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Y2 Clinical Pathology > Inflammatory Skin Pathology & Skin Tumours > Flashcards

Inflammatory Skin Pathology & Skin Tumours Flashcards

1
Q

What are the 2 categories of inflammatory skin disease and examples?

A

infectious

non-infectious inflammatory diseases:

  • dermatitis / psoriasis
  • blistering
  • connective tissue diseases
    • e.g. lupus erythematosus / dermatomyositis
  • skin lesions as a sign of systemic disease
  • skin lesions caused by metabolic disorders

plus some rare types

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2
Q

How common is eczema / dermatitis?

How severe it is?

A

it is very common and affects 5% of children in UK

it varies from trivial to severe

it is a reaction pattern rather than a specific disease

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3
Q

What are the 3 clinical stages of dermatitis (eczema)?

A

1. acute dermatitis:

  • red skin, weeping serous exudate +/- small vesicles

2. subacute dermatitis:

  • red skin, less exudate, lots of itching, crusting

3. chronic dermatitis:

  • skin is thick and leathery secondary to scratching
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4
Q

What are the 3 things seen in the microscopy in dermatitis?

A

spongiosis:

  • intercellular oedema within epidermis

chronic inflammation:

  • predominantly superficial dermis

epidermal hyperplasia & hyperkeratosis:

  • mild in acute dermatitis
  • marked in chronic dermatitis
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5
Q

What is visible in this image?

A

spongiosis in eczema

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6
Q

What is atopic eczema?

When does it occur?

A

it is a type 1 hypersensitivity reaction to an allergen

it usually starts in childhood, but occasionally occurs in adults

there is often a family history and it is often associated with asthma and hay fever

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7
Q

What are the 2 types of contact dermatitis?

What causes them?

A

contact irritant dermatitis:

  • direct injury to skin by an irritant
  • e.g. acid, alkali, strong detergent

contact allergic dermatitis:

  • e.g. nickel, dyes, rubber
  • act as haptens which combine with epidermal protein to become immunogenic
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8
Q

What are the morphological subtypes of dermatitis of unknown aetiology?

A

seborrhoeic dermatitis:

  • affect areas rich in sebaceous glands
  • e.g. scalp, forehead, upper chest

nummular dermatitis:

  • coin shaped lesions
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9
Q

What is psoriasis?

What % of the population are affected?

A

well defined, red oval plaques on extensor surfaces (knees, elbow, sacrum)

they have a fine silvery scale and Auspitz sign

removal of the scale causes small bleeding points

+/- pitting nails, +/- sero-negative arthritis

affects 1-2% of the population

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10
Q

What are the microscopic features of psoriasis?

A

“psoriasiform hyperplasia” has a distinct appearance:

  • regular elongated club shaped rete ridges
  • thinning of epidermis over dermal papillae
  • parakeratotic (contain nuclei) scale
  • collections of neutrophils in scale (Munro microabscesses)
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11
Q

What is the pathogenesis of psoriasis?

A

the clinical and microscopic features reflect massive cell turnover

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12
Q

What is shown here?

A

psoriasis

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13
Q

What are the genetic factors and environmental trigger factors involved in the aetiology of psoriasis?

A

genetic factors:

  • some have family history
  • multiple loci (psoriasis susceptibility or PSORS genes) with many in the region of MHC on chromosome 6p2 implicated
  • this is the same area involved in other autoimmune disorders

environmental trigger factors:

  • these are acquired factors
  • infection, stress, trauma, drugs
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14
Q

What is the associated comorbidity in psoriasis?

A
  • arthropathy (disease of the joints) associated in 5-10% cases
  • psychosocial effects
  • cardiovascular disease increased risk by 2-3 x
  • cancer - increased risk of non-melanoma skin cancer & lymphoma
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15
Q

What are the 2 different types of lupus erythematosus?

A

discoid LE

  • affects the skin only

systemic LE

  • this is a visceral disease that may or may not involve the skin
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16
Q

What does lupus erythematosus look like clinically?

A
  • red scaly patches on sun-exposed skin +/- scarring
  • scalp involvement causes alopecia
  • butterfly rash on cheeks and nose in SLE
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17
Q

What is lupus erythematosus?

What body parts can it affect?

A

an autoimmune disorder primarily affecting connective tissues of the body

autoantibodies are directed at various tissues

it may affect any part of the body, but importantly kidneys

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18
Q

What does lupus erythematosus look like microscopically?

A

thin, atrophic epidermis with inflammation and destruction of adnexal structures

IMF - LE band

IgG deposited in basement membrane

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19
Q

How does systemic lupus erythematosus (SLE) affect the body?

A
  • 30% CNS involvement
  • 50% butterfly erythema
  • 50% pleuropericarditis
  • 50% renal involvement
  • 20% discoid skin involvement
  • 90% arthralgia, arthritis
  • 80% common symptoms (fever, fatigue)
  • 70% vasculitis / skin involvement
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20
Q

what is shown here?

A

lupus erythematosus

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21
Q

What technique is used to detect lupus erythematosus?

A

immunofluorescence

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22
Q

What is dermatomyositis?

what test can be performed?

A

peri-ocular oedema and erythema (Heliotropic rash)

erythema in photosensitive distribution

myositis - proximal muscle weakness

(can check for creatinine kinase)

25% cases are associated with underlying visceral cancer

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23
Q

What is a heliotropic rash?

A

reddish purple rash on or around the eyelids

it is often accompanied by swollen eyelids

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24
Q

What does the microscopy look like in dermatomyositis?

A
  • similar to lupus erythematosus
  • often a lot of dermal mucin
  • negative IMF
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25
Q

What are bullous diseases?

A

formation of fluid filled blisters

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26
Q

What is the difference between pemphigus and pemphigoid?

A

pemphigus:

  • affects the outer layer of the skin (epidermis)
  • causes lesions and blisters that are easily ruptured

pemphigoid:

  • affects a lower layer of the skin, between the epidermis and the dermis
  • causes tense blisters that do not break easily
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27
Q

What is pemphigus?

What types of blisters does it involve in?

A

group of disorders characterised by loss of cohesion between keratinocytes resulting in an intraepidermal blister

all types cause fragile blisters / bullae which rupture easily

can be extensive +/- involve mucous membranes

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28
Q

What is the pathogenesis of pemphigus?

A

autoantibodies directed against intercellular material

can be detected by immunofluorescence (IMF)

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29
Q

What is bullous pemphigoid?

What are the blisters like?

A

a disease characterised by subepidermal blisters

elderly with large tense bullae which do not rupture easily

it can be localised or extensive disease

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30
Q

What is the pathogenesis of bullous pemphigoid?

A

autoantibodies to glycoprotein in the basement membrane

it can be detected by IMF

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31
Q

What is dermatitis herpetiformis?

What is it associated with?

A

small intensely itchy blisters on extensor surfaces

often affects young patients and is associated with coeliac disease

32
Q

What is the IMF and histopathology associated with dermatitis herpetiformis?

A

IgA deposition in dermal papillae on IMF

histopathology shows neutrophil microabscesses in dermal papillae

33
Q
A
34
Q

What is shown here?

A

dermatitis herpetiformis

small intensely itchy blisters on extensor surfaces

35
Q

What type of bullae are present in dermatitis herpetiformis?

A

subepidermal bulla

IgA is present in dermal papillae

36
Q

What systemic diseases can dermatomyositis and dermatitis herpetiformis be sign for?

A

dermatomyositis is a sign of visceral cancer

dermatitis herpetiformis is a sign of coeliac disease

37
Q

What is acanthosis nigricans and what systemic disease can it be a sign for?

A

dark warty lesions present in the armpits

it can be a sign of internal malignancy

38
Q

What is necrobiosis lipoidica and what systemic disease can it be a sign of?

A

red and yellow plaques on the legs

a sign of diabetes mellitus

39
Q

What is erythema nodosum and what systemic disease can it be a sign of?

A

red tender nodules on the shins

associated with infections elsewhere (especially in lungs), drugs and other diseases

40
Q

What type of skin tumours arise from the epidermis, melanocytes and Merkel cells?

A

epidermis:

  • basal cell carcinoma
  • squamous cell carcinoma

melanocytes:

  • naevi
  • melanoma

Merkel cell:

  • Merkel cell tumour (rare but dangerous)
41
Q

What type of skin tumours arise from adnexal structures, nerves/blood vessels and connective tissue?

A

adnexal structures:

  • sweat gland and hair follicle tumours and cysts

nerves & blood vessels:

  • haemangioma
  • neuromas

connective tissue:

  • dermatofibroma
42
Q

What is the aetiology of basal cell carcinoma?

Does it metastasise?

A

aetiology:

  • sun exposed site, especially on the face
  • occasionally can be secondary to radiotherapy
  • pale skin that burns easily
  • immunosuppression

it is the commonest malignant tumour and metastases are very rare

43
Q

What is a rare complication of basal cell carcinoma?

A

Gorlin’s syndrome

this is a condition that affects many areas of the body and increases the risk of developing various cancerous and noncancerous tumours

44
Q

What does BCC look like clinically in the early and late stages?

A
  • early - nodule
  • late - ulcer (rodent ulcer)

image shows rodent ulcer with rolled edges

45
Q

What does BCC look like microscopically?

A

tumour composed of islands of basalooid cells with peripheral palisade

46
Q

What is morphoeic BCC?

What does this look like clinically?

A

the morphoeic basal cell carcinoma (mBCC) is the most aggressive subtype

it spreads into the dermis beyond the clinically visible or palpable borders, making complete excision difficult

it is ill-defined and infiltrative

47
Q

What are the different causes of squamous cell carcinoma?

A

UV irradiation:

  • usually occurs in sun exposed sites with increased risk in tropical countries

radiotherapy

hydrocarbon exposure:

  • tars, mineral oils, soot
  • e.g. SCC was found in scrotum of chimney sweeps

chronic scars / ulcers:

  • SCC arises within these (Marjolins ulcer)

immunosuppresion:

  • renal transplant patients at increased risk

drugs:

  • some newer drugs for melanoma (BRAF inhibitors)
48
Q

What does SCC look like clinically and microscopically?

A

clinically:

  • nodule with ulcerated, crusted surface

microscopically:

  • invasive islands and trabeculae of squamous cells showing cytological atypia
49
Q

Does SCC metastasise?

What are other high risk features?

A

metastases in 5% to the lip, ear and perineum

high risk features:

  • > 2cm
  • > 4mm thick
  • high grade
50
Q

What is actinic keratosis?

What causes it?

A

a scaly lesion with an erythematous base that is very common on chronic sun exposed sites

it involves dysplasia to squamous epithelium

51
Q

What can actinic keratosis lead to?

A

it is a pre-malignant disease

it only rarely progresses to invasive squamous cell carcinoma

it may spontaneously resolve

52
Q

What is shown here?

A

actinic keratosis

(caused by chronic sun exposure)

53
Q

Where are melanocytes derived from?

What is their function?

A

melanocytes are derived from the neural crest

they form melanin

this is transferred to epidermal cells to protect the nucleus from UV radiation

54
Q

What tumours do melanocytes give rise to?

A

benign - naevi (moles)

malignant - melanoma

55
Q

What are naevi (moles)?

What are the different types?

A

local benign collections of melanocytes

superficial:

  • can be congenital or acquired

deep:

  • blue naevi (mongolian spot)
56
Q

What is atypical mole syndrome?

What are patients at an increased risk of?

A

multiple clinically atypical moles

histologically atypical / dysplastic naevi

seen in families with increased incidence of melanoma and associated with increased risk of developing melanoma

57
Q

What is shown here?

A

common naevus (mole)

58
Q

How dangerous and common is melanoma?

A
  • it is much rarer than BCC and SCC but incidence is rapidly rising
  • it is a very dangerous malignancy which can metastasize widely
59
Q

What is the ABCD approach to distinguishing between a naevus and melanoma?

A

Naevus:

  • symmetrical
  • Borders even
  • Colour uniform
  • Diameter < 6mm

Melanoma:

  • Asymmetrical
  • Borders uneven
  • Colour variation
  • Diameter > 6mm
60
Q

What 4 factors increase the risk of melanoma?

A

sun exposure:

  • especially short intermittent severe exposure

race:

  • celtic with red hair, blue eyes, fair complexions who tan poorly are most at risk
  • melanoma is rare in dark skinned people

family history:

  • atypical mole syndrome - multiple large atypical moles

giant congenital naevi:

  • small risk of turning malignant (<5%)
61
Q

What is lentigo maligna?

Who is usually affected?

A

a slow growing, flat, pigmented patch usually seen in elderly people

it is an early form of melanoma in which the malignant cells are confined to the tissue of origin (epidermis)

it occurs in sun damaged skin so is often found on the face or neck

62
Q

What is the microscopic appearance of lentigo maligna?

What happens late in the disease?

A

proliferation of atypical melanocytes along the basal layer of the epidermis

skin also shows signs of chronic sun damage

late in disease, melanocytes may invade the dermis with potential to metastasise (lentigo maligna melanoma)

63
Q

What is acral lentigenous melanoma?

Who is it most commonly seen in?

A

it is a specific type of melanoma that appears on the palms of the hands, the soles of the feet or under the nails (subungual)

the commonest form is seen in afro-carribbeans where it forms an enlarging pigmented patch

64
Q

What is the microscopy of acral lentigenous melanoma like?

A

similar to lentigo maligna except no marked sun damage

65
Q

What does superficial spreading melanoma look like?

A

it slowly grows horizontally across the top layer of skin before moving to the deeper layers

early - flat macule

late - blue / black nodule

most common type of melanoma

66
Q

What is the microscopy of superficial spreading melanoma like?

A

proliferation of atypical melanocytes which invade the epidermis [pategoid spread] and dermis

67
Q

What is meant by pategoid spread?

A

the “upward spreading” of normal cells in the epidermis

it is uncommon and a possible indication of a precancerous or cancerous condition

cells invade the upper epidermis from below

68
Q

What are the genetics implicated in superficial spreading melanoma?

A

often, BRAF mutations are the target for anticancer agents

69
Q

What is shown here?

A

melanoma

this image shows a melanoma with pagetoid spread

70
Q

What is a nodualr melanoma?

What is the prognosis like?

A

starts as a pigmented nodule +/- ulceration

it is a dangerous form of melanoma that grows quickly and has poor prognosis

71
Q

What is the microscopy of nodular melanoma like?

A

invasive atypical melanocytes invade dermis to produce nodules of tumour cells

72
Q

What is Breslow thickness?

How can it be used to predict 5-year survival rates for primary melanoma?

A

measure on microscope from granular layer of epidermis to the base of the tumour

it gives a 5-year survival rate for primary melanoma

73
Q

Which sites have a poorer prognosis in melanoma?

A

BANS

  • back
  • arms (posterior upper)
  • neck
  • scalp

all these sites have a poorer prognosis

74
Q

What are the other 3 prognostic factors implicated in melanoma?

A

ulceration

satellites / in-transits:

  • these are cutaneous deposits that occur before the first lymph node

sentinel node:

  • lymph node which drains from the melanoma first
  • it is removed, and if positive, the rest of the lymph nodes in that anatomic area are removed to try and halt disease progression
75
Q

What are the treatment options for melanoma?

A
  • surgery - excise primary melanoma and lymph nodes if the sentinel node is positive
  • BRAF inhibitors - 60% of melanomas have a mutation in the B-raf gene

Y2 Clinical Pathology (76 decks)

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