Dermatology Skin function: UV protection Mechanical functions ...

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Dermatology Skin function: UV protection Mechanical functions ...

  1. 1. Dermatology<br />Skin function:<br />UV protection<br />Mechanical functions<br />Thermoregulation (sweat glands, blood vessel constriction/dilation)<br />Chemical factor protection<br />Microorganism protection<br />Protection from water and ion escape<br />Vitamin D synthesis<br />SIS (skin immune system)<br />SALT (skin associated lymphoid tissue)<br />SISUVPilosebaceus unitT-cells - Th1 & Th2Photoaging sebaceus glandMast cells - histaminetumorshair follicleB-cellsImmunosuppressionpapillaNeutrophilsPhotodermatosis - prokoved by UVhair shaftEosinophils M. erector pililangerhans cells - search for antigens  <br />Cornified layer – pH 5.5desmosomes, corneocytes and lipids in layers<br />Granular layer – apoptosis, final process, dense structure of keratin<br />Spinous layer – produce keratin and differentiate<br />Basal membrane – some patients produce antibodies against basal membrane<br />Basal layer – cell producing layer, takes 30 days to travel to surface<br />Papillary layer – bed for epidermis, papillary plexus<br />Reticular layer – collagen fibers 1&2, elastic fibers and reticular fibers<br />Primary lesions:<br />MacculePapuleNodes/NodulesBlistersWheelsflatElevatedelevatedelevatedelevateddifferent colorepidermal changesskin/subcutisfluid contentsudden onseterythemaresolve & no scarringepidermal envolvebulla >0,5 cmspontanous resolutionvitiligoplane wart –epidermalscarringsmall vesiclesdermal edema lichen planus ruber - epi + dermis ex. Pemphigoidwhite/pink/redPustules - filled with pus, ex: Folliculitis  <br />Secondary lesions:<br />Erosion – ex: Pemphigus vulgaris<br />Ulcer<br />Crust – ex: Impetigo<br />Fissures<br />Scars<br />Scaling<br />Atrophy – aging<br />Microbilogy of skin: <br />Resident flora<br />Transient flora (depending on enviroment)<br />Temporary resident<br />-> corneocytes are died cells without nucleus or recpetors, bacteria can therefore not attach to this layer. This layer changes every 3 weeks as a natural defens.<br />Development of skin infections depends on:<br />pH <br />skin barrier<br />age – neonates don’t have enough Langerhans cells<br />profession<br />disease – immunosuppression<br />intake of antibiotic<br />3 groups:<br />staphylococcal skin infection - furunculus<br />streptococcal skin infection - erysipelas<br />mixed – impetigo(contagious)<br />Erysipelas – a bacterial infection of the dermis and upper subcutaneous tissue with cellulitis that may extend superficially.<br />Predisposing factors: Local - chronic inflammation, animal bites, surgery, balneotherapy, allergy, posthrombotic syndromes, lymphedema. General – immunesuppression, rheumatoid disease, etylinus and DM<br />Creteria: lower limb, face, elderly with CHD or DM, develop after surgery or car accident<br />Investigations: USG (exclude phlegma), US Doppler (exclude DVT), bacterial swab, lab test<br />Complications: bullae, hemorrhage, necrosis, edema, phlegma, thrombophlebitis, elephantiasis<br />Treatment: Cephalosporin (IV) for 12-14 days, Erythromycin<br />   Cellulitis    SuperficialProfoundErysipelasPeriorbicularisNecrotisansGazeus(face, limb, hand)(face)  (genital) (limb, hand)<br />“Fungal infection”<br />         Dermatophytes         Candidiasis         Malessesia <br />Signs:<br />red, round, oval like a coin<br />spread peripherally<br />crack & fissures between toes<br />crusty, scaly, bald on scalp<br />pustules around hair<br />white patches & plaques on mucous membrane<br />maceration ( white lesions centrally )<br />Id- allergic reaction:<br />Clinically course of fungal infection may be complicated by the secondary of Id-reaction. Appears on hands and face.<br />Predisposing factors: <br />injury<br />obesity<br />immune deficiency<br />metabolic disease<br />medications ( contraceptive or steriods)<br />practising sports<br />Increase occlusion (rubber shoes, synthetic fibers)<br />Remember that topical corticosteroids may cover thefungal infection and allow it to spread!!<br />“Dermatophytes”<br />DermatophytesGroupsDiagnosis1) MicrosporumAtropophylicWood's light(skin +hair)(person - person) T+MDirect examination2) TrichophytonZoophilicIndirect examination(skin + hair + nail)(animal - person) T+M 3) EpidermophytonGeophilic (skin + nails)(enviromental) M <br />Types / Localization:<br />Tinea pedis – Trichophyton rubrum, T. mentagrophytes, Epidermophyton floccosum<br />Swimming pool, foot wear, hot weather<br />Interdigitalis – “athlet’s foot”, papules and vesicles<br />Erythema, scaling, maceration, bulla formation<br />Most commonly between 4th & 5th toes<br />Dry type: chronic persistent – T.rubrum<br />Moist type: inlammatory recurrent – T. mentagrophyte<br />Tinea manuum – T. rubrum<br />Asymmetrical (unilateral)<br />Associated with tenia pedis<br />Minimal erythema<br />Dry powdery scaling on creases and fissures<br />Tinea corporis – Trichophyton rubrum & Micrisporum canis<br />Neck & upper trunk<br />Single/multiple plaques<br />Asymptomatic, mild pruritus<br />Periperal enlargement with central clearing<br />Tinea faciale <br />Treat with corticosteroid<br />Sharp-marginated annular lesion<br />Pseulopecia<br />Edema<br />Thickening of skin<br />Tinea cruris – T. rubrum, T. mentagrophyte<br />Men > women<br />Unilateral<br />Asymmetrical<br />Large, scaling dull red plaques with central maceration<br />Papule & vesicle<br />Tinea nail<br />Associated with pedis<br />Yellow crumby nails<br />Separation of nail from its bed<br />Subungual hyperkeratosis<br />Dystrophy<br />Not painful<br />Not itchy<br />Old men<br />Diabetes<br />Poor hygien<br />Immuneo deficiency<br />Therapy: systemic Itraconazole 2x200 mg/day for 1 week<br />Treatment of dermatophytes:<br />Topical Imidazole twice daily for 2-4 weeks<br />Systemic Fluconazole 150mg/day for 4-6 weeks<br />Itraconazole 100mg/day for 1-2 weeks “most safe”<br />Terbinafine 250mg/day for 2-4 weeks<br />“Candidiosis”<br />1) Intertrigo2) Candidal angular stomatitis3) Vulvovaginitis4) Tinea yeast penis<br />Diagnosis: microscopic and culture<br />Treatment: Nystatin topically, Fluconazole<br />Paronychia = infection of cuticle causing loss of cuticle, the skin is elevated due to edema & infiltration, pus, painful, and involve people with wet hands. Treatment is Imidazole or itraconazole.<br />Ptyriasis vesicolor (Pityrosporum orbiculare) = numerous lesions of different colour caused by inhibition of melanogenesis visible after sun exposure.<br />“Viral infection”<br />1) HHV2) HPV3) Poxvirus<br />Herpes simplex virus:<br />HSV-1 (upper) & HSV-2 (lower)<br />Personal contact<br />UV exposure<br />Menstruation<br />Fever, cold<br />Immunosuppression<br />Primary = newborn, symptomatic, person to person, severe pain, fever, lymphadenopathy, last 10-14 days, meningitis, sepsis, stomatitis, eczema<br />Secondary = last 7 days, hypersensitivity, itching before topical treatment<br />*Koebner phenomenon = linear distribution of skin lesions resulting from linear exposure or irritation. Conditions demonstrating linear lesions are warts, musculus contagiosum and rhus dermatitis.<br />Herpes zoster virus: “old people”<br />Dermatomal infection<br />Sensory ganglia<br />Direct contact, air-bourne<br />Contagious before vesicle appearance<br />Prodromal symptoms<br />Risk factors: age, malignancy, HIV+<br />Complications: postherpetic nauralgia, erosion, blindness, paralysis, death<br />Blister > 1cm<br />Unilateral<br />Treatment: Acyclovir systemic for 6-7 days<br />Human papilloma virus:<br />Verruca vulgaris (most common)<br />Plane warts – children, flat, multiple, painless, light brown, hand & face<br />Plantar warts – on feet<br />Mosaic warts<br />Anogenital warts (Condylomata accuminata)<br />“Syphilis”<br />Transmission:<br />Sexual transmission<br />T.p dies rapidly outside body<br />T.p penetrate damage skin and mucosa<br />Disseminated by lymphaties and bloodstream<br />Time of incubation depens on inoculum<br />Primary sore:<br />Develop in the morning<br />Macule, papule ulceration<br />Single, round, oval (5-10 cm)<br />Defined outline<br />Painless <br />Clean looking granulation<br />Inflammatory infiltrate of base<br />Exudate (dark field in microscopy)<br />Enlarge lymph node deep in the pelvis<br />Atypical type: mouth & anus, small irregular, painful<br />Constitutional symptoms:<br />Sore throat<br />Hepatitis jaundice<br />Neprhopathy<br />Stiffness<br />Photophobic<br />Phimosis - foreskin cannot be pulled back<br />Paraphimosis - foreskin cannot the pushed up (edema, blood canot leave gland)<br />Papular rash may mimic:<br />Psoriasis<br />Sarcoidosis<br />TB<br />Measles<br />Leukemia <br />Postular rash:<br />Seen in HIV+ and drug addicts<br />Looks like small pox<br />Alopecia ( type 1 – scalp) (type 2 – temporal & occipital)<br />Leukoderma in neck<br />Pink/white mucous patches<br />Angina, sore throat<br />Painless <br />“Urticaria”<br />Presence of atypical skin lesion utica & angioedema & subcutaneous tissue<br />Urtica (size, duration, itch) usually last 3 h<br />Subgroups:<br />AcuteSerum sicknessmost frequenttype 3IgE mediated (food, stress, immuno)drugs & immune areaallergens orallywheal, hand edemawheal, bronchospasmjoint pain, feveranaphylactic shocksymptoms occur 9 days after exposureQuinche edemalast 12-24 hSPT, RIST, RAST, for specific IgESustemic Prednisolone 30-40 mg 10-14 days<br />Treatment:<br />Quinche edema – adrenaline (sc), corticosteroid (iv), aminophiline<br />Wheal – laxative, remove diet, antihistamine, systemic corticosteroid<br />Aspirin urticaria<br />Aspirin intolerance – overproduction of leukotrienes (non-immunological)<br />Chronic 20-30% or asthma aspirin<br />Acetylosalicylic acid, NSAID, dyes, benzoic acid, sorbic acid, food<br />Diagnosis: exposure of small doses<br />Treatment: eliminate diet, antihistamines, antileukotriene drugs<br />Dermographism – cold urticaria – delayed pressure urticaria – cholinergic urticaria<br />URTICARIADIAGNOSTREATMENTstage:Coldice cube, waterCirpoheptadine 3x4 mg1) erythemaDermoscratchingAntihistamine, Ketotifen2) papuledelayedcube test, beltAntihistamine, Cimetidine 2x0,43) crustcholinergicexcerciseKetotifen 2x1 Bellergot4) post-inf. LesionsLightUVA, UVB testβ-caroten, tolerance to light <br />“Pemphigus”<br />Antibody binds to desmoglein (TMP) the extracellular domain of the desmosomes causing separation of the cytoplasmic plaque. Plaques are responsible for formation of epithelium in lungs, digestive tract etc. This also leads to erosion of respiratory tract and GIT.<br />Upper part (Dsg 1) = 160 kD = Pemphigus vulgaris<br />Lower part (Dsg3) = 130 kD = Pemphigus foliation<br />Ig G is found along basement membrane between epidermis and dermis<br />Paraneoplastic pemphigus: 190kD<br />Etiology <br />HLA-DR4<br />Drugs Captopril<br />Diet (garlic, onion, leads)<br />Burn induced penphigus<br />Pemphigoid gestation:<br />1st trimester<br />180 kD antigen<br />Disappears after delivery<br />Linear IgA dermatosis:<br />BP 180 kD antigen recognize 97 kD allergen<br />Mixed form of dermatitis + pemphigoid<br />Subepidermal bullocks disease:<br /> > 65years<br />180 kD antigen<br />Collagen type 7 connect lamina densa to skin<br />Treatment: Prednisone up to 3 months<br />180 kD molecules:<br />BP 180 – lamina lucida<br />PG – lamina densa<br />LABD <br />CP – damage lamina densa<br />”Psoriasis”<br />Chronic inflammation, non infectious skin disease affecting any part of skin<br />1-3 % affecting both sexes<br />30% of patien have positiv family history<br />Increase epidermal cell proliferation (short cell cycle time)<br />Activate keratinocytes (elevated TNF-α)<br />Infiltration of leukocytes<br />Stages:<br />Parakeratosis<br />Irregular thickening of epidermis<br />No granular layer<br />Leukocyte infiltration<br />Triggering factors:<br />Infection (streptococcus)<br />Stress<br />Hormone (pregnancy)<br />Drugs (β-blocker, alcohol, cigarett)<br />Trauma (scratch, surgical wound)<br />Other inflammatory skin diseases<br />Insect bites, seborrhagic dermatitis<br />Sunlight (may help)<br />Association with HIV<br />Types:<br />Ґ - < 40 years (12-20) 75% with positive family history<br />П - > 40 years (59) 25% caused by enviromental factors<br />Localization/Clinical: on scalp& elbow - red scaly papule ( plaque – erythroderma ) “well demarked”<br />Guttate psoriasis:<br />Young adult<br />Following infection<br />2-10 mm papule<br />Does not cause baldness!!<br />Diagnosis: seborrhagic dermatitis, erythroderma (drug induced) , hyperkeratosis on nails<br />Postular psoriasis:<br />Postules transform into plaque psoriasis<br />Palmar plantar psoriasis (PPP)<br />50-60 years<br />Tinea + eczema<br />High fever & elevated WBC<br />Psoriatic arthropathy<br />Seronegative arthropathy in skin & nails<br />Rh (-)<br />Any age<br />Single large joint (sausage digit)<br />Investigation: 1) clinical Plaque - ezcema, tinea2) histopathologyGutate - lichenoid , secondary syphilis3) mycologicalFlexural - candidiasis, tinea4) blood test <br />Therapy:<br />Tar preparation<br />Dithranol<br />Steroids<br />Vit D derivatives – calcitriol, tacalcitol, calcipotriol ( no skin atrophy)<br />Takrolimus<br />Salicylic acid containing preparation<br />Schampoo<br />Phototherapy: UVB 311 nm or PUVA 320-400 nm (+topical or retinoid for plaque psoriasis)<br />Retinoids (Neotigason) 40-50 mg/day *Teratogenic<br />Cyclosporin – plaque psoriasis 2,5 mg/kg<br />Anti TNF-α: Etanercept, Infliximab, Adalimumab<br />Anti activated T-lymphocytes: Alefacept & Efalizumab<br />“Cardiovascular syphilis”<br />Uncomplicated aortitis (linear calcification, < 40 years)<br />Aortic regurgitation (chest pain, dyspnea, angina pectoris)<br />Coronary ostial stenosis (syphalitiv asthma, CHF, nocturnal dyspnea)<br />Aortitis<br />Asymptomatic<br />Laboratory tests:<br />Group 1 /non-specific/ never false (-) / screening for cardiolopin<br />VDRL (veneral disease research laboratory)<br />USR (unheated serum reagent)<br />RPR (rapid plasma reagent)<br />Wasserman<br />Group 2 / specific antigen from T.p/ for confirmation<br />TPI (T.p immobilization)<br />FTA (florescent treponemal antibody)<br />FTA –ABS (florescent treponemal antibody absorption)<br />TPHA (T.p hemagglutination)<br />ELISA<br />If (+) test disappear within 6 months they are acute<br />False (+) can occur in SLE, leprosy, thyroiditis<br />Drug abusers may have false (+)<br />>70 years may have false (+)<br />VDRL test may be false in dehydrating patients<br />Captia syphilis is Ig M mediated and it is congenital<br />Treatment:<br />Cardiac surgery<br />Penicillin + steroids to avoid treatment paradox<br />“Nevi”<br />Vascular nevi:<br />Up to 40 % of infants ( no treatment needed)<br />Hemangioma<br />Port wine stain<br />Venous malformation<br />Melanocytic lesion:<br />Ephelis<br />Café-au-lait<br />Solar lentigo (numerous & bigger)<br />PUVA lentigo<br />Lentigines syndrome – Peutz Jacob<br />Melanocytic nevi:<br />1 Mongolian spot<br />Child<br />Blue grey<br />2 Blue nevi<br />Risk of melanoma<br />Dermal typ<br />3 Common melanocytic nevi<br />Normal<br />Sutton<br />Spitz<br />4 Congenital nevus<br />Spotted evils<br />Peculiar desire of mother during pregnancy<br />Present at birth or during 1st month<br />Hair present<br />5 Dysplastic nevi<br />Big, flat<br />Asymmetric<br />Multicolor<br />Trunk<br />Increase during puberty & pregnancy<br />Risk of melanoma<br />Sun exposure<br />Atypic<br />Dysplastic nevus syndrome – multiple, familiar, high risk of melanoma<br />A: asymmetry B: border C: colour D: diameter E: evolution (Staging system)<br />“Melanoma”<br />  Middle ageMmoles - nr?  female > maleMmoles - atypical?  face & lower extremitiesRred hair or freckles  M-trunkIinability to tan - type 1&2  sunburnSsunburn - children  genetic (CDKN2A - MTS1)Kkindered - family history<br />Superficial spreading melanoma (57%)<br />good prognosis<br />horizontal growth<br />Lentigo malignant melanoma<br />lentigo maligna<br />horizontal – vertigal<br />Nodular 21%<br />vertical growth<br />worst prognosis<br />Acral lentignous melanoma 4%<br />distal part of hands & feet<br />realted to LMM<br />Staging / treatment:<br />clinical + US<br />total excision<br />sentimental lynph node excision (from lesion region)<br />regional lymph node excision<br />adjuvant & chemotherapy (TNF-α, isolation)<br />paliative (chemotherapy and care, surgury for metastasis)<br />experimental immunotherapy<br />PET is the best method for metastasis<br />Halo nevi = Good BAD<br />“Precancerous lesions”<br />Actinic keratosis<br />Arsenic keratosis<br />Leukoplakia<br />Xeroderma pigmentosum<br />Epidermodysplasia verruciformis<br />Radiodermis<br /> Progression of lesion to cancer is higher if situated on lips<br />Keratokantoma is a pseudomalignant tumor that quickly develop lesion in young adult,in the face<br />Basal cell carcinoma – look for tiny nodules at the periphery of brain<br />Enviromental factors: UVB-UVA, HPV (16,18 + 5,8), immunosuppression<br />Epidermodysplasia verruciformis (EV):<br />Rare, multifocal<br />Early onset, infancy<br />Persistent flat warts & macules<br />50% of turning into carcinoma<br />Cancer 20 y after onset of disease<br />HPV 5 & 8<br />“Atopic dermatitis”<br />“Long-lasting chronic recurrent skin disease of both epi- & dermis”<br />AllergyRouteMediatorsimmidiatefood *most importanthistamine, chymasepolyvalentairborneIL 1,4,5,10 & TNF-αchronicextradigestiveLT, PG, PAFmultiorganskin contactIL 6 & 12<br />Features:<br />Atopy (IgE increase)<br />Hyperreactivity to environmental factors<br />Specific IgE to atopens<br />Polyvalent allergy (food –air)<br />Itch<br />Atypical location<br />Typical 1-2 lesions<br />Runs in the family<br />Onset: infant (60%), child (30%), adult (10%)<br />Minor criteriaMajor criteriaearly onsetchronicincr. Total IgEfamilialwool intolerancepruritusfood intolerancetypical(+) SPT recurrent <br />AD minor criteria related to dry skin:<br />Keratosis pilaris<br />Xerosis<br />Hand eczema<br />Mammal skin eczema<br />Pityriasis alba (desquamation of kin – white)<br />Cheilitis<br />Underlining hair follicles<br />AD criteria of neuropeptides:<br />White dermografin<br />Itch after sweating<br />Skin hyperpigmentation around eyes<br />Exacerbation upon stress<br />AD anatomic criteria:<br />Keratoconus<br />Cataract<br />Dennie – morgan sign (front neck fold)<br />Face edema<br />AD defect of horny layer skin barrier leads to defect in fillagrin causing formation of ceramides & lipids between keratinocyte layers.<br />Localization:<br />Phase 1<br />Exudation<br />Impeginisation<br />Cheek, neck , flexur, buttocks<br />Phase 2<br />Flexure, face<br />Papule, erythema, lichenification<br />Phase 3<br />Pathomechanism:<br />1 Allergen – food or animal hair<br />2 Skin irritation – chemicals<br />3 type 4 allergic mechanism – Th2 lymphocyte recognition<br />Urticaria in AD are seen as edematous papules and (+) SPT<br />Facilitated presentation of atopens due to specific IgE bound to FCER1 on langerhans cells<br />Normal level of IgE in the body is 100IU – in AD its 40 000IU <br />Treatment:<br />Systemic -pharmacotherapy -immunotherapy Local -drugs -prophylaxisAdditional -photochemotherapy -allergen removement<br />AntihistamineCyclosporin ALocalDiagnosiscetirizine1-2 monthsmacrolactamhistoryloratadineinhibit Th2ointment pH 5,5examinationebastine2,5 - 4 mg/kg IgE in serumaztemisol   terfonadine   feksofenadine   <br />Lupus erythematosus<br />= Autoimmune disease in the family of (CTD) of extremely broad clinical spectrum of symptoms<br />Clinical: <br />Discoid lupus erythematosus (DLE)<br />Subacute cutaneous lupus erythematosus (SCLE)<br />Systemis lupus erythematosus (SLE)<br />Skin involvement -> systemis disease, about 5-8% of patients develop skin disease<br />Features:<br />Skin lesions<br />Ig deposits on the dermal-epidermal junction (lupus band)<br />ANA – 95% SLE, 90% SCLE, 20-30% DLE<br />Hypersensitivity to UV, mainly UVB because:<br />Exacerbation of existing lesions<br />Provocation of new lesions<br />Exacerbation of stimulation of organ<br />Decrease MED (minimal erythemal dose) 50 %<br />Prolonged manifestation >10 days of persistent of erythemal reaction<br />Photo provocation of lesion<br />Photosensitivity of different intensity – dependent of LE form<br />Photoprotection (sunscreen) is obligatory<br />Lupus band:<br />Ig deposit (IgG & IgM) and component of complement of epidermal-dermal junction (EDJ)<br />CLE within skin lesion 90%<br />SLE within skin lesion 90% (in uninvolved skin 30-70%)<br />Depend on site of biopsy (best on dorsal hand)<br />Especially on sun exposed skin<br />Granular deposit<br />Immunological phenomena in collagen disease<br /> skin LBTserum ANASLE + + SS  + DM  + <br />≈ ANA does not correlate with the activity of disease<br />Method of detection<br />(IIF, DIF, ELISA)<br />DIF vs. IIF<br />skin biopsy within vivo bound autoantibodyhealthy tissue is used animal IgG & IgM - kinetoblast have DNA not only in nuclei0,9% NaCl - Hep - 2cell  - crithidium luciliae<br />Immunological marker in LE:<br />dsDNASLE( 50% have renal disease)  ssDNASLE    U1RNPSLESCLE  MCTDSmSLE( have CNS involvement) Ro SS-ASLESCLENLEsjögrenMCTDLA SS-BSLESCLENLE (neonate)sjögren nucleolar     AHA100% drug - induced LE   <br />DLE:<br />Most common skin form<br />F > M (2:1)<br />20 – 40 y onset<br />Clinical:<br />Erythema – disc shape on skin, cheek, nose<br />Infiltration<br />Follicular hyperkeratosis<br />Atrophic scarring without ulceration or necrosis<br />Localization:<br />LDLE – only head + permanent alopecia scarring<br />DDLE – neck & trunk<br />8-25 % involve mucus membrane<br />Treatment:<br />Photoprotection<br />Topical CS<br />Antimalarial drug (Arechine, Plaquenil)<br />Cryotherapy<br />Calcineurin inhibitors (Tacrolimus, Pinecrolimus)<br />Retinoids<br />SCLE:<br />Less frequent than DLE (acute onset!)<br />F> M 30-40 y<br />HLA –B8, DR-3<br />Does not fulfill 4 out of 11 ARA criteria for diagnosis of SLE<br />Clinical:<br />Erythemal edematous lesions<br />No follicular keratosis (like in DLE)<br />Inflammatory lesions<br />Heal without scarring<br />Hypopigmentation<br />Telangiectasis<br />Photosensitive<br />Leukopenia, joint symptoms, heart<br />Ro SS-A and La SS-B predominate (cross placenta)<br />Treatment:<br />Oral CS <br />Antimalarial <br />2 types:<br />Annular type – central regression expanding peripherally<br />Psoriasis type – papulosquamous, sharply-define, delicate scalp, red confluent plaque<br />SLE:<br />F > M, 20 – 30 y, (8:1)<br />Polyclonal activation of B – lymphocytes<br />Acquired & inbred deficiency of complement component (C1Q, C2, C3 & C4)<br />Circulating immunological complex<br />Related to HLA-B7, DR2, DR3, DR3-B8<br />Exacerbation factors:<br />UVA & UVB<br />Drugs (antiseizure, antiarrythmic, isoniazid)<br />Estrogen<br />Skin symptoms:<br />In 80% & is related to vasculitis<br />Butterly rash<br />Mucousmembrane erosion<br />DLE type lesion with atrophy<br />Erythemal lesion of palms & nails, tips of nails<br />Purpura<br />Urticaria vasculitis (last up to 3 days)<br />Raynaud’s <br />Diffuse alopecia (subcutaneous)<br />UV induced lesions<br />Diagnosis: 4 out of 11 ARA criteria<br />ARA criteria:<br />Face erythema – butterfly rash<br />DLE lesion – discoid rash<br />Photosensitivity<br />Oral erosion<br />Joint pain<br />Serositis – pleuritis, pericarditis<br />Renal involvement – protein >0,5 g/dl in urine<br />Hemolytic anemia, lymphopenia, thrombocytopenia<br />LE cells, anti –DNA, Sm<br />Neurologic symptoms (tremor, psychosis)<br />ANA if not drug induced LE syndrome (not specific)<br />-> Malar rash – erythematous lesion with no atrophy, no scarring, no follicular plugging<br />-> Lupus factor – antibody against DNA and histones<br />Types of autoantibody in SLE:<br />Anti-erythrocyte<br />Anti-leukocyte<br />Anti-platelet<br />Coagulation factor<br />Anti-phospholipids (thrombotic lesion)<br />SLE treatment:<br />UV protection<br />CS oral 1-2 mg/kg<br />Immunosuppressant’s (cyclophosphamide, metotrexate, azathioprin, imuran, cyclosporine A)<br />Plasmapheresis<br />Antimalarials<br />Topical CS & calcinurin inhibitors<br />NLE:<br />5% of children from mother with Ro –autoantibody passed through placenta<br />25% risk of NLE in the next pregnancy<br />Disappears completely when removing Ro<br />Child can develop heart block during 20 w of gestation<br />Hematologic manifestations<br />Drug eruptions<br />Cutaneous drug reaction:<br />2-3% hospitalized patients<br />5% outpatient<br />Mimic skin disease<br />Different type of lesions<br />Different drugs provoke similar skin lesions<br />Diagnosis:<br />Case history<br />Withdrawal of drug<br />Exposure/elimination test<br />lab test<br />Clinical:<br />maculopapular rash provoked by any drugs ampicillin)<br />9-10 days after onset of therapy<br />2-3 days after recharge<br />Exclude infectious diseases<br />Urticaria 36 h after exposure<br />Lichenoid reaction<br />Lichen – planus – erythroderma<br />Rare oral involvement<br />W – m after exposure?<br />Gold, antimalarials, NSAID, phenothiazine<br />Vascular changes<br />Purpura<br />Leucocytoplastic vasculitits<br />Urticaria vasculitits<br />Purpura hyperglobulinemica<br />Sulfonamides, NSAID, antidiuretic<br />5-7 days after exposure<br />Cutaneous necrosis<br />3-5 days after exposure<br />In subcutaneous fat region<br />Normal coagulation<br />Phototoxic / photoallergic<br />Ertyhematous, eczematous, lichenoid<br />Hyperpigmentation (amiodarone)<br />In sun exposed area<br />Pigmentation<br />Psot-inflammatory<br />Argyrosis - pathologic bluish-black pigmentation in a tissue resulting from the deposition of an insoluble albuminate of silver.<br />Acneform reaction<br />Acne without comedons<br />CS, anabolic steroids, halogens<br />Allergic reactions<br />25%<br />Type 4 hypersensitivity reaction<br />Min/hour/day after exposure<br />Sensitization:<br />Monovalent<br />Polyvalent<br />Group sensitization<br />Cross- reactivity<br />Non-allergic reactions<br />Pharmacological effects<br />Systemic CS<br />Mouth ulceration (metotrexate)<br />Overdose Ro (dermatitis)<br />Accumulation (argyrosis)<br />Poor elimination (elderly)<br />Genetic defect ( slow acetylator)<br />Pseudoallergic reaction<br />Non-immunological mast cell degranulation (aspirin)<br />Idiosyncrasy reaction - denotes a non-immunological hypersensitivity to a substance, without connection to pharmacological toxicity<br />Exacerbation of pre-existing dermatosis<br />Drugs may cause: <br />Steven – Jonson <br />Erythema nodosum<br />Erythema multiforme <br />Skin diseases provoked by drugs:<br />LE, SSc<br />Pemphigus<br />Pemphigoid<br />Bullous disease<br />Psoriasis<br />Acne<br />Dermatosis caused by drugs:<br />TEN<br />80% associated with sulfonamides, antibiotics, barbiturates<br />Onset 1-3 w<br />Cell-mediated reaction against epidermal cell<br />>30% skin surface affected<br />Nikolsky’s sign<br />Involve mucous membrane<br />Subepidermal bullae<br />Treat with intensive care or burn unit<br />Fixed erythema<br />Mainly skin without predilection<br />Same place if re-exposure<br />Barbiturate, paracetamol<br />Exposure test<br />Treatment not necessary<br />AGEP (auto generalized exthanmatous pustulosis)<br />7-10 days after exposure<br />Acute, generalized pustular eruptions, EM<br />No mucous membrane involvement<br />Unknown mechanism<br />Unilocular pustule<br />Differentiation from pustular psoriasis<br />Pseudolymphoma<br />By antiepileptic drugs<br />Enzymatic effects<br />Tumor mimic lymphoma<br />No monoclonality<br />DRESS (drug rush with eosinophilia & systemic symptoms)<br />Severe & acute<br />Maculopapular rash<br />Fever<br />Enlarge lymph node<br />Abnormal liver function<br />Renal impairment<br />Hypereosinophilia<br />Lymphocytosis<br />Circulation atypical lymphocytes<br />Drugs of DRESS: anticonvulsant, allopurinol, minocycline, sulfonamide, captopril, cyclosporine gold salt<br />Phosensitivity<br />UVAUVB320 - 400 nm290 - 320 nm1000 times weakerproduce sunburndose <10-20 J/cm2 <br />Acute changes:Erythema - sunburn = sunburn - tan = depens on melanin content - freckles = depens on skin thickness - solar lentigenes - scars - PHOTODERMATOSIS<br />Chronic changes: <br />Photo aging<br />Premalignant lesion – actinic kearatosis<br />Skin cancer BCC & SCC<br />Melanoma<br />Photo aging<br /> UVBUVAincrease epidermis +++ ++increase stratum corneum +++ +increase melanocytes +++ +collagen damage + +++infiltration  +++<br />Photodermatosis<br />Reactivity to UVB ≈ evaluation of minimal erythemal dose (MED) & establish the dose causing erythema<br />Reaction to UVA ≈ irradiation with 10 J/cm2 UVA <br />Albinism – vitiligo, XP (hypersensitivity to UVB, multisystem)<br />Idiopathic photodermatosis – PLE most common, solar urticaria rare (confirm with phototest, appearing upon sun exposure)<br />Endogenous – protoporphyria erythropoietica, porphyria cutanea tarda<br />Exogenous – phototoxic , photoallergic skin reaction<br />Xeroderma pigmentosum<br />Sun burn, freckle, telangiectasia, actinic keratosis<br />Defect DNA repair<br />Longer persistence of photoproduct<br />Mutation<br />Cancer development<br />Ocular – photophobia and cancer<br />Neuro – mental retardation and microcephaly<br />Treatment = lifelong sun protection<br />Erythropoietic protoporphyria<br />A mild form of porphyria arises from a deficiency of the enzyme ferrochelatase leading to abnormally high levels of protoporphyrin in the tissue, urine, blood and feces.<br />Painful photosensitivity<br />Presents first in childhood<br />Face and upper hands and feet<br />Prolong exposure leads to edema and blistering<br />Increase risk of gall stones<br />Accumulation in liver leads to liver failure<br />Treatment:<br />Protective clothes and sunscreen<br />Drug – induced photosensitivity<br />Mechanism: <br />Allergic<br />Toxic<br />UVA<br />In anybody<br />PhotoallergyPhototoxicPhototoxic drug reactionall contact dermatitisUVAacute - sunburneczema / xantheme / edemanon- immunologicalchronic - hyperpigmentationrarecommon 2nd exposure1st exposure <br />SystemicTopicalSystemic + Topicalantidiabetestarsulfonamides Athizidespsoralenstetracycline (Doxy + Mino)chinolonssalicylarilides A ??phenothiazine UV -filterNSAID synthetis natural fragment <br />HPV<br />-> Oncogenic type: 16 &18 - majority of cervical cancer<br />-> Non-oncogenic types: 6 & 11 - external genital warts<br />Determinants:<br />50-50% (F:M)<br />20-40 y (25-29 y for men)<br />Lifetime nr of sex partners (male more than female)<br />Early age of sexual intercourse<br />Smoking<br />Oral contraceptives<br />Male partner with many sex partners<br />Valvular intraepithelial neoplasia (VIN) 16 &18<br />Bowenoid papulosis - multiple, ill-defined, purple (16)<br />Bowen’s disease – single well-defined, red, painless, long lasting<br />Invasive vulvar cancer – progress to cancer<br />Anogenital warts (16 & 11)<br />Warts develop when exposed<br />Painful treatment<br />15-60% recurrency<br />Rapidly growing during pregnancy due to hormones<br />Transmission in children<br />Perinatal<br />In utero<br />Hetero- inoculation<br />Sexual abuse<br />Treatment <br /> Patient:<br />Podophyllotoxin (not for children)<br />Imiquimod (Aldara)<br />Immunomodulator<br />Doctor:<br />Cryotherapy<br />Podophyllin (not for pregnancy)<br />TCA / BCA<br />Surgery<br />Laser<br />Recurrent respiratory papillomatosis (RRP)<br />Children & adult<br />6 or 11<br />Can obstruct airway<br />Cause mobility<br />Possible causative role of RRP of head and neck<br />Treatment:<br />Surgery to remove affected tissue<br />Carbon dioxide laser<br />Tracheotomy<br />Photodynamic therapy<br />Antivirals<br />Vaccines that are used are with synthetic virus containing L1 gene. L1 proteins are produced from yeast or insect cells and then introduced into VLP (viral like particle) becoming HPVL1VLP vaccine. This does not contain any viral DNA. The vaccine is taken 3 times IM.<br />GardasilCervarixVaccines:6 , 11, 16, 1816 & 18<br />HSV<br />α = HSV-1 & HSV –2<br />β = CMV, HHV6, HHV7<br />γ = EBV<br /> PrimarySecondaryincibation2-14 days durationup to 21 days240 dayssign/symptomsulcerative lesionsprodromal symptoms multiple, bilateralitching, tingling inguinal lympho nodeneuralgia<br />Treatment:<br />PrimaryAcyclovir5 x 200 mg/day10 daysSecondareAcyclovir5 x 200 mg/day7 daysSuppressiveAcyclovir2 x 400 mg/daymonths<br />Acne<br />Pathogenesis:<br />Hair shaft are small in the ace surrounded by large sebaceous gland<br />Microcomedon formation cause by abnormal & differentiation of keratinocytes, increase or altered sebum secretion<br />Lipid composition cover opening of pores<br />Hormone level can be the cause of this (90% not)<br />P. acne proliferation in healthy people is another cause<br />Formation of comedo (accumulation of sebum) blocking<br />Severe, inflammation can form papule, pustule, nodule, cyst<br />Classification: <br />Acne vulgaris<br />Acne comedonica (non-inflammatory)<br />Acne papulo-pustulosa<br />Acne phlegmosa (nosulocystic acne – most important is to stop sebum production)<br />Acne fulminans<br />Acne inversa<br />Acne excoriate<br />Treatment:<br />Topical retinoidsOral IsotretinoinAntibioticBenzoyl peroxideregulate keratinizationnormalize keratinizationantibacterialantibacterialanti-inflammatoryanti-inflammatory / antiseborrhagicanti-inflammatoryincrease O2 level to kill P.acneAdapalen ErythromycinBrevoxylTretinoin ClindamycinBenzacneIsotretinoin TetracyclinAcneroxidTazaroten   <br />Epiduo treatment = retinoids + benzoyl peroxide – to normalize keratinization and reduce sebum production<br />Combined therapy = erythromycin + (topical) tretinoin = alcoholic vehicle causing dry skin<br />≈Tetracyclin is given for 3 months which can lead to resistant<br />≈Macrolides are not recommended because it can cause resistant<br />≈Benzoyl peroxide is good because it stops development of resistant strain<br />Nodulo – cystic acne<br />Oral isotretinoin (Roaccutane & Accutane)<br />Give permanent result<br />Decrease activity of sebaceous gland<br />Gland atrophy<br />120mg/kg<br />Teratogenic<br />ComplicationsTreatment of complicationhyperpigmentationsunscreenraised scartopical retinoidskeloidmicrodermabrasionatrophic scarchemical peelsfraxel lase (atrophic scar)pressure silicone dressing (keloid)<br />Scleroderma<br />≈ Autoimmune connective tissue disease with 3 pathologies:<br />Immunologic disturbance<br />Vasculopathy<br />Fibrosis<br />2 divisions:<br />Localized – skin & subcutaneous (Morphea)<br />Systemic – skin & internal organ<br />Morphea:<br />≈ A chronic condition that causes inflammation and thickening of the skin.<br />W:M ratio of 3:1<br />Onset 20-40 y (<10y 15%)<br />thickening and hardening of the skin and subcutaneous tissues from excessive collagen deposition <br />only involving the skin <br />classification divides morphea into five general subtypes: plaque morphea, generalized morphea, linear scleroderma, bullous morphea, and deep morphea<br />Case reports of morphea co-existing with other systemic autoimmune diseases such as primary biliary cirrhosis, vitiligo, and systemic lupus erythematosus lend support to morphea as an autoimmune disease<br />Treatment:<br />Penicillin procaine 72 million unit<br />cyclosporin<br />Vitamin E<br />PUVA<br />Vit D calcitriol orally<br />Topical calcipotriol<br />Topical Takrolimus<br />Morphea different from systemic scleroderma - no Reynaud - no organ involvement - no immuno markers - skin induration of clinical presentation<br />Systemic scleroderma:<br />≈Limited – diffuse skin involvement, central induration, short onset<br />≈Diffuse – primary (young), secondary (adult)<br />≈Etiology: unknown, genetic, environment<br />≈Characteristics: Reynaud, organ involve, skin indurations, Immunologic, malignant hypertension<br /> HandFaceLimited scleroderma:edemaedema 1/3 forearmtelangiectasia acroosteolysismask-like face atrophic scarradial furrowing lips finger atrohythin lips immobilizationmicrostomia erosion & ulcerationsharp nose<br />Immunological markers:<br />ANA > 90%<br />Antitopoisomerase 1 DNA (Scl 70 antibody), 23-76% (dSSc)<br />Anticentromere antibody 30-96% CREST<br />Organ involvements in systemic scleroderma:<br />MusculoskeletalAlimentary tractPulmonaryCardiacRenalacroosteolysisesophagus (90%)early onsetarrythmiarenal failureosteoporosisachalasiarestrictive lung diseasemyocardial fibrosismalignant hypertensionarthralgiaother parts rarePFT carbon monoxidepericardial diseasefatal prognosiscalcinosis - monometryHRcTdyspnea, palpitation myopathy - scintigraphyX-ray bibasilar pulmofibrosistachycardia   - X-ray ECG, Holet ECG, echo <br />Prognosis: <br />~ Limited Sc more chronic course but mild organ involvement<br />~ Diffuse Sc more rapid course and sever organ involvement<br />~ Reasons of death are pulmo- & cardiovascular involvements<br />Scleroderma-like conditions: (no Reynaud, no organ involvement, loose skin)<br />GVHD<br />Scleroderma diabeticorum<br />Porphyria cutanea tarda<br />Scleromyxedema<br />Phenylketonuria<br />Treatment:<br />Vascular drugs (pentoxyphyline, CCB, prostacyclin)<br />D- pencillamine (be aware of renal impairment & hypertension to stop fibrosis)<br />Immunosuppressants<br />CS<br />Anti TNF<br />UVA-1, photopheresis – high dose of Vit E<br />1 Malignant involvement of the skin<br />2 Paraneoplastic syndromes (not metastasis)<br />3 Enviromental carcinogenesis<br />glucaconome syndromealpha2 tumor of pancreas (movable)erythema nigricans malignaadenocarcinoma stomachacathosis paraneoplastiaupper GIerythema gyratum repensadenocarcinoma stomachxerosisHodgins disease, lymphomabullous phemphigoiddifferent tumor 20%dermatosis herpetiformisrare lymphomaeruptive seborrhagic wartsadenocarcinoma stomacherythrodermaleucemia, lymphomaflushing syndromestomach carcinomageneralized HZVleucemia, lymphomaparaneoplastic pemphigusthymomapruritusHodgins diseasepseudosclerodermaplasmocytoma, lymphomapyoderma gangrenosumplasmocytomadermatomyositiscacinoma (collagen disease)<br />HIV / AIDS<br />1) >500 ul>29%A1B1C1 2)200-499 ul14-28%A2B2C2 3)<200 ul<14%A3B3C3<br />Category A<br />Asymptomatic<br />Asymptomatic infection<br />Asymptomatic phase<br />Present for months /years<br />Persistent generalized<br />1-2 cm or more body region involve<br />Last for months<br />Acute retroviral infection<br />2-4weeks after infection<br />Enlargement of lymph node<br />Arthralgia /myositis<br />Headache<br />Maculopapular rash<br />Mucosal erosion<br />Category B<br />Unusual symptoms<br />Depress cell mediated immunity<br />Primary immunodeficiency<br />Bacterial angiomatosis<br />Candidiasis<br />Hairy leukemia<br />CIN 2/3 & CIS<br />Zoster ( >2 dermatosis >2 episodes)<br />Idiopathic thrombocytopenic purpura<br />Listerosis<br />Neuropathy<br />Other<br />Category C<br />Invasive cervical cancer<br />Severe HSv<br />Kaposi sarcoma<br />Toxoplasmosis<br />CMV<br />Other<br />Zoster<br />TB<br />Bacterial, fungal<br />AD<br />Acne<br />Psoriasis<br />Lichen planus<br />Vascular lesion<br />When to start treatment?<br />Category B & C<br />Asymptomatic CD4 < 350<br />CD4 - 350-500 kom/mm3<br />HIV > 100 000 copies or co-infection with HCV<br />CD4 > 500 treatment should be postpone<br />Post-exposure prophylaxis<br />Clean the skin<br />Introduce treatment (<72h)<br />Treat for one month<br />2NRTI or 2 NRTI + Pi<br />Kaposi sarcoma<br />Classical<br />Endemic<br />Iatrogenic (immunosuppressant)<br />Epidemic<br />Occupational risks: bullous fluid, plasma<br />~Serologic test in vertical transmission is not accurate because mother’s antibody may cross placenta. More accurate method is RT-PCR or culture of lymphocytes.<br />

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