Pemicu 8 Lenting2 pengganggu

Pemicu 8Lenting2 penggangguAdrian Pratama 405100018 Blok penginderaanLO 1Menjelaskan kelainan kulit akibat reaksi obat2anStevens johnson syndromeToxic epidermal necrolysis Epidermal necrolysis acute life-threatening mucocutaneous reactions (extensive necrosis & detachment of epidermis)

Pathogenesis CD8+ T killer lymphocytes in epidermis & dermis cytotoxicity against keratinocytes massive apoptosis IL-6, TNF-alpha, Fas-ligandAcetylation in patient with sulfonamide induced TENHLA-B1502 carbamazepine induced SJS >HLA-B5801 allopurinol induced SJS >

Clinical findingsHistory Begins 8 weeks after drugs exposure (usually 4-30 days)Fever, headache, rhinitis, myalgias 1-3 days before lesionPain on swallowing, burning / stinging in the eyes, heralding mucous membrane involvement Cutaneous lesionSymmetrically eruptionFace, upper trunk, proximal extremities (distal portion spared)Initial lesion erythematous, dusky red, purpuric macule, irregulary shapedAtypical target lesion with dark centersNikolsky sign flaccid blisters (spread with pressure & break easily) frictional trauma + pressure red, oozing dermis

SJS nikolskys 10% of body surface

TEN nikolskys > 30% of body surface Mucous membrane involvementErythema painful erosions of buccal, ocular, genital mucosaPainful hemorrhagic erosions coated by grayish white pseudomembranes & crusts of the lips

Ocular hyperemia, erosions, chemosis, photophobia, lacrimation, sheeding

Extracutaneous symptomsHigh fever, pain, weaknessVisceral involvementPulmonary dyspnea, bronchial hypersecretion, hypoxemia, hemoptysis Digestive (GIT) epithelial necrosis of esophagus, small bowel, colonRenal proteinuria, microalbuminuria, hematuria, azotemia

Approach to the patients

Laboratory testsEvaluation of respiratory rate & blood oxygenationTransient peripheral CD4+ lymphopeniaAnemia Massive transdermal fluid loss electrolyte imbalance, hypoalbuminemia, hypoproteinemia, prerenal azotemiaHypercatabolic state insulin resistance blood glucose >>

Histopathologic test

DDLimited EN (SJS)Erythema multiforme majorVaricella Widespread ENAcute generalized exanthematous pustulosis Generalized bullous fixed drug eruptionComplications Acute phase sepsisPulmonary complications & multiple organ failuresLate ophthalmic complicationsChronic inflammation, fibrosis, entropion, trichiasis, symblepharonhypo/hyperpigmentationHyper/atrophic scarsNail changesPigmentation of nail bed, ridging, dystrophic nails, anonychiaVulval & vaginalDryness, itching, pain, bleedingGenital adhesion (severe cases), other sticturesTreatment Symptomatic treatment Withdrawal of the offending drugsFluid replacementRaise the environment temperature (28C 30C)early nutritional support Skin, blood, urine specimen cultured Wound dressingsArtificial tears + antibiotic eyedrops + vit A every 2 hoursMouth rinsing antiseptic/antifungal solution

Specific treatment Corticosteroids IVIgCyclosporin APlasmapheresis / hemodialysisAnti-tumor necrosis factors extreme cautions !!Prognosis

LO 2Menjelaskan infeksi parasit & gigitan serangga Hookworm related cutaneous larva migrans~creeping eruption

Epidemiology Tropical & sub-tropical areasContact with sand/soil contaminated with animal feces

Etiology & pathogenesis3rd stage larvae of Ancylostoma braziliense & Ancylostoma caninum penetrate humans (dead-end host) skin between stratum germinativum & corneum migrate severeal cm per day localized eosinophilic inflammatory reaction die after days - months

Clinical findings Related physical findingsWheezing, dry cough, urticaria Cutaneous lesionsErythematous, raised, vesicular, serpentine cutaneous trailIntensely pruritic & may be painfulEruption lasts 2-8 weeks

Laboratory findings Transient peripheral eosinophilia

Special testsSkin scrappings dead end nematode larvae with light microscope Nematode larvae also be seen in the dermis on sections of skin biopsy specimens

Treatment Single dose of ivermectin / 3 day course of albendazoleTopical therapy thiabendazole / 10% albendazole

Prevention Avoiding direct skin contact with fecally contaminated soilScabies Epidemiology Urban areas; nursing home, prisons, hospital wardsTransmission through close personal contact

Etiology & pathogenesis Sarcoptes scabiei var. HominisFemale mite burrow into stratum corneum (20 min) lays 3 eggs/day eggs hatch in the 4th day larvae migrate to the skin surface & become mature female & male copulate males falls of the skin female continue the cycle

Clinical findings Pruritus & rash (6-8 weeks)Itching is severe worst at night Lesions appear red, scaly, crusted papules & nodulesPathognomonic lesion burrow (thin, thread-like, linear structure)Vesicles & bullae may develop

Crusted scabiesHyperkeratotic plaques, xerotic skin, pruritus may absent

DiagnosisMineral oil over the burrow scraping longitudinally with scalpel microscopic identification of mites, eggs, pellets

DDAtopic dermatitisInsect bite reactionsContact dermatitis Dermatitis herpetiformisDyshidrotic eczema

Treatment

PreventionsTreat all the individuals which has close contact with patientBed sheet, pillow cases, towels, clothes worn during the past 5 days should be washed & dried in the hot cycle

Arthropod bites & stings Treatment principlesWounds should be cleansed + remove any remaining arthropod parts ASAP< discomfort ice packs/ topical corticosteroids/ antipurirtics/ injection of local anesthetic/ systemic analgesicsSupportive measures for systemic toxicSecondary infections antibiotics + tetanus prophylactic (several)Black widow antivenin distribution

LO 3Menjelaskan infeksi virus dengan efluoresensi vesikobulosaVaricella Epidemiology 90% children < 10 yo, 5% > 15 yo

Etiology & pathogenesis Entry of varicella zoster virus upper respiratory tract & oropharynx initial multiplications small dissemination via blood & lymphatics (primary viremia) cleared by reticuloendothelial system incubation periods (2 weeks)Immune < overwhelming virus replication secondary viremia skin lesions occur Clinical findings ProdromeFever, chills, malaise, headache, anorexia, severe backache, sore throat & dry cough Rash Face & scalp trunk (relative sparing of extremities)More profuse on the medial aspects Nose colored macule papules vesicles pustules crusts (in 12 hours)Vesicles of varicella: 2-3 mm in diameter & elliptical; long axis parallel to the folds of the skinEarly vesicles: superficial, thin, surrounded with irregular erythema (dewdrop on the rose petal)Soon become cloudy (inflammatory cells) pustule drying on the center umbilicated pustule crusts

Diagnosis Appearance & evolution of rash, history of exposure (2-3 weeks)

Laboratory tests Histopathology multinucleated giant cells & epithelial cells containing acidophilic intranuclear inclusion bodiesIsolation of virus in cells culture definitive diagnosis PCR VZV DNAImmunofluorescent staining of cellular material from fresh vesicles Serologic tests antibody to VZV-induced membrane antigenDD Vesicular exanthems of coxsackie viruses & echovirusesImpetigo Insect bitesContact dermatitis

Complications Secondary bacterial infections staphyllococci / streptococciSecondary bacterial pneumonia, otitis media, suppurative meningitis (rare)Varicella during pregnancy intrauterine VZV infection congenital abnormalitiesTreatmentCool compresses, calamine lotion, orally antihistamines

Prevention Varicella vaccineVZ-Ig

Herpes zoster Epidemiology Older age (>= 60 yo) 7-11%/1000 persons/yearImmunosuppressive patients risk >

PathogenesisVZV passes from lesion in skin & mucosa into the contiguous ending of sensory nerves & transported centripetally up the sensory fiber sensory ganglia virus persists for life reactivation dermatomal lesion (N. V1 & spinal sensory ganglia from T1-L2)

Clinical findingsProdrome Pain & paresthesia in the involved dermatome eruption in several days itching, tingling; burning, severe, deep, boring, lancinating painRashUnilateral & dermatomal (area of V1 nerve & T3-L2 nerve are most frequent)Macules & papules grouped vesicles in erythematous base (12-24 hours) pustules (3rd day) crusts (7-10 days, persists 2-3 weeks)Pain Burning, deep aching, tingling, itching, stabbingImmunocompromised Necrosis & scarring; chronic verrucous, hyperkeratotic, ecthymatous cutaneous lesion (acyclovir resistant VZV)

Diagnosis Characters of eruption & dermatomal distributions + dermatomal pain/discomfortCluster of vesicles + history of recurrences

Laboratory tests = varicella

DDZosteriform herpes simplexContanct dermatitisInsect bites Burns Complications

TreatmentCool compresses, calamine lotion drying

Treatment to postherpetic neuralgiaTopical anesthesia (lidocaine 5% patch; capsaicinOral agents Gabapentin (moderate & greater pain relief); Pregabalin (faster onset of action)TCAs (Nortryptiline & desipramine)Scheduled opioid

Prevention Vaccination

Herpes simplexEtiology & epidemiology HSV-1 childhood, rates of infection increase with ageHSV-2 sexual behaviour

Pathogenesis 3 stages Acute infection replication at the site of inoculation on mucocutaneous surfaces rapidly spread to infect sensory nerve terminals neuronal nuclei (ganglia)Establishment & maintenance of the latencyHSV gene expression severely restricted Reactivation of the virusConcomitant anterograde axonal transport peripheral site

HSV-1 reccurent site trigeminal ganglia

HSV-2 reccurent site sacral ganglia Clinical findingsOrofacial infectionFever, malaise, myalgias, pain on swallowing, irritability, cervical adenopathy Clusters of tiny ulcers & vesicles lesion on hard & soft palate, tongue, buccal mucosa, neighbouring facial areas (gingivostomatitis)Reactivation lips, outer one-third of lower lipPain, burning, itching on the site Trigger emotional stress, illness, sun exposure, trauma, fatigue, menses

Developmental stage: prodromal, erythema, papuleDisease stage: vesicle, ulcer, hard crustResolution stage: dry flaking & residual swelling

Genital infectionVesicles, pustules, erythematous ulcers 2-3 weeks to resolveSite in malesGlans penis / penile shaftSite in femalesVulva, perineum, buttocks, vagina, cervix, Pain, itching, dysuria, vaginal & urethral discharge, tender inguinal lymphadenopathy Fever, malaise, headache, myalgias

Small erymathous lesion, fissures, pruritus, urinary symptoms

Laboratory testsCulture of HSVPCRDirect fluorescent antibody staining of the lesion scrapingsTzanck smear scarping the base of the ruptured lesion + giemsa / wright staining multinucleated giant cellsSerologic detection of antibodies to HSV

PreventionsAntiviral: acyclovir, famciclovir, valacyclovirVaccines proved that no vaccine that proved to protect adequately

Molluscum contagiosumEtiology & epidemiology MCV generally affects young childrenMCV transmision via direct skin / mucous membrane contact / vomites, bath towels, swimming pool

Pathogenesis 4 subtypes of MCV MCV 1 (98% in US)Virus replicates in cytoplasm of epithelial cells MCV genesA homolog major histocompatibility class 1 heavy chain interfere with antigen presentationChemokine homolog inhibit inflammationGlutathione peroxidase homolog protect virus from oxidative damage by peroxidase

Cutaneous lesionSmall pink, pearly, flesh-colored papules then enlarge; can be to 3 cm large (giant molluscum)As they enlarge dome-shaped, opalescent morphology become appearentCentral dell / umbilicationWhite curd-like substance can be expressed with pressurePredilection intertriginous sitesGrouped in cluster result of koebnerization Erythema & eczematous around lesion molluscum dermatitis

Special tests Giemsa staining hypertrophied & hyperplastic epidermis + large intracytoplasmic inclusions (Henderson-Paterson bodies)

DDVerucae Pyogenic granulomaPapular granuloma annulareEpidermal inclusion cyst

ComplicationsPruritus Chronic conjunctivitis & punctate keratitisSecondary bacterial infection

Prognosis & clinical courseSpontaneous clearance (months to years)

Warts Etiology

Pathogenesis Infection through inoculation of virus into the viable epidermis through defects in the epitheliumVerucca appears within (2-9 months)Viral replication in upper level of epithelium composed of non-replicating keratinocytes viral proteins (E5, E6, E7 proteins)Alter cells proliferation & inhibit cells death via apoptosisE5 Stimulate epidermal growth factors receptorsE6 Stimulates expression of hTERT protects the end of chromosomes blocks cells senescence

Cutaneous lesionCommon warts (verruca vulgaris)Scaly, rough, spiny papules/nodules on the cutaneous surfaceSingle grouped papules on the hands & fingersFiliform verruca cutaneous hornFlat warts verruca planaSlightly elevated, flat topped papules, minimal scalePlantar & palmar wartsThick, endophytic, hyperkeratosis papules, painful with pressureMosaic wartsCoalescence of plantar & palmar warts into large plaques

Diagnosis Clinical appearanceHistologic examinationAcanthotic epidermis with papillomatosis, hyperkeratosis, parakeratosisBasket-weave-like hyperkeratosis, with many large clear cells in the granular & spinous layers

DDSingle lesion verruca vulgaris, callus, epidermal inclusion cyst, pyogenic granuloma, milkers nodules (palms), orf (palms)Multiple lesions arsenical keratoses, verruca vulgaris, palmoplantar keratoderma, psoriasis, pits in basal cell nevus syndrome

Treatment Physical destruction of the infected cellsCryotherapy using liquid nitrogenCurretage & surgically excisedChemotherapeutic agents Topical podophyllin resinTopical 5-fluorouracilIntralesional bleomycinCaustics & acids Salicylic acid, lactic acid, trichloroacetic acidIntralesional interferonLO 4Menjelaskan infeksi bakteri dengan efluoresensi vesikobulosa Scrofuloderma subcutaneous tuberculosis leading to cold abscess formation & secondary breakdown of the overlying skinPrevalence children, adolescents, aged

Clinical manifestationsParotidal, submandibular, supraclavicular; may be bilateralfirm, subcutaneous nodule, well defined freely movable, asymptomatic enlarge & softens liquefaction + perforation linear & serpiginous ulcers & sinuses + inverted, bluish edges, soft & granulating floors scar tracts develop & bridge ulcerative areas/normal skin

Histopathology Massive necrosis & abscess formation in the center + tuberculoid granulomas in the margins of sinuses & abscess

Diagnosis Clinical appearance + underlying tuberculous lymphadenitis / bone & joint disease

DDMycobacterium-avium intracellulare lymphadenitisM. Scrofulaceum infectionSyphilitic gummasSporotrichosis Actinomycosis Severe forms of acne conglobataHidadenitis suppurativa

Course Spontaneous healing Bullous impetigoe/ phage group II S. Aureus

3 types of skin lessionbullous impetigoexfoliative disease (staphylococcal scalded-skin syndrome)nonstreptococcal scarlatiniform eruption (staphylococcal scarlet fever)

Epidemiology more commonly in the newborn and in older infants, and is characterized by the rapid progression of vesicles to flaccid bullae Several decades ago, extensive bullous impetigo (ritters disease/ impetigo neonatorum) within neonatal nurseries

Clinical manifestationarise on areas of grossly normal skincontain clear yellow fluid that subsequently becomes dark yellow and turbid margins are sharply demarcated bullae are superficial, and within a day or two, they rupture and collapse thin, light-brown to golden-yellow crusts

Examination Gram stain of exudates from bullous impetigo gram-positive cocci in clustersS. aureus belonging to phage group II can be cultured from the contents of intact bullaeHistologically vesicle formation in the subcorneal or granular region, occasional acantholytic cells within the blister, spongiosis, edema of the papillary dermis, a mixed infiltrate of lymphocytes and neutrophils around blood vessels of the superficial plexus

DDContact dermatitis Bullous insect bitesBullous tineaBullous fixed drug reactionBullous drug eruptionSSSSThermal burnsPemphigus vulgarisBullous pemphigoidErythema multiformeDermatitis herpetiformis

Treatment

Superficial folliculitis~Bockhart impetigo

Clinical manifestationsSmall, fragile, dome shapped pustule occurs at infundibulum of hair follicle (scalp & beard, axilla, extremities, buttocks)

DDSeborrheic dermatitis rosacea of the eyelids

Furuncles & carbunclesFurunclesMay complicate pre-existing lesion (atopic dermatitis, excoriation, abrasions, scabies, pediculosis) or occur spontaneouslySite High friction, occlusion, perspiration: neck, face, axillae, buttocksCutaneous lesionHair bearing skin hard, tender, red folliculocentric nodule painful & fluctuant (abscess formation)Rupture pus dischargePain surrounding the lesion

Carbuncles Larger, more serious inflammatory lesionDeeper base, extremely painful lesionSite Nape of the neck, the back, thighsFever, malaise often present, quite illInvolved area is indurated & redMultiple pustules draining around multiple hair follicle yellow gray irregular center slowly granulating area may remain deeply violaceous for prolonged period

DDCystic acneKerion Hidradenitis suppurativaRuptured epidermal inclusion cystFuruncular myasis Apical dental abscessosteomyelitis

Laboratory testsLeukocytosis Histologic examination dense PMN inflammatory process in dermis & subcutaneous fatCarbuncle multiple abscess seperated by connective trabeculae Gram stain of pus gram (+) cocci Culture S.aureus

Prognosis & clinical courseBacteremic spread Reccurence

Lesion on lip & nose spread via facial & emissary vein cavernosus sinus

Carbuncle osteomyelitis, endocarditis, brain abscessTreatmentSimple furunculosisMoist heatCellulitis present systemic antibioticsSevere Antibiotic via parenteral routeMRSAVancomycin 1-2 g IV/ day in divided doseLarge, painful, flucutant lesion incision & drainage

References Fitzpatricks dermatology in general medicine; 7th edition