skin disease

7/17/2019 Skin Disease

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DERMATOLOGY

MICHAEL CHEERAN DAVID PAGE 1 23/08/200 8

CONTENTS

Contents ............................................................................................................................... 1

Benign Epidermal Tumours................................................................................................ 2

Seborrhoeic Wart (Basal Cell Papilloma) ............................. ................................. ................................. ........... 2

Skin Tags ......................................................................................................................................................... 2 Epidermal Cysts ............................. ................................ ................................ ................................. ................. 2 Milium ................................ ................................ ................................ ................................ ............................. 2

Benign Dermal Tumours..................................................................................................... 3

Dermatofibroma ................................................................................................................................................ 3

Pyogenic Granuloma ......................................................................................................................................... 3

Keloid ............................................................................................................................................................... 3

Campbell de Morgan Spot (Cherry Angioma) ................................. ................................. ............................... .. 3

Lipoma ............................................................................................................................................................. 3

Chondrodermatitis Nodularis ............................... ................................. ................................ ............................ 3

Naevi .................................................................................................................................... 4

Melanocytic Naevi ................................ ................................ ................................. ............................... ............. 4

Epidermal Naevi ............................ ................................ ................................ ................................. ................. 4

Connective Tissue Naevi.................................................................................................................................... 4

Differential Diagnosis ....................................................................................................................................... 4

Malignant Melanoma .......................................................................................................... 5

Basal Cell Carcinoma .......................................................................................................... 6

Squamous Cell Carcinoma .................................................................................................. 6

Disorders of Pigmentation .................................................................................................. 7

Urticaria ............................................................................................................................... 8

Leprosy ................................................................................................................................ 9



DERMATOLOGY


BENIGN EPIDERMAL TUMOURS

SEBORRHOEIC WART (BASAL CELL PAPILLOMA)

Common proliferation of basal keratinocytes; pigmented

Clinical presentation: Often multiple Affect elderly or middle-aged Mostly on trunk and face Generally round or oval in shape Start as small papules, often lightly pigmented or yellow Become darkly pigmented, warty nodules; 1-6 cm in diameter Have a stuck-on appearance, with keratin plugs and well-defined edges.

Differential Dx: Actinic keratosis (2° to sun exposure and damage)

Melanocytic naevus Pigmented basal cell carcinoma Malignant melanoma

Mx: Liquid nitrogen cryotherapy Thicker seborrhoeic warts need curettage, or shave biopsy with cautery. Histological examination advised if doubts on Dx. Shows a hyperkeratotic epidermis, thickened by basal cell proliferation, with keratin

cysts.

SKIN TAGS

Pedunculated benign fibro-epithelial polyps; a few millimetres in length Common in elderly or middle-aged Common sites: neck, axillae, groin, eyelids Often found in obese patients

Can be confused with small melanocytic naevi or seborrhoeic warts Rx for cosmetic purposes – cryotherapy or local excision.

EPIDERMAL CYSTS

Usually seen on the scalp, face or trunk

Sometimes incorrectly called sebaceous cysts Keratin filled and derived from the epidermis Pilar cyst is derived from the outer root of the hair follicle

Presentation – firm, skin coloured, mobile cysts; 1-3 cm in diameter May be complicated by infection

Rx = excision

MILIUM

Small white keratin cysts (1-2 mm in size)

Around the eyelids and upper cheek; often seen in children Can be extracted by a sterile needle.



DERMATOLOGY


BENIGN DERMAL TUMOURS

DERMATOFIBROMA

Common dermal nodules; asymptomatic usually

Caused by a proliferation of fibroblasts, with dermal fibrosis and epidermal hyperplasia May be 2° to an insect bite or other trauma

Presentation – lower legs of young women Firm, dermal nodules 5-10 mm in diameter May be pigmented Enlarge slowly (if at all)

Mx: May be confused with a melanocytic naevus or a malignant melanoma Excise lesion if symptomatic or if in doubt.

PYOGENIC GRANULOMA

Rapidly developing bright red or blood-crusted nodule may be confused with malignant melanoma it is neither pyogenic nor granulomatous; but is an acquired haemangioma

Presentation: Develops at a site of trauma (e.g. prick from thorn) Bright red, or pedunculated nodule – bleeds easily Enlarges rapidly over 2-3 weeks Is usually seen on a finger; but also occurs on the lip, face and foot

Occurs in young adults or children

Mx = excision; histological analysis to exclude a malignant melanoma.

KELOID

An excessive proliferation of connectivetissue in response to skin trauma

Differs from a hypertrophic scarbecause it extends beyond the limit ofthe original injury

Presents as protuberant and firmsmooth nodules or plaques

Occur mainly over the upper back,chest and ear lobes

Develop more commonly in Black Africans

Have their highest incidence in 2nd to4th decades

Rx = injection of steroid into keloid.

CAMPBELL DE MORGAN SPOT (CHERRY ANGIOMA)

Benign capillary malformations Commonly seen as bright-red papules

on the trunk in elderly or middle-aged Often mistaken for petechiae!

LIPOMA

Benign tumours of fat; soft masses insubcutaneous tissue

Multiple; found on trunk, neck andupper extremities

CHONDRODERMATITIS NODULARIS

Small painful nodule on the upper rimof the helix of the pinna.

Usually in elderly♂

2° to inflammation in the cartilage, 3°to degenerative Δ in the dermis R x = excision



DERMATOLOGY


NAEVI

MELANOCYTIC NAEVI

A benign proliferation of 1+ normal constituents of the skin = pigmented mole.

Common, usually multiple

Congenital naevi – present at birth; protuberant or hairy? Small risk of malignant Δ

Junctional naevi – flat macules; round/oval; found on soles, palms or genitalia Intradermal naevi – dome shaped, skin-coloured papules; typically affects the face Compound naevi – pigmented nodules or papules; warty or hairy?

Blue naevi – solitary and usually found on hands/feet; blue colour is an optical illusion caused by pigment deep within the dermis.

Spitz naevi – firm, reddish-brown, rounded nodule on the face of a child Initial rapid growth; dilated dermal vessels

Halo naevi – depigmentation where a naevus has involuted (2° immune destruction) Mostly seen on the trunk

EPIDERMAL NAEVI

Present at birth or develop shortly after Warty, often pigmented Frequently linear – a few centimetres long R x = excision, but recurrence is common A rare variant on the scalp carries a small risk of malignant Δ ( naevus sebaceous )

CONNECTIVE TISSUE NAEVI

Smooth skin-coloured papules composed of coarse collagen, in the dermis

DIFFERENTIAL DIAGNOSIS

Freckle – tan-coloured macules on sun-exposed sites Lentigine – sun-exposed sites in elderly, also in Peutz-Jeughers; increased melanocytes Seborrhoeic wart - stuck-on appearance Haemangioma – vascular, but may show pigmentation Dermatofibroma – elevated, firm and pigmented nodules on the legs (? 2° insect bites)

Pigmented Basal Cell carcinoma – often on the face Pearly edges Increase in size, and can ulcerate

Malignant Melanoma – variable colour and outline Increase in size May be inflamed or itchy.



DERMATOLOGY


MALIGNANT MELANOMA

Incidence is 10 per 100,000 per year;♀:♂ is 2:1 Incidence rising by 7% per year, and doubling every decade

Prognosis is related to tumour thickness and staging according to the Breslow Thicknessscale: The length (mm) between the granular cell layer to the deepest identifiable melanoma

cell.

4 Presentations:

Superficial spreading

50%,♀ predominance Macular with variable pigmentation

Nodular 25%,♂predominance commonest on the trunk grow rapidly and ulcerate

Lentigo Developing in long-standing lentigo maligna 15%; lentigo maligna arises in sun-damaged skin (e.g. face of elderly person) Irregular outline and pigmentation

Acral Lentiginous 10%

Affects palms, soles and nail beds Often diagnosed late, with a poor prognosis

Risk factors: Sun exposure Dysplastic naevus with a FHx of malignant melanoma

Diagnosis: Size? Shape? Colour? Inflammation?

Crusting – ooze/bleed? Itch?

A asymmetry B borders C colour Δ D diameter Δ

Mx – surgical excision Tumour thickness < 1mm needs a 1cm clearance margin Tumour thickness > 1mm needs a 2-3 cm clearance, often with a skin graft to close. Recurrence can be local or via lymphatic/haematogenous spread. ? Prophylactic clearance of local lymph nodes ? α-Interferon and dacarbazine vs. thick malignant melanomas. Avoid burning in the sun; use high strength sun protection. Report early on, any changes in a mole.



DERMATOLOGY


BASAL CELL CARCINOMA

Rodent ulcers typically seen on the face in elderly/middle-aged.

Arise from basal keratinocytes at the epidermis, in light exposed areas

Grow slowly and destroy local bone, cartilage and soft tissue Locally invasive, but rarely metastasise.

Causes: Prolonged UV exposure Arsenic ingestion (e.g. in tonics) X-rays Chronic scarring Genetic predisposition

Nodular – commonest from Usually starts as a small skin-

coloured papule Pearly edges, fine telangectasia and

central crusting Usually < 1 cm in diameter Exclude intradermal naevus and

molluscum contagiosum

Cystic – tense and translucent

Multi-centric – superficial tumours, often multiple, plaque-like and extensive Frequently pigmented Exclude discoid eczema and psoriatic plaques.

Morphoeic – scarring variant often shows white/yellow morphoea-like plaques Centrally depressed

Mx: Excision

Incisional biopsy with radiotherapy, if excision not possible. Cryotherapy Regular follow-up, since recurrence is 5% at 5 years.

SQUAMOUS CELL CARCIN OMA

Malignant tumour derived from keratinocytes in an area of damaged skin

♂>♀ in patients > 55 years; may metastasise.

Malignant keratinoyctes retain the ability to produce keratin Destroy the dermo-epidermal junction to invade the dermis in an irregular manner.

Keratosis -derived type – starts within an actinic papule, which progresses to ulcerate andform a crust

Nodular – dome shaped More invasive varieties often develop at the edge of pre-existing ulcers and at sites

of radiation damage. Metastases found in 10%.

Differential: kerato-acanthoma, actinic keratosis, seborrhoeic keratosis.

Mx:

Surgical excision with lymph node examination Radiotherapy.



DERMATOLOGY


DISORDERS OF PIGMENTATION

Vitilgo Autoimmune disease, associated with pernicious anaemia, thyroid and Addison’s

diseases.

Well-defined, depigmented macules Often symmetrically distributed on the hands, wrists, knees, neck, and mouth. No good R x camouflage cosmetics In dark-skinned individuals, steroids/PUVA/oral psoralens to induce re-pigmentation?

Albinism Autosomal recessive defect in tyrosinasefailure to synthesise melanin Lack of skin and eye colour

Premature skin photo-ageing, and↑ risk of squamous cell carcinoma. Mx: strict sun avoidance.

Phenylketonuria Autosomal recessive deficiency in phenylalanine hydroxylase cannot make tyrosine Accumulation of phenylalanine leads to mental retardation and choreoathetosis Impaired melanin fair skin and hair Atopic eczema is common Mx = a low phenylalanine diet to prevent early neurological damage.

Freckles & Lentigines Freckles are light-brown macules which darken on sun exposure; normal melanocytes

Lentigines are also brown macules, but do not darken in the sun;↑no of melanocytes

Melasma

Patterned, macular, facial pigmentation Associated with hormonal Δ e.g. pregnancy ( chloasma ) or the use of OCP

Avoid sunshine, use SPF, and “fade-out” cream (over the counter) for 6-8 months.

Peutz-Jeughers Syndrome Rare autosomal dominant condition Lentigines around the lips, buccal mucosa and fingers Associated with small bowel poyps Intersusseption and rare malignant Δ.

Addison’s Disease

Autoimmune 1° hypoadrenalism with 2° hyperpituitarism ( ↑ ACTH)

ACTH synthesised from pro-opiomelanocortin ↑melanogenesis Generalised pigmentation

Or localised to buccal mucosa, palmar creases, scars, flexures and areas of↑friction

Drug-induced Amiodarone Chloroquine Chlorpromazine Psoralens



DERMATOLOGY


URTICARIA

Common eruption of transient pruritic wheals

Associated dermal oedema is usually the result of mast cell degranulation and the release of vasoactive amines IgE mediated (type I) hypersensitivity Complement activation Direct release of histamine (e.g. opiates and contrast media) Blocking of prostaglandin pathway (e.g. aspirin and NSAIDs) A serum histamine – releasing factor?

Chronic Idiopathic urticaria: Itchy pink wheals, anywhere on the skin Number varies from a few to many, appearing in a day Angioedema of the lips and tongue can co-exist

? Pharmacological provoking factors. Spontaneous resolution within a few months

Acute urticaria: Sudden onset 2° to IgE mediated reaction Commonly associated with a food allergen (e.g. nuts, egg, prawn) or a drug allergen.

Physical urticaria: Cold, heat, sun exposure Dermographism = whealing induced by firm stroking of the skin

Cholinergic urticaria = small intensely itchy papules in response to sweating

Eruptions last from a few minutes to hours.

Hereditary angioedema: Rare, potentially fatal, autosomal dominant condition. Can cause respiratory obstruction and/or abdominal pain & vomiting C1-esterase inhibitor deficiency allows unchecked complement activation R x = i.v. FFP vs. acute attacks; anabolic steroids (e.g. Danazol ) used to promote hepatic

synthesis of C1-esterase inhibitor.

Urticarial vasculitis Acute onset with widespread lesions Persist > 24 hours, and fade leaving purpurea.

Mx: Conservative (avoidance of allergens) Desensitisation Antihistamines: cetirizine (Zirtek) , terfenadine (Triludan) Corticosteroids Adrenaline vs. anaphylaxis (along with slow i.v. chlorpheniramine/Piriton ) Diet – avoid salicylates, azo dyes and benzoic acid preservatives.



DERMATOLOGY


LEPROSY

Also known as Hansen’s disease – chronic disease of peripheral nerves caused by M. leprae

3 cardinal features:

Hypo-pigmented / erythematous, hypo-aesthetic patches Thickening of peripheral nerves sensory or motor deficits Acid fast bacilli (AFB) from skin lesions

Incubation for 2-5 years inside histiocytes and schwann cells Spread by inhalation, direct contact, ingestion and insects.

Classification by degree of immune competence: Tuberculoid tuberculoid (TT) greatest cell-mediated immunity Borderline tuberculoid (BT) Borderline borderline (BB)

Boderline lepromatous (BL) Lepromatous lepromatous (LL) least cell-mediated immunity

TT: 3 patches – anaesthetic, well-defined macules or plaques <3 cm 1 peripheral nerve may be thickened

AFB smear – ve; ↓ bacterial load Lepromin test +ve; biopsy shows tuberculoid granuloma

BT: 3-10 patches – partially anaesthetic, hypo-pigmented, ill-defined large macules/plaques

Satellite lesions Asymetrical peripheral nerve thickening AFB smear 1+ Lepromin test +ve

BB: AFB smear 2+ Lepromin test +ve or – ve

BL: Tendency towards symmetrical plaques AFB smear 3+

Lepromin test – ve

LL: Extensive disease – symmetrical, numerous macules, nodules, papules Shiny, infiltrated skin lesions Nasal involvement – epistaxis, septal perforation, collapse of nasal bridge Pedal oedema Laryngeal oedema – hoarse voice and dyspnoea Peripheral nerve thickening with glove & stocking anaesthesia and ?motor deficits Gynaecomastia and testicular atrophy AFB smear 6+

Lepronin test – ve; biopsy shows foam cell granuloma with numerous organisms.



DERMATOLOGY


Type 1 Lepra reactions: (BT, BB and BL) Type IV hypersensitivity (delayed) Erythema, oedema and hyperalgesia in pre-existing skin lesions Tender and thickening of nerves palsies and sensory deficits If mild sx R x = analgesia

Severe sx

R x

= 30 –

40 mg oral prednisolone

Type 2 Lepra reactions: (BL and LL) Type III hypersensitivity (immune complex deposition) Triggered by infection, vaccines and stress Fever Joint tenderness Lymphadeopathy Erythema Nodosum Leprosum – over face and extensor surfaces ; not legs Iritis, Conjunctivitis Epistaxis, rhinitis Acute epididymo-orchitis

Laryngeal odema death Glomerulonephritis R x = steroids and thalidomide

Complications: Nerve palsies – ulnar claw hand, carpal tunnel, Bell’s palsy, foot drop, claw otes

Anaesthetic complications: Trophic ulcers and osteomyelitis Distortion of toes Shortening of foot Tarsal disintegration

Malignancy

Mx:

Paucibacillary TT/BT = 100mg Dapsone + 600mg Rifampicin for 6 months2 years of follow-up

Multibacillary BB/BL/LL (or AFB smear +ve)100mg Dapsone + 600mg Rifampicin + 300mg Clofazimine for 2 years5 years of follow-up

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