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Year 3 Pathology > Skin 1, 2 and 3 > Flashcards

Skin 1, 2 and 3 Flashcards

1
Q

What do each of the arrows point to in this picture?

A

Top- superficial keratin

Down right side top to bottom-
stratum granulosum
langerhans cells
basal layer
basal lamina

Bottom-
melanocytes
blood vessels

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2
Q

What do melanocytes do?

What are the different stages of hair follicles, what do the stages change?

A

Melanocytes- produce melanin to protect against UV

Hair follicles- papilla and length varies depending on time and season

Anagen, Catagen and telogen

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3
Q

What is acantholysis?

What is acanthosis?

What is alopecia?

What is atopy?

A

Acantholysis- loss of keratinocytes cohesion

Acanthosis- increased thickening of the stratum spinosum

Alopecia- hair loss or failure to grow

Atop- allergic skin disease

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4
Q

What is the name for these two tissue alterations?

What is folliculitis?

What is furunculosis?

What is hyperkeratosis?

A

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

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5
Q

Which image shows the following?:

Pustule

Pigmentary incontinence

Seborrhoea

Spongiosis

Vesicle

A

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

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6
Q

What are the three categories of vascular skin pathology?

A

Vasculitis

Local trauma effect (bruise)

Septic or non-septic thromboembolism

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7
Q

What causes skin vasculitis?

How do they grossly appear?

What is the histological hallmark?

A

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

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8
Q

What are the different types of vasculitis?

A

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

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9
Q

What can cause inflammation of the skin?

A
  • bacteria
  • viruses
  • arthropods
  • viruses
  • protoza
  • fungi
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10
Q

What three conditions are superficial bacterial pyodermas?

A

Impetigo

Exudative epidermitis

Dermatophilosis

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11
Q

What is impetigo?

How does it grossly and histologically appear?

A

Impetigo- superficial pustular dermatitis with no involvement of the hair follicle

Gross- erythematous pustule to papules

Histology- subcorneal pustules composed of mainly neutrophils

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12
Q

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?

A

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

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13
Q

What condition does dermatophilus congolenis cause?

What kind of bacteria is it?

What conditions are favourable for its infection?

Describe its clinical presentation

A

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

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14
Q

What agent most commonly causes deep pyoderma?

How does it appear and progress?

How does it appear histologically?

A

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

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15
Q

What are abscesses and cellulitis?

What symptoms are they associated with?
What causes them?

How do they appear histologically?

A

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

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16
Q

What agents can cause cutaneous bacterial granulomas?

How do the different agents presentation and pathogenesis differ?

A

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

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17
Q

What 3 different types of viruses can infect the skin?

A

Poxviruses

Herpes virus

Papillomaviruses

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18
Q

What poxvirus causes cowpox?

How do lesions appear and distribute?

How does it appear histologically

A

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

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19
Q

What type of poxvirus causes orf?

Where do lesions distribute and appear

How does it appear histologically?

A

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

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20
Q

Other then orthpox (cowpox) and parapoxvirus (orf)

What other poxviruses can infect the skin with high epitheliotropism?

A

Avipoxvirus- fowlpox

Lepovirus- myoma

Suipoxvirus- swinepox

Molluscipoxvirus- molluscum

Yatapoxvirus

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21
Q

What causes herpes dermatitis in cats?

Describe gross lesion distribution and appearance

How does it histologically appear?

A

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

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22
Q

What do papillomaviruses cause?

A

Typically associated with proliferative disease of squamous epithelia in most domestic species

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23
Q

How are fungal (mycoses) of the skin divided?

What allows mycoses infection?

A

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

24
Q

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?

A

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

25
Q

What two protozoa commonly infect the skin?

A

Leishmania

Besnoitosis

26
Q

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?

A

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

27
Q

What are common physical and chemical cutaneous injuries?

A

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

28
Q

What different types of parasites can infect the cutaneous?

A

Flies

Lice

Fleas

Mites

29
Q

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?

A

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

30
Q

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?

A

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

31
Q

Where do demodex mites complete their lifecycle?

Where are there lesions found and how do they grossly appear?

How do the lesions appear histologically?

A

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

32
Q

What is the difference between autoimmunity and hypersensitivity?

A

Hypersensitivity is an immune reaction to an external irritant- pollen

Autoimmunity is a pathological immune reaction against self-antigens

33
Q

What are common hypersensitivities of the skin?

A

Uticaria

Atopic dermatitis

Food hypersensitivities

Insect hypersensitivties

34
Q

What is urticaria?

What are frequent causes?

How do lesions appear and distribute?

How does it appear histologically?

A

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

35
Q

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?

A

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

36
Q

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?

A

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

37
Q

What is pemphigus complex- pemiphigus foliaceus?

How do lesions grossly distribute and appear?

How do they histologically appear?

A

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

38
Q

What are the two forms of Dr Houses least favourite disease (Lupus erythematous)?

A

Systemic lupus erythematosus (SLE)
multiple organs with skin lesions in 1/3

Discoid lupus erythematous (DLE)
​localised cutaneous form

39
Q

How does discoid lupus erythematous grossly appear and distribute?

How does it appear histologically?

A

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)

40
Q

How does the skin respond following hypovitaminoses?:

Vitamin A

Vitamin B

Vitamin E

What mineral deficiencies can affect the skin?

A

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

41
Q

What hormonal imbalances cause dermatoses?

A

Hyperadrenocorticism

Hypoestrogenism

Hypothyroidism

42
Q

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?

A

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

43
Q

What do endocrinopathies cause grossly and histologically?

A

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

44
Q

What is cushings disease?
what can cause it?

How does it appear and distribute grossly?

How does it histologically appear?

A

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

45
Q

What causes hyperoestrogenism in male and female dogs?

A

Polycystic ovaries and functional ovarian neoplasms in female dogs

Oestrogen secreting tumours in intact males (sertolioma)

46
Q

What idiopathic eosinophilic diseases can affect cats and horses?

A

Feline-

  • eosinophilic plaque
  • eosinophilic granuloma
  • indolent ulcer

Equine

  • eosinophilic granuloma
  • multisystemic eosinophilic epitheliotropic disease
47
Q

What are the three presentations of feline eosinophilic dermatoses- granuloma complex

A

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

48
Q

What are the three different equine eosinophilic nodular disease?

A

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

49
Q

What are epidermal cysts?

What causes them?

A

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

50
Q

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

A
  • 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

51
Q

What causes a papilloma?

What causes susceptibility and regression?

What are the two types?

Why can they easily be associated with secondary infection?

A

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

52
Q

What are koilocytes?

A

Keratinocyes with eccentric pyknotic nucleus and peripheral clear halo (ballooning degeneration)

53
Q

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?

A

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

54
Q

How are follicular tumours classified

What are the different types?

A

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

55
Q

How do pilomatricomas appear?

What are they derived from?

A

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

56
Q

What are the different sebaceous gland tumours?

What types are A, B and C?

A

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

Year 3 Pathology (21 decks)

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