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Clinical Pathology > Inflammatory skin diseases, skin tumours and the eye > Flashcards

Inflammatory skin diseases, skin tumours and the eye Flashcards

1
Q

Which infections can cause inflammation of the cornea and conjunctiva?

A

Herpes varicella zoster of trigeminal nerve

Chlamydia (2 forms)

  • Trachoma: tropical disease. Common cause of blindness
  • Mild disease due to Chlamydia types d-k, aquired during birth from infection in genital tract
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2
Q

What are the causes of cataracts?

A

Senile degeneration

Rubella

Down’s Syndrome

Irradiation

Diabetes Mellitus

Uveitis

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3
Q

What are the causitive agents in retina infections?

A

Toxoplasma: Cat is host and oocyst in faeces.

  • Congenital infection cause severe bilateral disease.
  • Acquired causes focal inflammatory disease.

Toxocara canis: from infected dog faeces, larva may migrate to retina and die causing localised inflammation.

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4
Q

What are the possible causes of retinal vascular disease?

A

Ischaemia

  • atheroma
  • vasculitis
  • embolis of retinal artery.
  • Can look for changes using ophthalmoscope

Hypertensive retinopathy:
- flame shaped haemorrhages and exudates

Diabetic retinopathy
- dot and blot haemorrhages and exudates

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5
Q

What is macular degeneration?

A

Damage to macule, the central part of vision

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6
Q

What are the two forms of macular degeneration?

A

1] Dry macular degeneration [age related]

  • 90% cases
  • Affects >60years old
  • progressive visual impairment
  • no treatment

2] Wet macular degeneration

  • 10%
  • due to new vessel growth beneath retina
  • treat with drugs and lasers
  • drugs inhibit vessel growth injected directly into the eye.
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7
Q

What is retinoblastoma?

A

Rare. 10% familial. Genetics, deletion of long arm chromosome 13, loss of RB gene.

Tumour occurs in retina. Treat with enucleation and DXT

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8
Q

How does melanoma arise in the eye?

A

Arise melanocytes of Uveal tract [Iris, ciliary body or choroid].

2 types on genetic profiling

  • type 1 , good prognosis
  • type 2; poor prognosis.

Treat with radiotherapy and surgery.

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9
Q

Which common viral infections cause inflammatory skin diseases?

A

HPV
- warts, condylomas

HSV

  • 1 cold sores
  • 2 genital herpes

Herpes Varicella zoster

  • chickenpox
  • shingles
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10
Q

What are the three stages of dermatitis (eczema)?

A

Acute dermatitis

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

Subacute dermatitis

  • skin is red
  • less exudate
  • itching ++, crusting.

Chronic dermatitis

  • skin thick and leathery
  • secondary to scratching.
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11
Q

What is seen on microscopy in eczema?

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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12
Q

What is atopic eczema?

A

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

Type 1 hypersensitivity reaction to allergen.

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13
Q

What is contact irritant dermatitis?

A

Contact irritant dermatitis
- direct injury to skin by irritant, eg acid, alkali, strong detergent, etc

Contact allergic dermatitis

  • nickel, dyes, rubber
  • act as haptens which combine with epidermal protein to become immunogenic.
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14
Q

What are the other forms of dermatitis?

A

Seborrhoeic dermatitis

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

Nummular dermatitis
- coin shaped lesions.

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15
Q

What are the features of psoriasis?

A

Well defined, red oval plaques on extensor surfaces

  • knees, elbows, sacrum
  • fine silvery scale.

Auspitz sign.

Removal of scale causes small bleeding points.

+/- pitting nails.

+/- sero-negative arthritis.

1-2% of the population

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16
Q

What is seen on microscopy in psoriasis?

A

“Psoriasiform hyperplasia” - 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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17
Q

What is the pathogenesis of psoriasis?

A

Clinical and microscopic features reflect massive cell turnover

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18
Q

What is the aetiology of psoriasis?

A

Genetic factors

  • Some have family history. - Multiple loci [PSORS] in region of major histocompatibility complex on Chromosome 6p2 implicated
  • Same area involved in other autoimmune disorders eg IBD,MS

Environmental trigger factors

  • infection,
  • stress
  • trauma
  • drugs
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19
Q

Which comorbidities are associated with psoriasis?

A

Arthropathy
- 5-10% associated

Psychosocial effects

Cardiovascular disease

  • 2-3x risk
  • ?inflammation
  • drugs
  • stress
  • smoking

Cancer

  • increased risk Non-melanoma skin cancer [eg BCC]
  • Lymphoma
  • ? Disease or treatment effect.
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20
Q

What is lupus erythematosus?

A

Discoid LE
- skin only

Systemic LE (SLE)
- visceral disease
+/- involves skin.

Clinically
- red scaly patches on sun-exposed skin
+/- scarring
- scalp involvement causes alopecia.

SLE
- Butterfly rash on cheeks and nose.

Auto-immune disorder primarily affecting connective tissues of the body [CT disorder].
- Auto antibodies directed at various tissues.

May affect any part of the body, but importantly kidneys

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21
Q

What is seen microscopically in SLE?

A

Thin atrophic epidermis. - Inflammation and destruction of adnexal structures.

IMF

  • LE band
  • IgG deposited in basement membrane.
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22
Q

What is dermatomyositis?

A

Peri-ocular oedema and erythema
- Heliotropic rash

Erythema in photosensitive distribution

Myositis

  • proximal muscle weakness
  • can check for creatinine kinase

In adults 25% associated with underlying visceral cancer.

23
Q

What is seen on microscopy in dermomyositis?

A

Similar to L.E.

Often a lot of dermal mucin.

Negative IMF

24
Q

What are bullous diseases?

A

Formation of fluid-filled blisters

25
Q

What is bullous phemigus diseases?

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.

26
Q

What is the pathogenesis of bullous phemigus diseases?

A

Autoantibodies, directed against intercellular material.

27
Q

What is bullous phemigoid disease?

A

Disease characterised by subepidermal blisters:

Elderly with large tense bullae which do not rupture easily.

Can be localised or extensive disease.

Pathogenesis:
- Autoantibodies to glycoprotein in basement membrane. Can be detected by IMF.

28
Q

What is dermatitis herpetiformis?

A

Small intensely itchy blisters. Extensor surfaces

Often young patients. Associated with Coeliac disease.

IgA deposition in dermal papillae on IMF.

Histopathology;
- Neutrophil microabscesses in dermal papillae.

29
Q

Which skin lesions are can be sign of systemic disease?

A

Dermatomyositis and visceral cancer

Dermatitis herpetiformis and Coeliac disease

Acanthosis Nigricans [ dark warty lesions in armpits] and internal malignancy.

Necrobiosis Lipoidica [red + yellow plaque on legs] and Diabetes Mellitus

Erythema Nodosum [red tender nodules on shins] associated with infections elsewhere esp.lung, drugs, and other diseases

30
Q

Which skin lesions are caused by metabolic disorders?

A

Xanthoma’s [yellow plaques often eyelids] and hyperlipaemis’s

Gout, tophi

Porphyria. Group of disorders caused by defective synthesis of haem, part of haemoglobin

Symptoms vary depending on type [abdo.pains, psychiatric disturbance ,skin lesions]

31
Q

What is porphyria cutanea tarda (PCT)?

A

Commonest type. 20% inherited, A.D., 80% acquired [hepatitisC]. Alcohol can precipitate.

Enzyme deficiency

  • uroporphyrinogen decarboxylase deficiency (UROD)
  • leads to build up of porphyrin compounds in the skin
  • these cause tissue damage when exposed to sunlight.

Causes Blisters and scarring of skin

Diagnosis, can look for porphyrins is urine [goes dark on light exposure].

32
Q

What is basal cell carcinoma (BCC)?

A

Commonest malignant tumour
- Metastases very rare.

Aetiology

  • Sun exposed site, especially face
  • Occasional secondary to radiotherapy
  • Pale skin that burns easily
  • Immunosuppression

Rare - Gorlin’s syndrome

33
Q

What is the clinical presentation of BCC?

A

Early: nodule.

Late: ulcer (rodent ulcer).

Morphoeic BCC - ill defined and infiltrative.

34
Q

What are the microscopic features of BCC?

A

Tumour composed of islands of basaloid cells with peripheral palisade

35
Q

What is squamous call carcinoma?

A

U.V. irradiation

  • Usually occurs in sun exposed sites.
  • Increased risk in tropical countries.

Radiotherapy.

Hydrocarbon exposure

  • tars, mineral oils, soot.
  • Percival Pott noted SCC scrotum in chimney sweeps.

Chronic scars/ulcers
- SCC arises within these (Marjolins ulcer).

Immunosuppression
- renal transplant patients at increased risk.

Drugs, some newer drugs for melanoma

36
Q

What is the clinical presentation of SCC?

A

Nodule with ulcerated, crusted surface

37
Q

What is the microscopic appearance of SCC?

A

Invasive islands and trabeculae of squamous cells showing cytological atypia.

38
Q

How common are metastases in SCC?

A

5% (lip, ear, perineum)

39
Q

What are the other high risk features of SCC?

A

> 2 cm, >4mm thick, high grade

40
Q

What is actinic keratosis?

A

Pre-malignant disease; actinic [solar]keratosis.

Dysplasia to Squamous epithelium.

Very common on chronic sun exposed sites.

Scaly lesion with erythematous base

Only rarely progresses to invasive disease.

May spontaneously resolve

41
Q

What are melanocytes?

A

Melanocytes derive from neural crest

Function; to form melanin which is transferred to epidermal cells to protect the nucleus from UV radiation.

Give rise to tumours

  • Benign; naevi [moles]
  • Malignant; Melanoma
42
Q

What are melanocytic naevi?

A

Local benign collections of melanocytes

43
Q

What are the two types of naevi?

A

Superficial; congenital or acquired

Deep; Blue naevi.[ mongolion spot]

44
Q

What is dysplastic naevus syndrome?

A

Families with increased incidence of melanoma

Multiple clinically atypical moles

Histologically atypical

Increased risk of developing melanoma.

45
Q

What are the features of melanoma?

A

Much rarer than BCC and SCC.

Incidence is rising rapidly.

Very dangerous malignancy which can metastasize widely.

46
Q

How can you tell the difference between a naevi and a melanoma?

A

Asymmetrical

Borders uneven

Colour variation

Diameter >6mm

47
Q

What are the main risk factors for melanoma?

A

Sun exposure

  • especially short intermittent severe exposure
  • Australia.

Race

  • Celtic with red hair, blue eyes, fair complexions who tan poorly most at risk.
  • Melanoma rare in dark skinned people.

Family history

  • Dysplastic naevus syndrome
  • multiple large atypical moles

Giant congenital naevi
- small risk (10%) turn malignant.

48
Q

What is lentigo maligna?

A

Face, elderly people. Slow growing, flat, pigmented patch.

Micro: Proliferation of atypical melanocytes along basal layer of epidermis. Skin also shows signs of chronic sun damage.

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

49
Q

What is acral lentigenous melanoma?

A

Palms and soles, occasionally subungual.

Commonest form in afro-caribbeans. Forms enlarging pigmented patch.

Micro: Similar to lentigo maligna except no marked sun damage.

50
Q

What is superficial spreading melanoma?

A

Commonest type in Britain.

Early: flat macule. Late: blue/black nodule.

Micro: Proliferation of atypical melanocytes which invade epidermis [pagetoid spread] and dermis.

Genetics; Often BRAF mutations ? Possible target for anticancer agents.

51
Q

What is nodular melanoma?

A

Starts as pigmented nodule. +/- ulceration. Poor prognosis.

Micro: Invasive atypical melanocytes invade dermis to produce nodules of tumour cells.

52
Q

What is Breslow thickness?

A

Predicts 5 year prognosis

Measure on microscope from granular layer of epidermis to base of tumour

4 = 45-60%

% = 5 year survival

53
Q

Aside from Breslow, what are the other prognostic factors in

A

Site - BANS - back, arms (posterior upper), neck, scalp. All poorer prognosis

Sentinel Node. Lymph node which drains from melanoma first. Good indicator of prognosis. Removed and if positive, rest of lymph nodes in that anatomic area removed to try and halt disease progression.

54
Q

What is the treatment for melanoma?

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.

Clinical Pathology (65 decks)

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