Skin 1, 2 and 3 Flashcards
What do each of the arrows point to in this picture?
Top- superficial keratin
Down right side top to bottom-
stratum granulosum
langerhans cells
basal layer
basal lamina
Bottom-
melanocytes
blood vessels
What do melanocytes do?
What are the different stages of hair follicles, what do the stages change?
Melanocytes- produce melanin to protect against UV
Hair follicles- papilla and length varies depending on time and season
Anagen, Catagen and telogen
What is acantholysis?
What is acanthosis?
What is alopecia?
What is atopy?
Acantholysis- loss of keratinocytes cohesion
Acanthosis- increased thickening of the stratum spinosum
Alopecia- hair loss or failure to grow
Atop- allergic skin disease
What is the name for these two tissue alterations?
What is folliculitis?
What is furunculosis?
What is hyperkeratosis?
Top- bullae- collection of fluid >1cm in diameter
Bottom- ballooning degeneration- intracellular oedema
Folliculitis- luminal, mural or perifollicular inflammation of the hair follicle
Furunculosis- perifollicular inflammation due to hair follicle wall rupture
Hyperkeratosis- increased thickness of the keratin layer
Which image shows the following?:
Pustule
Pigmentary incontinence
Seborrhoea
Spongiosis
Vesicle
A- seborrhoea- increased scale formation- dandruff
B- spongiosis- epidermal intracellular oedema
C-Vesicle- fluid filled blister <1cm in diameter
D- Pustule- cavitation of the epidermis filled with inflammatory cells
E- pigmentary incontinence- melanin granules and melanophages within the dermis
What are the three categories of vascular skin pathology?
Vasculitis
Local trauma effect (bruise)
Septic or non-septic thromboembolism
What causes skin vasculitis?
How do they grossly appear?
What is the histological hallmark?
Causes-
endotheliotropic organisms
deposition of immune complexes
septic emboli
Gross appearance-
erythematous plaques, macules, purpura, oedema and ulcers
chronic lesions- ulcers and dermal atrophy
Histological landmark- karyorrhectic cell debris and fibrinoid necrosis of the vessel wall surrounded by fibrin exudation and haemorrhages
What are the different types of vasculitis?
Neutrophilic- suggestive of type III hypersensitivity or septicaemia
Lymphoplasmacytic- mainly based on cell-mediated immune response
Eosinophilic- suggestive of a type I hypersensitivity reaction of eosinophilic dominated dermatoses
What can cause inflammation of the skin?
- bacteria
- viruses
- arthropods
- viruses
- protoza
- fungi
What three conditions are superficial bacterial pyodermas?
Impetigo
Exudative epidermitis
Dermatophilosis
What is impetigo?
How does it grossly and histologically appear?
Impetigo- superficial pustular dermatitis with no involvement of the hair follicle
Gross- erythematous pustule to papules
Histology- subcorneal pustules composed of mainly neutrophils
What is greasy pig disease?
How does it affect pigs and grossly appear?
What are the three clinical forms of the disease?
How does it appear histologically?
Greasy pig- exudative epidermitis- is a superficial exudative pyoderma of young pigs caused by staphylococcus hyicus
High morbidity low mortality, exotoxin produces cleavage between stratum corneum and granulosum
Greasy dark brown exudate over eyes, snout, chin and ears
Clinical forms-
Acute- rapid spread to the whole body (death in 3-5 days)
Subacute- lesions confined to head and % of survivors
Chronic- high surviving rate, poor growth
Histo- subcorneal pustular dermatitis- epidermis covered with ortho and parakeratoic serum, neutrophils and bacterial colonies
What condition does dermatophilus congolenis cause?
What kind of bacteria is it?
What conditions are favourable for its infection?
Describe its clinical presentation
Dermatophilosis- acute to chronic exudative superficial dermatitis
Gram +ve coccoid bacterium producing branching filaments
Skin trauma and wet are favourable
Continuous and cyclic epidermal invasion, inflammation and regeneration leading to thick parakeratotic crusts
What agent most commonly causes deep pyoderma?
How does it appear and progress?
How does it appear histologically?
Staphylococcus spp mainly
Appearance and progression of gross lesions-
follicular papula to pustule to crust formation and coalescing ulcers/alopecia
leads to dark red nodules, ulcers and fistulae
leads to lymphadenopathy and fever
Histo-
neutrophilic folliculitis and furunculosis with bacterial colonies- free keratin fragments- foreign body reaction and haemorrhage
What are abscesses and cellulitis?
What symptoms are they associated with?
What causes them?
How do they appear histologically?
A and C- focal non-specific severe suppurative inflammation of the deep dermis and panniculum
Associated with fever and lymphadenopathy
Contaminated wounds or contaminated foreign bodies
Histology-
Abscess- circumscribed central core of necrotic material and degenerate neutrophils surrounded by granulation
Cellulitis- poorly circumscribed extensive suppurative or pyogranulomatous inflammation with oedema, haemorrhage or thrombosis
What agents can cause cutaneous bacterial granulomas?
How do the different agents presentation and pathogenesis differ?
Actinomyces and nocardia-
pyogranulomatous dermatitis and panniculitis [subcut adipose inflammation]
grossly- large fibrotic and ulcerated nodules often with draining fistulous tracts
Mycobacterial infections-
M. tuberculosis and bovis- disseminated infections to the skin
Saprophytic mycobacteria often to the skin since acquired from wound
What 3 different types of viruses can infect the skin?
Poxviruses
Herpes virus
Papillomaviruses
What poxvirus causes cowpox?
How do lesions appear and distribute?
How does it appear histologically
Orthopox
Distribution- single with a predilection for face and forepaws
Lesion appearance- ulcers to papules and pustules in secondary lesions
Histo- focal sharp demarcated ulcer covered with fibrinecrotic exudate
What type of poxvirus causes orf?
Where do lesions distribute and appear
How does it appear histologically?
Parapoxviruses
Lambs and kids
Lips and muzzle affected
Multifocal to coalescing raised and flat grey crusts
Histo- ballooning degeneration and spongiosis with prominent epidermal hyperplasia and crust formation
Other then orthpox (cowpox) and parapoxvirus (orf)
What other poxviruses can infect the skin with high epitheliotropism?
Avipoxvirus- fowlpox
Lepovirus- myoma
Suipoxvirus- swinepox
Molluscipoxvirus- molluscum
Yatapoxvirus
What causes herpes dermatitis in cats?
Describe gross lesion distribution and appearance
How does it histologically appear?
felid herpes type 1
the common pathogen of the airways, skin lesions often occur in the absence of respiratory signs
Gross lesion- primarily on the nasal planum and haired skin of the face
Gross appearance- persistent of recurring crusts, ulcers and vesicles
Histo-
ulcerative and necrotising dermatitis, large intranuclear glassy inclusion bodies
What do papillomaviruses cause?
Typically associated with proliferative disease of squamous epithelia in most domestic species
How are fungal (mycoses) of the skin divided?
What allows mycoses infection?
Cutaneous, subcutaneous and systemic
Cutaneous- most common and confided to cornified tissues- dermatophytosis
Subcutaneous- huge variety of saprophytic fungi, remain localised- zygomyocsis
Systemic- haematogenous dissemination- cryptococcus
Skin usually non-permissive- immunological dysfunctions are facilitating the conditions
What is the common name for dermatophytosis and what type of infection is it?
What are the three main genera?
What are the favourable conditions for this infection, how is it transmitted?
Describe the pathogenesis of infection after transmission
How do lesions distribute and appear?
How does it appear histologically?
Ringworm- confined to the keratin layer of skin, claws and hair
Genera- Microsporum, trichophyton, epidermophyton
Favourable conditions- micro-abrasions, maceration, prolonged corticosteroid, transient or permanent immune deficiencies
Transmission- infected hair or keratin fragments
Fungi migrate to the follicular lumen and proliferate along the entire follicle- using keratin as nutrient
Gross lesion- circular expanding areas of scaling and alopecia, often furunculosis and chronic pyogranulomatous develop and mimic tumours
Histo- ortho and parakeratotic hyperkeratosis and acanthosis. Luminal folliculitis, furunculosis and pyogranulomas
What two protozoa commonly infect the skin?
Leishmania
Besnoitosis
What is leishmania and how is it transmitted?
What are the two clinical forms?
When is skin most affected from infection?
How do lesions distribute and appear?
How does it appear histologically?
Obligate intracellular apicomplexan parasite of macrophages, transmitted by blood-sucking sandflies
Two clinical forms:
Alopecic- stronger Th1 response and fewer parasites
Nodular- predominant Th2 response and numerous parasites
Gross- mainly on head, limbs and dorsal midline, nodules, alopecia, ulcers or pustules
Histo-
nodular to diffuse superficial and deep granulomatous dermatitis, variably dominated by plasma cells
What are common physical and chemical cutaneous injuries?
Physical- mechanical forces, cold, hot, burns
Chemical- primary irritant contact dermatitis, ergotism
Actinic injuries- solar light exposure, photosensitisation
Bruise- subcutaneous accumulation of extravasated erythrocytes
haemosiderin-laden macrophages remain visible locally for a very long period of time after clinical resolution
What different types of parasites can infect the cutaneous?
Flies
Lice
Fleas
Mites
What is myiasis?
Why can it cause limited local penetration or potentially anaphylactic shock?
What are migrating larvae from flies associated with?
What species can lead to cysts in what animals?
Myasis- refers to the infestation of living tissues by the larval stages (maggots) of dipterous flies
- Some species remain localised to the site of injury (limited, local penetration)
- other species after penetrating through intact/wounded skin or migrating from the GI colonise and develop cyst-like dermal structures with a central pore
- Accidental rupture of the cysts can lead to anaphylactic shock
Migrating- associated with eosinophilic and lymphocytic inflammation and fibrous capsule with eosinophils and granulation tissue in the cystic dermal cavity
Cuterebra- rabbits, rodents
Hypoderma bovis/lineatum- cows (warble fly)
Blow flies- sheep
What species causes sarcoptic mange?- shout out to scabies girl
What is important to note about this disease?
What species is it common in?
What is the gross lesion distribution?
Briefly describe its life cycle
How does it look histologically?
Sarcoptes scabei
Zoonotic, highly contagious, notifiable, extremely pruritic
Common in pigs and dogs
Gross lesion distribution- the inner surface of the pinna, spreading to head, neck and legs
Life cycle- within tunnels burrowed within and under the stratum corneum- scales and crusts
Histo- severe acanthosis, patchy parakeratosis, spongiosis, leukocyte exocytosis and eosinophilic pustules
Where do demodex mites complete their lifecycle?
Where are there lesions found and how do they grossly appear?
How do the lesions appear histologically?
Demodex mites are obligate parasites completing their life cycles within the lumen of hair follicles and adnexa
Gross lesion appearance-
alopecia, scaling, comedones in the squamous form
pustules, folliculitiss and furunculosis in pustular form (secondary bacteria)
Distribution-
localised form- well-circumscribed, self-limiting lesions on ears, lips, eyes and extremities
generalised form- diffuse alopecia and scaling
Histo- severe suppurative folliculitis and furunculosis
What is the difference between autoimmunity and hypersensitivity?
Hypersensitivity is an immune reaction to an external irritant- pollen
Autoimmunity is a pathological immune reaction against self-antigens
What are common hypersensitivities of the skin?
Uticaria
Atopic dermatitis
Food hypersensitivities
Insect hypersensitivties
What is urticaria?
What are frequent causes?
How do lesions appear and distribute?
How does it appear histologically?
Acute, variably pruritic, oedematous skin lesions- type 1 hypersensitivity, caused by mediators of basophils and mas cells
Drugs, foods and food additives are frequent causes
Distribution- variable from localised to widespread
Appearance- discrete, well-circumscribed round erythematous and oedematous plaques
Histo- variable and non-specific, subtle or prominent dermal oedema of the superficial dermis
What causes atopic dermatitis and what predisposes for it?
How do animals present?
How do lesions distribute and how do they appear?
How does it appear histologically?
Increased production of IgE against ‘innocuous’ antigens, genetically based on a predisposition for an immunoregulatory balance.
Prominent Th2 reactivity- IgE hypersecretion and deficient cell-mediated immune response- highly susceptibility to local infections
Clinically intense pruritus
Lesion distribution- variable, typically ventral sparsely haired skin
Appearance- excoriations, papules, pustules, hyperpigmentation, licheninfication
Histo- perivascular to interstitial lymphoplasmacytic dermatitis with oedema, eosinophils, macrophages and variable degree of epidermal hyperplasia
What specifically causes insect hypersensitivity?
What kind of reactions are they?
What are the names of the different conditions?
How do lesions distribute and appear?
How do they histologically appear?
Antigens from saliva, venom, whole body or faeces
Type I and IV reactions- seasonal and pruritic lesions
Sweet itch in horses, Flea allergic dermatitis
Distribution- sparsely haired body regions, lumbosacral for flea-bite
Appearance- pruritic crusted papule- hyperkeratosis, lichenification, seborrhoea and excoriation
Histo- eosinophils dominated dermal perivascular to diffuse dermatitis with lymphocytes and fewer macrophages
What is pemphigus complex- pemiphigus foliaceus?
How do lesions grossly distribute and appear?
How do they histologically appear?
Autoantibodies against desmoglein 1
Distribution- restricted to the skin (no mucosa), starts from periocular and nasal skin (cat, dog) to ears, neck and ventral abdomen
Appearance- erythematous maculae to pustules to erosion and crusts
Histo- acantholytic subcorneal or intragranular pustular dermatitis
What are the two forms of Dr Houses least favourite disease (Lupus erythematous)?
Systemic lupus erythematosus (SLE)
multiple organs with skin lesions in 1/3
Discoid lupus erythematous (DLE)
localised cutaneous form
How does discoid lupus erythematous grossly appear and distribute?
How does it appear histologically?
Distribution- restricted to nasal planum
Appearance- erythema, depigmentation, scaling, crusting, alopecia and ulcers
Histology- similar to SLE, but more epidermal hyperplasia, denser interface infiltrate dominated by lymphocytes (few plasma)
How does the skin respond following hypovitaminoses?:
Vitamin A
Vitamin B
Vitamin E
What mineral deficiencies can affect the skin?
Vitamin A- squamous epithelial hyperkeratosis (follicular keratosis)
Vitamin B- dry seborrhoea with alopecia
Vitamin E- panniculitis due to steatonecrosis (lack of antioxidant protection)
Zinc deficiencies can affect the skin
What hormonal imbalances cause dermatoses?
Hyperadrenocorticism
Hypoestrogenism
Hypothyroidism
What is the alternative name for red, white and blue epidermal disease?
Why does it have the name red, white and blue?
What is the pathogenesis?
How are lesions distributed and appear?
Superficial necrolytic dermatitis
Alternating severe parakeratotic hyperkeratosis (red), spongiosis and oedematous spinous layer (white), and basal layer (blue)
Unkown pathogenesis but highly associated with glucagon secreting pancreatic tumours and end stage liver
Distribution- symmetrical and bilateral on lips, periocular skin, pinna and distal extremities
Appearance- areas of erythema, erosion, ulcers and crusts
What do endocrinopathies cause grossly and histologically?
Gross- bilateral and symmetrical alopecia, easily epilated hair with failure to regrow
Histologically- follicular atrophy, orthokeratotic hyperkeratosis, follicular keratosis with lumen distension
Both- dermal atrophy and epidermal hyperpigmentation
What is cushings disease?
what can cause it?
How does it appear and distribute grossly?
How does it histologically appear?
Dermatological changes associated with hyperadrenocorticism
pituitary tumour, adrenal tumour, iatrogenic administration
(calcinosis cutis is often present and commonly due to iatrogenic corticosteroid administration)
Distribution and appearance- bilateral and symmetrical hypotrichosis and alopecia of trunk and abdomen, skin is diffusely thinned and less elastic, hyperpigmentation, comedones and calcinosis also seen
Histo- diffuse cutaneous atrophy with orthokeratosis hyperkeratosis and follicular keratosis
What causes hyperoestrogenism in male and female dogs?
Polycystic ovaries and functional ovarian neoplasms in female dogs
Oestrogen secreting tumours in intact males (sertolioma)
What idiopathic eosinophilic diseases can affect cats and horses?
Feline-
- eosinophilic plaque
- eosinophilic granuloma
- indolent ulcer
Equine
- eosinophilic granuloma
- multisystemic eosinophilic epitheliotropic disease
What are the three presentations of feline eosinophilic dermatoses- granuloma complex
Eosinophilic plaque-
Pruritic lesion associated with hypersensitivity
Haired skin of inguinal, axillary and lateral thigh areas
Diffuse and perivascular eosinophilic dermatitis with epidermal acanthosis and spongiosis
Eosinophilic granuloma-
raised, pink variable pruritic nodular lesions on both haired skin (linear) and oral mucosa (nodular)
Diffuse eosinophilic inflammation with granulomas centred around degenerated collagen bundles covered with degenerate and degranulating eosinophils (flame figures)
Indolent ulcer-
uni or bilateral ulcerated plaque-like lesion on the upper lip
non-pruritic and non-painful
What are the three different equine eosinophilic nodular disease?
Collagenolytic granuloma-
single or multiple nodular, non-painful, non-pruritic lesions
foci of collagen degeneration surrounded by granulomas, sometimes with macrophage palisading and numerous eosinophils
Axillary nodular necrosis-
nodular non-painful, non-pruritic lesion on the trunk behind the axilla (girthgalls)
foci of coagulative necrosis with numerous eosinophils and fewer flame figures
Unilateral popular dermatosis-
seasonal and uncommon unilateral nodules on the lateral trunk
small foci on folliculoconcentric coagulative necrosis
What are epidermal cysts?
What causes them?
Clinically recorded as single, rarely multiple, dermal masses but not neoplastic
Cystic cavities filled with lamellar keratin and lined by continuous squamous epithelium
Cause-
enormous abnormal distension of follicles, traumatic dermal implantation of epidermal fragments
What are the different neoplasms deriving from the epidemic and adnexal structures?
What are the two main aetiologies that have been associated with epidermis and adnexa neoplasms
- Papilloma
- Squamous cell carcinoma
- Basal cell carcinoma
- Tumours of the hair follicles
- Sebaceous and modified sebaceous gland tumours
sebaceous gland adenoma/epithelioma/adenocarcinoma, perianal gland tumour - Sweat gland and modified sweat gland tumours-
sweat gland adenoma/adenocarcinoma, ceruminous gland tumours
Aetiologies- UV light, pappillomavirus
What causes a papilloma?
What causes susceptibility and regression?
What are the two types?
Why can they easily be associated with secondary infection?
Papilloma- virus-induced
idiopathic squamous- older animals, no cytopathic effects
Immune system competence is linked with susceptibility and regression
Cutaneous papillomas- one or multiple filiform exophytic and hyperkeratotic projections of the epidermis supported by thin dermal stalk
Fibropapillomas- plaque-like lesions with the predominant dermal proliferation
They can bleed easily and therefore cause secondary infection
What are koilocytes?
Keratinocyes with eccentric pyknotic nucleus and peripheral clear halo (ballooning degeneration)
What is associated with and predisposes to squamous cell carcinomas?
What are the typical characteristics?
How does it grossly appear and where are they most commonly found?
How does it appear histologically?
UV light is directly involved in white/pale animals, viral papilloma can predispose
Locally invasive and destructive- rarely metastatic
Appearance- single expansile hyperplastic ulcerated or nodular skin lesions
Distribution- everywhere but mainly on the head
Histo-
invasive islands and cords of neoplastic cells within the dermis, anisocytosis, anisokaryosis and mitotic index high, keratin pearls often present, inflammation and pronounced desmoplasia, neutrophilic pustules due to abnormal keratin formation and necrosis
How are follicular tumours classified
What are the different types?
Histologically, follicular tumours are classified according to the segment of origin as assessed by differentiation patterns observed
Infundibular keratinising acanthoma-
infundibular differentiation with keratohyalin granules in the granular layer
Tricholemmoma- clear keratinocytes similar to the isthmic outer root sheath cells
Pilomatricoma- signs of matrical differentiation as seen in the hair bulb
Trichoblastoma- formation of primitive hair germ cells
How do pilomatricomas appear?
What are they derived from?
Solitary benign tumour, localised on the lower dermis and subcutis
Chaulky white on cut surface, multilobulated and sometimes pigmented
Central portion abruptly filled with ghost cells
Derived from follicular matrix cells
What are the different sebaceous gland tumours?
What types are A, B and C?
Adenoma- well-differentiated, with preponderance of sebocytes with few basaloid cells and ducts
Epithelioma- a preponderance of basaloid cells with few sebocytes and ducts- intermediate degree of malignancy
Adenocarcinoma- cells with variable degrees of sebaceous differentiation
irregular lobar formations, pleomorphism, local infiltration
A- adenoma
B- epithelioma
C-carcinoma
