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Clinical pathology > Inflammatory skin pathology and skin tumours > Flashcards

Inflammatory skin pathology and skin tumours Flashcards

1
Q

Eczema/Dermatitis stages

A

Clinically 3 stages:

  • Acute dermatitis = Skin red, weeping serous exudate +/- small vesicles
  • Subacute dermatitis = Skin is red, less exudate, itchier, crusting
  • Chronic dermatitis = Skin thick and leathery, secondary to scratching
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2
Q

Eczema/Dermatitis histology

A
  • Spongiosis = = intercellular oedema within epidermis

- Chronic inflammation – predominantly superficial dermis

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3
Q

Atopic eczema

A
  • Usually starts in childhood, Often FH and associated with asthma and allergic rhinitis
  • Type 1 hypersensitivity reaction to allergen
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4
Q

Contact irritant dermatitis

A
  • Direct injury to skin by irritant; affects anyone in contact with irritants e.g. acid, detergent
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5
Q

Contact allergic dermatitis

A
  • Affects those with hypersensitivity to irritant; combines with epidermal proteins to become immunogenic; e.g. nickel, dyes, rubber
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6
Q

Dermatitis of unknown aetiology

A
  • Seborrheic dermatitis – affects areas rich in sebaceous glands – scalp, forehead, upper chest
  • Nummular dermatitis – coin shaped lesions
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7
Q

Psoriasis definition

A
  • 1-2% of population
  • Well defined, red oval plaques on extensor surfaces (knees, elbows, sacrum)
  • Fine silvery scale
  • Auspitz sign = small bleeding points after removal of scale layers
    o+/- pitting nails. +/- sero-negative arthritis
  • Cancer – increased risk of non-melanoma skin cancer
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8
Q

Psoriasis histology

A
  • Psoriasiform hyperplasia
  • Regular elongated club shaped rete ridges
  • Thinning of epidermis over dermal papillae
  • Collection of neutrophils in scale – Munro micro-abscesses
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9
Q

Psoriasis aetiology

A
  • Genetic – FH: multiple loci e.g. PSORS gene in MHC of Chromosome 6p2
  • Environmental – infection, stress, trauma, drugs
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10
Q

DLE =

A
  • Discoid lupus erythematosus – skin only
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11
Q

SLE =

A
  • Systemic–visceral disease

- Butterfly rash on cheeks and nose

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12
Q

Lupus Erythematosus

A
  • Red scaly patches on sun-exposed areas, scalp involvement
  • Autoimmune disorder primarily affecting connective tissue
  • Histology:
    Thin atrophic epidermis with thickened basement membrane
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13
Q

Dermatomyositis

A

Symptoms:

  • Peri-ocular oedema and erythema (Heliotropic rash)
  • Erythema in photosensitive distribution
  • Myositis – proximal muscle weakness - can check for CK
  • 25% associated with underlying visceral cancer
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14
Q

Bullous pemphigoid

A
  • Formation of fluid filled blisters
  • Sub-epidermal
  • Ends in D = deep
  • Autoantibodies to glycoprotein in basement membrane. Destruction causes blister formation which do not rupture
  • Elderly
  • Can be localised or extensive disease
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15
Q

Dermatitis Herpetiformis

A
  • Small intensely itchy blisters on extensor surfaces
  • Often young patients - associated with coeliac disease
  • IgA deposition in dermal papillae on immunofluorescence
  • Histology – neutrophil micro-abscesses in dermal papillae – sub-epidermal bulla
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16
Q

Basal Cell Carcinoma

A
  • Commonest malignant tumour of skin
  • Aetiology = sun exposure, radiotherapy, Gorlin’s syndrome
    Clinically:
  • Early – nodule
  • Late – rodent ulcer
  • Morphoeic BCC = ill-defined and infiltrative
  • Histology - islands of basaloid cells
17
Q

Squamous cell carcinoma aetiology

A
  • UV irradiation
  • Radiotherapy
  • Hydrocarbon exposure
  • Chronic scars/ulcers (SCC arises with these)
  • Immunosuppressed – renal transplant patients at increased risk
  • Drugs – e.g. BRAF inhibitors for melanoma
18
Q

Squamous cell carcinoma features

A
  • Clinically - nodule with ulcerated crusted surface

- Histology - invasive islands wit trabeculae of squamous cells with cytological atypia

19
Q

Acitinic Keratosis

A
  • Pre-malignant disease of SCC
  • Dysplasia to squamous epithelium
  • Very common on chronic sun exposed sites
  • Scaly lesion with erythematous base
20
Q

Melanocyte tumours

A
  • Melanocytes derive from neural crest
  • Function – produce melanin which is transferred to epidermal cells to protect the nucleus from UV radiation
  • Give rise to naevi/moles (benign) and melanoma (malignant)
21
Q

Naevi/moles

A
  • Local benign collections of melanocytes
    Several types:
  • Superficial – congenital or acquired
  • Deep – blue naevi (Mongolian spot)
22
Q

Atypical mole syndrome

A
  • Families with increased incidence of melanoma
  • Multiple clinically atypical moles
  • Histologically atypical/ dysplastic
  • Increased risk of developing melanoma
23
Q

Melanoma risk factors

A
  • Sun exposure – especially short intermittent severe exposure
  • Race – celtic with red hair, blue eyes, fair skin who tan poorly most at risk.
  • Family history – atypical mole syndrome
  • Giant congenital naevi
24
Q

Lentigo Maligna Melanoma

A
  • Face, elderly people, slow growing, flat, pigmented patch
  • Proliferation of atypical melanocytes along basal layer of epidermis
  • Skin also shows signs of chronic sun damage
  • Late in disease, melanocytes may invade dermis which can metastasise
25
Q

Acral Lentiginous Melanoma

A
  • Palms and soles; commonest form in afro-Caribbean people
  • Forms enlarging pigmented patch
  • No marked sun damage
26
Q

Superficial spreading melanoma

A
  • Commonest type of melanoma in UK
  • Early – flat macule
  • Late – black/blue nodule
  • Histology – proliferation of atypical melanocytes which invade epidermis and dermis
  • Genetics – often BRAF mutations targets for anticancer agents.
27
Q

Nodular melanoma

A
  • Starts as pigmented nodule +/- ulceration
  • Poor prognosis
  • Histology – invasive atypical melanocytes invade dermis to produce nodules of tumour cells
28
Q

Prognosis of melanoma

A
  • Most important factor = Breslow thickness
  • Measure on microscope from granular layer of epidermis to base of tumour
  • Back, arms, neck, scalp = poorer prognosis
  • Sentinel node - first to be drained and tested
29
Q

Treatment of melanoma

A
  • Surgery – excise primary and lymph nodes if sentinel node is +ve
  • BRAF inhibitors – 60% of melanomas have B-RAF gene mutations
30
Q

Breslow thickness thresholds

A 
Breslow thickness (mm)	5yr survival %
<1	91-95
1-2	75-90
2-4	60-75
>4	45-60

Clinical pathology (69 decks)

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