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Y3 - Skin pathology > Dermatopathology 2 > Flashcards

Dermatopathology 2 Flashcards

1
Q

Mycoses affecting the skin can be divided into which 3 types?

A
  • Cutaneous
  • Subcutaneous
  • Systemic
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2
Q

Describe cutaneous mycoses and give 2 examples

A
  • The most common mycoses types
  • Confined to the cornifies tissues
  • E.g. Malassezia dermatitis and Dermatophytosis
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3
Q

Describe subcutaneous mycoses

A

Huge variety of saprophytic fungi, remain localised

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4
Q

Describe systemic mycoses and name example causes

A

Haematogenous dissemination (e.g. Cryptococcus, Blastomyces, Coccidioides spp)

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5
Q

What is Dermatophytosis?

A

Superficial mycotic infection (“ringworm”) confined to the keratin layer of skin, claws and hair.

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6
Q

What are the 3 favourable conditions for Dermatophytosis?

A
  • Microabrasions or maceration of the stratum corneum in moist skin
  • Prolonged corticosteroid treatment
  • Transient or permanent immune deficiencies
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7
Q

How is Dermatophytosis transmitted, how does it then cause infection?

A
  • Via infected hair and keratin fragments

- Fungi migrate to the follicular lumen and proliferate along the entire follicle

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8
Q

How are Dermatophytosis lesions distributed?

A

Head and extremities

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9
Q

How do Dermatophytosis lesions appear grossly?

A

Gross: Circular expanding areas of scaling and alopecia. Often furunculosis and chronic pyogranulomas (kerion) develop and mimic tumours
First appears as a red colour and as the epidermis thickness (thickened keratin layer) increases the colour becomes greyish – this is the infectious part as it is covered in fungal spores

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10
Q

How does Dermatophytosis appear histologically?

A

Hyperkeratosis and acanthosis.
Luminal folliculitis, furunculosis and pyogranulomas.
Fugal spores lining the hair shaft.
Fungal hyphae admixed with serous crusts of the epidermal surface.

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11
Q

Describe the features of Leishmania parasite

A
  • Causes skin and systemic lesions
  • Obligate intracellular apicomplexan parasite of macrophages
  • Transmitted by blood sucking sand flies
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12
Q

Describe the two clinical forms of Leishmania

A

Alopecic: stronger Th1 response and fewer parasites
Nodular: predominant Th2 response and more numerous parasites

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13
Q

Describe the gross lesions distribution and appearance of Leishmania

A

Distribution: head, limbs and dorsal midline
Appearance: Variable. Nodules, alopecia, ulcers or pustules. Bilateral.

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14
Q

Describe the histological appearance of Leishmania

A

Hyperkeratotic, nodular to diffuse superficial and deep granulomatous dermatitis, variably dominated by plasma cells.

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15
Q

What is Myiasis?

A

The infestation of living tissues by the larval stages of dipterous flies

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16
Q

Describe how some dipterous spp migrate?

A
  • Some remain localised to the site of injury with limited local penetration
  • Others migrate from the wounded skin or the GI tract after ingestion and colonise -> development of cyst-like dermal structures with a central pore -> emerge from the pore and pupate in the environment
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17
Q

Describe inflammation associated with myiasis

A

Eosinophilic and lymphocytic inflammation (along migration tracks) and fibrous capsule with eosinophils and granulation tissue in the cystic dermal cavity

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18
Q

Name some examples of parasites that cause myiasis

A
  • Hypoderma bovis and H. Lineatum : cattle (warble)

- Blowflies (lucilia, calliphora, etc): sheep

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19
Q

Sarcoptic mange is caused by which parasite?

A

Sarcoptes scabei

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20
Q

What are some features of sarcoptic mange

A
  • Zoonotic, highly contagious and notifiable disease
  • Extremely pruritic
  • Common in pigs and dogs
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21
Q

How are sarcoptic mange lesions distributed?

A

Inner surface of the pinna, spreading to head, neck and legs

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22
Q

Where does Sarcoptes scabei live in the skin?

A

The parasite lives between the keratinocytes – it doesn’t go into the dermis it only lives within the dermis

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23
Q

Describe the histological appearance of sarcoptic mange

A

Severe acanthosis, parakeratosis, spongiosis, leukocyte exocytosis, eosinophilic pustules

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24
Q

Where do Demodex mites complete their life cycle?

A

Within the lumen of hair follicles

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25
Q

Describe the gross lesion appearance of Demodectic mange

A

Alopecia, scaling and comedones in the squamous form; pustules, folliculitis and furunculosis in pustular form (complicated by bacteria)

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26
Q

Describe the gross lesion distribution of Demodectic mange - localised and generalised forms

A

Localized form: Well-circumscribed self-limiting lesions on ears, lips, eyes and extremities
Generalized form: diffuse alopecia and scaling (face and legs)

27
Q

Describe the histological lesion appearance of Demodectic mange

A

Severe suppurative folliculitis and furunculosis (deep infection of the hair follicle leading to abscess formation with accumulation of pus and necrotic tissue)

28
Q

Give some examples of traumatic and chemical injuries

A
  • Mechanical forces
  • Hot temperatures/burns
  • Primary irritant contact dermatitis
  • Photosensitisation
29
Q

What are bruise?

A

The local effect of vigorous pressure (blunt trauma) can cause the occurrence of acute intradermal and/or subcutaneous haemorrhages

30
Q

What are the 3 molecular components of a bruise as it heals?

A

Haemoglobin -> biliverdin -> bilirubin

31
Q

How does a bruise occur?

A
  • Lesion will evolve rigorously following the steps of erythrocyte removal (recruited leukocytes and phagocytes) and haemoglobin catabolism (typical lesion colour)
  • Haemosiderin-laden macrophages can remain visible locally for a very long period of time after clinical resolution of the trauma
32
Q

What are the 3 types of blood discolouration?

A
  • Petechia (1mm)
  • Purpura (up to 1cm, coalescing petechiae)
  • Ecchymosis (> 1cm)
33
Q

How does haemorrhage resolution occur?

A

Incoming macrophages phagocytose extravasated erythrocytes

34
Q

Explain the steps involved in a bruise becoming yellow over time

A

3 – days after a bruise has occurred, inflammatory cells produce Haemosiderin because Hb produced by erythrocytes isn’t going anywhere, only macrophages can clear it, they keep the iron from Hb and the rest of it becomes bile (why a bruise becomes yellow over time)

35
Q

Define hypersensitivity

A

Any excess of immune response targeting an antigen from the outside world that would normally be unharmful to most of the population

36
Q

Give 4 examples of hypersensitivity reactions

A
  • Urticaria
  • Atopic dermatitis
  • Food hypersensitivity
  • Insect hypersensitivity
37
Q

Define autoimmunity

A

Pathological immune reaction against self-antigens

38
Q

Name some examples of autoimmune reactions

A
  • Pemphigo-complex diseases
  • Bullous pemphigoid
  • Lupus erythematosus
  • Erythema multiforme
  • Alopecia areata
39
Q

Why keratinocyte type make up most of the population?

A

Spinous keratinocytes

40
Q

Which layer of keratinocytes lies beneath spinous keratinocytes? What is their function?

A

Tiny cuboidal cells = basal keratinocytes – these continually proliferate

41
Q

Describe the top layer of the epidermis

A

The top layer is much flatter and contains a lot of granules which lead to the formation of keratin which is the final layer called the stratum corneum

42
Q

Describe the mechanism of action of hypersensitivity reactions

A
  • Macrophages (that liver permanently in the skin) are exposed to the antigen
  • They educate immune cells from the lymph node that arrive in the skin and lead to the production of immunoglobulins from plasma cells (IgE)
  • These attach themselves to muscles and lead to oozing of the muscle contents and blood (eosinophils)
43
Q

What is the name given to the mildest hypersensitivity reaction?

A

Urticaria

44
Q

How is urticaria characterised?

A

The oozing of a very protein poor fluid from the holes between endothelial cells - caused by the release of granules from muscles

45
Q

Describe the features of urticaria

A

Acute, variably pruritic, oedematous skin lesions -> Type I hypersensitivity reaction

46
Q

What are the causes of urticaria

A
  • Caused by mediators of basophils and mast cells

- Drugs, foods and food additives are frequent causes

47
Q

Describe the gross lesion distribution and appearance of urticaria

A

Distribution: variable, localised to widespread
Appearance: Discrete, well-circumscribed round erythematous and oedematous plaques

48
Q

Describe the histological appearance of urticaria

A

Variable and non-specific.

Subtle or prominent dermal oedema of the superficial dermis

49
Q

What is the cause of atopic dermatitis?

A

Increased production of IgE against “innocuous” antigens

50
Q

Atopic dermatitis is common in which spp?

A

West Highland terriers

51
Q

How does atopic dermatitis present clinically?

A

Intense pruritus (due to large eosinophil numbers)

52
Q

Describe the gross lesion distribution and appearance of atopic dermatitis

A

Distribution: Variable, but typically on the ventral sparsely-haired skin (head, paws, distal extremities and ventrum)
Appearance: excoriations, papules, pustules, hyperpigmentation and lichenification are considered secondary to trauma induced by pruritus

53
Q

Describe the histological appearance of atopic dermatitis

A

Perivascular to interstitial lymphoplasmacytic dermatitis with oedema, eosinophils, macrophages and variable degree of epidermal hyperplasia

54
Q

Where do antigens causing insect hypersensitivity come from?

A

Insect saliva, venom, whole body or faeces

55
Q

Insect hypersensitivities are which 2 classes of hypersensitivity reaction?

A

I and IV

56
Q

What are 2 examples of insect hypersensitivity reactions?

A
  • Flea-bite hypersensitivity: (“flea allergic dermatitis”)

- Culicoides hypersensitivity: horses (“sweet itch”).

57
Q

Describe the gross lesion distribution and appearance of insect hypersensitivity reactions

A

Distribution: Sparsely haired body regions. Lumbosacral region for flea-bite hypersensitivity
Appearance: Pruritic crusted papule -> hyperkeratosis, lichenification, seborrhoea and excoriation (secondary lesions)

58
Q

Describe the histological appearance of insect hypersensitivity reactions

A

Eosinophil dominated dermal perivascular to diffuse dermatitis with lymphocytes and fewer macrophages

59
Q

Describe the gross lesion distribution and appearance of Pemphigus foliaceus

A

Distribution: restricted to the skin (no mucosa). Starts from periocular and nasal skin (cat, dog) -> ears, neck and ventral abdomen
Appearance: erythematous maculae -> pustules -> erosion and crusts

60
Q

Describe the histological appearance of Pemphigus foliaceus

A

Acantholytic (loss of cohesion between keratinocytes) subcorneal or intragranular pustular dermatitis

61
Q

Name the two forms of lupus erythematosus

A
  • Systemic lupus erythematosus (SLE)

- Discoid lupus erythematosus (DLE)

62
Q

Describe the gross lesion distribution and appearance of Discoid lupus erythematosus

A
  • Restricted to the nasal planum

- Erythema, depigmentation, scaling, crusting, alopecia and ulcers

63
Q

Describe the histological appearance of Discoid lupus erythematosus

A

Epidermal hyperplasia, denser interface infiltrate dominated by lymphocytes (few plasma cells)

Y3 - Skin pathology (4 decks)

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