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    Dermatitis & Urticaria: Department of Dermato Venereology Faculty of Medicine Gadjah Mada University

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    This document discusses various types of dermatitis and urticaria. It begins by defining dermatitis as inflammation of the skin that is not caused by infections or malignancy, and is characterized by itching, burning or stinging skin lesions. Dermatitis is divided into exogenous and endogenous forms, as well as acute and chronic types. Allergic contact dermatitis is the most common in developed countries and is caused by repeated skin exposure to a sensitizing substance. Urticaria is a transient skin swelling and itching caused by capillary leakage. It is classified based on physical triggers, underlying causes, and the presence of angioedema. The pathogenesis involves immunological mechanisms such as autoimmune reactions and

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    Dermatitis & Urticaria: Department of Dermato Venereology Faculty of Medicine Gadjah Mada University

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    adysti
    33 views34 pages
    This document discusses various types of dermatitis and urticaria. It begins by defining dermatitis as inflammation of the skin that is not caused by infections or malignancy, and is characterized by itching, burning or stinging skin lesions. Dermatitis is divided into exogenous and endogenous forms, as well as acute and chronic types. Allergic contact dermatitis is the most common in developed countries and is caused by repeated skin exposure to a sensitizing substance. Urticaria is a transient skin swelling and itching caused by capillary leakage. It is classified based on physical triggers, underlying causes, and the presence of angioedema. The pathogenesis involves immunological mechanisms such as autoimmune reactions and

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    DERMATITIS

    Original Title

    Dermatitis Dan Urtikaria Final

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    This document discusses various types of dermatitis and urticaria. It begins by defining dermatitis as inflammation of the skin that is not caused by infections or malignancy, and is characterized by itching, burning or stinging skin lesions. Dermatitis is divided into exogenous and endogenous forms, as well as acute and chronic types. Allergic contact dermatitis is the most common in developed countries and is caused by repeated skin exposure to a sensitizing substance. Urticaria is a transient skin swelling and itching caused by capillary leakage. It is classified based on physical triggers, underlying causes, and the presence of angioedema. The pathogenesis involves immunological mechanisms such as autoimmune reactions and

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    33 views34 pages

    Dermatitis & Urticaria: Department of Dermato Venereology Faculty of Medicine Gadjah Mada University

    Uploaded by

    adysti
    This document discusses various types of dermatitis and urticaria. It begins by defining dermatitis as inflammation of the skin that is not caused by infections or malignancy, and is characterized by itching, burning or stinging skin lesions. Dermatitis is divided into exogenous and endogenous forms, as well as acute and chronic types. Allergic contact dermatitis is the most common in developed countries and is caused by repeated skin exposure to a sensitizing substance. Urticaria is a transient skin swelling and itching caused by capillary leakage. It is classified based on physical triggers, underlying causes, and the presence of angioedema. The pathogenesis involves immunological mechanisms such as autoimmune reactions and

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    Dermatitis & Urticaria

    dr. Fajar Waskito, Sp.KK(K), M.Kes

    Department of Dermato Venereology


    Faculty of Medicine
    Gadjah Mada University
    DERMATITIS
    Inflammation of the skin
    Not because of infections or malignancy
    Itching, burning or stinging
    Skin lesions are polymorphic

    Dermatitis are divided into


    Exogenous
    Endogenous or

    Acute
    Chronic
    Prevalence :
    Exogenous dermatitis are the most prevalence
    Irritant contact dermatitis is the most prevalence in
    most part of Asia, Africa and south America
    Allergic contact dermatitis is the most prevalence in
    US and most European countries

    Pathology :
    The histologic changes are often similar among
    dermatitis
    Biopsy are usually done to rule out other conditions
    Histopathology can differentiate between acute and
    chronic dermatitis, eventhough most are
    overlapping.
    Microscopic findings :

    Acute dermatitis Chronic dermatitis


    Epidermis Epidermis
    Intercellular edema (Spongiosis) Spongiosis quietly absent
    Intraepidermal vesicles Intraepidermal vesicles are not
    Mononuclear infiltrates dominant
    Mononuclear infiltrates
    Acanthosis more dominant
    Parakeratosis are appear
    Dermis Dermis
    Vasodilatations Vasodilatations & perivascular
    Perivascular infiltrates infiltrates are decrease
    Thickening in sub-basal collagen
    Allergic contact dermatitis
    Dermatitis
    Repeated skin contact with substance
    Elicit sensitisation via cell mediated immunity

    Some factors that influence the occurrence :


    Human : genetics (HLA), immune responses are in
    normal function
    Substance : antigenisity (potency), the degree of exposure
    Potency : Mol. Weight 5000 Da, antigenicity appears when bind to autolog skin
    protein.
    More frequent and longer contact of substance to the skin the probability of
    the appearance of allergic reactions are more bigger
    Skin : the degree of penetration
    Sensitisation is easier on the damage or inflammed skin or in occluded
    skin
    Mechanisms of sensitization
    Combining the substance (hapten) with skin
    protein to form antigen
    Processing antigen by Langerhans cell (APC)
    Presenting antigen to lymphocytes in Lymph
    nodes
    Lymphocytes are altered and proliferate
    Altered Lymphocytes are travelled throughout the
    body to produce sensitivity of entire skin

    It requires a minimum of 8 – 10 days for clinical allergy to be


    demonstrated after the sensitization process has started.
    Pathology :
    The histologic are not diagnostic
    Biopsies are just to rule out other conditions
    Acute stages :
    3 hours after application of allergen
    Vasodilatation and perivascular infiltrates in the dermis
    At 6 hours, changes in the dermis more pronounced.
    Spongiosis of the lowermost epidermis and exocytosis.
    12 – 24 hours, the changes in the epidermis more marked
    (vesicles), acanthosis. Perivascular infiltrate in the dermis
    more pronounced
    After 2 days, spongiosis disappears; intraepidermal vesicles
    and acanthosis are the main features with parakeratosis

    Chronic stages :Acanthosis, hyperkeratosis, variable


    inflammatory cell infiltrates.
    Clinical manifestations :
    Polymorphic, not well demarcated, lateralisation
    Evaluate the locations & pattern of the lesions.

    Confirmation test : Patch test or repetitive open


    epicutaneous test
    Example of substance that cause ACD in dentists :
    Some substances have been used by dentists, may be have
    same effects to dental assistants, dental laboratory
    technicians and patients

    The substances are : Glutaraldehyde, latex gloves, procaine,


    Lidocaine, Eugenol, dental composite resin products
    (Bisphenol A & Acrylate), the catalysts from the two
    impression materials Impregum and Scutum. Mercury and
    Metals in modern alloy (rare)
    Treatment :
    Non pharmacotherapy : Eliminations
    Pharmacotherapy :
    Systemic : antihistamin ?, short course steroid
    Topical : Steroid
    Irritant contact dermatitis (ICD)
    ICD are divided into acute & chronic cumulative irritant
    The mechanisms are non immunologic
    Acute irritant can be sufferred on every individu (eg. strong acid
    or strong alchali)
    Chronic cumulative can elicit reactions if the substances are in
    repeated contact and on skin damage (eg. The weak acid or
    alchali, detergent)

    Clinical manifestations :
    The lesions usually are well demarcated on the skin contact.

    Treatment are the same with ACD


    Atopic dermatitis :
    Genetic background
    Disfunction of immune system (Tend to form IgE in
    contact with common antigens)
    Tend to suffer Asthma bronchiale, Hay fever,
    urticaria both in theirselves or their parents, and dry
    skin.
    Response to Delayed type hypersensitivity are
    decrease
    Defects on neutrophiles chemotactics

    Trigger factors : Climates, temperatures, humidity and


    the conditions inwitch allergens are too much in their
    environments
    Atopic dermatitis in clinical setting are divided
    into :

    Infantil (age 2 – 6 months)


    The lesions are commonly occur on the face,
    diaper area and on extensor surface. The lesions
    tend to wet

    Childhood (age 2 – 12 years)


    The lesions are commonly flexural distributed,
    and the lesions tend to dry

    Adulthood
    Lichenifications on the fold area, palmar and
    areola mammae
    Diagnostic criterias of atopic dermatitis (Hanifin &
    Rajka)
    Minimally have been found 3 major criterias and 3
    minor criterias
    Major criterias :
    Pruritus
    Characteristic morphology and distribution of
    the lesions
    Chronic recalcitrans dermatitis
    History of atopic in their parents or theirselves
    Minor criterias :
    Xerosis
    Keratosis pilaris
    Hiperlinearis palmaris
    Reactivity to type I hypesensitivity testing
    Serum IgE is increase
    Tend to get bacterial infections (S. aureus, H.
    simplex
    Hand & foot dermatitis
    Dermatitis on areola mammae
    Conjunctivitis
    Dennie Morgan folds
    Keratoconus anterior/Subcapsulair cataract
    Periorbital darkening
    Facial pallor,
    Pirtyriasis alba,
    Anterior neck fold,
    Itching when sweating,
    Woolly toleransion,
    Perifolicular papules,
    Food intolerance,
    Influenced by environment and emotion,
    white dermographisme
    Seborrheic dermatitis : is dermatitis that distributed on
    seborrheic area

    Clinical manifestations :
    White to yellow scales with erythema on well
    demarcated area. Males are more prevalence

    Seborrheic dermatitis is divided clinically into :


    Infant type : appears on the first 2-3 months of their
    lives, and the peak is on 6-8 weeks (may because of
    hormonal effects from their mother)
    Adult type : appears after puberty and the peak is on
    18-40 years. Dandruff is one of the manifestations of
    seborrheic dermatitis.
    Dermatitis intertrigo is dermatitis on the fold areas

    Predisposition factors are :


    Sweating/humidity
    Obesity
    Friction between two surfaces of the skin
    Occlusions

    Clinical manifestations :
    Circumscribed patch erythematous,
    Sometimes this is superinfected with yeast
    (Candida albicans)
    Nummular dermatitis is dermatitis in nummular
    (=coin, discoid) configurations and very itchy

    Predilections are especially on the extensor surface of


    lower extremities

    Predispositions are females on middle age. Trauma is


    one of the initiating factors beside of emosional stress

    Clinical manifestations are almost the same with tinea


    corporis (ringworms), but the borders of the lesions
    tend to vesiculous
    Neurodermatitis = Lichen simplex chronicus

    The chief of clinical manifestations are itching,


    lichenifications without atopic predisposition that
    appears especially on the nape of neck, lower
    extremities, vulva, pubis, scrotum and ankle.

    Lichenifications is as manifestation of repeated


    scrubbing or scratching.

    Emosional stress is known as aggravating factors


    Napkin dermatitis is a general term to discribe
    some dermatoses on the lower abdomen, genitalia,
    buttock and upper thigh of the baby, children,
    incontinentia and paralytic patients

    Causatives :
    As combinations of some factors eg. Wet, friction,
    irritation, napkin and sometime the candida
    infections.
    Dermatitis venenata = cantharides dermatitis =
    Primary irritant contact dermatitis

    Dermatitis as manifestation of contact with strong


    irritant (eg. Cantharidin)

    Stasis dermatitis is dermatitis that appeared on the


    distal site of varicous veins. It will appeared especially
    on the medial part of lower extremities, inwitch the
    vascularitations are not good if compare with
    another regions.
    Management urticaria

    Urticaria (1) :
    • Urtica
    • Transient edema in the upper dermis
    • Transient leakage of plasma

    Angioedema(1) :
    • Edema in the upper/lower dermis and/or
    subcutis
    Four stages in the management of
    urticaria

    • Knowing the tipology of urticaria


    • Knowing the causative factors
    • Knowing the risk factors and some factors that
    influence the uricaria
    • Treatment and counceling stage
    Tipology, causative factors and factors
    that influence the urticaria (2)

    Classifications Type

    Physical urticaria

    Ordinary urticaria Acute and chronic


    episodic
    Vasculitis urticaria

    Angioedema without Def. C1 inh,


    urtica Normal C1 inh
    Contact urticaria
    Frequency of the type ofurticaria (3)

    Type % ase

    Ordinary urticaria 60

    Physical urticaria 35

    Vasculitis Urticaria 5
    Pathogenesis of urticaria (4)
    Idiopathic

    Immunology
    • Autoimmune (autoantibody FcɛRI or IgE)
    • Ig E dependent (Type I hipersensitivitas)
    • Immune complex (vasculitis urticaria)
    • Complement dependent (def. C1-esterase inhibitor)

    Non-immunology
    • The substances that have direct effect on Mast cel (opiat,
    codein, radiocontras, venoms, physical stimuli, estrogen, ACTH,
    Thiamin)
    • Aspirin, NSAID, pseudoalergen in the food (Salisilat, azo dyes,
    food preservatives)
    • ACE inhibitor
    Diagnosis of urticaria
    are based on clinically
    Laboratorium :
    • Urticaria vaskulitis
    • Deficiency of C1-esterase inhibitor
    Simple clinical diagnosis of urtikaria
    Onset Duration Urticaria
    10 mnt. after < 1 hour Physical urticaria
    stimulation
    > 1 hour after > 1 day Delayed pressure
    continously urticaria
    pressure
    10-30 mnt > 2 hours Contact urticaria k
    exposed to
    contactant
    2 -24 Ordinary urticaria
    hours
    1–7 Vasculitis
    days urticaria
    Laboratory examinations
    class Ax FBC SPT RAST WCD
    Physical
    Ord-acute
    Ord-chron
    Vasculitis
    Angioedem
    Contact

    Klas ESR TA/TFT C4 ASST Biopsi Provok

    Physical
    Ord-acute
    Ord-chronic
    Vasculitis
    Angioedema
    Contact
    Non farmacologic treatments

     Avoid the aggravating/precipatating factors (2)

     Inform how to prevent (2)


     Give symptomatic medicamentous (2)
     Consider for using NSAID (5)
     Consider for using codein, opiat (6)
     Consider for using ACE inhibitor (7)
    Farmacologic treaments
    First line
    • Antihistamin H1
    • Have sedative effects : Chlorpheniramin maleat,
    Hidroksisin, diphenhidramin
    • Have non sedative effects :Cetirizine, Loratadine,
    Desloratadine, Fexofenadine
    • Doxepin 10 mg
    • Antihistamin H2
    • Nifedipine
    • Ketotifen fumarat
    • Sodium chromoglycate
    Second line
    • cortikosteroid
    • Stanozolol
    • Sulfasalazine
    • Methotrexate
    Urticarial Vaskulitis
    • Colchicine
    • Dapsone + corticosteroid
    • Indomethacine
    • Hidroxychloroquine

    All severe angioedem except of def. C1 ersterase inhibitor


    can be given Adrenalin im/sc : 0,5 mL (pengenceran 1 :
    1000) or inhalation
    Third line
    • Auto antibody hitamine-releasing :
    • Plasmapharesis
    • Cyclosporin A
    • Immunoglobulin iv

    Deficiency of C1-inh
    Concentrate of C1 or fresh frozen plasma

    Profilaksis
    Steroid anabolic or plasmin inhibitor tranexamine acid
    Development of treatment methode

    • Imunomodulator that inhibit cytokine production


    • Be careful on using of NSAID
    • Downregulate production of autoimun antibodi
    • Blocker of FcεRI mast cell
    • Anti IgE substances

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