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Peer Teaching

Peer Teaching. Dermatology & Miscellaneous. Basic skin structure. Ulcers. Arterial Venous Neuropathic Traumatic Vasculitic. Arterial Vs Venous. What might delay healing?. oedema immobility (poor calf muscle pump and oedema ) anaemia or malnutrition corticosteroids

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Peer Teaching

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  1. Peer Teaching Dermatology & Miscellaneous

  2. Basic skin structure

  3. Ulcers • Arterial • Venous • Neuropathic • Traumatic • Vasculitic

  4. Arterial Vs Venous

  5. What might delay healing? • oedema • immobility (poor calf muscle pump and oedema) • anaemia or malnutrition • corticosteroids • repetitive trauma • heavy colonization with bacteria

  6. ECZEMA • Superficial skin inflammation with vesicles (when acute) • redness • oedema • oozing • scaling • pruritus

  7. TYPES

  8. 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) ORherpes simplex virus (small blisters or punched out lesions = eczema herpeticum which is FATAL)

  9. EXOGENOUS • Unusual pattern of rash with clear-cut demarcation • Odd-shaped areas of erythema and scaling

  10. 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 immunomodulatorsiecalcineurin inhibitors (tacrolimus and pimecrolimus) for eyelids • Abx if superinfection • Second line: If severe and unresponding • prednisolone • azathioprine • ciclosporin

  11. For exogenous eczema: !!Remove causative agents!!

  12. ACNE • Increased sebum production by sebaceous glands • Blockage of pilosebaceous units • Follicular epidermal hyperproliferation • Infection with propionibacterium

  13. 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.

  14. WORST CASE SCENARIO • ACNE FULMINANS = young man develops severe nodulocystic acne + • fever • malaise • joint pain • swelling

  15. 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)

  16. Side effects of Isotretinoin • mild alopecia • dry skin • raised blood fat levels • teratogenicity • psychological disturbances

  17. Skin Cancer • Malignant melanoma • Squamos cell cancer • Basal cell carcinoma (rodent )

  18. 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

  19. GLASGOW SCALE • Assymetry • Border-irregular • Colour – non uniform • Diameter >7mm • Elevation • (=Glasgow scale) + Clarks staging to stratify depth URGENT EXCISION

  20. 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)

  21. Ulcerated lesion • Hard, raised edges • Sun-exposed sites • Keratotic nodule with granulating base and rolled border • Regional lymphadenopathy • Treatment: • Excision (curretage) • Photodynamic therapy (PDT) for superficial tumours • Mohs microscopic surgery if need to preserve skin in recurrent cancers e.g. eyelid

  22. Squamos cell cancerBasal cell carcinoma (rodent ) • Very slow grower • Never metastasizes • Locally invasive (hence rodent) • Middle aged • Caucasians

  23. 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: waxuindurated plaque that looks like a scar

  24. Treatment: • Excision (curretage) • Photodynamic therapy (PDT) for superficial tumours

  25. INFECTIONS OF SKIN

  26. MISCELLANEOUS

  27. 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

  28. Paracetamol metabolized in liver by conjugation with glucoronateor sulphate excreted by kidneys. • Cytochrome P450 metabolises some of it to highly reactive N-acetyl-p-benzoquinonimine(can inactivated by conjugation with glutathione)

  29. WITHIN 8 HOURS OF OD: N-acetylcysteine IV

  30. Breast Cancer

  31. STAGING OF BREAST Ca

  32. 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) • 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 • Reconstruction: implants • Latissimusdorsi flap • TRAM flap

  33. Mental Capacity Act 2005

  34. 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.

  35. HIV Human immunodeficiency virus Transmission Sexual intercourse/Infected blood/IVDU/Vertical Pathophysiology GP120 – CD4+ CD4+ migrates Lymphoid tissue Replication, producing billions virions New CD4+ cells infected, numbers delete 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

  36. HIV 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 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

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