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Peer Teaching Dermatology & Miscellaneous Basic skin structure Ulcers • • • • • Arterial Venous Neuropathic Traumatic Vasculitic Arterial Vs Venous ARTERIAL VENOUS Gaiter area above lateral malleolus Tips of toes To start with irregular then becomes demarcated Deep ulcer, round Pre tibial areas Peripheral on borders or sides of feet. Large but shallow cool, shiny pale or dusky skin with loss of hair. Peripheral gangrene Reduced peripheral pulses Delayed cap refill BETTER WITH LEG DOWN PAIN HIGH Haemosiderin deposits on tibial areas varicose eczema with hyperpigmentation and lipodermatosclerosis BETTER WITH LEG UP MINIMAL PAIN Type of Ulcer What to know: Neuropathic Pressure sites on foot: under second metatarsal head surrounded by callus limited joint mobility? Deformity? Ie Charcots joints Check footwear for source of trauma/ pressure NB: osteomyelitis complicates deep neuropathic ulcers Traumatic Including IV drug abuse Vasculitic Purpuric wound edges Palpable purpura Nodules Livedo Ass.w/ connective tissue disorders What might delay healing? • oedema • immobility (poor calf muscle pump and oedema) • anaemia or malnutrition • corticosteroids • repetitive trauma • heavy colonization with bacteria ECZEMA • Superficial skin inflammation with vesicles (when acute) • redness • oedema • oozing • scaling • pruritus TYPES ATOPIC EXOGENOUS Hereditary Acute or chronic skin inflammation Abnormal epithelial barrier function antigenic and irritant agents to penetrate and come into contact with immune cells. Due to primary chemical irritants such as: Primary irritants -acids & alkalis -detergents -petroleum Delayed Type IV hypersensitivity -nickel -rubber additives -hair dyes -topical medicaments Filaggrin mutation (Caucasians) IgE in serum Preferential activation of Th2 CD4 lymphocytes ATOPIC • Itchy • Erythematous • Scaly patches seen in flexures behind knees and around the neck. • Can become secondarily infected by Staph Aureus (crusted, weeping impetigo-like lesion) OR herpes simplex virus (small blisters or punched out lesions = eczema herpeticum which is FATAL) EXOGENOUS • Unusual pattern of rash with clear-cut demarcation • Odd-shaped areas of erythema and scaling Treatment • • EDUCATION – family AND patient Emollients (aqueous cream or emulsifying ointments) • • Mild steroids (hydrocortisone) used for face Potent steroids used for body and soles (betamethasone) • Topical immunomodulators ie calcineurin inhibitors (tacrolimus and pimecrolimus) for eyelids Abx if superinfection • • Second line: If severe and unresponding • prednisolone • azathioprine • ciclosporin • For exogenous eczema: !!Remove causative agents!! ACNE • Increased sebum production by sebaceous glands • Blockage of pilosebaceous units • Follicular epidermal hyperproliferation • Infection with propionibacterium • Androgens (in normal amounts) stimulate increased sebum production • Hair follicles with large sebaceous glands (face, neck, chest & back) become blocked due to hyperkeratosis • closed ‘comedo’ • Within the follicle an obligate anaerobe proprionibacterium acnes proliferates • Acts on sebum releasing inflammatory chemicals • Leak into surrounding dermis • Body mounts an intense acute inflammatory response • PAPULE: rapid pustular development. Red base. • PUSTULE: evolved papules • NODULES: increasing severity to become deep-seated nodule V. uncomfortable and cysts develop. COMEDONES OPEN Felt rather than seen dilated blocked hair follicles. Always seen in acne in younger patients. WORST CASE SCENARIO • ACNE FULMINANS = young man develops severe nodulocystic acne + • fever • malaise • joint pain • swelling Treatment • • • • • • • • • • First-Line Keratolytics (benzoyl peroxide) Topical retinoids (tretinoin or isotretinoin) Retinoid-like agents (adapalene) Abx (erythromycin, clindamycin) Second-line: Low dose oral Abx (oxytetracycline, trimethoprim) Hormonal Rx + cyproterone acetate + co-cyprindol is good if CI to oral contraceptive. • • Third-line: • Oral retinoid (isotretinoin or acitretin) Side effects of Isotretinoin • • • • • mild alopecia dry skin raised blood fat levels teratogenicity psychological disturbances Skin Cancer • Malignant melanoma • Squamos cell cancer • Basal cell carcinoma (rodent ) Malignant Melanoma • • • • • • • Sunlight is major cause F>M Metastasise early!! Can occur in pre-existing moles Nodular melanomas: invade deeply and metastasise early • • Superficial spreadingmelanomas: grow slowly and metastasise GLASGOW SCALE • • • • • Assymetry Border-irregular Colour – non uniform Diameter >7mm Elevation • (=Glasgow scale) + Clarks staging to stratify depth URGENT EXCISION Squamos cell cancer • Begins as solar (actinic) keratoses on the forehead • OR • Found on lips of life-long smokers • OR • In long-standing ulcers (marjolin’s) • • • • • • Ulcerated lesion Hard, raised edges Sun-exposed sites • • • • • Treatment: Excision (curretage) Photodynamic therapy (PDT) for superficial tumours Keratotic nodule with granulating base and rolled border Regional lymphadenopathy Mohs microscopic surgery if need to preserve skin in recurrent cancers e.g. eyelid Squamos cell cancer Basal cell carcinoma (rodent ) • • • • • • Very slow grower Never metastasizes Locally invasive (hence rodent) Middle aged Caucasians Types • Nodulocystic: • Dome shaped pearly papule • Telangiecstasia across surface • • • • Superficial: 1 + scaly erythematous plaques (on trunk) well-defined raised pearly edges Bowen’s or fungal?? • Pigmented: if heavily pigmented then think malignant melanoma. • Morphoeic: waxu indurated plaque that looks like a scar Treatment: • Excision (curretage) • Photodynamic therapy (PDT) for superficial tumours INFECTIONS OF SKIN Necrotizing fasciitis Cellulitis & erysipelas LIFE-THREATENING soft tissue infection rapidly progressive necrosis that spreads subcutaneously to deep fascia Due to streptococcus pyogenes (or staph.aureus if immunosuppressed) Secondary to organ failure AND streptococcal toxic shock syndrome (TSS) Consider if sick patient not responding to treatment for cellulitis and pain out of proportion to signs Erysipelas = often involves the face. Due to group A streptococci beta-haemolytic. Cellulitis = lower extremities normally. Common in patients with chronic lymphoedema. Due to streptococcus or sometimes CA-MRSA. Necrotizing fasciitis Cellulitis & erysipelas Hx of recent trauma Ill patient with high temp, tachycardia, low BP Pain> signs Altered LoC Rapidly spreading poorly demarcated purplish erythema Erythema in involved area Poorly demarcated margins Swelling Warmth Tenderness Dishwater pus (malodorous serosanguineous exudate) Crepitation in soft tissue (gas from aerobic/anaerobic) blisters Low-grade fever Necrotizing fasciitis Cellulitis & erysipelas MISCELLANEOUS Paracetamol OD • Exceed max recommended dose = 2 X 500mg QDS in 24h • Intake of >12g or >150mg/kg hepatic necrosis • • • • • • Risk factors: alcohol abuse enzyme inducing drugs (anticonvulsants or anti-TB drugs) malnourished anorexia nervosa HIV more susceptible to toxic • Paracetamol metabolized in liver by conjugation with glucoronate or sulphate excreted by kidneys. • Cytochrome P450 metabolises some of it to highly reactive N-acetyl-p-benzoquinonimine (can inactivated by conjugation with glutathione) 0-24 h Asymptomatic or mild nausea Vomiting Lethargy malaise 24-72 h Asymptomatic Mild nausea Vomiting Liver enlargement & tenderness > 72 h Increasing confusion (encephalopathy) Jaundice, coagulopathy, hypoglycaemia, renal angle pain • WITHIN 8 HOURS OF OD: N-acetylcysteine IV Breast Cancer STAGING OF BREAST Ca Staging 1 Confined to breast mobile 2 Growth confined to breast Mobile Lymph nodes in ipsilateral axilla 3 Tumour fixed to muscle (not chest wall) Ipsilateral lymph nodes matted/fixed Skin involved> tumour 4 Complete fixation chest wall Distant METS Management is MDT-based! • Surgery: wide local excision OR masectomy + breast reconstruction • • • Radiotherapy: post-op to avoid recurrence If lymph node +ve also (SE: pneumonitis, pericarditis, rib fractures, lymphoedma, brachial plexopathy) • • • • • Chemotherapy: good if younger and lymph node +ve Antrhacycline 5FU cyclophosphamide Methotrexate • • • • • • • • • Endocrine agents: To decrease oestrogen (ER) activity: Tamoxifen (ER blocker) • • • Reconstruction: implants Latissimus dorsi flap TRAM flap Anastrozole (aromatase inhibitors that target ER synthesis good if post-menopausal Ovarian ablation or GnRH analogues ‘GOSERELIN’ if young and ER +ve tumour. Support: breast care nurses Mental Capacity Act 2005 5 magic principles – learnt them! • 1. Presumption of capacity – everyone has the capacity to make their own decision until proven otherwise • 2. The right for support to be given to help make those decision – ie get all info before conclude they are incapable. • 3. Individuals retain right to make what might seem like unwise decisions • 4. Must retain patients best interests if make it on their behalf ie they lack capacity • 5. The least restrictive option in their best interested must be chosen on their behalf. HIV Human immunodeficiency virus Transmission Sexual intercourse/Infected blood/IVDU/Vertical Pathophysiology 1. GP120 – CD4+ 2. CD4+ migrates Lymphoid tissue 3. Replication, producing billions virions 4. New CD4+ cells infected, numbers delete 5. Immune function falls. Stages 1. Acute infection Asymptomatic 2. Seroconversion 2-6 weeks post exposure. 3. Asymptomatic phase * can get PGL 4. AIDS CD4+ count <200mm3 HIV Diagnosis ELISA = HIV-Ab if 1-3 weeks post exposure PCR = HIV RNA or core p24 antigen - All HIV diagnoses given tuberculin test. Complications • LUNGS: Pneumocystis jiroveci pneumonia - give IV co-trimoxazole and pred • GI: candidiasis, HSV, anorexia, weight loss, Diarhhoea, hepatomegaly, anaemia • EYE: CMV retinitis. Fudoscopy shows ‘mozzarella pizza’ sign • CNS: - acute= transient meningoencephalitis - chronic= dementia, meningitis, CMV encephalitis Management HAART: highly active antiretroviral therapy 1 NNRTI ( non - nucleoside reverse transcriptase inhibitor) e.g NEVIRAPINE and EFAVIRENZ 2 NRTI e.g ZIDOVUDINE OR PI (protease inhibitor) e.g INDINAVIR 2 NRTI