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CLINICAL PATHOLOGY > Theme 10 - INFLAMMATORY SKIN PATHOLOGY > Flashcards

Theme 10 - INFLAMMATORY SKIN PATHOLOGY Flashcards

1
Q

eczma/ dermatitis is most commonly caused by what hypersensitivity reaction?

A

Type 1 hypersensitivity to allergen(s)

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2
Q

when is atopic eczema onset?

A

Usually starts in childhood
Often family history
Often associated with asthma and hay fever.

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3
Q

what are the three clinical stages of dermatitis?(eczema)

A

acute dermatitis (red skin, weeping exudate with small vesicles)

subacute dermatitis - skin is red, less exudate and there is more itching and crusting

Chronic dermatitis - skin is thick, leathery and there is secondary scratching

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4
Q

what is spongiosis?

A

microscopy of eczema = spongy appearance of the blistering of skin

characterised by rounding of keratinocytes and widening of intercellular spaces

formation of small intraepidermal vesicles.

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5
Q

what is contact irritant dermatitis?

A

direct injury to the skin by irritant like acid

type 4 hypersensitivity

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6
Q

what is contact allergic dermatitis?

WHAT HYPERSENSITIVITY REACTION IS IT?

A

nickel, dyes, rubber -

act as haptens that combine with epidermal protein to become immunogenic

type 4 hypersensitivity

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7
Q

aetiology of dermatitis

A

unknown

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8
Q

what is psoriasis presented as?

A

scaly patches on the extensor surfaces and hair bearing areas like the scalp

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9
Q

aetiology of psoriasis

A

GENETICS:

  1. family history
  2. susceptibility genes (PSORS)
  3. major histocompatability complex on chromosome 6p2
  4. environmental - stress, trauma, drugs and infection
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10
Q

associated comorbidity of psoriasis is

A

arthropathy

psychological effects on self esteem

cardiovascular disease

cancer

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11
Q

Lupus erythematosus types

A

Discoid LE - skin only

Systemic LE - visceral disease that involves skin

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12
Q

Lupus erythematosus clinical signs and symptoms

A

Red scaly patches on skin
Scarring
Alopecia
Butterfly rash on cheeks and nose (in SLE)

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13
Q

microscopy of lupus

A

thin atrophic epidermis

Inflammation and destruction of adnexal structures

IgG deposited in the basement membrane

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14
Q

dermatomyositis -

A

an autoimmune condition
that causes skin changes and muscle weakness.

Symptoms can include:

periocular oedema and erythema

(swelling around the eyes called a heliotropic rash)

Myositis - proximal muscle weakness

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15
Q

What are bullous diseases?

A

disorders that cause blistering of the skin

diagnosed by fluoresence in microscopy

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16
Q

what is pemphigus?

A

there is a loss of cohesion between keratinocytes that result in intra-epidermal blisters

blisters are more soft and tend to break & can involve mucous membranes

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17
Q

what is pemphigoid?

A

Sub epidermal blisters that are tough and don’t easily rupture

Intermediate filaments are detected in the basement membrane

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18
Q

dermatitis hepatiformis - how does it present?

A

intensely itchy rash
sub-epidermal blisters
IgA deposition in dermal papillae

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19
Q

EXAMPLES of skin lesions and them being signs of systemic disease

A
  1. Dermamyositis - sign of visceral cancer
  2. Dermatitis hepatiformis - coeliac disease
  3. Acanthosis nigricans - dark warty lesions are associated with internal malignancy
  4. Necrobiosis lipoidica - (red and yellow plaques on the legs) associated with diabetes
  5. Erythema nodosum - red tender nodules on the shins
    associated with infections around the body especially lungs
20
Q

How common are skin tumours?

A

Skin tumours are the most common type of malignancy

21
Q

Which elements of the skin can tumours arise from? (6 examples)

A

All elements of the skin:
EPIDERMIS - basal cell carcinomas and squamous cell carcinomas
MELANOCYTES - Naevi and melanoma
MERKEL CELL TUMOUR - rare but dangerous
ADNEXAL STRUCTURES - sweat gland and hair follicle tumours and cysts
NERVES AND BLOOD VESSELS - haemangioma and neuromas
CONNECTIVE TISSUE - dermatofibromas

22
Q

Basal cell carcinoma - how common is it, what is the aetiology?

A

Commonest malignant tumour
due to sun exposure - Usually in pale skin that burns easily e.g. of the face but can be secondary due to radiotherapy

usually disease of the elderly but Gorlin’s syndrome can cause multiple BCCs in any age

23
Q

What is the clinical appearance of basal cell carcinomas?

A

Early stages - nodule

Late stages - ulcer (rodent ulcer)

They are often ill defined and infiltative.

24
Q

what is the microscopic appearance of BCCs?

A

tumour is composed of islands of basaloid cells with peripheral palisade

(palisade looking like a picket fence with basaloid cells inside forming a tumour)

25
Q

Do BCC metastasize?

A

Basal cell carcinomas do not met. but they grow in size and on the face this can reach the eye/ear/nose

26
Q

Squamous cell carcinomas - where do they occur and who gets it?

A

UV irridiation
occurs in sun exposed sides
Can occur secondary to radiotherapy and exposure to hydrocarbons e.g. tars and mineral oils

CAN BE CHRONIC ULCERS and those who are immunocompromised are at high risk

27
Q

What is the clinical appearance of SCC?

A

Nodule with ulcerated and crusted surface

Can metastasise e.g. in lips, ear and perineum

28
Q

what is the microscopic appearance of SCC?

A

Invasive islands and columns of squamous cells

These cells show cytological atypia

29
Q

what is Actinic keratosis?

A

Pre malignant disease to SCC

Caused by:
Dysplasia to squamous epithelium

30
Q

what are melanocytes?

A

derived from neural crest embryologically

form melanin which is transferred to epidermal cells to protect nucleus from UV

31
Q

What is Naevi (moles)?

A

local benign collections of melanocytes that can be:

Superficial: congenital or acquired

Deep: blue naevi (mongolion spot) because they have stopped the process of maturation

32
Q

what is atypical mole syndrome?

A

Families have increased incidence of melanoma

Histologically atypical and dysplastic naevi (abnormal growth and morphology)

33
Q

what are giant congenital naevi?

A

immatured melanocytes that appear as a large blue/black spot on an infant

34
Q

Epidemiology of melanomas - How rare is it and what is the incidence like?

A

Much rarer than BCC and SCC

Incidence is rising rapidly

Very dangerous malignancy which can metastasize widely

35
Q

What are the observational differences between Naevi and melanomas?

A

Naevi are:

Symmetrical
Borders are even
Uniform in colour
Have a diameter below 6mm

Melanomas:
Asymmetrical
Borders uneven
Colour variation
Diameter greater than 6mm
36
Q

What are the risk factors for melanoma?

A

Sun exposure - short intermittent severe exposure (australia)
Race - pale skin and blue eyes are most at risk
Family history - atyptical mole syndrome are at risk
Giant congenital naevi - small risk of turning malignant

37
Q

What is superficial spreading melanoma, how does it appear clinically and microscopically?

A

The most common type of melanoma in the UK

Early - flat macule
Late - blue/black nodule

Proliferation of atypical melanocytes which invade epidermis and dermis

38
Q

BRAF mutations are…

A

target for anti cancer agents

39
Q

What is nodular melanoma?

A

Pigmented (blue black) nodules with ulceration

Invasive atypical melanocytes that invade the dermis

Produce tumour cells in the dermis - poor prognosis

40
Q

What is lentigo maligna?

A

Slow growing, flat and pigmented patches in the faces of elderly people.

41
Q

Lentigo maligna microscopic appearance and clinical appearance

A

Proliferation of atypical melanocytes along basal layer of epidermis

Skin shows signs of chronic sun damage

42
Q

What is acral lentigenous melanoma?

A

melanoma found on palms of hands, soles of feet and in afro-caribbean patients.

No marked sun damage

43
Q

Breslow thickness

A

Measure on microscope from granular layer of epidermis to base of tumour.
5 year survival rates for primary melanoma
Breslow tumour
< 1 91-95
1 - 2 75-90
2 - 4.00 60-75
>4.00 45-60

44
Q

Prognostic factors of skin malignancies

A
  1. Site - BANS - back, arms (posterior upper), neck, scalp.
    All poorer prognosis
  2. Ulceration
  3. Satellites/ in-transits [cutaneous deposits]

Sentinel Node. (Lymph node which drains from melanoma first)

Removed and if positive, rest of lymph nodes in that anatomic area removed.

45
Q

What treatment options are available for skin malignancy?

A

Surgery –
excise primary and + lymph nodes if sentinel node positive

BRAF inhibitors-
60% melanoma’s have mutation in B-raf gene. Can use BRAF inhibitors.
Mutations conferring resistance almost inevitable

Immunotherapy –
can provide sustained remission
does not require a specific mutation

CLINICAL PATHOLOGY (56 decks)

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