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Y4 SA dermatology > Scale > Flashcards

Scale Flashcards

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Dermatology Board Prep flashcards
1
Q

What is scale?

A
  • the presence of flakes of keratinized skin in the hair coat and on the skin
  • it can be adherent (well attached to the epidermis) or loosely attached
  • thickened stratum corner
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2
Q

What does scale result from?

A

▪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

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3
Q

Are scale and crust the same thing?

A
  • no
  • crusts result from the hardening of pus, serum and/or blood with scale to form a solid material which like scale is variably adherent to the skin
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4
Q

Diseases where scale is seen as a primary problem

A

▪ 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

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5
Q

Diseases where scale is seen as a secondary problem

A

▪ 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

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6
Q

Is primary or secondary scale more common?

A
  • secondary scale is much more common that primary dz
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7
Q

Is scale in bacterial infections common?

A
  • yes
  • it is 1 of the most common forms of scale seen in dogs (may be the O main concern/presenting complaint)
  • Staphylococcus pseudintermedius causes folliculitis and following rupture of the pustule and central hair loss a spreading circle of scale is seen moving from the central area
  • The amount of scale depends on bacterial toxins (esp. exfoliative toxins)
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8
Q

Diagnostic plan

A
  1. Check for parasites
  2. Check for infection
  3. In older dogs perform general health screening (e.g. urinalysis, haematology & biochem)
  4. Biopsy
  5. Genetic testing if indicated
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9
Q

Checking for parasites

A

a. Clinical examination
b. Coat brushings, hair plucks, skin scrapes
c. Consider parasite treatment trial

Particularly important in young animals, don’t rely on reported ectoparasite use

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10
Q

Checking for infection

A

a. Clinical examination
b. Skin surface cytology

If infection, what is the primary dz?

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11
Q

Genetic testing

A

a. Ichthyosis of the Golden retriever†, Great Dane and American Bulldog
b. Pedal hyperkeratosis of the Dogue de Bordeaux
c. Nasal parakeratosis of Labrador Retrievers (NPLR) †

† Common in the UK

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12
Q

Zn-responsive dermatosis - which animals are affected?

A

▪Genetically predisposed breeds eg Husky (type I)
– Often young adult onset
▪In nutritional restriction seen in young rapidly growing large breeds (type II)

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13
Q

Zn-responsive dermatosis - what is type I?

A

▪Genetic poor Zn absorption

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14
Q

Zn-responsive dermatosis - what concurrent dz do you need to be aware of with type I?

A
  • hypothyroidism (older animals - later onset)
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15
Q

Zn-responsive dermatosis - CS

A

▪Dull coat and specific hard plaques with marked scale and crusting
▪Crusted hyperkeratosis (bacterial infection common)
▪Bacterial infection
▪Variable pruritus
– due to infection
▪Crusted lesions where they bash their skin

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16
Q

Zn-responsive dermatosis - histologically (from biopsy)

A

▪Parakeratosis is key finding
▪Zinc is required for normal keratinisation – disease most common at areas of trauma
▪In parakeratotic hyperkeratosis nuclei are retained in the stratum corneum
– This is seen to a lesser extent in bacterial pyoderma and in superficial necrolytic dermatitis (hepatocutaneous syndrome)
– Normal squares should not have nuclei

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17
Q

Zn-responsive dermatosis - tx

A
  • Zn supplementation, correct diet (consider steroids in type 1 if poor response)
    – steroid in v low doses can increase the absorption of zinc
  • Zinc sulphate traditionally used
    – may cause v+
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18
Q

Ichthyosis of the Golden Retriever - History & CS

A

▪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
▪ Fine in themselves, just v scaly
▪ Can get wax ears as exfoliates out of the skin/ear less well
▪ Scale easily brushed off
▪ Can see shiny adherent material on ears and ventral abdomen
▪ Ichthyosis = fish scale dz

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19
Q

Ichthyosis of the Golden Retriever - tx

A

▪Symptomatic treatment only
▪Recently retinoids used with some success

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20
Q

Ichthyosis of the Golden Retriever - what is it?

A

A 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
▪Abnormal cleavage of the corneodesmosome

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21
Q

Ichthyosis of the Golden Retriever - Major ddx in young animals

A
  • parasites
    – if several in litter affected, consider skipping biopsy and performing genetic test after ruling out mites
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22
Q

Is canine ear margin seborrhoea common?

A
  • no it is relatively uncommon
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23
Q

Canine ear margin seborrhoea - breed predilection

A
  • Marked breed predilection in Dachshunds
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24
Q

Canine ear margin seborrhoea - CS

A

▪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
▪ Very sore

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25
Q

Canine ear margin seborrhoea - ddx

A

▪Secondary causes of pinnal seborrhoea
▪ hypothyroidism
▪Trauma due to pinnal flapping
▪Early vasculitis
– But not vasculitis as no notches/necrotic tissue due to lack of blood supply
▪Early localised scabies

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26
Q

Canine ear margin seborrhoea - diagnosis

A

▪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
-> Notch ends up with compromised blood supply -> more problems that before
– Retract skin before resection to ensure adequate closure
– Bilateral so O doesn’t really notice once hair grows back
– Resection can also be sent away for histopath if concerned

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27
Q

Canine ear margin seborrhoea - tx

A

▪incurable condition
▪topical anti-seborrhoeic shampoos, combined with moisturisers.
▪Fissures should be treated with surgery if steroids (e.g. hydrocortisone aceponate) are not useful.

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28
Q

Nasodigital hyperkeratosis - what is it?

A

▪A broad term for dogs with non- inflamed, quiescent and tightly adherent hyperkeratosis affecting the nose and sometimes the feet

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29
Q

Nasodigital hyperkeratosis - history

A

▪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

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30
Q

Nasodigital hyperkeratosis - nasal lesions

A

▪frond-like projections to a hard
pavement-like surface
▪the nose is dry
▪cracks and fissures can occur leading to irritation

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31
Q

Nasodigital hyperkeratosis - pad lesions

A

▪all the pads
▪most prominent at the edges - weight bearing
▪lack of flexibility, cracking and the formation of corns lead to lameness

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32
Q

Nasodigital hyperkeratosis - ddx

A

▪Superficial necrolytic dermatitis
– Painful, systemically unwell
– Often more widespread disease ▪Epitheliotropic cutaneous lymphoma
– Hypopigmentation
– Ulceration
– Progression beyond the nose and pads
▪Demodicosis (foot pad disease)
– Rare – look for signs of mites elsewhere on dog

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33
Q

Nasodigital hyperkeratosis - diagnosis

A

▪ 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

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34
Q

Nasodigital hyperkeratosis - tx

A

▪ cutting off prominent fronds with
scissors or a scalpel blade
▪ hydrating the keratin using shampoos and soaks as described elsewhere
▪ Essential fatty acids

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35
Q

Nasal parakeratosis of Labrador Retrievers - history

A

▪First observed between 6 & 12 months
▪ Affects all colours
▪ Often several members of the family affected

36
Q

Nasal parakeratosis of Labrador Retrievers - CS

A

▪ Roughening of the nasal skin
▪ Moderate hyperkeratosis
▪ Some (often diffuse) hypopigmentation
▪ Clear demarcation on bridge of the nose (sometimes affected by previous topical agents)

37
Q

Nasal parakeratosis of Labrador Retrievers - ddx

A

▪ Discoid lupus erythematosus and mucocutaneous pyoderma

38
Q

How to tell the difference between nasal parakeratosis and pemphigus or lupus

A
  • pemphigus/lupus: wouldn’t expect the clarity between the nose and face
  • discoid lupus: ulceration and pigmentation
  • nasal parakeratosis: nothing on lips or down towards mouth
39
Q

Nasal parakeratosis of Labrador Retrievers - diagnosis

A

▪ Biopsy
▪Genetic testing

40
Q

Nasal parakeratosis of Labrador Retrievers - tx

A

▪Treatment is for life and affected dogs should not be bred from
▪ 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

41
Q

Footpad hyperkeratosis of the Dogue de Bordeaux - History

A

▪ 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

42
Q

Footpad hyperkeratosis of the Dogue de Bordeaux - CS

A

▪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
– Very painful
▪ Often signs of bacterial infection (cytological or pedal swelling and peripheral lymph node enlargement)

43
Q

Footpad hyperkeratosis of the Dogue de Bordeaux - diagnosis

A

▪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)

44
Q

Footpad hyperkeratosis of the Dogue de Bordeaux - tx

A

▪50% propylene glycol soaks (requires an obedient dog and willing owner)
– Problems occur when dog aggressive
▪Retinoids – very expensive in 60-80 kg dog
– Also associated with a worry about psychotic episodes in people
– Difficult to get hold of
▪Antibiotics for secondary infection ▪Affected dogs should not be bred

45
Q

What is a callus?

A

▪ Callus is the normal response to pressure induced ischemia and inflammation
▪ Reactive epidermis that results in scale build up on top

46
Q

Callus - history & CS

A

▪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
▪Secondary infection is common.

47
Q

Callus - diagnosis

A

▪typical clinical signs and
position, combined
▪Biopsy* especially if needed for tissue culture
▪Skin surface and exudate cytology and bacterial culture should be employed

  • Care with biopsy
    – Small punch biopsy to not lose integrity of the area
    – Histology ± tissue culture
48
Q

Callus - histopathology

A

▪epidermal hyperplasia
▪moderate to severe acanthosis
▪variable epidermal hyperkeratosis sometimes parakeratotic.
▪Follicles are often cystic with keratin and hair fragments leading to furunculosis)

49
Q

Callus - tx

A

▪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
– Limbs ones refer

50
Q

When do you know you need to treat a callus?

A
  • Pick it up and roll it
  • Deep pyoderma = ricey grainy bits
51
Q

Thymoma induced exfoliative dermatitis - signalment

A

▪Rare paraneoplastic syndrome ▪Middle to older age

52
Q

Thymoma induced exfoliative dermatitis - CS

A

▪Diffuse, non-pruritic erythema and exfoliation (large 1+ cm flakes if skin) +/- alopecia
– Can peel the scale away, brings the hair with it
▪Concurrent signs from respiratory compromise
– High resp rate due to chest mass

53
Q

Thymoma induced exfoliative dermatitis - diagnosis

A

▪ Biopsy
▪Chest radiography / CT
– Cranial thoracic mass on imaging

54
Q

Thymoma induced exfoliative dermatitis - tx

A

▪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

55
Q

What is exfoliative dermatitis reported in?

A
  • rare cases of FASS
56
Q

Idiopathic canine sebaceous adenitis - background

A

▪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
▪ Vislas commonly affected, and present with segmental alopecia and scale

57
Q

What dz might you see histological sebaceous adenitis?

A
  • a variety of diseases
  • particularly Leishmaniasis
58
Q

Idiopathic canine sebaceous adenitis - CS

A

▪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

Diffuse partial alopecia with lots of scale, if pluck hairs see follicular casts

Symmetrical

Alopecia and scale can be segmental

59
Q

Idiopathic canine sebaceous adenitis - diagnosis

A

▪Clinical signs highly suggestive
▪Rule out possible differential diagnoses and confounding co-morbidities
▪Biopsy: Absent sebaceous glands gives a clear diagnosis

60
Q

Idiopathic canine sebaceous adenitis - tx

A

▪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 (initiates anagen)
▪Steroids may be used, but reduction in hair cycling not useful

61
Q

Idiopathic canine sebaceous adenitis - prognosis

A

▪Good if seen early
▪Some cases do well for many years and then develop alopecia in old age despite treatment – unknown mechanism

62
Q

Non-specific treatment – topicals

A
  • Keratoplastic / keratolytic products
  • Moisturising and emollient products

Most cases need both types of products

63
Q

Keratoplastic/keratolytic products - what do they do? When to use them

A

▪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 moisturising products

64
Q

Moisturising and emollient products - what do they do? When to use them

A

▪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

65
Q

Forms of topical treatments & their action

A

▪Shampoos
– used with water & rinsed
– some have residual action

▪Foams
– residual action

▪Sprays
– residual action (lipophilic agents bind to lipid = reservoir)

▪Wipes
– physical interaction and residual action in some

▪Creams
– local treatment (water based)
– easily absorbed

▪Gels
– local treatments (often contain mixture of components to aid absorption)

▪Ointments
– local treatment (oil based) occlusive and remain in place

▪Spot-on products
– provide drugs for surface or systemic absorption

66
Q

Keratoplastic vs keratolytic

A

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

67
Q

What do emollient agents do? Types

A
  • They moisturise and restore barrier function
    ▪Occlusive (greasy agents e.g. lanolin) ▪Hydrophilic (molecules that bind/trap water
    e.g. urea or propylene glycol)
  • Can be combined
68
Q

Important topical agents for scaling conditions

A

▪Sulphur
▪Salicylic acid
▪Selenium sulphide
▪Hydrocortisone aceponate
▪Betamethasone (and other
steroids in ear creams)

69
Q

Sulphur - properties & use

A

▪ 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

70
Q

Salicylic acid - properties & use

A

▪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

71
Q

Typical use of sulphur-salicylic acid shampoo

A
  • to remove scale
  • reduction in skin barrier function increases natural water loss and causes inflammation
  • a moisturiser is essential after scale removal
72
Q

Selenium sulphide - properties & use

A

▪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)

Irritant and old school, but very keratoplastic. Use in extreme need

73
Q

Emollients and Moisturisers - properties & use & examples

A

▪Include fats / hydrocarbons / humectants / oils
▪Act as vehicles for other ingredients
▪Soften / protect skin
– Form a thin film of oil on stratum corneum
– Decrease water loss
– Occlusive function
▪Act to bind water in the skin
– Hydroscopic function

Examples:
* Zinc gluconate
* D-panthenol
* Liposomes
* Glycerin
* Propylene glycol

74
Q

Common moisturisers

A
  • Urea
  • Glycerin
  • Propylene glycol
  • Vaseline
75
Q

Urea - mechanism of action, notes re use

A

Binds water
* Promotes hydration
* Anti-bacterial
* Keratolytic
* Proteolytic digestion of fibrin

Used in shampoos such as Sebocalm in combination with glycerin

76
Q

Glycerin - mechanism of action, notes re use

A

Hygroscopic / absorbed into skin

Used in shampoos and conditioning foams and sprays and wipes (e.g. with chlorhexidine in Clorexyderm range)

77
Q

Propylene glycol - mechanism of action, notes re use

A

Potent softening and hydroscopic agent

Used neat or diluted 50% in water for severe pad hyperkeratosis
Common component of conditioning products

78
Q

Vaseline - mechanism of action, notes re use

A

Petroleum jelly, is a safe occlusive agent

Can be greasy and mark clothes and soft furnishings

79
Q

Other agent that improve barrier function

A
  • topical essential fatty acids
  • colloidal oatmeal
  • lanolin
  • phytosphingostine
80
Q

Topical essential fatty acids - mechanism of action, notes re use

A

Attempt to restore lipid layers in stratum corneum

Expensive and controversial efficacy e.g. Allerderm Spot-on

81
Q

Colloidal oatmeal - mechanism of action, notes re use

A

Hygroscopic and soothing
Reduced pro-inflammatory cytokines
aka anti-pruritic and anti-inflammatory

Used in shampoos e.g. Coatex Aloe and oatmeal shampoo

82
Q

Lanolin - mechanism of action, notes re use

A

Occlusive agent

Common in creams and conditioners

83
Q

Phytosphingosine - mechanism of action, notes re use

A

Natural product found in epidermis (SC) and in various plants and fungi Increases barrier function and may reduce pro-inflammatory cytokines

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.

84
Q

Systemic agents that may affect keratinisation (& how they work)

A

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

85
Q

Why does hypothyroidism result in scale?

A
  • change in epidermal turnover
86
Q

What do Dalmations or pale dogs get after pustules and scale?

A
  • black pigmentation / post inflammatory macule

Y4 SA dermatology (22 decks)

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