MALLENOUS Flashcards
EXPLAIN ECZEMA , DF ,TYPES , CLASSIFICATION
-Def : severe dermatitis (inflammation of the skin) characterized by itching, oozing & burning sensation. induced by external or internal factors
-Stages of eczema:
1. Acute eczema: characterized by erythema, vesicles, exudate crust.
2. Subacute eczema: there is less erythema, involuting vesicles, papules, and scaling.
3. chronic eczema: there is thickening (lichenification) of the skin, scaling, and fissuring.
-Classification:
1. Exogenous eczema :Contact dermatitis
2- Endogenous eczema: Atopic dermatitis ,Discoid eczema ,Pityriasis alba,seborrehic,stasis.
explain Contact dermatitis (C.D.)
-def inflammatory skin disease induced by exogenous agent (chemical or physical).
-Types:
1-Irritant Contact Dermatitis:
-Cause : Skin exposure to irritant
-C/P :Strong irritant: acute eczema Mild repeated irritant: chronic eczema
-Example : Alcohol
-Diagnosis
1. Localization of the eruption on the site in contact with the causative agent.
2. Improvement of lesion on elimination of the contact recurrence on re-exposure.
3. Patch test: sensitizer on adhesive patch on back positive if dermatitis occur
-Treatement : 1- Removal of the cause. 2. Topical steroids.
3- Oral antihistamines. 4- Systemic steroids in extensive cases.
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2-Irritant Allergic contact dermatitis :
-Cause : Skin exposure to sensitizer(contact allergen)
-C/P : Acute ,subacute or chronic
-Example : Nickel , neomycin
-Diagnosis
1. Localization of the eruption on the site in contact with the causative agent.
2. Improvement of lesion on elimination of the contact recurrence on re-exposure.
3. Patch test: sensitizer on adhesive patch on back positive if dermatitis occur
-Treatement : 1- Removal of the cause. 2. Topical steroids.
3- Oral antihistamines. 4- Systemic steroids in extensive cases.
explain Atopic Dermatitis , def ,etiology,Clinical picture,Regional variants,Diagnostic criteria,Complications,Treatment,
-def: chronic relapsing pruritic inflammatory skin disease
frequently associated with other atopic diseases in the patient or other family members.
-N.B: atopic diseases e.g. hay fever, asthma , atopic dermatitis , allergic rhinitis(atopic triad)
-etiology: Atopy is a genetically determined state of hypersensitivity to environmental triggers
-Clinical picture:The cardinal symptom is itching(especially at night) ,dryness (increased by wool, pollen, climate changes)
-The distribution and characters of lesions differ depending on the age:
-infantile atopic dermatitis:
Age: 2 months - 2 years.
Lesions: The primary lesion is erythematous, oedematous, papulovesicles, oozing ,crustation
Sites: face , extensors
Course: remissions ,relapse ,50% of cases clear by the age of 2 years or to child hood phase
-Childhood atopic dermatitis:
Age: 2 - 10 years.
Clinical presentation:
* Sites: pattern changes to involvement of the antecubital and popliteal fossae, neck, wrists,
ankles, around the mouth and around the eyes. Sometimes, only one site is involved. The
lesion may affect the extensors & face.
* less exudative , tend to lichenify especially in flexures (flexural eczema, Besnier’s prurigo).
* Prurigo of Hebra: affects the extensor aspects of the limbs with excoriated shotty papules
and lichenified skin, beside superficial lymphadenopathy (axillary and inguinal).
* Xerosis typically becomes pronounced and widespread.
* Pityriasis alba is common in this stage.
-Course: may clear by the age 12 years in about 50% of cases or changes into the adult phase. This means that about 60%-75% of all cases of infantile and childhood AD go into remission
by 12 years of age.
-Adulthood atopic dermatitis:
- lichenified plaques in flexor areas.
- Other changes seen in adult phase are: affect scrotum,vulva , nipple, pomphlyx
-Erythroderma
-Prognosis: It is difficult to assess the prognosis in individual case. It is worse if both
parents are affected. About 30-50% of infantile eczema subsequently develops asthma About
60% of infants and young children with AD go into remission by 12 years of age, but in
others disease activity persists into adolescence and adulthood
—–Regional variants of AD:
1. Eczema of the lips.
2. Perioral eczema (lip-licker’s eczema).
3. Eyelid eczema: characterized by lichenification of the periorbital skin.
4. Head and neck dermatitis: after puberty.
5. Juvenile plantar dermatosis: dry, glazed, fissured dermatitis of the soles
6. Atopic hand eczema
7. Nummular (discoid eczema) on the extremities
8. Chronic nipple eczema
-Diagnostic criteria:
1. Intense pruritus is the cardinal symptom.
2- Chronic with remission and relapse.
3. Typical morphology and distribution
Flexural lichenification in adults and children.
-Facial and extensor involvement in infants.
4. Personal or family history of atopic disease (asthma, hay fever, atopic dermatitis).
5. Other important criteria: generalized xerosis (dry skin) and onset before the age of 2 years.
-Complications:
1. Bacterial infection: Staph
2. Viral infection: warts , molluscum,
3.Eczema herpeticum (herpes simplex on top of atopic eczema).
—Treatment:
a) General measures:
- Avoid exposure to irritants, wool, synthetic cloths or other rough fabrics, dust mites.
- Careful drug taking particularly with penicillin, antitetantic serum , drugs induce
anaphylactic reaction.
b) Regular Emollient therapy (ointment or water in oil creams):the basic line in all cases
c) Topical Anti-inflammatory Therapy
- Topical corticosteroids ointment: the main line
- Topical calcineurin inhibitors: Tacrolimus 0.03% , 0.1% oint , pimecrolimus 1% cream.
d) Systemic therapy:
* Systemic anti-inflammatory :
- Oral steroids: only for short period in severe uncontrollable flares.
- Other immunosuppressive drugs as cyclosporine and azathioprine
* Phototherapy (PUVA, or NUVB)
* Oral sedating antihistamines.
* Antibiotics: in extensive lesions or bacterial superinfection
explain Urticaria , def , pathogenesis , causes , clinical pic ,Course, treatment
—Def : vascular reaction pattern characterized by formation of wheals.
—Pathogensis :
*liberation of histamine , other mediators of inflammation.
* from the mast cells through allergic or non-allergic reactions,
* which produces vasodilatation and increased vascular permeability,
—Causes:
1 - Food (fish, egg, milk), and food additives
2. Drug:- non-immunologic (eg. direct release of histamine from mast cells by opiates and radiocontrast media):
-immunologic mechanisms (e.g., antibiotics, NSAIDs,ACEIs)
3. Infections: e.g
Viral: hepatitis (HBV or HCV).
Bacterial: H. pylori, sinusitis, cystitis. prostatitis, cholecystitis. dental abscess.
Fungal: dermatophytosis, candidiasis (may be asymptomatic vaginal candidiasis).
Protozoal: trichomonas
Parasitic: ascaris.
4. Inhalants: dust, pollen, perfumes, feather, tobacco
5- Collagen diseases eg. SLE, dematomyositis and rheumatoid arthritis.
6- Neoplasms: lymphoma, leukemia, and internal malignancy.
7- General diseases: thyrotoxicosis, uremia, liver diseases, polycythemia vera.
8. Physical factors: sun, water, cold , heat, pressure.
9 Psychogenic causes: stress, anxiety.
10- Idiopathic: 50% of acute urticaria and 90% of chronic urticaria are either idiopathic or autoimmune urticaria
–Clinical picture:
** wheals: Pruritic ,Evanescent (less than 24 hours) , Edematous ,Erythematous
-may be localized or generalized,
-The size is variable from pinpoint to many inches across.
-The shape of the lesion may be bizarre, geographic & or annular.
** Angioedema : diffuse swelling in certain areas of thin skin &loose SC tissue such as eye
lids,lips,genitalia) may occur with wheals.
**General symptoms : GIT (nausea,vomiting) & respiratory tract (horseness, wheezing and dyspnea).
–Course:
> acute urticaria : disappear within a few hours or days
> In chronic urticaria : persists for more than 6 weeks.
> Spontaneous improvement may occur in absence of diagnosis or treatment
-Treatment: Treatment of cause if possible
1. Antihistamines
2.Systemic steroids in severe cases resistant to other treatments).
3. Local soothing agent
