?
Background
* Inflammation in the sebaceous glands resulting in reduced activity to complete loss
* Not uncommon
* Autosomal recessive mode of inheritance in poodles and Akitas
* Considered by some to be brought about by a stressful event
Note histological sebaceous adenitis may be seen in a variety of diseases and particularly Leishmaniasis
Clinical signs
* Dry scale: Fine, white and non-adherent
* Hair loss (variable): Hair breakage and matting together and secondary infection
* Perifollicular hyperkeratosis is prominent
* Follicular casts are common
* Pruritus when 2˚ infection present
Diagnosis
* Clinical signs highly suggestive
* Rule out possible differential diagnoses and confounding co-morbidities
* Biopsy: Absent sebaceous glands gives a clear diagnosis
Treatment
* Use emollient and lubricating shampoos
- Improve cosmetic appearance
- Consider the ‘cling film wrap’
* Fatty acid and oil supplementation
- Topically
- Systemically
* Ciclosporin
- Drug of choice
- Direct action on T-cell destruction and may also promote hair cycling
* Steroids may be used, but reduction in hair cycling not useful
What non-specific topical products are used in scale cases?
Keratoplastic / keratolytic products
* These reduce scale production (keratoplastic [e.g. sulphur and coal tar shampoos]) or remove scale (e.g. salicylic acid shampoos])
* Delicate balance between removing scale and causing excessive drying.
* Used before moisturizing products
Moisturising and emollient products
* These reduce transepidermal water loss and prevent inflammation (e.g. products containing oils, propylene glycol and urea).
* Best used after other products have removed scale (e.g. keratolytic shampoo) and/or shampoo has been used to treat secondary skin surface infection
Most cases need both of these types of products
What are the different types of anti-seborrheic shampoos?
- Keratoplastic (reducing cell turnover in the skin to reduce scale production) e. g. sulphur & tar
- Keratolytic in which the shampoo removes cells from the surface of the skin e. g. salicylic acid
Properties
* Emollient agents moisturize and restore barrier function
- Occlusive (greasy agents e.g. lanolin)
- Hydrophilic (molecules that bind water e.g. urea or propylene glycol)
What is the role of sulphur in scale?
- Keratoplastic
- Cytostatic on basal cell layer of epidermis so slows down epidermal cell proliferation
- Keratolytic
- Forms hydrogen sulphide / pentathionic acid that damage corneocytes softening stratum corneum causes shedding of cells
- Antibacterial / antifungal
- Not very degreasing so doesn’t dry out skin
- Used for mild grease, scale and proliferation
- e.g. primary seborrhoea (over productions of scale with marked reduction in skin turnover time)
- Combined with salicylic acid to increase degreasing power (synergistic activities)
- Recommended to use moisturiser if skin dry
What is the role of salicylic acid in scale?
- Often combined with sulphur as synergistic
- Treatment of seborrheic conditions (1˚ and 2˚)
- Keratolytic
- Lowers pH of skin
- Hydrates keratin / causes swelling of corneocytes
- Stabilises inter-cellular cement in stratum corneum -> desquamation
- No effect on mitotic rate of basal keratinocytes
- Mildly anti-pruritic
- Mildly anti-inflammatory
- Recommended to use moisturiser if skin dry
What is the role of selenium sulphide in scale?
- Older anti-seborrheic but can be used to treat severe cases of oily greasy skin non-responsive to other agents
- Keratolytic
- Inteferes with hydrogen-bond formation in keratin
- Keratoplastic
- Depresses epidermal growth
- Antimicrobial
- Fungicidal at higher concentrations
- Causes marked skin drying (irritation potential)
- Stains coat (pink)
What are common moisturisers used in scale? What is their mechanism?
Urea
Mechanism:
* Binds water
* Promotes hydration
* Anti-bacterial
* Keratolytic
* Proteolytic digestion of fibrin
Comments: Used in shampoos such as Sebocalm in combination with glycerin
Glycerin
Mechanism: Hygroscopic / absorbed into skin
Comments: Used in shampoos and conditioning foams and sprays and wipes (e.g. with chlorhexidine in Clorexyderm range)
Propylene glycol
Mechanism: Potent softening and hydroscopic agent
Comments:
* Used neat or diluted 50% in water for severe pad hyperkeratosis
* Common component of conditioning products
Vaseline
Mechanism: Petroleum jelly, is a safe occlusive agent
Comments: Can be greasy and mark clothes and soft furnishings
What agents can be used to improve barrier function? What is their mechanism?
Topical essential fatty acids
Mechanism: Attempt to restore lipid layers in stratum corneum
Comments: Expensive and controversial efficacy
* e.g. Allerderm Spot-on
Colloidal oatmeal
Mechanism:
* Hygroscopic and soothing
* Reduced pro-inflammatory cytokines
Comments: Used in shampoos e.g. Coatex Aloe and oatmeal shampoo
Lanolin
Mechanism: Occlusive agent
Comments: Common in creams and conditioners
Phytosphingosine
Mechanism:
* Natural product found in epidermis (SC) and in various plants and fungi
* Increases barrier function and may reduce proinflammatory cytokines (see comment)
Comment:
* Anti-inflammatory and antipsoriatic activities of the phytosphingosine derivatives inhibited NF-κB, JAK/signal transducer and activator of transcription (JAK/STAT), and mitogen-activated protein kinase (MAPK) signaling
* Now largely removed from the veterinary market for commercial reasons.
Ophytrium
Mechanism: derived from the root of the Japanese mondo grass plant
Comment: Moisturising and anti-inflammatory effects
What are systemic agents that may effect keratinisation?
Steroids
* Reduce the turnover of epithelial cells
* May reduce scale in some cases
* Local application useful (e.g. ear margin seborrhoea)
Retinoids
* Normalise skin development, used in a variety of disorders of hyperkeratosis
* High number of adverse effects e.g. dry eye, hepatopathy
* A referral medication
