Dermatology - summary medicine PDF

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summarized from Davidsons' & from ward rounds...

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Dermatology Always describe first the morphology Primary lesions Macule: circumscribed area of altered skin colour, not raised Plaque: Discrete, elevated, flat topped lesion, wider>tall Papule: Discrete elevation in skin wide Nodule: Discrete elevation in skin >0.5cm wide. Taller>wide Papilloma: Projecting nipple like mass – skin tag Erosion: Partial loss of surface epithelium Ulcer: Complete loss of surface epithelium Abscess: Localised collection of pus in a cavity Cyst: Abn filled area that has an epithelium lining Petechiae: Pinhead sized macules due to extravascular blood in the dermis Purpura: Larger macules agv blood in the dermis Ecchymosis: Blood deeper in the underlying structures Telangiectasia: Visible dilatation of small cutaneous blood vessel Vesicle: Small 0.5cm fluid filled blister Pustule: Visible accumulation of pus in a blister Weal: Evanescent discrete area of dermal edema, usually white 2nd lesions Atrophy: Area of thin translucent skin due to loss of epidermis, dermis or SC fat Crust: Dried exudate of blood or serous fluid Excoriation: Linear erosion agv scratching Lichenification Scar: replacement of normal structures by fibrous tissue at the site of an injury Stria: linear, atrophic, pink, purple, or white band due to connective tissue changes Violaceous?

Skin lesions are common, affect wide range of ages

Acne vulgaris Very common, GP must be able to Rx, only severe cases should be referred

Comedo: white ball, no inflammation Papules: white ball, inflammation surrounding Pustule: Contains pus, inflammation Factors  Moisturizers & oils  Stress (↑ androgens)  Diet  Mechanical manipulation  GM  B12  Iodine Pathogenesis 1. Androgens lead to sebaceous gland hyperplasia 2. Hyperkeratosis of intra-follicular sebum duct - blocked 3. Comedo forms 4. Inflammatory mediators (Interleukin 1) 5. Rupture of comedo 6. Propionibacterium acnes 7. Free fatty acids (pro-inflammatory) 8. Neutrophil chemotaxis – pus formation GM & acne  Steroids (local & systemic) anabolic steroids  Progesterone (Contraception – P only)  Lithium  TCA  B12  Iodine Grading: type of lesion determines, not number I: Only Comedo II: Comedo & papules III: Pustules additionally IV: Nodules/ cysts/conglobate Topical retinoids Adapalene, isotretinoin, tretinoin, tazarotene For all cases of acne – ideal for long term maintenance. Apply at night – UV lights inactivates GM. Apply to whole face – initially irritating start slow Comedo Rx Topical Retinoids Benzoyl peroxide – kills acne bact. Works well with topical retinoids Comedo extraction, anti-androgens Papular acne Rx Topical: comedolytic drugs. Benzoyl peroxide/erythromycin combination (Never antibiotic alone) Systemic: tetracycline’s, erythromycin Oral contraception, Anti-androgens: Drosperinone (Yaz?) or 2mg cyproterone acetate Pustular acne: Always systemic antibiotics + topical preparations Nodulo-cystic acne Always systemic

Antibiotics: lymecycline, minocycline, doxycycline Anti androgens 10mg cyproterone acetate Systemic Isotretinoin (full course) Additional Rx Comedo extraction Intralesional steroids – cysts >2cm Scars: laser/abrasion – once acne has cleared up Sequence of Rx 1. Comedolytics + antibiotics 2. Oral contraception & anti androgens (if F) 3. isotretinoin Isotretonoin systemic Indications  Nodulocystic/ conglobate acne  Non-responsive: 3months of lymecycline or 4 cycles anti androgens  Scarring acne  Gram neg folliculitis  Dysmorphofobic pt – crazy, threatens suicide over pimples (real or imagined) Dosage Total dose 120-150mg/kg over the entire period. Tablets come in 20mg doses 0,5-1,0mg/kg/day Bv Pt 60 kg Total dose: 7200 – 9000mg Daily dose: 30-60mg/day Thus 7200/40 = 180days or 7200/60 = 120days Side effects  Teratogenic  Initial acne flare  Dry skin, lips, eyes  Dermatitis  Raised lipids  Liver function disturbance  Photosensitivity  Myalgia/arthralgia  Night blindness  Osteoporosis  Depression: Rare but serious. Report mood swings Precautions Pregnancy test – negative. Start contraception, then start isotretinoin 1month later on the 3rd day of menstruation. Negative pregnancy test every month LFT & triglycerides/cholesterol before Rx and repeat after 1 month

Rosacea Older pts. Red face, no comedos Stimuli

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Heat Psychological stress Sunlight Alcohol - exacerbates Spices (MSG) Hot beverages Hormonal factors

Rx  Tetracyclines  Topical metronidazole – maintenance  H. pylori eradication  Ice compress  Avoid stimuli NEVER TOPICAL STEROIDS Peri-oral dermatitis Not a true dermatitis, form of rosacea around the mouth Caused by overuse of moisturizers, topical steroids Rx: tetracycline 6weeks The only people that need moisturizers are pt with atopic dermatitis

Atopic dermatitis & other inflammatory skin sicknesses Atopic dermatitis Genetic defect auto dominant. Defective skin barrier (water & other molecules). Not an allergy

Pathogenesis: Th1 immune system doesn’t develop, stays Th2 as in a fetus. More prone to allergies later (atopic march), sometimes raised IgE. Genetic major component (esp maternal agv imprinting). Environmental Manifest as asthma, hay fever, food & other allergies. Affects 1 in 10 schoolchildren Defective barrier allows greater penetration of allergens and causes inflammatory response to common environmental Ag Problem list 1. Very dry skin, rough. Often in flexures, neck. Can have lichenifcication 2. Pruritus + rash: worsens with going to school, winter, at the coast History  Respiratory symptoms  Reaction against certain foods  Pet allergies  Rx to this point & response Further investigations FBC, IgE, Rast-tests, patch test Dx of atopic dermatitis  Chronicity  Pruritus  Typical skin involvement  Atopy in family Triggers  Cold, dry air  Warm water  Soap  Stress  Wool  Food intolerance (protein contact dermatitis)  House dust mite  Pets  Malassezia furfur (adults)  Staphylococcal infections Rx  Emollients (moisturizers)  Sedating anti-histamines  Topical steroids  Pimercrolimus  Antibiotics Refer: respiratory symptoms Avoid the triggers, Breastfeeding lessens incidence Follow-up: initially often, later less. 60% is outgrown by 6year, but never normal skin Foods to avoid peanuts, tomatoes, pineapple. Citrus fruit, chocolate, Sulphur dioxide (dried fruit, mixed cool drinks), avocado, mango, banana, soya Seborrheic eczema Red scaly rash Affects scalp (dandruff), central face and nasolabial folds, eyebrows and central chest. Severe may resemble psoriasis

Discoid eczema Discrete annular eczematous lesions Irritant eczema Strong irritants elicit an acute reaction at site of contact, weak irritants cause chronic eczema after prolonged exposure Allergic contact eczema Delayed hypersensitivity reaction following contact with Ag. Requires previous sensitization and reaction is specific to allergen. Often getting the original site is important to determine cause eg earlobes or bra clips or wrists Rx Topical corticosteroids 1% hydrocortisone Sedative antihistamines

Psoriasis Non-infectious, chronic inflammatory disease of the skin. Well defined erythematous plaques with silvery scale. Likes extensor surfaces & scalp, chronic fluctuating course. Any age Keratinocytes hyperproliferate with a grossly increased mitotic index – retention of nuclei in stratum corneum. Disordered cell proliferation. Genetically inherited. Triggers from environment, not the cause

Nail signs: Pitting, onycholysis, subungual hyperkeratosis

Triggers  Stress  Infection: streptococcus  Trauma/friction  Alcohol (lots)  Drugs: ACE inhibitors, chloroquine, B-blockers, lithium, NSAIDs, penicillin

Patterns  Plaque psoriasis (psoriasis vulgaris): 80-90%. Patches/plaques that are tender and appear as thick red swollen, inflamed. Dry, covered with crusty silver scale. May be itchy. Seen on knees, elbows, scalps, trunk but can appear anywhere  Inverse psoriasis: smooth red & swollen areas. Grows in folds like under breast, navel, groin & buttocks. High possibility of complications such as yeast or fungi infection  Pustular psoriasis – palmo-plantar; generalized: Red edge and yellowish/whitish pus filled blisters. Mostly only the hands & soles of feet Rx  Topical steroids – medium/potent  Coal tart preparations  Vit D analogues  UV light  Systemic: methotrexate, acitretin, cyclosporine A, biologicals Nummular dermatitis (discoid eczema). Distinct coin shaped (nummular) sores on skin. May appear after a skin injury such as burn, abrasion or insect bite. May be itchy or not, dry & scaly or wet & open

Lichen planus Skin rash triggered by immune system. Chronic recurrent rash. Pruritic, flat topped, violaceous papules and characteristic fine white network on surface. Rash may generalize, coalesce into rough, scaly plaques. Often leaves post-inflammatory pigmentation. Intensely itchy polygonal papules, violaceous hue. Some hyperkeratosis. Starts on distal limbs – volar aspect of wrist & lower back Nail changes: longitudinal grooving to destruction of nail fold & bed Rx: Spontaneous resolution, systemic corticosteroids, ciclosporin, retinoids

Cutaneous hypersensitivity Hypersensitivity reactions (Gell & Coombs ) I: Allergy – Anaphylactic. IgE mediated. Allergens induced IgE Al. Quick response within minutes. Urticaria

II: Cytotoxic. Al bependant. IgM or IgG. Al-Ag interaction on cell surface. Ag binds to host cell – cell seem as forgein = lysis via membrane attack complex. Eg toxic epidermal necrolysis III: Immunecomplex. IgG (mediator) binds to free Ag = insoluble immune complex (occurs in Ag overflow). Immune complex cant be removed from circualtion (fagocytosis). Precipitates on basal membranes = inflammatory response agv complement-activating via chemo-activating factors. eg vasculitis IV: Delayed (cell mediated). Lymphokines from sensitifsied T-cells. Lesion 24-48hrs after Ag exposure. TH cells activated via APC. When Ag is seen again the Th cells become activated, macrofages activate and a inflammtory response occurs. Eg allergic contact dermatitis History  GM: aspirin, NSAIDs, laxatives.  Associated symptoms/diseases  Rx & response Further examination Systemic physical exam – throat. LN The following are for chronic urticaria – only a small chance for finding source  Total IgE, selective RAST  FBC + ESR  Collagen disease screen serology  Sinus-X-rays  Orthopantomogram Cutaneous hypersensitivity  Urticarial – disappears within a day  Contact dermatitis: allergic, irritation  Photosensitivity  GM reactions: most common Acute urticaria 6weeks. Idiopathic, autoimmune, spontaneous IgG aimed against IgE. Not an allergic base even though its an IgE mechanism Causes: GM, infection, infections, food, inhalations, auto-immune sickness, chronic autoimmune urticaria, idiopathic Rx therapeutic Anti-histamines Sedating: hydroxyzine, promethazine – good for nervous pt Non-sedating: loratadine, cetirizine, ebastine H2 blockers – cimetidine Systemic corticosteroids Referral – selective Identify cause. Avoid all GM, diary of attacks Follow-up: maintenance Rx. GM works better to prevent than to Rx – take GM even without an attack Prognosis. Most burn out in 2-3years but may keep going for decades.

Non-allergic mast cell degranulation Aspirin, ethanol, curare, codeine, ACE inhibitors, heat, cold, vibration, water, pressures, viral infection Photosensitivity GM: thiazides, doxycycline, isotretinoin, amiodarone, NSAIDs, promethazine SLE, HIV, porphyria (cutanea tarda, variegata), pellagra, albinism

Allergic contact dermatitis Cell mediated response. Previous sensitization, reacts with minimal exposure, itches intensely. Red, raised vesicular if acute. Scaly lichenified when chronic. Can spread beyond area of contact. Metals (nickel, chromium, cobalt), perfumes, colorants, glues, preservatives, formaldehyde, plants, antibiotics – aminoglycoside, quinolone Photodermatitis: Form of allergic. Light activates the allergen?

Patch testing Tests for cell mediated hypersensitivity, blood tests are useless

Irritation contact dermatitis No allergy – like a sun burn. No previous sensitization. Large exposure necessary - almost everyone is vulnerable. Burning sensation, little itching. Reddish, not raised, no vesicles. Fissures, scaly when chronic

Sebaceous dermatitis In sebaceous glands – axillary, nasolabial folds, groin Common after puberty or 25hr after sun exposure eg thiazide, enalapril, chloroquine metabolic  Porphyrias  Pellegra: Exacerbation of pre-existing disease  SLE  DLE  Herpes

HIV skin lesions Early signs  Acute seroconversion syndrome  Herpes zoster  Serborreuse dermatitis  Psoriasis Acute seroconversion syndrome 2-6w post infection, duration of ±1w

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Vasculitis Acquired igtiosis Retroderma

Morbilliform rash (measles like - macular lesions that are red and usually 2–10 mm in diameter but may be confluent). Fever, sweat, malaise, myalgia, arthralgia, pharyngitis, generalized lymphadenopathy Herpes zoster Reactivation of virus. Pre-eruptive phase has pain/itching/paresthesia’s along dermatome Eruptive: Grouped herpetiform vesicles with erythematous base over dermatomal spread. Unilateral. Vesicles are initially clear – cloud, rupture, crust. Painful, induration (an increase in the fibrous elements in tissue commonly associated with inflammation and marked by loss of elasticity and pliability). Herpes keratitis: If tip of nose is affected – same nerve. Dull pain, acute dryness. Blepharo-conjunctivitis. Derma & ophthalmology emergency Seborrheic dermatitis Chronic, relapsing, mild dermatitis. Affects sebaceous gland rich areas of skin Gradual progression. Flaky skin and scalp – face, behind ears skin folds. Patchy, scaly skin lesions, mild redness. Scales are white or yellow – big fatty dandruff Ichthyosis vulgaris: dry, scaly or thick skin. Fish scale appearance, symmetrical. Hyperkeratosis of soles Psoriasis: Atypical presentation in HIV +ve. Palmoplantar psoriasis. Biopsy to confirm Retroderma: Neologism in the Freestate. Dermatitis in HIV. Red form head-to-toe. Often other disease with eg photosensitivity or atopic Photo dermatosis: Skin fold sparing - Nasolabial, eyelid, lower lip, upper chin Cutaneous vasculitis: Non-blanching ALLMD: Actinic lichenoid leucomelanoderma of HIV. New disease, specific for HIV. Sun exposed areas get lichenification. Slightly grey + spotty pigmentation. Rx ARV’s Drug interactions Toxic epidermal necrosis (TEN): >30% of body surface affected, not just mucosa. Steven Johnson Syndrome (SJS): 5cm in diameter with central keratin plug (volcano shaped) Rx: curettage or excision to rule out squamous cell and avoid scarring of spontaneous resolution

Melanoma Most malignant tumor. Caused by high exposure to UVA in childhood, family predisposition. Early and rapid metastasizes Risk: >30 melanocytic nevi, 3+ dysplastic nevi, fair skin, 3+ blistering sunburn episodes as child, family history, previous melanoma, tanning beds

Dysplastic nevi and melanocytic nevi are seldom pre-malignant. Melanoma is mostly de novo. Types: Superficial spread, nodular, acral lentiginous (on soles & palms), lentiomaligna, a-melanocytic Starts with a superficial and radial growth phase then invasion Macro: A – Asymmetrical B – Border, irregular C – Color, different shades of brown and black D – Diameter >6mm E – Evolution, change in appearance is NB Diagnosis Clinical - changing, pigmented lesion Incision biopsy of thickest/blackest part. No punch biopsy – doesn’t stage Rx: wide surgical excision according to Breslow thickness. Sentinel LN dissection for tumor 1-4mm thick (no prognosis >4mm thick). Examine rest of skin, check for mets. 6m lifelong follow-up Marjolin ulcer Aggressive ulcerating squamous cell carcinoma presenting in an area of previously traumatized, chronically inflamed or scarred skin. 10-25years later Slow growing, painless ulcer. No lymphatic spread as lymph channels are destroyed Rx: Surgical, wide excision. 1cm margin. Radiation therapy is an alternative

Porphyria Porphyria

Rare disorder of heme biosynthetic pathway partial enzyme deficiencies and mutation in relevant genes. Hepatic or erythropoietic depending on whether the major site of excess porphyrin production is in the liver or the red cell 2 broad categories  Cutaneous: Photosensitive skin manifestations attributable to excess production and accumulation of porphyrins in skin – causes pain, erythema, bullae, erosions, hirsutism and hyperpigmentation. Predominantly sun exposed areas. Skin becomes very sensitive to damage from minimal trauma  Neuro-psych: acute relapsing and remitting neurological syndrome. Presents with acute abdominal pain and features of autonomic dysfunction – tachycardia, HT, constipation Dx: Porphyrins and porphyrin precursors found in blood, urine and faeces. All taken simultaneously and wrapped in black plastic or whatever to prevent photodegradation. Send to lab quickly Porphyria variegate Settler sickness of South-Africans of Dutch heritage. Mostly whites, some coloured’s. Autosomal dominant. Genetic predisposition + precipitating e.g heavy alcohol use, HIV, estrogen, Hep B & C Porphyria cutanae tarda The cutaneous features are increased skin fragility, blistering, erosions and milia occurring on light-exposed areas such as the backs of the hands. Facial hypertrichosis Skin signs Variegate has similar signs to cutanea tarda  Skin becomes weak, sensitive and mechanically susceptible especially in sun exposed areas. May lead to blisters, erosions (not normal reaction – mechanobullous)  Skin shows accelerated ageing. “Weather beaten” almost leonine face (porphyria is more generalized vs leonine - central) periorbital mottled hyperpigmentation  Hands rough abused hands. Bullae  Atrophic, depigmented lesions. Fibrosis (scarring agv dermal damage)  Scleroderma-like skin: Looks like connective tissue disease – keep on diff  Hypertrichosis: symmetrical ‘sideburn area’ not really rest of body. Semi-specific of porphyria Management  Confirm biochemical Dx  Mechanical protection – avoid trauma  Sun avoidance  Venesection 6weekly – remove porphyrins from blood  Chloroquine ½ tablet 3 per week  Local wound care for ulcers Acute intermittent porphyria No skin lesions – just avoid precipitating items Porphyria crisis Mimics acute abdomen – severe non-focal abdominal pain, vomiting, HT, tachycardia sometimes motor neuropathy, partial ileus. Absent peritoneal signs Drugs to avoid Benzo’s, barbiturates, anticonvulsants, rifampicin, halothane

Cutaneous fungal infections Dermatophytes Keratolytic fungi - Break down keratin

Three anamorphic genera cause: Trichophyton, Microsporum, and Epidermophyton

Tinea  Corporis – body: 2nd rings. Annular. Red edge, scaly, raised., central resolution o Incognito – atypical presentation agv steroid Rx Capitis – scalp: Circumscribed Hair loss, Scaling with/without exudation/pustules, systematic Rx (follicle in SC). Rare in adults – think

immunosuppresion

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Cruris – groin: Skin folds, little scaling. Low grade Inguinal -does not involve scrotum. Bilateral or

annular lesions. unilateral.

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Pedis – feet. Asymmetrical. Groups of vesicles.

Diffuse dryness, scaly.

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Unguium – nails, asymmetrical, onycholysis, thick nail plate. Subungual hyperkeratosis, yellow, white, brittle. Complete nail destruction. Nail folds normal, no oil spots Rx hands – 2m, feet – 3m

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Macro: Lesion begins as a large, erythematous, scaly plaque with raised edge. Following central resolution, the lesion may become annular in

shape. Usually hair loss

Dx Clinical, culture Wood’s light – certain species fluoresce, good for sifting potassium hydroxide (KOH) examination of skin scrapings, used to visualize fungal elements removed from the skin's stratum corneum for hyphus & spores Rx Single lesions: Topical - imidazole, terbinafine Immune compromised or multiple lesions: Ketoconazol...