63 Diseases of the skin + eye Flashcards
Which inflammatory diseases affect the cornea and conjunctiva? (3)
Herpes zoster.
Chlamydia A-C: blindess. D-K: conjunctivitis.
Acanthamoeba.
What increases cataract risk? (6)
Senile degeneration. Rubella. Downs syndrome. Irradiation. Diabetes mellitus. Uveitis.
Which infections affect the retina? (2) How?
Toxoplasma: congenital is bilateral, acquired is focal.
Toxocara gondis: dog faeces, local inflammation.
Which vascular diseases affect the eye? (2)
Appearances?
Hypertensive retinopathy: flame shaped haemorrhage.
Diabetic retinopathy: dot + blot haemorrhage.
Where do melanomas of the eye occur?
Prognosis?
Uveal tract (iris, ciliary body, choroid). Type 1: good prognosis. Type 2: bad.
Differentiate between Herpes Simplex 1 + 2.
1 primarily causes cold sores.
2 primarily causes genital herpes.
Differentiate between a furuncle and a carbuncle:
Abscesses. Furuncle involves one follicle, carbuncle involves more than one.
What are the three stages of dermatitis (eczema)?
- acute - red skin, serous exudate ± vesicles
- subacute - red, less exudate, itching, crusting
- chronic - skin thick + leathery from itching
What is seen in microscopy from eczematous skin? (3)
Spongiosis: intracellular oedema in epidermis.
Chronic inflammation.
Epidermal hyperplasia + hyperkeratosis.
What is the appearance of psoriatic plaques?
Sign?
Associated with?
Well defined red, oval plaques on extensor surfaces with silvery scale.
Auspitz sign: removal of scale causes small bleeding points.
± pitting nails, sero-negative arthritis.
What is seen in microscopy of psoriatic skin? (4)
Psoriasiform hyperplasia:
Elongated club shaped rete ridges.
Thinning of epidermis over dermal papillae.
Parakeratotic scale.
Collections of neutrophils (Munro micro abscesses).
What is the aetiology of psoriasis?
PSORS in MHC on 6p2 implicated.
Infection, stress, trauma, drugs.
What co-morbidities are associated with psoriasis? (4)
Arthropathy.
Cardiovascular disease.
Non melanoma skin cancers (BCC).
Lymphoma (rx effect?).
What is the clinical appearance of SLE? (3)
Red scaly patches on sun exposed areas.
Alopecia.
Butterfly rash on cheeks + nose.
What is seen on microscopic examination off skin from SLE? (3)
Thin + atrophic epidermis.
Inflammation + destruction of appendages.
IgG deposition on BM - immunofluorescence.
How does dermatomyositis affect the skin?
Microscopically?
Associated with?
Heliotropic rash.Erythema in photosensitive distribution.
Lots of dermal mucin.
25% have visceral cancer.
Differentiate between pemphigus and pemphigoid.
Pemphigus: intraepidermal bullae.
Pemphigoid: subepidermal bullae.
What is pemphigus caused by?
Loss of cohesion between keratinocytes, causing intraepidermal blister. Autoantibodies directed against intercellular material.
Skin appearance in dermatitis herpetiformis?
Who?
Microscopically?
Small, intensely itchy blisters.
Young women, often coeliacs.
IgA deposition in dermal papillae. Neutrophil microabscesses.
Appearance of Necrobiosis Lipoidica?
Associated with?
Red + yellow plaques on legs.
Diabetes mellitus.
Appearance of Erythema Nodosum?
Associated with?
Red tender nodules on shins.
Lung infections, drugs.
Appearance of Acanthuses Nigricans?
Associated with?
Dark warty lesions on armpits.
Internal malignancy.
What is Porphyria Cutanea Tarda caused by?
Precipitators factors? (2)
Appearance? (2)
Uroporphyrinogen decarboxylase deficiency. Porphyrin build up causes skin damage on exposure to sunlight.
Alcohol, Hep C.
Blisters + scarring.
What are porphyrias?
Clinical features? (3)
Group of disorders caused by defective synthesis of haem.
Abdo pain, psychiatric disturbances, skin lesions.
What is the aetiology of basal cell carcinoma? (4)
Sun exposed site, especially face.
Pale skin.
Immunosuppression.
Gorlin’s syndrome.
Appearance of basal cell carcinoma -
Macroscopically:
Microscopically:
Nodule, later transforms into ulcer.
Islands of baseloid cells with peripheral palisade.
Behaviour of basal cell carcinoma?
Malignant.
Metastases very rare.
Risk factors for squamous cell carcinoma: (6)
UV radiation. Hydrocarbon exposure. Radiotherapy. Chronic scars/ulcers. Immunosuppression (esp renal transplant). Drugs (melanoma drugs).
Appearance of squamous cell carcinoma -
Macroscopically:
Microscopically:
Nodule with ulcerated + crusted surface.
Invasive islands and trabeculae of squamous cells showing cytological atypia.
Metastases behaviour of squamous cell cancer?
Metastases in 5%, risk if:
Lip, ear, perineum.
> 2cm, > 4mm thick, high grade.
What is actinic keratosis?
Appearance?
Behaviour?
Pre-malignant stage of SCC.
Dysplasia. Common in sun exposed areas.
Scaly lesion with erythematous base.
Rarely develops further, may resolve.
Where do melanocytes derive from?
Neural crest.
What are naevi?
Local benign collections of melanocytes.
What is dysplastic naevus syndrome?
Multiple clinically atypical moles with atypical histology.
Increased risk of melanoma.
What is the appearance of a melanoma? (4)
Asymmetrical.
Borders uneven.
Colour variation.
Larger than 6mm.
What are the risk factors for melanoma? (4)
Short, intermittent sun exposure.
Race - celts at high risk (pale).
Dysplastic naevus syndrome.
Giant congenital naevi.
What is lentigo maligna?
Who?
Microscopic?
Risk?
Slow growing pigmented patch.
Elderly.
Proliferation of atypical melanocytes along basal layer of epidermis + marked sun damage.
May invade dermis + metastasise.
Where does acral lentigo maligna develop?
Who?
Miscroscopic?
Palms and soles.
Afro-carrribeans.
Proliferation of atypical melanocytes along basal layer of epidermis, no sun damage.
Appearance of superficial spreading melanoma:
Microscopic:
Genetics:
Flate macule, develops into blue/black nodule.
Atypical melanocyte proliferation invading epidermis + dermis.
BRAF.
What is the appearance of a nodular melanoma?
Prognosis?
Pigmented nodules ± ulceration.
Poor.
What is used to determine the prognosis of melanomas? (3)
Breslow thickness (microscopic distance from granular layer to of epidermis to base of tumour).
BANS (back, arms, neck, scalp) - poor.
Sentinel node.
How are melanomas treated?
Surgery (primary and sentinel node).
BRAF inhibitors.
