LALA Megatable Derma

8/19/2019 LALA Megatable Derma

1/39

!"!"!"# LALAϋ

FLAT LESIONS

1. MACULE - Flat discoloration- < 1 cm

2. PATCH - Larger (> 1cm) macule- Ex. vitiligo, nevus flammeus

ELEVATED SUPERFICIAL

3. PAPULE - Elevated, circumscribed, solid- No visible fluid- < 1cm in size- May appear white (milia), red (eczema), yellowish

(xanthoma), black (melanoma)- Usually found in the dermis

! Opening of sweat ducts! Root of hair follicles

- If associated w/ scales: papulosquamous - May last for a year- Papules that are equidistant: follicular papules (ma y also see

hair sticking out)4. PLAQUE - Broad papule or confluence of papules

- >1cm- Center may be depressed or may have normal skin- May also be centrally depressed

ELEVATED DEEP -

5. NODULE - Large papule (>1cm)- Deep on palpation (centered in dermis and subcutaneous fat)

6. TUMOR - Soft/firm, fixed/movable, elevated/deep/pedunculated(fibromas)

- Usually >2cm- Usually round7. WHEALS (HIVES) - Plateau – like, edematous elevations

- Evanescent (do not last > 1 day)- Associated with angioedema- May be pink to red, surrounded by a flare of macular

erythema- May be discrete/coalesce- Prototype lesion of urticaria- Dermatographism or pressure – induced whealing may be

seen

!"#$%"& ()*#+,*- original skin lesions; unaltered by any factors


2/39


3/39

!"!"!"# LALAϋ

1. SCALES (exfoliation) - Implies a pathologic process in epidermis- Parakeratosis (persistence of nuclei in keratinocytes in

stratum corneum of skin) often present- Dry, greasy, laminated masses of keratin- We normally shed little amounts of stratum corneum

- Occurs due to:! Rapid epidermal cell formation! Interruption in the normal process of keratinization

-

Fine & branny or powdery: Tinea versicolorCoarser: eczema, ichthyosisStratified: scalded skin syndrome & infection – associated desquamations (scarlet fever)Silvery squames (due to trapping of air between

layers): psoriasis – described as plaque with thickscales

2. CRUSTS/SCABS - Dried serum, pus, ,or blood with epithelial/bacterial debris- When removed, there is erosion/ulcer/wound underneath

Dry, superficial, golden – yellow: impetigoHard and tough: third – degree burns

Elevated brown/black/green masses: latesyphilis (oyster – shell crusts: rupia)

3. EXCORIATIONS & ABRASIONS Excoriations- Punctate/linear abrasions- Superficial (usually only involves epidermis but may reach

papillary dermis)- Due to scratching with fingernails in an effort to reduce

itchiness- Inflammatory areola- May allow entry of microorganisms -> may cause crusting,

pustules, cellulitis & enlargement of neighboring lymphglands

- Elevated, long & deep excoriations = severe pruritus(except lichen planus where there is severe pruritus but rareexcorations)

Abrasions- If due to mechanical trauma or constant friction

4. FISSURES (CRACKS/CLEFTS) - Linear cleft in epidermis or dermis following skin lines- Common in skin that is thickened & inelastic from frequent

inflammation & dryness (especially in areas of frequentmovement)

! Ex. tips & flexural creases of thumb, fingers, palms;edges of heels; clefts between fingers & toes, anglesof mouth, lips, nares, auricles, anus

- May be single or multiple- Exposure to cold, wind, water, or cleaning products may

produce a stinging burning sensation = indicates microscopicfissuring

! Referred to as chapping (chapped lips)- Pain often produced by movement of the parts involved ->

may open, deepen or form new fissures- Painful but NOT bacterial! No need for oral antibiotics. May

apply topical antibiotics or wait it out

*).+,/%"& ()*#+,*- altered by external factors (ex. scratching); modified by evolution, regression, trauma or other external factors


4/39


5/39

!"!"!"# LALAϋ

1A & 1B: NAIL LESIONS

SKIN LESION Description Cause/PrecipitatingFactors/Risk

Factors

Age & Area ofPredilection

Diagnosis Treatment Also know this Other info

Dermatophyteonychomycosis

Yellow discolorationNail becomes thick &brittle due tokeratinNail may separatefrom nail bedMay involve skin ofthe toe & soles(scaling,erythematous, well – defined patches mayappear)Usually starts distallygoing proximally

Superficial withoutparonychialinflammationChalky white spots onor in the nail plate thatis easily shaved off

Asymptomatic in thenails (reservoir forinfection); Px willusually complain ofthe alipunga than thechanges in the nail

Fungal infection by adermatophyte

T. rubrum – mostcases

T. mentagrophyte

Scrape on top of nail:do KOH test & lookfor long, septatehyphae

If subungual: getkeratin under brittlenail

REMEMBER: KOH isnot highly reliablebecause it has pooryield since keratinhas to be dissolved toactually see thehyphae

Oral:ItraconazoleKetoconazole – only give for 10days for tineaversicolor due tohepatotoxicityTerbinafineFluconazole

2 – 4mos: timeneeded to growfingernails4 – 6 mos: growtoenails

Duration of anti –fungal treatment

Onychomycosis is fungalinfection of the nail

Onycholysis is separationof the nail from the nail bed

3 types:1. Distal subungual

– most common- usually causedby T rubrum

2. White superficial- leukonychiatrichophytica- usually due to Tmentagrophytes- invasion oftoenail plate onnail surface

3. Proximalsubungual- involves nailplate fromproximal nailfold- usually due to Trubrum & Tmegninii- may be anindication of HIVinfection

Candidaonychomycosis

Pain or swelling inproximal foldPink & tenderDescribed as a yuckynailGradual thickening &brownishdiscoloration of nailplates

Candida albicans

Common inhomemakers, andfrequent/prolongedexposure of handsto water

Usually seen in DMpx

Fingernailscommonlyaffected

Seepseudohyphae/yeasts

Anticandidalagents + topicalcorticosteroid

Avoidance of wetwork & otherirritantsIf topical tx fail,give oralfluconazole 1x/wkor itraconazole

Check proximal part firstwhen treating candida

With paronychia (swellingof nail fold; pressing on itmakes fluid come out)


6/39

!"!"!"# LALAϋ

Produces destructionof the nail & massivenailbedhyperkeratosis

**Remember, it is very important to differentiate a dermatophyte type of onychomycosis from a candidal one.

SKIN LESION Description Cause/PrecipitatingFactors/Risk

Factors



Psoriaticonychomycosis

Pits on the nailsFurrows/transversedepressions (Beau’slines)Nail bed splinterhemorrhagesYellowish greendiscoloration mayoccur in area ofonycholysisOil spots (start in themiddle)

Pathology is in thenail plate

86.5% of patientshave psoriaticarthritis

Characterized bypitting of nails +symptoms ofdermatophyteonychomycosis

The px usually comeswith psoriatic plaquesin other parts of thebody (ex. scalp)

Intralesionalinjection ofTriamcinoloneacetonidesuspension, 3 – 5mg/ml

Topical 1% 5 – F Usolution, MTX,PUVA,cyclosporine oracitretin

Features of psoriasis:1. Distal

onycholysis2. Brittle3. Nail pits4. Oil spots

Dermatophyteonychomycosis

Candida onychomycosis

Brittle Not brittleNo paronychia With paronychiaLong septate hyphae Pseudohyphae

Why is it important to differentiate?Drug of Choice

Dermatophyte: TerbinafineFluconazole & Itraconazole can be used forboth dermatophytes and candida


7/39

!"!"!"# LALAϋ

2A: ERYTHEMATOUS LESIONS: Non Scaly Papules

SKIN LESION Description Cause/PrecipitatingFactors/Risk Factors



Miliaria Rubra(prickly heat,heat rash)

Discrete, extremelypruritic,erythematouspapulovesicles May also becomeconfluent

Accompanied byprickling, burning, ortingling sensation

Retention of sweat asa result of occlusionof eccrine sweat ductsand pores

S. epidermidis

Infants due toimmature eccrinegland

Antecubital & poplitealfossae, trunk,inframmary areas,abdomen (waistline),inguinal region ->areas usuallymacerated due toimpedance in theevaporation ofmoisture

Control temperature todecrease sweatingGood aeration

Anhydrous lanolin – resolves occlusion ofporesCalamine lotion

AntihistaminesTopical corticosteroids

Non – folliculardistribution

- No hair iscoming out,therefore doesnot involve hairfollicles

Problem in kidsdue to itching(may presentwith bacterialinfectionalready)

Scabies Pruritic papularlesions, excoriations& burrows w/c housethe female mite & heryoung (burrows appearas slightly elevated,grayish, tortuous linesin the skin)

Vesicle or pustulecontaining mite maybe seen at end ofburrow

Presentation:F – itching of nipplesM – itchy papules onscrotum & penis

2 – 4 wks afterinfection:sensitization period

Nodular scabies:Dull red nodules (3 – 5mm diameter)appearing duringactive scabies,may/may not itch

Sarcoptes scabei (itchmite, causativeorganism)

Close personalcontact, fomites(clothing, bedsheet)

Immunocompromised,institutionalized,malnourished patients

Young childrenM = F

Circle of Hebra:axillae, elbow,flexures, wrists, hands,crotchFinger webs

Scalp & face spared (adults)Entire cutaneoussurface involved(infants)

Nodular scabies:Scrotum, penis, orvulva

See mite undermicroscope (usuallyburrows in stratumcorneum & depositseggs here)

Majority of mitesfound on hands &wristsLess frequently in(decreasing order):elbows, genitalia,buttocks, axillae

India ink or gentianviolet applied toinfested area =allows identificationof burrows easily

Permethrin 5% cream- safest, most effective(C/I: pregnancy)- apply neck – downbecause most lesions arehere- treat all householdcontacts- repeat after 1 week(wait for eggs to hatchagain)

6 – 10% precipitatedsulphur in petrolatum- safe in pregnancy- doesn’t smell good

Ivermectin – not used

For nodular scabies:Intralesional steroids, tar,excision

Features of scabies:1. Circle of Hebra2. Nocturnal itch3. Contact w/

person at home

Reinfections may occurearlier and in moresevere forms

May bemistaken forLangerhans cellhistiocytosis

Suspect scabiesif more than 1famly memberhas pruritus

In animal orzoonoticscabies,burrows areusually absent &is self – limited


8/39

!"!"!"# LALAϋ

Crusted scabies(Norwegian orhyperkeratotic) : seeninimmunocompromisedor debilitated px

Crusted scabies: Face & scalp,genitalia, buttocks,pressure bearingareas

Acne Vulgaris Chronic inflammatorydisease of thepilosebaceous

follicles

Comedo (primarylesion of acne) – non

– inflammatory lesion(ex. blackhead oropen comedo;whitehead or closedcomedones)

May also present aspapules, pustules,cysts, nodules, scars

Remember that alllesions of acne will ALWAYS have aplug

No pruritus in acne!

Propionibacteriumacnes- metabolize sebum to

free fatty acid ->cause inflammation ofcyst wall -> rupture

Androgenicstimulation ofsebaceous gland

External factors:mechanical trauma,cosmetics, topicalcorticosteroids

Hereditary (keratinous

plug in lowerinfundibulum of hairfollicle – primarydefect)

Begins at puberty (signof increased sexhormone production) –

usually 8 – 12 y/o- Lesions are

comedonal incharacter

Adolescents (15 - 18y/o) – majority of cases

- Lesionsbecomeinflammatorypustules

- Involution ofdiseasebefore 25 y/o

Acne may also beginat 20 – 35 y/o inpeople who did nothave teenage acne

Face (most common incheeks), neck, uppertrunk, upper arms andother oily seborrheicareas

TOPICAL (long – termusage is the rule, and applyto entire acne – affected

area, not just the lesions; 6 – 8 wks) Benzoyl peroxide (mosteffective for inflammatoryacne)Topical retinoidsClindamycinErythromycin + benzoylperoxideSulfur, resorcin, salicylicacid

Azeleic acid

SYSTEMIC (inhibitsformation of new lesion; formoderate to severe acne;usually 3 – 6 monthsduration) Tetracycline (safest &cheapest; may causestaining of teeth if takenby kids < 9 or 10 y/o)Minocycline (mosteffective oral antibiotic intreating acne vulgaris)DoxycyclineErythromycinClindamycinSulfonamides

OCPsSpironolactoneDexamethasoneIsotretinoin (do not givein childbearing age dueto teratogenicity)

- Indicated forsevere acne thatimproves by lessthan 50% after 6mos of therapyw/ combined

Remember that acne isone of the folliculardiseases

Keep px disease free for1 – 2 mos first, beforedecreasing dosage to

prevent flaring

Major advantage: ONLYacne therapy that is notopen ended (leads toremission of months oryears)


9/39

!"!"!"# LALAϋ

oral & topicalantibiotics

Give keratolytics toslough off corneum w/hopes of removingcomedones




PEDICULOSIS(Phthiriasis)PediculosisCapitis

Intense pruritus ofthe scalp w/ posteriorcervicallymphadenopathy

Affected hairbecomes lustreless &dryVisible nits – whitishconcretions on thehair shaft but most

common in theretroauricular area

Pediculus humanusvar. capitis (headlouse)

Children (but may alsooccur in adults)

GOAL: eliminate both lice& ova

Permethrin (most widelyused pediculicide)

- Someassociation withcongenitalleukemia inpermethrin

abuse

Pyrethrins + piperonylbutoxide

Enzymatic egg remover(Clear)

Secondary complications

with impetigo &furunculosis – commonduring itching

Pediculosiscorporis(pediculosisvestimenti,“vagabond’sdisease”)

Generalized itching +erythematous &copper – coloredmacules or urticarialwheals andlichenification

See nits on clothingor beddings

Pediculid reaction

Pediculus humansvar. corporis (bodylouse)

Due to body lice thatlay their eggs in theseams of clothing

Indigent, homelessindividuals

Upper back; noinvolvement of hands& feet

Established bygeneralized itching+ parallel linearscratch marks +hyperpigmentation +erythematousmacules

2 – 6wks:sensitization periodfor first timeinfections

Supported by findinglice in the seams ofclothing or inbeddings

Bathe thoroughly withsoap & water

Destruction of lice- Wash bedding &

clothing- Disinfection

(placing clothesin dryer for 30mins at 65 oC orironing them)

Body louse infestation isdifferent from scabies, inthat there is noinvolvement of hands &feet

Body lice vectors for

relapsing fever, trenchfever, epidemic typhus

Secondary impetigo &furunculosis are common

Problem: KnockdownResistance (commonmechanism of resistancethat manifests as lack ofimmobilization of lice


10/39

!"!"!"# LALAϋ




Pediculosispubis (crabs)

Nits are attached tohairs at an acuteangle

See sky bluemacules ( maculaeceruleae) in side of

trunk and inneraspects of thighs(due to altered bloodpigments)

Phthirus pubis

Transmission throughsexual intercourse &close physicalcontact; notinfrequently from

bedding

Adults

Genital region &hypogastriumhairy areas of the legs,abdomen, chest, arms,axillae (rare)

If diagnosed withcrabs, search forother STDs

Permethrin

Pyrethrins combined w/piperonyl butoxide

Enzymatic egg remover(Clear)

Retreatment in 1 weekrecommended

INSECT BITES Immediate reaction:inflammatory reactionat the site of thepunctured skin, tothe insect’s venom orsaliva containinghistamine, enzymes,agglutinins,serotonin, formic

acid, or kinins. Accompanied bypruritic localerythema & edema

Delayed reaction:host’s immuneresponse toproteinaceousallergens

Present as pruriticred papules typicallywith a surroundingswelling & a centralpunctum (minuteround spot indicatingan opening)

CLASS INSECTAOrder Lepidoptera (caterpillar, moth)Order Hemiptera (bedbug, reduviidbugs)Order Anoplura (louse)Order Diptera

(mosquito, flies)Order Coleoptera (beetles)Order Hymenoptera (bees, wasps, ants)Order Siphonaptera (fleas)

a) Pruritus: camphor,menthol lotions, gelformulations, topicalanesthetic preparationsb) Persistent bitereactions: topicalcorticosteroidpreparationsc) If topical agents fail,

give intralesional injectionof corticosteroids orexcision of pruritic nodule

Prevention: Protectiveclothing & inset repellant

Recurrent bacterialinfection may be due toinsect bites

Bedbugbites/Cimicosis(OrderHemiptera)

Severalerythematouspapules or urticariallesions groupedtogether or in rows(breakfast, lunch,dinner)

Cimex lectularius:most common intemperateC hempiterus: tropicalclimates

Suspected vectors forChagas’ disease &

Arms, legs, ace Diascopic examshows hemorrhagicdot (site of bite) inthe middle of mostlesions

Topical antipruritics orcorticosteroidsZinc lotion with 2 – 4%polidocanol or 1%methanolSevere cases: systemicantihistamines


11/39

!"!"!"# LALAϋ

Hepa B

Often infest bats &birds & usually residein cracks & crevicesand descend to feedwhile victim sleeps

Eliminate bird nests & batroosts, cracks & crevicesTreat area withinsecticide (dichlorvos &permethrin)

Permethrin – impregnated bednets:effective in tropical

climatesReduviid bites(OrderHemiptera)

Typically painlessRomana’s sign :unilateral eyeswelling after anighttime encounterwith Trypanosomacruzi (transmitted byfeces & rubbed intobite)

Poor housingconditions

Exposed areas of skin




Mosquito bites(Order Diptera)

Multiple pruritic oftenexcoriated papules

Bullous reaction(culicosis bullosa)

Large blisters(pemphigushystericus)

Moisture, warmth,CO2, estrogens, lactic

acid in sweat, drinkingalcohol attractmosquitos

Exposed areas of thebody; arms & legs

Antipruritics/corticosteroidcreams

Oral antihistaminesInsect repellatns (diethyltoluamide)

Protective clothing &mosquito netting

Attack mosquito habitats(sprays/disposingstagnant water)

Secondary infectioncommon in children

Mosquito bites are acommon cause of papularurticaria & may also playa role in reactivation oflatent EBV infection

Severe local reactionsseen in young children,immunodeficientindividuals

Fleabites/Pulicosis(OrderSiphonaptera)

Multiple, irregularlydistributed wheals &papules that aregrouped and may bearranged in zigzaglines

Hypersensitivereactions appear asnodules or bullae

4 species that mostcommonly attack

humans:

1. Cat flea(Ctenocephalides felis)

2. Human flea(pulexirritans)

3. Dog flea (Ccanis)

4. Oriental ratflea

Legs & covered bodyregions (waist)

Diascopic exam:central hemorrhagicbite site (purpurapulicosa)

Topical & systemicantipruritic treatment;corticosteroidsPet grooming :DInsect repellent


12/39

!"!"!"# LALAϋ

(Xenopsyllacheopis)

Usually present inhouses with cats ordogs

Ant bites (OrderHymenoptera)

Painful stings withinseconds of biteaccompanied by

whealing

Later: intense pruriticsterile pustuledevelops at the sitewith an erythematoushemorrhagic halo

Severe cases maycause anaphylaxis,seizures,mononeuropathy

Any body part Ice packsOral antihistaminesTopical antipruritics or

corticosteroids

If w/ secondary i nfection:antibiotics

Bee (OrderHymenoptera)

Reaction to venom =ranges from pain &

mild local edema toexaggeratedreactions that maylast for days

Serum sickness(fever, urticaria, jointpain) occur 7 – 10days after sting

Severe anaphylacticshock and death mayoccur w/in minutes ofsting

Bee venom containshistamine, mellitin,

hyaluronidase, HMWsubstance with acidphosphatase, &phospholipase A

Usually exposed areas For local reactions:Immediate application of

ice packs or topicalanesthetics

For chronic reactions:Injection withTriamcinolonesuspension diluted to5mg/mL with 2%lidocaine

For severe reactions:Oral prednisone

For severe systemicreactions:0.3mL of epinephrine IMCorticosteroids


13/39

!"!"!"# LALAϋ

2B: ERYTHEMATOUS LESIONS: Non – Scaly Nodules

SKIN LESION Description Cause/Precipitating Factors/Risk

Factors


Diagnosis Treatment Also know this

Furuncle (boil)/Caruncle

Furuncle Acute, round, tender,circumscribedperifollicularstaphylococcal abscess;nodular & with centralsuppuration

Carbuncle 2 or more confluentfuruncles, w/ separateheads

Lesions begin in hairfollicles, continue byautoinoculation (carriersin nose/groin)

Most will undergo centralnecrosis & rupture thruskin

S aureus

Predisposingfactors:Disruption of skinsurface integrity(pressure, irritation,friction, dermatitis,shaving, etc)

Systemic disorders(alcoholism,malnutrition, blooddyscrasias,immunosuppression)

Atopic dermatitis(predisposes

individual to carrierstate)

Nasal carriers are atrisk for chronicfurunculosis

Nape, axillae,buttocks (but mayoccur anywhere)

Warm compress may arrestearly furuncles

Penicillinase – resistantpenicillin or 1 st gencephalosporin (1 – 2g/day)

– oral!

Bactobran – applied toanterior nares to preventrecurrence (apply daily for 5days)

If localized with definitefluctuation: incision &drainage

If lesion is in EAC, upper lip

or nose, I & D will only bedone if antibiotics fail

To eradicate carrier state: 1. Daily use of

chlorhexidine wash2. Rifampin +

Dicloxacillin (10days)

3. Sulfa – TMP forMRSA (10 days)

4. Low doseclindamycin (3 mos)

Vs. acne: furuncle is extremely painful

Furuncle is deep so topical medswill not work

Similarities between erysipelas &furuncle:

1. + signs of inflammation2. Painful3. Acute

DO NOT do I & D ifacutely inflamed, givemoist heat instead.


14/39

!"!"!"# LALAϋ

2C: ERYTHEMATOUS LESIONS: Non – Scaly Plaques




Fixed DrugEruption (FDE)

Begins as a red patch thatsoon evolves to aniris/target lesion (~1cm),identical to erythemamultiforme & mayeventually blister & erode

Known as “fixed” becauseit occurs at the same sitew/ every exposure tomedication

Usually causesprolonged/permanentpostinflammatoryhyperpigmentation

A non – pigmenting FDEis usually caused by

Pseudoephedrine HCl (“Baboon syndrome” – buttocks, groin, axilla)

Medications takenintermittently

HLA – B22

Young boys

Oral & genitalmucosa (50%)

- NSAIDS:usually lips

- Sulfa – TMP:usuallygenital

Stop takingoffending drug.

Features:1. Normal stratum corneum2. Chronic changes in

dermis:a. Papillary fibrosisb. Pigment

incontinence3. Eosinophils & neutrophils4. No anesthesia or

hyposthesia

With first intake of drug:1. Redness2. Hyperpigmentation3. Redness + increasing size

+ pruritus

FDEs may progress to Steven – Johnsons syndrome

- Usually associated withanticonvulsant intake

ErythemaMultiforme(EM)

Begin as sharplymarginated, erythematousmacules, which becomeraised, edematouspapules over 24 – 48 hrs

Target or iris lesions with3 zones:

1. Central duskypurpura

2. Elevated,

edematous, palering3. Surrounding

macularerythema

Px may present withconjunctivitis

Herpes simplexinfection (usuallyorolabial HSV)

In the Phils: usuallydrug – induced

HLA – DQ3

Young adults

Dorsal hands (initialinvolvement), dorsalfeet, extensor limbs,elbows & knees,palms & soles (siteof typical iris/targetlesions)

Prevention:cornerstone oftreatment (if due toHSV)

Sunblock creams(may prevent UVBinduced outbreaks)

Antiherpeticantibiotic (in oral,chronic, suppressivedoses)

- Acyclovirmay preventlesions

Prednisone (mayreactivate HSV andincrease frequencyof attacks)

Features:1. Target/iris lesions2. Cellular necrosis3. Basketweave stratum

corneum4. Mononuclear infiltration

FDE vs. EMFDE: < 6 lesionsEM: many generalized lesions

For severe erythema multiforme,give oral steroids.

1

2

3


15/39

!"!"!"# LALAϋ




Erysipelas (“St. Anthony’s fire orignis sacer”)

Fiery – red swelling withcharacteristic raised,indurated border; onsetusually w/ prodromal sx

Distinctive feature:advancing edge of patch

PAINFUL!

Spreads peripherally;more superficial thancellulitis

Any inflammation ofthe skin (esp iffissured/ulcerative)may provide entrancefor beta – hemolyticstreptococcus

Newborn, postpartumwomen

Face (lesion starts incheek near nose & infront of ear lobe)Legs (more likely to

need hospitalization)Perineum &abdomen (inpostpartum women)

Systemic penicillin(vigorous tx for 10days; improvementseen in 24 – 48h)

ErythromycinLocally: ice bags &

cold compresses

Acute tuberculoid leprosy may looklike erysipelas BUT acutetuberculoid leprosy has no fever,pain, or leukocytosis.

Cellulitis Suppurative inflammationinvolving thesubcutaneous tissue

No central suppuration (Sinong may centralsuppuration?Furuncle/carbuncle )

Ill – defined borderindicates deepness

S pyogenes/ S aureus

Usually follows somediscernible wound

Leg: Tinea pedis asmode of entry

IV penicillinase – resistant penicillinsor 1 st gencephalosporin (oral!)

Erysipelas & cellulitisare both deep – see neutrophils reaching thedermis w/c is why topical medswon’t work :(

Possible complications:- Gangrene- Metastatic abscess

- SepsisMay present with chills & fever

Urticaria Wheals, white/redevanescent plaques,surrounded by a red haloor flare; pruritic!

May be accompanied byangioedema

Rarely lasts >12 hrs

Mast cell degranulation =increased histamine

Drugs (most frequentcause: Penicillins)

- Aspirin mayexacerbatechronicurticaria

Food, food additives,emotional stress,menthol, neoplasms(carcinomas,Hodgkins, CLL),inhalants, infections(acute urticaria: strep,TB; chronic urticaria:hep B & C)

Covered areas:trunk, buttocks, chest

If individual wheal persistsfor > 24 hrs = do s kinbiopsy

Antihistamines

Avoidance of thetrigger

For chronic:antihistamine daily

Features:1. Mild dermal edema2. Margination of neutrophils

w/in postcapillary venules3. No karyorrhexis & fibrin

deposition (compared tovasculitis)

Acute: < 6wksChronic: >6wks

ExfoliativeDermatitis(erythroderma,pityriasis rubra)

Extensive erythema &scaling; may ooze a straw

– colored exudates

Itching appears w/systemic toxicity (fever)

Possible causes:1. Generalizatio

n of a pre – existingchronicdermatoses

2. Drug

Face & extremities Topical steroids,soaks, compresses

SystemiccorticosteroidsImmunosuppresants

Features:No vesicles or pustulesCourse of disease may beprotracted, last years, or maypersist & resist therapy


16/39

!"!"!"# LALAϋ

eruptions3. Idiopathic

Predisposing Factors: Psoriasis, eczema,drug allergy, otherdermatoses




Hansen’s

Disease(Leprosy)

Important feature:

Neurotropism

Mycobacterium leprae

- Weakly acidfast

- Grows best(30 oC)

- Intracellular

2 peaks of

presentation:1. Children 10

– 20 yrs2. Adults 30 –

60 yrs

Areas of predilection: Cooler areas of thebody (spares scalp &midline)

Early diagnosis is

essential!

Lepromin skin test (todetermine type of leprosy)

- Multibacillary (if+ organisms onskin smear)

- Paucibacillary (ifskin smear is (-)or px has < 5lesions)

PGL – 1 (for pure neuralleprosy)

Dapsone

(cornerstone of tx)

Dapsone + Rifampin

Clofazimine (sideeffect: skindiscoloration)

Compared to TB txregimens, meds aregiven once a month for leprosy.

Leper reaction:Upon starting tx, px m ay experiencethe ff:

- Fever- Joint pains- Nerve damage due to

inflammation of nerve

- Skin becomes swollen &erythematous- New lesions appear

Management of leper reaction:Prednisone

Early &IndeterminateLeprosy(indeterminatebecause course ofdisease cannot bepredicted yet)

First lesion: solitary, ill – defined hypopigmentedpatch w/ slight anesthesia

90% initially present withnumbness (cutaneousfindings may appear yearslater)

Loss of cold & light touch – earliest sensorychanges (usuallyfeet/hands)

Cheeks, upper arms,thigh, buttocks

Usually no/few bacilli Peripheral nerves not enlargedNo plaques/nodules

Few cases stay in this state; mostwill become l epromatous,borderline, or tuberculoid. Somemay spontaneously resolve.




Before starting tx, do a CBCbecause Dapsone maycause hemolytic anemia

Do liver function tests &chest xray (check for TB)


17/39


18/39

!"!"!"# LALAϋ

Lepromatous macules Symmetrical & diffuselydistributed over the bodySmall & numerousIll defined, blend intosurrounding skinLittle or no loss ofsensation, no nervethickening, no sweating

Lepromatousinfiltrations3 types: diffuse, plaque,nodular**Diffuse – diffuseinfiltration of face,madarosis, waxy/shinyappearance of skin

May manifest as lepromas (ill defined nodulesoccurring in acral parts:ears, brows, nose, chin,elbows, hands, buttocks,knees)

Nerve disease is bilateral& symmetrical (stocking – glove pattern)

disease3. Anesthesia on a lesion –

leprosy is the onlydermatologic disease thatwill cause this

4. Hypopigmented patches inkids – early sign!

Present with loss of hair ineyebrows (madarosis) ->eyelashes -> body (scalphair spared)

Misdiagnosed as diabeticneuropathy


19/39

!"!"!"# LALAϋ

2D: ERYTHEMATOUS LESIONS: Non – Scaly Patch




PhototoxicDermatitis

Exaggerated sunburnreaction: erythema, edema,vesicles, bullae, burning,stingingFrequently resolves withhyperpigmentation

Mechanism: Direct tissueinjury

Phototoxic agents:- Coal tar

(cosmetics, drugs,dyes, insecticides,disinfectants)

- Furocoumarins inplants

- Bergapten (lotion,aftershave)

- Yellow cadmiumsulfide (tattoos)

- Drugs:doxycycline,naproxen,ibuprofen,amiodarone,phenothiazine

Sun – exposed areas:- Face- V of neck- Extensors of

upperextremities

- Dorsum ofhands

- Often lowerlegs & feet

Topical agent: clinicalSystemic agent:clinical + phototests

Symptomatic tx:corticosteroids

Avoid sun exposureProtective clothing isessentialSunscreen with broadestUVA coverage

Onset: minutes to hours afterexposure; usually occurs after1 st exposure

PhotoallergicDermatitis

“Rash”

Usually eczematouslesions & pruritic

Mechanism: Type IVdelayed hypersensitivityreaction

Photoallergic agents:- Drugs:

phenothiazines,chlorpromazine,quinidine,sulfonylureas,NSAIDs

- Topicalantimicrobials/antibacterialsoaps(hexachlorophene, bithionol)

- Sunscreens(PABA,

benzophenones)- Fragrances (mustambrette, 6 – methylcoumarin)

- Aftershave (oil ofsandalwood)

Sun – exposed areas:- Face- V of neck- Extensors of

upperextremities

- Dorsum ofhands

Often lower legs & feet

Topical agent:photopatch testsSystemic agent:clinical + phototests;photopatch tests

Same Onset: 24 – 48hrs afterexposure

No occurrence after 1 st exposure


20/39

!"!"!"# LALAϋ

2E: ERYTHEMATOUS LESIONS with Eczema




AtopicDermatitis

Hallmark of AD: pruritus (itching usually precedeslesions)

Diagnostic criteria ofHanifin & Rajka:Major criteria: PruritusTypical morphology &distribution (adults: flexural,infants: facial & extensors)Chronically relapsingdermatitisPersonal or family hx ofatopic disease

Minor criteria (at least 3):XerosisIchthyosis

Elevated serum IgEEarly age of onsetNipple eczemaCheilitisRecurrent conjunctivitisDennie – Morgan foldsKeratoconus

Anterior subcapsularcataractPeriorbital darkeningPityriasis albaItch when sweatingBlanching phenomenonWhite dermographism

Food hypersensitivitySusceptibility to infection (Saureus, eczemaherpeticum – HSV 1, HIV)

Risk factors:1. Polygenic

inheritance/personal or family hx ofatopic disease

2. Environmentalfactors

3. High level of IgEantibodies tohousemites

Adults: flexurallichenificationInfants: facial &extensors

Topical therapy 1. Corticosteroids –

dominant method oftx for AD- Potent steroid

duringweekend, mildersteroid duringthe week

2. Calcineurin inhibitors(Tacrolimus) – alternative tosteroids

Systemic therapy1. Antihistamines – for

sedative effect2. Antistaph antibiotics

during flares

(cephalosporins &semisyntheticpenicillins)

3. Systemic steroids – only for controllingacute exacerbations

4. Azathioprine,mycophenolatemofetil,methotrexate – fordebilitating diseaseunresponsive toother tx

5. Phototherapy –

hospital based; goodfor control of severe AD

Associated features &complications: 1. Dennie – Morgan folds

- Linear transverse foldbelow edge of lowereyelids

2. Hertoghe’s sign - Thinning of lateral

eyebrows3. Headlight sign

- Perioral, perinasal &periorbital pallor

4. Pityriasis alba- Subclinical dermatitis- Poorly marginated,

hypopig mentedslightly scaly patches

5. Keratosis pilaris- Horny follicular

lesions- Refractory to tx


21/39

!"!"!"# LALAϋ




Infantile AD 60% present in 1 st yr of life(usually >2 mos of age)

Usually begins as erythema& scaling of cheek

Lesions may be papular or

exudative

Worsened afterimmunizations & viralinfections

2 mos – 2 yrs of age

Cheek, scalp, neck,forehead, wrists,extensor extremities(areas involved

correlates withcapacity of child toscratch/rub site & withbaby’s activities likecrawling)

Blinded foodchallenges

Assays for food – specific IgEPrick testing

Partial remission duringsummer & relapse duringwinter (due to therapeuticeffects of UVB and humidity& aggravation by wool & dryair)

Evaporation barrierimmediately after bathingWhite petrolatum

Aquaphor & vegetableshorteningProtection of affected partfrom scratching & rubbing

Childhood AD Less exudativeOften lichenified, induratedplaques

Itch – scratch cycle: Pruritus leads to scratching& scratching causessecondary changes that

causes itching

- Antecubital & poplitealfossa, flexor wrists,eyelids, face, neck

Scratching impulse is usuallybeyond control of px (itching issame as lichen simplexchronicus -> compelling,paroxysmal) – inability to feelpain during paroxysms

Severe AD (>50% body

surface area involved) – associated with growthretardation

- Topical calcineurininhibitors(macrolactams)/phototherapy may allow forrebound growth

Adult AD Localized, erythematous,scaly, papular, exudative,or lichenified plaques

Staphylococcal colonizationis universal

Hand dermatitis: mostcommon problem for adultsw/ hx of AD

1. Wet work- Especially

implicated in handeczema

2. After birth of 1 st child3. Soaps

Adolescents: Antecubital & poplitealfossa, front & sides ofneck, forehead, areaaround eyes

Adults: chronic handeczema is common

Dermatitis is uncommonafter middle life

Topical corticosteroid:mainstay of tx

Avoid extremes of cold &heat

Avoid overbathingTepid showers, not hot

Itching usually occurs inresponse to heat/stress, duringthe evening when trying torelax, or at night

Flares may be due to acuteemotional stress (decreasesitch threshold)

Mild stigmata of dry skin &irritation remain even afterrecovery


22/39

!"!"!"# LALAϋ




SeborrheicDermatitis

Moist plaques w/ chronic,superficial, inflammatorydisease of the skin

Scaling on anerythematous base +severe itching

Pityrosporum ovale Scalp, eyebrows,eyelids, nasolabialcreases, lips, ears,sterna area, axillae,submammary folds,umbilicus, groin,gluteal crease

Cradle cap – seen ininfants asyellow/brown scalinglesions of the scalpwith adherent epithelialdebris

Differentiate frompsoriasis (moresevere scaling, +

Auspitz sign: removalof scales disclosesbleeding points, nailpitting)

Antifungal agents(Ketoconazole) & topicalcalcinearia inhibitors -mainstay

Corticosteroid creams,gels, sprays, foam

Be careful with use ofsteroids due to sideeffect of steroid rosacea

Dandruff (pityriasis sicca) – mild form of SD

Lesions may becomegeneralized -> generalizedexfoliative erythroderma/erythroderma desquamativum

(esp in infants)

Atopic D has more severeitching than seborrheic

NummularEczema

Discrete, coin - shaped ,well – circumscribederythematous, edematous,vesicular & crusted plaques

+ Koebner’s phenomenon:formation of lesions aftertrauma

Severe, paroxysmal &nocturnal pruritus

Emotional stress Alcohol AtopyTrauma (Koebner’sphenomenon)

Young adulthood & oldage

Lower legs, dorsa ofhands, extensorsurfaces of arms

Lower legs (older men)Trunk, hands, fingers(younger females)

Initial tx: simple soaking& greasing w/ occlusiveointment OR applicationof potent steroid

Antihistamine Antibiotics if w/ staphinfectionIntralesional or systemicsteroids (if refractory totopical meds)

Recurrent staph infection maybe present

As new lesions appear, oldlesions expand by tinypapulovesicular satellitelesions at the periphery fusingwith the main plaque

May be very similar to AD butdifferent in site of predilection& presentation (coin shaped).

Although AD may benummular in adolescents, ADis more chronic & lichenified.

InfectiousEczematous/Autosensitiza-tionDermatitis

Widespread dermatitis ordermatitis distant from alocal inflammatory focus

Generalized acutevesicular eruptionsassociated with chroniceczema of the legs w/ orw/o ulceration

Often in linear configuration

Cause of the distantdermatitis is not the sameas the cause of the localone

Autosensitization to thedischarge

Precipitating factors:- Diabetics w/ non –

healing wounds- Chronic otitis

media, eye, nose,vaginal discharge

AntibioticsOral glucocorticoids

Usually develops about a:- Discharging abscess- Ulcer- Sinus- Fistula


23/39

!"!"!"# LALAϋ




ContactDermatitisIrritant CD Inflammatory reaction to a

substance that causeseruptions in most people

Hallmark: Pain & burning!

Lesions: necrosis &ulceration

Acids Alkaline materials(soaps/detergents)SolventsDiaper

Acute: direct cytotoxicdamage to keratinocytes

Chronic: slow damage tocell membranes by CHONdenaturation & cellulartoxicity

Hands

Lesions sharplycircumscribed tocontact area; no

distant lesions

Topical steroids(betamethasone,clobetasol propionate)

This is a non – allergicinflammatory response. Noprevious exposure necessary.

Effect is evident w/in mins/hrs

Allergic CD Inflammatory reaction onlyamong people who havebeen previously sensitized(delayed reaction)

Delayed contact

hypersensitivity Acquired sensitivity tovarious substancesErythematous papules,vesicles, linear &symmetrical lesions w/inscratch marks

Hallmark: Itch!

Lesions: edema, vesicles,

Poison ivy, poison oak,poison sumacNickel/other metalsMedications (antibiotics,anesthetics, topical meds)Rubber/latex

CosmeticsFabric & clothingDetergents

AdhesivesPerfumesJewelryShoes

More intense incontact areas but mayhave distant lesions

Topical steroids Lesions appear 24 – 72 hrsafter exposure, but maydevelop as early as 5 hrs or aslate as 7 days after exposure

Diaper/NapkinDermatitis

Alkaline irritative effects ofammonia formed in wetdiaper

Risk factor: frequentmaceration

Highest incidence :6 – 12 mos of age

Lower abdomen,genitals, thighs,convex surfaces ofbuttocks

Use diaper w/superabsorbent gel

Frequent change ofdiaper

Topical hydrocortisoneZinc oxide paste

Irritant HandDermatitis/Housewife’s

Eczema

Dryness/redness of fingers

Chapping at back of hands,erythematous hardening ofpalms, fissuring

Under rings when notremoved duringwashing

BetamethasonedipropionateClobetasol proprionate

Triamcinolone


24/39

!"!"!"# LALAϋ




Intertrigo Superficial inflammatorydermatitis occurring where2 skin surfaces are inapposition

Result of friction, heat,moisture -> affected fold

becomes erythematous,macerated, secondarilyinfected

Hot & humid weatherObesityDM & hyperhidrosis

Children & elderly

Retroauricular areas,folds of upper eyelids,creases of neck,axillae, antecubitalareas, finger webs,

inframammary areas,umbilicus, poplitealspaces, toe webs,gluteal folds

Inframammary area inobese women: mostfrequent site ofintertriginouscandidiasisGroin: fungal infection

Eliminate macerationLocalantibiotics/fungicidesSeparate apposing skinsurfaces w/ gauze orother dressings

Castellani paint,polysporin ointment, lowpotency topical steroid

StasisEczema

Erythema/yellowish/ lightbrown pigmentation oflower 1/3 of legs espsuperior to medialmalleolus

Hyperpigmentation due tomelanin & hemosiderin

Cutaneous marker forvenous insufficiency

Venous insufficiency

Persons with heart failure,varicose veins, recenttrauma of legs – greaterrisk

Elderly (rarely occursbefore 5 th decade oflife)

Lower 1/3 of lower leg(superior to medialmalleolus)

Symptom reliefTx of underlying venousinsufficiencyEmollients – for pruritus& eczemaTopical corticosteroidsSupport stockings

Swelling may be noted late inthe afternoon withspontaneous resolution in themorning


25/39

!"!"!"# LALAϋ

2E: ERYTHEMATOUS LESIONS: Dry, Chronic Eczema




LichenSimplexChronicus(Neuroderma-titisCircumscripta)

Paroxysmal pruritus

Criss – cross pattern:between is a mosaiccomposed of flat – topped,shiny, smooth, quadrilateralfacets (lichenification)

Circumscribed, lichenified,pruritic patches

Excoriated papules(sometimes w/ bleeding),slightly scaly & moist, rarelynodular

Chronic rubbing &scratching

Associated with topic orallergic contact dermatitis,anxiety, nervousness,depression

Nuchal area (female),scalp, ankle, lowerlegs, upper thighs,exterior forearms,vulva, pubis, anal area,scrotum, groin

Goal: cessation ofpruritus

Stop scratching!Cover affected areas atnight to preventscratching while asleepTopical steroids :Clobetasol propionate,betamethasonedipropionatecream/ointment – usedinitiallyTriamcinolonesuspension

With habitual itch – scratchcycle

PrurigoNodularis

Multiple severe itchingnodules (pea – sized orlarger; 3 – 20mm)

Chronic disease, lesionsevolve slowly

Symmetrical & usuallylinear arrangement

Unknown

Atopic dermatitis, anemia,Hep C, pregnancy, stress,

etc.

Chronic renal failure: most common internalcause of pruritus

Any age but mainly inadults (20 – 60 y/o)M = F

Anterior surfaces ofthighs & legsForearms, trunk, neck

Visual examinationBiopsyBlood tests, liver,kidney, thyroid fxn

tests

Initial tx: intralesional ortopical administration ofsteroids

Other measures:Keep in cool areas,avoid hot baths orshowers and woolclothingUse soap only in axilla& inguinal area

Antihistamines Antipruriticlotions/emollientsPUVAVit D3, tacrolimusCryotherapy

Prurigo Mitis Mild form of chronic

dermatitis characterized byrecurrent, intensely itchingpapules & nodules

Severe itching ->excoriation, eczematisation

Worsened after

immunizations & viralinfections

Early childhood Blinded food

challenges Assays for food – specific IgEPrick testing

Same


26/39

!"!"!"# LALAϋ

2F: ERYTHEMATOUS LESIONS: Papulosquamous Disease




Tinea Capitis Scalp ringworm

Incubation period: 2 – 4days

Pathogenic dermatophytes(Except: Epidermophytonfloccosum &Trichophytonconcentricum)

Most common: T tonsurans& M canis

ChildrenBoys > Girls

Scalp, glabrous skin,eyelids, lashes

Wood’s light Fungal fluorescenceFluorescentsubstance: pteridine(+) if bright green oryellow green

10 – 2% KOH solutionFindings: pattern ofendothrix/ ectothrix

Culture (growth in 1 – 2 wks)

Griseofulvin (2 – 4 mos)Terbinafine (fortricophyton infections; 1

– 4 wks)Itraconazole/fluconazole(2 – 3 wks)Selenium sulfideshampoo orketoconazole shampoo(adjunct)

Kerion celsii: systemicsteroids + antifungal

Kerion celsii : deep tenderboggy plaques exuding pus;cause scarring & permanentalopecia

Favus: concave, sulfur – yellow crusts around loose,wiry hairs; atrophic scarringresults to smooth, glossy,paper – white patch

Scutulae: cupshaped crust onglabrous skin, < 2cm, mousyodor

T tonsurans Black – dot ringwormSubtle seborrheic – likescalingInflammatory lesion

Large spore endothrix

(-) fluorescence inWood’s light

Culture:granular/powdery,

yellow to red, browncolonyM canis Scaly, erythematous,

papular eruptions withloose & broken – off hairs -> inflammatory

Small spore ectothrix

(+) fluorescence inWood’s light

Culture: profuse,cottony, aerial mycelia;buff to light brown

TineaCorporis(TineaCircinata)

1 or more circular, sharplycircumscribed, slightlyerythematous, dry, scaly,hypopigmented patches

With progressive central

clearingDepth of infection usuallylimited to epidermis & itsappendages

See annular outlines(ringworm)

T rubrum – most commonM canis – causes moisttypeT mentagrophytes

Mode of transmission:

Contact w/ infected human(most common)Contact w/ contaminatedhousehold pets, farmanimals, fomites

Widespread tinea corporismay be a presenting sign of

AIDS or related to the useof a topical steroid orcalcineurin inhibitor

PreadolescentsF > M

Neck, extremities,trunk

KOH exam of skinscrapings (get fromactive border of lesion-highest yield of fungalelements)

Fungal culturePCRSkin biopsy (seeseptate branchinghyphae in stratumcorneum)

TOPICAL: localizeddisease w/o fungalfolliculitis

- Sulconazole,miconazole,itraconazole

(give 2 – 4wks)- Terbinafine,

Ketoconazole – give for 1 wk

Combination with apotent corticosteroidmay cause widespreadtinea & fungalfolliculities so avoid

Variants:1. Fungal folliculitis

(Majocchi granuloma)- Infection of hair

follicles w/ granulomaformation

- Usually in F whoshave legs- T rubrum/

mentagrophyte2. Tinea imbricate

- Concentric ring ofscales, extensivepatches w/ polycyclicborders

- T concentricum3. Tinea incognito


27/39

!"!"!"# LALAϋ

using CS!

SYSTEMIC: forextensivedisease/fungal folliculitisGriseofulvin, terbinafine,itraconazole,fluconazole

- Atypical presentationdue to corticosteroidtx

4. Tinea gladiatorum- Skin to skin contact in

wrestlers

Tinea Cruris

(jock itch,crotch itch)

Begins as small,

erythematous scaling orvesicular & crusted patchthat spreads peripherallyand partly clears in center

Patch: curved, well – defined border, particularlyon lower edge

T rubrum – common

Epidermophyton floccosumT mentagrophytes

They produce keratinasesthat allow invasion ofcornified cell layer ofepidermis

Risk factors:Warm & moist areasTight – fitting clothes

Autoinoculation (athlete’sfoot & ringworm)Direct skin-to-skincontact/fomitesObesity, DM,immunocompromised

Adult men

Upper & inner surfaceof thighsPerineum & perianalareas

KOH wet mount

Growth onMycosel/Saboraudagar plates

Treat all areas of active

infectionKeep groin area clean &dryLoose – fitting clothingLose weightUse plain talcumpowder

Antifungal creams

Candidal infection may mimic

this (difference is the presenceof satellite pustules in candida)




TINEA PEDIS(athlete’s foot)

Dermatophytosis of the feet

Characterized by erythema,scaling, vesicular & crustedpatch spreadingperipherally with partialcentral clearing

Most common fungaldisease

Chronic w/ exacerbations inhot weather

T rubrum – causemajority of infection;usually non – inflammatory type

T mentagrophytes – cause inflammatorylesions

Risk factors:Hyperhidrosis (sweatbetween toes and soles)Hot, humid weatherOcclusive footear

Late childhood to youngadulthoodYounger indvls:inflammatoryOlder: non - inflammatoryM > F

Site: usually 3 rd toe webDistribution: usuallybilateral; may involve onehand, both feet

Dry toes thoroughlyafter bathingGood antiseptic powderFungicides

May become a portal of entryfor lymphangitis whenpyogenic cocci infect fissuresbetween toes & in the vesicles

T rubrum Moccasin type lesions:non – inflammatory type w/dull erythema &pronounced scaling thatmay involve entire sole and

This type of lesion may also becaused by E floccosum


28/39

!"!"!"# LALAϋ

sides of foot =moccasin/sandalappearance

T mentagro -phytes

A. Inflammatory/ bulloustype

- Plantar arch &along sides of feet

- Burning/itchingsensation

- Least common- Involves sole,instep, webspaces

B. Interdigital type- Erythema, scaling,

maceration extendup to dermis

- Complicated bysecondarybacterial infection

C. White superficialonychomycosis




TINEAMANUM

Dermatophytosis of thehands

Dry, scaly, erythematoustype OR moist, vesicular,eczematous type

T rubrum – morecommon; produces dry,

scaly erythematous typeT mentagrophytes – dermatophytosis of handsecondary to tinea of feet;produces vesicular type;both hands involved

Unilateral if associated withtinea pedis & crurisOften associated with tineaunguium of fingernails (ifchronic)

Direct microscopicexam of scrapings

(instep, heel, sidesof foot, palms)

10 – 20% KOHsolutionFungal culture

Oral antifungal agents(topical don’t usually

work because of thethick palmar stratumcorneum) – Griseofulvin, terbinafine,itraconazole,fluconazole

Prevention:Dry toes thoroughlyafter bathingGood antiseptic powderbetween toes (tolnaftateor zeasorb powder)Plain talc, cornstarchdusted into socks

PITYRIASISROSEA

Usually begins with single 2 – 4cm thin oval plaque w/fine collarette of scaleinside the periphery(herald patch/motherpatch)

Salmon – colored papules& macules., oval/circinatepatches, covered with finely

UnknownSome evidence points to aviral cause – reactivationof HHV7 & HHV6

Spring & autumn months

15 – 40 y/oF > M

KOH wet mountGrowth onMycosel/Saboraudagar plates

SupportiveTopical CS orantihistamines forassociated pruritusUV treatment mayexpedite involution oflesions

Usually asymptomatic but maybe pruritic & haveconstitutional symptoms


29/39

!"!"!"# LALAϋ

crinkled, dry epidermis thatoften desquamate

TINEAVERSICOLOR

Hypopigmented,coalescing, scaly macules(due to abnormally small &poorly melanisedmelanosomes) in dark skin

Hyperpigmented on pale

skin

Malassezia furfur (skinlesions area producedwhen in hyphal phase)

Risk factors:Genetic predispositionWarm, humid envt

ImmunosuppressionMalnutritionCushing disease

Sterna region, sides ofchest, abdomen, back,pubis, neck, intertriginousareas, oily areas of skin

Face & scalp (usually ininfants &

immunocompromised px)

Wood’s light exam Culture (rarely usedfor dx)

Anti – fungal agents(selenium sulfide,imidazoles, triazoles,sulfur preparations,salicylic acid, benzoylperoxide, etc)

Ketoconazole:400mg/1x a monthItraconazole: 200mg for7 daysTerbinafine: topical

Hypopigmentation may persistfor wks/mos after fungaldisease is cured

Most cost effective tx:selenium sulfide & zincpyrithione soap




PSORIASIS Common, chronic,recurrent, inflammatorydisease of the skin

Round, circumscribed,erythematous, dry scalingplaques of various sizes,covered by gray or silverywhite imbricated l amellarscales

Symmetrical, solitarymacule to > 100 macules

May be accompanied byitching/burning

Nail pitting & oil spots

Unknown Mean: 27 y/o

Scalp, nails, extensorsurfaces of limbs

(shins), elbows, knees,umbilical & sacralregion

Depends on site,severity, duration, age

Topical:

- Corticosteroids- Tars- Vit D- Salicylic acid- UV- Tazarotene

Systemic- CS- Methotrexate

Koebner’s phenomenon:appearance of lesions at areasof injuries

Auspitz’s sign: bleeding pointssecondary to thinning ofepidermis over dermalpapillae; bleeding uponremoval of scales

Woronoff ring: concentricblanching of erythematous skinnear periphery of healingpsoriatic plaque

Types

Seborrheic – like psoriasis

W/ prominent features ofseborrheic dermatitis

W/ minimal amount of soft& greasy micaceous scales

Flexure areas(antecubital areas,axillae, under breast)

Inversepsoriasis

“flexural psoriasis” – palms& toes

“volar psoriasis”

Folds, recesses, flexorsurfaces: ears, axillae,groin, inframammaryfold, palms, soles, nails


30/39

!"!"!"# LALAϋ

Napkinpsoriasis

Increases risk for adultpsoriasis infection

Infants between 2 – 8mos of age

Psoriaticarthritis

5 clinical patterns:1. asymmetrical distalinterphalangeal jointinvolvement w/ naildamage2. arthritis mutilans w/osteolysis of phalanges &

metacarpals3. symmetrical polyarthritislike RA, with claw hands4 . oligoarthritis w/swelling & t enosynovitisof 1 or few hand joints – most common5. ankylosing spondylitisalone or with peripheralarthritis

Distal & proximalinterphalangeal joints(relative sparing ofmetacarpal &metatarsal phalangeal

joints)

Aspirin, NSAIDs, oralretinoids, PUVA

Guttatepsoriasis

Typical lesions: size ofwater drops (2 – 5mm)

Abrupt erosion following aninfection (ex. streppharyngitis)

Usually px


31/39

!"!"!"# LALAϋ

3: SKIN COLORED PAPULES




Verrucavulgaris(common wart)

Benign epidermalproliferations

Elevated round papules w/a rough grayish surface

(“verrucous”) - If in palms &

soles, not veryverrucous

Linear configuration ofverruca

See black dots(thrombosed dilatedcapillaries) on surface

HPV type 1, 2, 4, 27, 57,63

Transmission: simpledirect contact;

autoinoculation

Predisposing factors:Frequent immersion ofhands in water(makes skin soft, easierfor virus to enter)Meat handlers

5 – 20 y/o

Hands, peri – ungal(esp in nail biters),elbows, knees, plantar

surfaces, anogenitalareas

Generally self – limited

In the Phils:Electrocautery (completeremoval)

- Give xylocainebefore doingthis becausewarts in palmsare painful(many painreceptors – Meissner &Pacini)

Topical keratolytics(salicylic acid/lactic acidpreparations)

Usually asymptomatic:painless & no itching

Larger than verruca plana

No dermatoglyphics(fingerprint folds) – in calluses,these lines are accentuated

Verruca Plana(flat warts)

Flat – topped papules thatare slightly erythematous

Brown on light skin &hyperpigmented on darkskin

Multiple & grouped

No rough surface, no blackdots

HPV type 3, 10, 28, 41

Transmission: directcontact & autoinoculation(in men who shavebeards, women whoshave their legs)

Children & young adults

Forehead, cheeks,nose, neck, dorsa ofhands, wrists, elbows orknees

Light cryotherapy (mayproduce loss of color) –

because nitrogen cancause death ofmelanocytes in coloredskin

Topical salicylic acid(may cause burning ofnormal skin = applypetroleum jelly)

Topical tretinoin

W/ Koebnerization (alsofound in psoriasis) – tend to

form linear, slightly raisedpapular lesions

Lesions are small andnumerous & spread fast

Of all HPV infections, flat wartshave the highest rate ofspontaneous remission

Molluscumcontagiosum

Painless, itching notprominent

Smooth surface, firm,dome – shaped pearlypapules (3 – 5mm) withcentral umbilication

Poxvirus (MCV 1 – 4)MCV 1: childrenMCV 2: HIV

Usually in kids, sexuallyactive individuals,immunosuppressed px(HIV infected)

Kids: face, trunk,extremities

Adults: lower abdomen,upper thighs, penileshaft in menImmunosuppressed:face (cheeks, neck,eyelids), genitalia

If px is healthy: usuallyself – limited

Kids : no tx OR topicaltretinoin/cantharidin (4 – 6hrs)Adults: cryotherapy orcurettage; sexual partnersshould be examinedImmunosuppressed :aggressive tx with HAART;curettage or core removal w/blade; cantharone or 100%trichloroacetic acid;cryotherapy

DO NOT DO CAUTERY. Docurettage! Scrape off infectedarea with curette w/c willremove abnormal tissue. Try toalso remove the molluscumbody


32/39

!"!"!"# LALAϋ




Acne Vulgaris(review nalang:D)

Comedo as basic lesion

Follicular disease w/ akeratinous plug

Propionibacterium acnes Adolescents (15 – 18y/o)

Involution of diseasebefore 25 y/o

See acne vulgaris (p. 8)

MiliariaPustulosa

Distinct, superficialpustules that are

independent of the hairfollicle

Pruritic

Preceded by anotherdermatitis that has

produced injury,destruction, or blockingof the sweat duct

Commonly associateddiseases:Contact dermatitisLichen simplex chronicusIntertrigo

No particular age

Intertriginous areas,flexure surfaces ofextremities, scrotum,back of bedridden px

Usually self – limitedPlace px in cool envt

Circulating air fans Anhydrous lanolin – helpresolve occlusion ofpores & helps restorenormal sweat secretionsHydrophilic ointmentSoothing, cooling bathsDusting powders

No need for antibiotics (because pustules aresterile; contain non-pathogenic cocci)

Recurrent episodes may be asign of type I

pseudohypoaldosteronism(salt – losing crises mayprecipitate miliaria pustulosa orrubra)

Difference from acne: nokeratinous plug

Gram (-)

Folliculitis

Superficial pustules (3 –

6mm)Fluctuant, deep – seatednodules

Enterobacter, Klebsiella,

Proteus, SerratiaPredisposing factors:Long term – antibiotictherapyContinuous scratchingOccurs in areas ofirritation (shaving,friction, clothes rubbing)

Anterior nares, face Isotretinoin

Sulfa – TMP

P AeruginosaFolliculitis

Pruritic, follicular,maculopapular, vesicular,or pustular lesions

Usually occurs 1 – 4days after bathing in hottub

Sides of trunk, axilla,buttocks, proximalextremities, apocrineareas of breast & axilla

Involutes w/in 7 – 14days

3 rd gen cephalosporins(oral), fluoroquinolones ifw/ fever

Some may present with fever& prolonged disease (“hot footsyndrome”)

Staphyloco-ccalFolliculitis

Atypical plaquePustular erythematousfollicular lesion

S aureus Eyelashes, axilla, pubis,thighs

Thorough cleansing ofaffected area withantibacterial soap andwater (3x/day)Deep lesions should bedrainedMupirocin ointmenttopically1 st generationcephalosporin (if

4: PUSTULAR DISEASE


33/39

!"!"!"# LALAϋ

drainage or topicaltherapy fail)

Anhydrous formulation ofaluminum chloride (forchronic folliculitis)




Superficial

PustularFolliculitis(impetigo ofBockhart)

Superficial folliculitis w/ thin

– walled pustules at follicleorifice

Fragile, yellowish – white,domed pustules

S aureus

May secondarily arise inscratches, insect bites,other skin injuries

Extremities, scalp, face

Ecthyma Begins with vesicle orvesicopustule w/erythematous base &surrounding halo thatenlarges over days &crusts

Becomes superficial saucer – shaped ulcer with rawbase

Indurated ulcer margin;granulating base mayextend deeply into d ermis

Beta hemolyticstreptococcusS aureus

Predisposing factors:UncleanlinessMalnutritionTraumaIV drug usersHIV infectionDM

Children

Lower extremities,shins, dorsal feet

Lesions may heal butmay leave a scar

Good hygieneMuciprocin or bacitracinointment1 st generationcephalosporin or oraldicloxacillin

PyogenicParonychia

Inflammatory reaction ofthe nail folds

Purulent, painful swelling oftissues around the nail

May be acute/chronic

Primary predisposingfactor: separation ofeponychium from nailplate (due totrauma/frequent wettingof hands)Manicure/pedicure

Secondary bacterialinfection due to: Saureus, Strep pyogenes,Candida albicans

No particular age

Folds of skinsurrounding nail

Smears of purulentmaterial will confirmimpression

Protection againsttrauma & keeping handsdry

Acutely inflamedpyogenic abscess:incision & drainage (dothis first before givingpenicillin orcephalosporin)

Candida (usuallyimplicated in chronicparonychia) – topical/oralantifungal (miconazole) +topical steroids

IntertriginousCandidiasis

Pruritic pink to redintertriginous moist patchessurrounded by a thincollarrette scale & pustules

Candida albicans(seen inimmunocompromisedpx,& conditions that favor

No particular age

Inframammary area (forobese women)

10% KOH microscopicexam (seepseudohyphae)

Goal: reduceinflammation!

Topical terbinafine will


34/39

!"!"!"# LALAϋ

closely adjacent to thepatchesHallmark: Satellite lesionson surrounding healthy skin(satellite pustules)

growth: warm, moist,high skin pH, reducedmicrobial flora due toantibiotic therapy),obesity, poor hygiene,restrictive clothing

Axilla, groin,overhanging abdominalfolds, intergluteal folds,interdigital spaces,umbilicus

not work; only AZOLES will work


35/39

!"!"!"# LALAϋ

5: VESICULAR DISEASE




MiliariaCrystallina

Small, clear, verysuperficial vesicles w/ noinflammatory reaction

Asymptomatic, short – lived, self – limited

Increased perspirationClothing that preventsdissipation of heat &moistureBedridden px & bundledchildren

Neonates ( < 2 wks)

Infants: head, neck,upper trunk

Adults: trunk

Self – limitedNo medical treatmentrequiredSymptom relief (keep pxin cool envt)

Impt features to remember:1. Rupture spontaneously2. Normal skin w/

desquamation3. No mucosal involvement4. Acute5. No target lesions6. No erythema ! – most

importantImpetigoContagiosa

Discrete, thin – walledvesicles that becomepustular & rupture

Very weepy lesions (freshexudates) covered byyellow/orange crusts

Gyrate pattern/gyrateerythema (round, ring –

like polycyclic or arcuate)

S aureus (most common)Streptococci(group B strep – newbornimpetigo)

Predisposing factors:Temperate zones

Sources of infection:Kids: pets, dirty

fingernails, other kids Adults: barber shops,beauty parlors, swimmingpools, etc

Children

Exposed body parts:face, hands, neck,extremities (palms &soles spared)

Histopathology:1. Superficial

inflammation inupper part ofpilosebaceousfollicles

2. Subcornealvesicopustule

3. Mild inflammationin dermis (PMNs,

edema)

Clean area beforeapplying meds

Systemic antibiotics(semisynthetic penicillinsor 1 st gencephalosporins) w/topical therapy(Bacitracin & muciprocinointment)

Recurrent: 10 daysRifampin (600mg/d)

Impetigo on the scalp:complication of pediculosiscapitis

Acute glomerulonephritis – complication following betahemolytic strep skin infection

- Usually in kids <6y/o

- Absent in staph

impetigo

Steven – Johnson’sSyndrome

Flat, erythematous,purpuric macules that formincomplete “atypicaltargets” that may blistercentrally(Erythema multiforme minormay also appear as targetlesions, may be drug induced,and may have the same areasof predilection. Difference is inNikolsky sign)

Evolution of lesions:Macules -> vesicles &bullae

Fever & influenza likesymptoms precede

Drug allergy (1day – 3wks latent period):antibiotics, NSAIDs,allopurinol,anticonvulsants

Oral mucosa &conjunctiva

Skin biopsy:Lymphocytic infiltrateat dermoepidermal

junction w/ necrosis ofkeratinocytes

Similar to px withextensive burn1. IV immunoglobulin2. Systemic

corticosteroids(dexamethasone,methylprednisolone)

- Stops spread &skin loss3. ICU4. Increase caloric

enteral intake

Cause of mortality indermatology

Px usually go to the hospitalbecause of pain

+ Nikolsky sign: application

of very slight pressure causesthe skin to slough off; usuallyseen in vesicular lesions (dueto weakening of intercellularattachments)

- This is absent inerythema multiformeminor becauselesions here aremore papular

5: VESICULAR DISEASE


36/39

!"!"!"# LALAϋ

eruption/skin lesions(rapidly spread w/in 4 days)

Mucosal involvement (>2mucosal surfaces eroded – oral or conjunctiva)

Not pruritic

2 causes of mortality in SJS:1. Sepsis2. Electrolyte

imbalance

SJS involves less than 10%body surface. (Toxicepidermal necrolysis involves>30% body surface & it’s amore severe SJS)

HerpesSimplex

Intraepidermal vesicles

Acantholysis (ballooningdegeneration of epidermalcells)

Types of infection:Primary infection : virusreplicates in site ofinfection; usually resides intrigeminal ganglion

Nonprimary initialepisode: initial clinicallesion in a personpreviously infected w/ thevirus

Recurrent infection

HSV 1: orolabial herpes;more commonHSV 2: genital herpes

Risk factors:ImmunocompromisedPrior infectionOccupation (esp inherpetic whitlow)Minor trauma & sunexposure

Transmission: intimateskin to skin contact, bodilyfluids

Tzanck smear – mostcommon procedure- Not specific (HSV,VZV)- Multinucleatedepidermal giant cells

Direct fluorescentantibody test – moreaccurate

Viral culture – veryaccurate & rapid(results ini 48 – 72 hrs)

PCRSkin biopsySerology

Drug of choice:Acyclovir (oral)

Indications for oral meds:- Recurrence- Dissemination

(inimmunocompromised)

Features:1. Acute2. Clustered lesions (In

SJS, not clustered)3. Can have mucosal

involvement

Other manifestations:Herpetic whitlow

- Infection of digits- Tenderness &

erythema of lateralnail fold

Herpetickeratoconjunctivitis

- Punctate/marginalkeratitis

- May impair visionHerpes gladiatorum

- HSV 1- Seen in wrestlers,

rugby players- Face, sides of neck,

inner armsHerpes Sycosis

- Affect primarily thehair follicle

- Close razor shaving

Recurrent EcthymaMultiforme

- Presents withpapules laterbecome targetlesions in palms,elbows, knees andoral mucosa

Neonatal Herpes- Passage through

birth canal


37/39

!"!"!"# LALAϋ

- Skin lesions,microphthalmos,encephalitis,chorioretinitis,intracerebralcalcifications

HSVEncephalitis/Meningitis

- Headache, fever,mild photophobia,autonomicdysfunction

OrolabialHerpes

Lesions in mouth: brokenvesicles that appear aserosions or ulcers coveredw/ white membrane

Frequent m anifestation:cold sore or fever blister

Erosions may spread tooral mucosa, tongue,tonsils = herpeticgingivostomatitis

95%: recurrent HSV1infection

Frequent trigger: UVBexposure

Lips near vermillionborder

If untreated, may last 1 – 2 wks

Upon onset: high fever,lymphadenopathy, malaise

GenitalHerpes

Vesicles in erythematousbase that ulcerate & crust

Grouped blisters &erosions w/ continueddevelopment of newblisters over 7 – 14 days

Course:

HSV2

Spread by skin-to-skincontact during sexualintercourse

Labia, vulva,perineum, perianalareas, shaft, glanspenis

Usually resolves in 21days

Asymptomatic shedding mayoccur between outbreaks

Can present as severesystemic illness

- Fever & flulikeillness

- Vaginal pain &dysuria (herpeticvulvovaginitis)


38/39

!"!"!"# LALAϋ




Herpes Zoster Shingles

Cutaneous eruptionsfrequently preceded by oneto several days of pain inaffected area

Papule & plaques oferythema -> blisters

Reactivation of varicellazoster virus

Risk factors: AgeImmunosuppression

F > M

Sensory dorsal rootganglion cells

Usual sites:

Thoracic (55%)Cranial – trigeminal(20%)Lumbar – 15%Sacral – 5%

Ophthalmic zoster :involvement ofophthalmic division of5 th CN

Ramsay huntsyndrome: involvement of facial &auditory nerves

Tzanck smear AcyclovirIndications:

- Immunocompromised px

- To preventcomplications in

elderly (give 1st

3 days)- Ophthalmic

involvement

Features:1. More painful than

simplex2. Dermatomal3. Not recurrent4. Unilateral w/in

distribution ofcranial/spinal nerve5. Neuralgic

Postherpetic NeuralgiaMajor complication; occurs 1month after onset of zosterinfection

Scabies See page 7 for completedetails

Features:1. Pruritic2. No target lesions3. No mucosal

involvement4. Px usually comes

to you the lesionhas been there forseveral weeksduration


39/39

!"!"!"# LALAϋ

6: BULLOUS DERMATOSIS




Fixed DrugEruption (FDE)

See p 13/14

ContactDermatitis

See p. 22

Bullous

Impetigo

Strikingly large, fragile

bullae

Ruptures & leavescircinate, weepy orcrusted lesions (impetigocircinate)

Other manifestations:Constitutional symptomsappear laterDiarrhea w/ green stoolsBacteremia, pneumonia,or meningitis

S aureus

Predisposing factor:Insect bitesCutsNursery w/ infectedchildren

Any age but usually in

newborn infants- Neonatal type is

highly contagious- Begins in 4 th –

10 th days of lifew/ appearance ofbullae

Early: face & hands Adults: axillae, groin,hands(spares scalp)

Systemic antibiotics

IV fluid resuscitation – if w/ large areas ofinvolvement w/denuded skin fromruptured bullae

Sources: Andrews ’ Clinical DermatologyDra. Ismael ’s lecThe original megatable from MH :D Thank you

Documents

LALA Megatable Derma