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Dermatologyn osce for reg phg sr selection
- 1. Short cases andspots in Dermatology for MD
- 2. Examination of theskin • Consent • Proper exposure • Adequate environment • Primary skin lesions • Secondary skin lesions • Systemic examination
- 3. Skin lesion morphology– Primary skin lesions • Macule – circumscribed flat skin lesion – seen but not felt. Can be ill defined or well defined. Hyperpigmented, hypopigmented or erythematous • Papule – solid elevated lesion < 0.5 cm • Vesicle – fluid filled lesion < 0.5 cm • Nodule – solid elevated lesion > 0.5 cm • Pustule – vesicle filled with pus • Blister (bullae) – fluid filled lesion > 0.5 cm • Plaque – A large > 1cm raised lesion, can be distinct or merging into the surrounding skin • Wheal – dermal edema with papule or plaque • Purpura and ecchymosis – erythematous macule with extravasation of blood - < 0.5cm – purpura, > 0.5cm ecchymosis • Lesions due to dilation of blood vessels – Telangectasia and poikiloderma (atrophy of skin, telangiectasia and reticulate hyperpigmentation
- 4. Papules and nodules– further morphology • Vertical profile – dome shaped, flat topped, umbilicated, acuminate, verrucous, pedunculated • Horizontal profile – discoid, annular, circinate, arcuate, reticulate
- 5. Skin lesion morphology– secondary skin lesions • Scale • Crust • Erosion • Excoriation • Ulcer • Sinus • Atrophy • Lichenification – thickening of the skin, hyperpigmentation, increased skin markings
- 7. Psoriasis Describe the skinlesions • Well defined, erythematous plaques with large silvery loose scales • Initial lesions – discoid, gyrate, polycyclic and annular • Positive auspitz sign • Positive Koebner phenomenon • Predilection – pressure points, scalp, nape of the neck, extensor surfaces
- 13. Describe the hands •Well defined, erythematous plaques with large silvery loose scales • Confluent plaques • Nail changes – nail pitting, thickening of the nail plate, sub-ungual hyperkeratosis, nail plate dystrophy, onycholysis, oil spots
- 15. Describe the hands Whatare the clinical types of articular involvement in psoriasis? • Asymmetrical oligoarthritis • Distal interphalangeal joint arthritis • Symmetrical polyarthritis • Arthritis mutilans • Spondyloarthritis
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- 25. What are thecommon precipitants of the disease? • Physical trauma, infection – Streptococcal, HIV, drugs – antimalarials, lithium, beta blockers, NSAIDs What are the pathological hallmarks of the disease? • Increased epidermal cell proliferation and parakeratosis, dermal capillary and fibroblast proliferation
- 26. What are theprinciples of therapy? • Counselling and reassurance • Topical agents – coal tar with salicylic acid, dithranol, calcipotriol, steroids • Systemic agents – MTX, acitretin • Immunosupression – CyA • Biologics • Photochemotherapy – PUVA
- 27. Describe the skinlesions
- 31. • Herald patch– oval lesion wrinkled, salmon pink center and a colarette of scales at the periphery • Scaly papules arranged peripherally – fir tree appearance (Christmas tree appearance) • Trunk • Diagnosis – Pityriasis rosea
- 32. What is thepathogenesis of this condition? • Viral agents implicated in the pathogenesis (HHV) What are the principles of treatment? • Is usually a self limiting condition
- 37. Describe the skinlesions • (Pruritic), polygonal, purple (violaceous), plane papules • Flexor aspect of the forearm and wrist • Also shins • Wickham’s striae on the lesions • Oral lesions
- 38. • Oral lesions– white, reticulate pattern in the oral mucosa, purplish • Wickham’s striae
- 39. • Scalp andnail lesions • Nail – Thinning and splitting of the nail plate, longitudinal ridging, pterygium formation • Scalp demonstrates scarring alopecia • Note – LP can also affect the mucosal surfaces
- 43. What are theprinciples of therapy? • Localized Lichen planus – topical steroids (medium potency) • Extensive – oral steroids, acitretin • Hypertropic LP – Potent topical steroids and salicylic acid with antihistamines • Nails – oral steroids
- 54. Allergic contact dermatitis •The typical features of eczema depend on the time course of the disease • Acute – erythematous and edematous plaques, ill defined and surrounded by papules, vesicles, pustules and exudates with subsequent crusting • Chronic – lichenification – hyperpigmentation, skin thickening and increased skin markings
- 55. What is theclassification of eczema?
- 56. How would youevaluate this patient? • Patch test What are the principles of management? • Remove trigger • Hydration and use of emollients • Acute phase – Soaks of potassium permanganate as topical treatment, topical steroids, rarely systemic steroids • Chronic phase – Topical steroids, combined with salicylic acid/urea for lichenified lesions • Antibiotics for superadded infection
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- 67. Pemphigus Bullous pemphigoidDermatitis Herpetiformis Linear IgA disease Introduction Autoimmune blistering intraepidermal skin disease More common than pemphigus Blistering disease Papulovesicular disease Pathogenesis Antibodies against Desmoglein III Antibodies against hemidesmosomal proteins Strong association with HLA B8, DR3 and Clinical manifestations Males= Females Occurs in middle age P. Vulgaris – flaccid blisters in oropharynx, mucus membranes head, neck and intertrigonous areas Positive Nikolsky sign P. Foliaceus – seborrhoeic distribution Can occur as a paraneoplastic syndrome of lymphoreticular malignancies Age of onset later (>60) Tense blister and urticarial lesions on flexor surfaces of arms, legs and groin Pruritic Can develop on erythematous and edematous skin or normal skin Young to middle aged patient Pruritic – grouped in the scalp, posterior neck and extensor surfaces of the upper and lower limbs Buttocks Associated with gluten enteropathy Occurs throughout adulthood Lesions common in the mucus membranes of the oral cavity Investigations Skin biopsy and tzank smear – intraepidermal split P. Vulgaris – suprabasilar acantholysis P. Foliaceus = subcorneal acantholysis Immunoflorescence IgG deposition Skin biopsy Dermoepidermal split Subepidermal blister with eosinophillic infiltrate Linear IgG and C3 deposition IgA deposition Dermal papillary neutrophilic microabscesses IgA deposition Subepidermal vesicle formation Treatment Steroids – local (f), systemic (V), IV IG, HCQ, MMF Topical steroids, oral steroids, MTX, AZP Dapsone Dietary modifications Dapsone Steroids
- 68. Features Limited cutaneousSSc Diffuse cutaneous SSc Skin involvement Limited to fingers, distal to elbows, face Slow progression Diffuse involvement Rapid progression Calcinosis cutis Frequent, prominent Rare, mild Raynaud’s phenomenon Precedes skin involvement: critical ischaemia common Onset concomitant with skin involvement Pulmonary fibrosis Rare, late, may be isolated Frequent, early and severe Visceral involvement Rare Common PAH Frequent, late, may be isolated May occur, associated with pulmonary fibrosis Scleroderma renal crisis Very rare Can occur early ; 15% Antibodies Anticentromere Antitopoisomerase-1
- 69. What are theinvestigations you would like to perform in this patient? • Skin biopsy – sclerosis of the dermis • Serological – Anti centromere antibodies in LcSSC and Scl-70 in DSSC • Other investigations for organ evaluation What are the principles of management? • General management for RP • Nifedipine • Treat esophageal reflux • Immunosupression – steroids, MTX, AZA • D- penicilamine in diffuse disease
- 71. PRP • Plaques withcoalescing follicular scaly papules • Orange colored thickening of the palms
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- 76. DPN • Seborrheic keratosisand DPN • Typical stuck on brown/black verrucous papules
- 78. Keratoacanthoma • Dome shaped/nodularwith central firm keratin core. • Usual sunexposed sites—face, forearms, hand, dorsae, etc. Heal with hypopigmented scar
- 80. Pyogenic granuloma • Fleshylesion • Erythematous
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- 88. Bowen’s disease • Squamouscarcinoma in situ
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- 95. Melanoma Basal cellcarcinoma Squamous cell carcinoma Introduction Skin malignancy arising from melanocytes Arises from undifferentiated epidermal cells Malignant proliferation of keratinocytes Pathogenesis and epidemiology Incidence increasing Risk factors Exposure to UV radiation Family history Multiple pigmented melanocytic naevi, giant melanocytic naevi Severe burns in childhood Common in Europe Risk factors Exposure to UV radiation Arsenic, immunosupression Genetic predisposition – Xeroderma pigementosum Risk factors Exposure to UV Arsenic, immunosupression From long standing ulcers From existing lesions – Bowen’s disease (intraepidermal lesion confined to hair follicle, actinic keratosis Clinical manifestations Sites – over the back (males) and lower limbs (females) Change in a melanocytic naevus Increase in size (>6mm), irregular outline, asymmetry, alteration of colour, bleeding and ulceration, satellite lesions, change in symptoms Subtypes Superficial spreading – flat/nodular lesions Lentigo melanoma – face of elderly patients Acral melanoma – hands and feet Amelanocytic melanoma Sun exposed areas of the face – especially the nose Subtypes Nodulocystic – dome shaped, pearl colour with superficial telengectasia, central ulceration and rolled edges Superficial – plaque like lesion commonly in the trunk Sclerosing – late presentation Pigmented Metastasis rare – local destruction common Indurated nodule or ulcer in sun exposed areas Local infiltration, lymphatic metastasis Investigations Skin biopsy and sentinel node biopsy Skin biopsy Skin biopsy Management Prognosis depends on depth of invasion – Breslow thickness Surgical resection Chemotherapy, alpha interferron for metastatic melanoma - Resection for high risk lesions – facial, sclerosing Cryotherapy, radiotherapy, PDT, imiquomod - immunotherapy Surgical resection, radiotherapy
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