Post on 03-Apr-2018
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DERMATITIS EKSEMATOSA
Dr. Kristo A. Nababan, SpKK
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Nummular eczema
Characteristic: Oval patches with
crusted papulovesicles
Localisation: Trunk
Extremities
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Dermatitis Numularis
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Differential Diagnosis
Acute vesico papular dermatitis:
Contact dermatitis
Infections: Dermatophyte, HS virus,
Varicella Zoster, Bacteria
Chronic vesico papular dermatitis:
Chronic CD, psoriasis, drug eruption,
fungal infect
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Biopsy
- Intercellular edema widening
intercellular spaces sponge like
appearance epidermal (spongiosis) - Acute & severe : intra epidermal
vesicular
- Chronis: Epidermal hyperkeratoticThickened (acanthotic)
Dermis: lymphocyte infiltration
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Therapy
1. Corticosteroid:
- topically
- injectable intralesional
- sistemic2. Wide spread acute/ subacute eczematous:
prednisone/ triamcinolone 40 mg/i. m
wet dressing/bath: acute dermatitis3. Chronic: baths containing oil moisturizers
4. Itching: hydroxyzine/ diphenhydramine
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ATOPIC DERMATITIS
Chronic relapsing inflammatory skin
disease.
It is frequently associated with asthma,
allergic rhinitis.
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Debate
AD is primarily an allergen induced disease
or
Simply an inflammatory skin disorder foundin association with respiratory allergy
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Atopy
Familial hypersensitivity of skin and m.
membrane against environmental substances
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Atopy / Atopic Syndrome
Sindrome consist of :
Bronchial asthma
Allergic rhinitis
Atopic Dermatitis
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Epidemiology
Prevalence: AD Common health
problem
10%> in children
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Natural history
AD start early in life ( 60% of the patients
develop the disease in infancy
Majority improve < 5 years
>> pats: resp. allergic disease: asthma &allergic rhinitis
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Prognosis
- Depend of the severity
- Start early in life
more severe
persist
- recurrent of AD adolescent
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Ethiology
Texture o/ t skin is abnormal with defective
lipid barrier---> TEWL increase
( Transepidermal Water Loss)
This is due to abnormal metabolism of
fatty acid is not clear
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Factors Contribute to the Development
of A. D.
Genetics
Environmental
Immunological
Pharmacologic
A. D.
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Genetics Factors
- Immunological abnormalities/ atopy
- Hypersensitivity o/ t skin
important development AD
-genetic influence elevated Ig E productT cell disregulation
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Role of Allergen
Food: Milk, Egg infancy
Aeroallergen
late childhood(house dust mite) 80% (+) skin prick test
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Food
-50% children AD clinical reactivity tofood protein
-Young children allergic to food: Milk
Peanut
soy
wheat
75% (+) to food
-Fooddirect contact provoke AD
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Aero allergen
Older children, adultaero allergen
(house dust mite, mould)
Food allergy less important
- Prick test and patch tes20-60% (+) tomite
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Role of Infection
Pat AD develop viral, bacterial, fungal
Skin infection
- Staphylococcus Aureus, Beta haemolytic
strept common cutaneous pathogens
- Staphy Aureus exotoxn, exoenzymeinflammatory skin lesion
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Atopic Dermatitis
AD can be divided into three stages:
1. Infantile atopic dermatitis:
2 months-2 years of age2.Childhood atopic dermatitis:
2 years-10 years
3. Adolescent and adult atopic dermatitis
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Infantile Atopic Dermatitis
60 % In the first year of life
Usually . 2 month of age
Clinic: Itchy erythema of the cheeks
Intraepidermal vesiclesrupture
moist, crusted areas extend to
other part of the body (scalp, neck,
forehead, wrist, extensor extremities
buttocks and diaper area spared
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Chidhood Atopic Dermatitis
Childhood
Clinic: less acute lesions
Lesions less exudative, drier,
>papularLocations: antecubital, popliteal
fossae, flexor wrist, eyelids, face,
around the neck
lichenified, slightly scaly/ infiltrated
plaques
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Adolescents and adult AD
Older patients
Clinic: Localized erythematous, scaly, papular/vesicular plaques
Pruritic, lichenified plaquesLocation: antecubital and popliteal fossae, frontand sides of neck, forehead, area about theeyes
Eruptions generalized more severe inflexures lichenified
Plaques often erythematous/ hyperpigmented
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Major Clinical features of AD (base on
Hanifin and Rajka)
- Intense pruritus & excoriation
- Typical morphology and distribution of skin
lesions:-facial and extensor involvement in
infant and early childhood
-flexural lichenification in adult
- Chronic or chronically relapsing dermatitis
(>6 weeks)- Personal and family history of atopic disease
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Minor features -Dryness of the skin (xerosis)
-Ichthyosis, keratosis pilaris, hyperlinear
palms
-Non specific hand/foot dermatitis
-Scalp dermatitis e.g. cradle cap
-Allergic shiners -Recurrent conjunctivitis and keratoconus
- IgE reactivity
-Dennie-Morgan infraorbital fold
-Orbital darkening -Pityriasis alba
-Food hypersensitivity
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Intense pruritus
Itching, Scratching the day worse atnight sleep disruption
Pat AD threshold of itching decreased
Humidity
Excessive sweating
Exposure to allergens, irritants (soap,
detergent acrylic, wool) itch
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Whats the etiology of pruritus in
AD ?
- Not well understood
- Local release of proinflammatory mediators &
cytokines
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Rukwied and Heyer (1999)
Pruritus:
- Histamine
- Cytokines
- leukotrienes
- neuropeptide
- proteases
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Morphological characteristic of AD
-Acute lesions are papules, vesicles on
erythematous background with sign of erosion,
bleeding and serous exudate
-Sub acute lesions are erythematous and scaly
papules on dry background
-Chronic lesions are fibrotic papules on lichenified
(thickened) back ground
-Excoriation due to scratching in a all stage
-Infection may alter the appearance with the presence of
oozing or local abscess
-Even uninvolved skin is often dry and scaly
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Investigation
Total Ig E > not helpful diagnosis
Skin prick test (SPT) Specific Ig E (RAST) more helpful
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Diagnosis
3 or more major criteria
3 or more minor criteria
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Atopic Dermatitis in Child
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Basic Treatment
Skin care Emollients
Avoidance of irritants, sudden
changes of temperature, humidity
Identification of
specific
Exacerbating factors
Anti inflammatory
Treatment
TREATMENT OF ATOPIC DERMATITIS
Allergens
Microbes
Emotional factors
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Avoidance of trigger factors
1. Irritants detergents
soap
2. Allergens: Food allergen
Airborne allergensChild < 5 years : Usually allergy to 1 or > foodcows milk, egg, wheat, bean
3. House dust mite: older children
young adult
4. Emotional stress
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TOPICAL EMOLLIENT
BASIS TOPICAL TREATMENT :
2 3 X / DAY
WATER LOSS
ITCHING
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Topical treatment
CREAM / LOTION : EARLY PHASE
OINTMENT : LICHENI FIED SKIN
SEVERE CASE :
AFTER OINTMENTWETWRAP DRESSING
EPIDERMAL WATER LOSS
TOPICAL CROMOLYN IN WATER SOLUBLEEMOLLIENT VEHICLE ANTI INFLAMATORYEFFECT
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ANTIBIOTIC FUSIDIC ACID
GRAM (+)
TETRA CYCLINE
SKIN CLEANSER 10% POVIDONE
IODINE
GENERALIZED INFECTION :ANTIMICROBIAL BATH (CHLORHEXIDIN 0,005%)
SISTEMIC ANTIBIOTIC : FLUCLOCXACILLIN :
MUPIROCIN
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OTHER TREATMENT
STRATEGIES
UVA PHOTOTERAPY
CICLOSPORIN
IF
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Atopic Dermatitis in Child
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Atopic Dermatitis in Infant and Child
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Atopic Dermatitis in Child
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CONTACT DERMATITIS
An inflammatory reaction of
the skin precipitated by an
exogenous chemical
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Contact Dermatitis
1. Irritant CD: produced by
substance that has direct toxiceffect on the skin
2. Allergic: trigger an
immunologic reaction
tissueinflammation
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Pathogenesis
Irritant CD: nonspecific inflammatory
reactions due toxic injury of the skin
Allergic CD: Cell mediated immunity/
type IV
A. Sensitization phase
B. Elicitation PhaseSensitization: hapten + protein LCs Th1
t IV
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type IV
antigens
T
inflammatory
mediatorslymphokines
activated macrophage
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Irritants
Subtances direct toxic effect of the skin
Acids
Alkalis Solvents
Detergents
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Allergens
Triggers immunologic reactiontissue
inflammation
Metals
Plants
Rubber chemicals Medicines
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Clinical appearance
Acute (vesicles) Chronic (lichenification)
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Incidence:
- Frequent problem
- 50% occupational illness
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History
First determine: ACD/ICD
Strong irritant several hours skin damage
Weaker irritants multiple application & days
dermatitis Allergic Contact Dermatitis:
Requires 24-48 hours
Often exposure Clinical disease
Occasionally dermatitis (8-12 hours) up to 4-7 hours
Detailed history of occupation, hygiene habits, hobbies
Th t S iti
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The most common Sensitizers
Poison Ivy
Para phenylenediamine
Nickel
Rubber compounds Ethylenediamine
Poison ivy: in the summer
Allergen: pentadecylcatechol (oleoresin of the plant)
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PPD
Permanent coloring of hair
Cross reaction : Azo, aniline dye,
Benzocaine, procaine,
Hydrochlorothiazine
Sulfonamides
When completely oxidized (fur coat), PPD not allergenic
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Nickel
Most commonly in woman
Ear piercing
In all metals
Hypoallergenic earring: one cannot be
certain that they are free of nickel
Stainless steel: nickel bound so tightly
ACD (-)
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Rubber compound
Shoes ACD on dorsa of the feet
Allergen: Mercaptobenzothiazole
Thiurams
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Ethylenediamine
Preservative in Mycolog cream, ointment (-)
Dyes, insecticides,
Rubber accelerators,Synthetic waxes,
In aminophyllin
Sensitive individualgeneralizedeczematous dermatitis
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Physical Examination
Acute/chronic
Depend upon the nature of the exposure
patches/plaque, angular corner, geometric on
lines, sharp margin Localization:
Head& neck: cosmetics, hair dyes, permanentwaves, shampoos
Eyelid: eye cosmetic, nail polishPhoto allergic: produce by a photoreactionbetween SUV & allergen, of the neck, arms
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Physical Examination
The dorsum of the hands: industrial
chemicals (irritants): petroleum, solvents
The dorsum of the feet: shoes (rubber,
leather tanning agents)
Groins and buttocks in infants: Diaper
dermatitis: moisture and feces
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DD
Other eczematous eruptions
Atopic dermatitis
Seborrhoic dermatitis
Stasis eczema
Superficial fungus infections
Bacterial cellulitis
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Diagnosis
Patch test: The test material, in different vehicles
(commonly white petrolatum)
Is applied to the skin under a metal disc, called a
Finn chamber A test battery of 20-24 allergens is used as
standard allergens
The sheet is placed on the upper back, scaled
with adhesive tape
The patch is removed after 48 hours read
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Therapy
Prevention
Avoidance of irritant/allergen change in life
style & occupation
Protective clothing Occupational: protective, barrier cream little
benefit
Substituted Topical steroid
Antihistamine
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Dermatitis Kontak Iritan
DKI pd tangan & ujung-ujung jar i akibat asam
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Dermatitis Kontak Alergi
DKA akibat kalung nikel DKA akibat semen
Seborrheic Dermatitis/ Morbus
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Seborrheic Dermatitis/ Morbus
Unna
Definition: a chronic, superficial, inflammatoryprocess affecting the hairy regions of the body
Etiology: unknown/ Pityrosporum ovale
Dandruff is scaling of the scalp withoutinflammation
Incidence: a common problem, 2-5%adult 18-40 years, baby (cradle cap),
children 6-10 years, woman> man
S b h i D i i
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Seborrheic Dermatitis Predilection hairy
region: scalp, eyebrow
eyelid
Nasolabial creases,
ears, chest
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History
The occurrence of Seborrheic
Dermatitis parallels the increased
sebaceous gland activity occurring in
infant, after puberty, pruritus
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Physical examination
Predilection for the hairy regions where thereare numerous sebaceous gland: scalp,eyebrows, eyelids, nasolabial creases, ears,chest, intertriginous area: axilla, groin, buttocks,
infra mammary folds Bilateral and symmetrically
Most mild form, dandruff, fine whittis scalingwithout erythema.
Patch/plaque: indistinct margin, erythema,yellowish, greasy scaling, uncommon hair loss
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Physical examination S.D
Mild form: dandruff fine whitish scaling
without erythema / Pityriasis sica
Mild Moderate: erythema, yellowish
greasy scaling
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DD
1. A.D (infantile eczema)if infant Loc: diaper area & axilla
diagnosis S.D
If lesion: forearms, shins AD
2. Psoriasis: scalp, groin, other area
papilosquamous patches &
plaque
3. T. capitis: hair loss, urban blackBiopsy : non diagnostic
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Therapy S.D
Anti seborrheic shampoos (sulfur, salicylic
acid, selenium sulfide, zinc pyrithione)
Shampoos must be rubbed in to the
scalp 5-10 minutes
Inflam. Seborrrheic:
topical steroid lot/gel in hairy area;
hydrocortisone cream non hairy skin
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Course & Complication
Infancy : to remit after 6-8 months
Adult : chronic, unpredictable
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STASIS DERMATITIS
Defination:
An eczematous eruption of thelower leg secondary to peripheralvenous disease
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STASIS DERMATITIS
Venous incompetence hydrostaticpressure, capillary damage extravasation ofred blood cell & serum inflammatoryeczematous process
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Incidence
Adults (middle age old age)
History: Chronic
pruritic eruption
precede by edema & swelling
Patients with Stasis dermatitis have oftenhad thrombophlebitis
Physical examination
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Physical examination
Varicose vein are prominent1. Edema
2. Brown pigmentation3. Petechiae
4. Sub acute and chronic dermatitis
5. Thickened skin, scaling and /or weeping6. Any portion of the leg prominent site is
above the medial malleolus
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DD
1. Contact Dermatitis
2. Peripheral Arterial Disease
3. Superficial Fungal Infection
4. Bacterial cellulitis
Examination of peripheral pulses, history of
topical agent, KOH, gram steins, bacterialculture should be done
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Biopsy
Sub acute or chronic dermatitis with
hemosiderin, fibrosis, and dilated capillariesin the dermis
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Therapy
- Prevention of venous stasis and edema use of supportive hose
- Standing should be restricted
- Patients who are obese weight reduction- If this fails bed rest with elevation of legs- Topical steroid
- Wet compresses if there is oozing orcrusting
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Course and Complications
Dusky erythema
Ulceration total bed rest with legelevation with antiseptic cleansingSystemic antibiotics not helpfulApplication of skin grafts
Allergy to topical preparation 60% ( topical
antibiotics)
LICHEN SIMPLEX
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CHRONICUS/Neurodermatitis
-Definition:
A chronic eczematous eruption o/ t skin, that isresult of scratching
Pruritus scratching lichenification & itching
LSC
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SC
Pruritus scratching and precipitated byfrustration, depression and stresslichenification further itching, resultingitch-scratch-itch cycle
History
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History
- Patient may have history of emotional or
psychiatric problem
Ph i l E i ti
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Physical Examinations
Patients: anxious
Lichenified plaque, scratching (+)
Liken Simplek Kronikus/
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Liken Simplek Kronikus/
Neurodermatitis
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DD
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DD
1. Chronic dermatitis2. Psychodermatoses (factitious
dermatitis, delusion of parasitosis
Factitious dermatitis: self inflicted injury o/ t
skin
bizarre eruption (often ulcerated), linearand geometric outlines
Delusion of parasitosis: in disturbed/
anxious eccentric individual
Begins intractable pruritus crawling sensation, thatthey are harboring parasites & bring specimens
Active lesions: excoriated, crusted papule secondary to picking
DD
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DD
3. Neurotic excoriations
Linear :dug out lesions:
Upper mid back (Where scratching
fingers cannot reach.
Neurotic woman
Therapy
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Therapy
Difficult
Tranquilizer and anti depressants
Topical steroid and intralesional steroid
Tabel ECZEMATOUS ERUPTIONSIncidence* History Physical Differential
Di i
Lab.
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Diagnosis
Nonspeciffic
eczematous
dermatitis
11.4 Pruritus Acute-vesicles, weeping, crusted
patches
Subacute-juicy papules
Chronic-lichenified, scaling plaques
Contact dermatitis
Atopic dermatitis
Seborrheic dermatitis
Fungal infection
PsoriasisDrug rash
-
Contact
dermatitis
2.8 Irritant-contact
precedes rash by
hours to days
Allergic-contact
precedes rash by 1-4
days
Vesicles, juicy papules, lichenified
plaques
Sharp margins
Geometric or linear configuration
Conforms to area of contact
Eczematous dermatitis
Fungal infection
Cellulites
Patch test
Atopic
dermatitis2.6 Allergic rhinitis
AsthmaVesicles, juicy papules-infants
Lichenified plaques-adults and
older children
Head, neck, antecubital and
popliteal fossa
Contact dermatitis
Scabies
IgE
Seborrheic
dermatitis
3.7 Dandruff Scaling papules and patches
Scalp, eyebrows, nasal, sternum
Atopic dermatitis
Psoriasis
Fungal infection
Histiocytosis XLupus erythematosus
-
Stasis
dermatitis
0.4 Varicose veins
Leg swelling
Thrombophlebitis
Juicy papules
Lichenified plaques
Brown pigmentation
Lower legs
Cellulitis
Contact dermatitis
Arterial disease
Fungal infection
-
Lichen
simplex
chronicus
0.8 Rash subsequent to
pruritus
Lichenified plaque
Within reach of fingers
Psoriasis -
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