Acne

ACNE VULGARIS

Objectives:
Explain etiology and Pathogenesis of Acne vulgaris. Label different types of Acne. List available modalities to treat acne. Compare acne to rosacea.

Acne vulgaris

Definition: a chronic inflammatory disease of pilosebaceous unit. It is a polymorphic disorder(comedons, papules , pustules, nodules, pseudocysts, and sometimes scarring) The sites of predilection face, upper trunk and upper arms. It usually affect adolescent. is of multifactorial aetiology.

The etiology and Pathogenesis of Acne vulgaris:

*These changes occur on a hormonal background of androgen. I – Increase sebum production. II- Obstruction of the pilosebaceous duct (comedogenesis). III- colonization of the duct with (P.acnes). IV- The production of inflammation.

Other factors affecting the pathogenesis:

A. Endogenous factors Genetics. Stress and anxiety.++ Menstruation.+
B- Exogenous factors: UV. radiation. Hot humid environment and sweating.+Diet.*’’Occupation.

Clinical Presentation of Acne:

Unsightliness. Psychological impact.
The types of lesions in Acne: A – Non inflammatory lesions: (comedones) which consist of: White heads (closed comedones). Black heads (open comedones). B – Inflammatory lesions include: The superficial lesions are usually papules and pustules. The deep lesions are deep pustules, nodules and pseudocysts & Sinuses

ذ

Acne varients

Pomade acne Cosmetic Acne. Acne venenata. Drug induced acne. Endocrine acne. Acne astevalis

Neonatal acne

Persistent acne


Complications of acne:1- Scarring.2-Psychological impact. Types of acne scarring:Atrophic scars.Ice pick scars.Hypertrophic scars. Keloid scars. .

Differential diagnosis of acne:

1-Rosocea. 2-Perioral dermatitis. 3-Pitrosporum folliculitis. 4-Folliculitis barbae and Psudofolliculitis barbae. 5-Acneform drug eraption 6-Acneform secondary syphilis.

Treatment of Acne:

A-General measures. B-Topical treatment. C-Systemic therapy. The choice of therapy. Mild acne:topical therapy. Moderate acne:topical and oral therapies. Severe acne: isotretinoin unless it is contraindicated.

A - General measures: Gentle cleansing. Avoidness of comedogenic applications. Reassurance . B- Topical treatments: 1- Those directed towards microorganisms. 2- Those directed towards comedogenesis.

1- Topical treatments directed towards microorganisms: 

Topical antibiotics: erythromycin (1.5-2% gel or cream). clindamycin (1% lotion) Benzyl peroxide.

2-Topical treatment directed towards comedogenesis:

Retinoids: 1- Anti-seborrheic effect. 2- Anti-comedonal effect. 3- Anti-inflammatory effect. 4- Inhibiting the growth of P. acne . Tretinoin may be used as solution, cream or gel. It is available in 0.025% , 0.05% and 0.1% concentration (2). Tazarotene (0.1% gel) applied once daily. Adapalene: Adapalene (0.1% gel). Azelaic acid: cream with 20%

C) Systemic Treatment of acne:

1-Those directed against microorganisms (antibiotics). 2-Those directed against comedogenesis and seborrhea (retinoids). 3-Those acting on hormonal bases (antiandrogens).

Systemic antibiotic:* Moderate or severe inflammatory acne.*Acne resistant to topical treatment.*Acne that covers large area of the body. Tetracycline: Tetracycline dose for an adult is 250 mg four times daily. Doxycycline: It is usually given in a dose of 100 mg once or twice daily . Minocyclin: The usual dose is 50-100 mg once or twice daily. Erythromycin and Azithromysin: Clindamycin: In a dose of 75-150 mg.

2- Systemic Retinoids:

(Isotretinoin) is the single most effective treatment. Indications: 1- Severe acne. 2- Moderate unresponsive acne. 3- Acne with scarring. 4- Acne with severe depression or dysmorphophobia. 5- High sebum excretion rate. 6- Some unusual variants, such as acne fulminans, gram-negative folliculitis .


3- Hormonal therapy:
Acne is not responding to conventional therapy. If there are signs of hyperandrogenism. A- Androgen production inhibitors: glucocorticoids and oral contraceptives. B-Androgen receptor blockers: cyproterone acetate, spironolactone and flutamide.

acne vulgaris

MILD

Rosacea

Rosacea (Latin: “like roses”) is a chronic inflammatoy disorder of the facial pilosebaceous units, with an increased reactivity of capillaries to heat, leading to flushing and telangiectasia... Age of incidence between 30 to 50 years, Sex Females predominantly; Race WHITE peoples.DISTRIBUTION Characteristic is a a symmetrical localization on the face

Skin Symptoms/ facial appearance?; Flushing, “heat” in the face. Stages of Evolution // episodic (flushing) in response to (hot liquids), spicy foods; alcohol ,exposure to sun, heat and emotional stress. *Episodic erythema, “flushing and blushing” Stage I: Persistent erythema with telangiectases Stage II: Persistent erythema, telangiectases, papules, tiny pustules Stage III: Persistent deep erythema, dense telangiectases, papules, pustules, nodules; marked sebaceous hyperplasia edema of the central part of the face "glandular rosacea"causing disfigurement of the nose {Rhinophyma (enlarged nose) }


Eye Lesions/// “Red” eyes ,chronic blepharitis, conjunctivitis, and episcleritis. Rosacea keratitis Differential Diagnosis Acne, (note: in rosacea No comedones) Perioral dermatitis, folliculitis, and SLE Dermatopathology 1-Dilated capillaries.2-Marked sebaceous gland hyperplasia 3-Inflammatory infiltrate with foci of neutrophils within the follicle 4 -epithelioid granuloma without caseation,

Course Prolonged. Recurrences are common. After a few years, the disease tends to disappear spontaneously. Management Reduction of alcoholic and hot beverages. Topical :\Metronidazole gel or cream, 0.75 %, twice daily orTopical antibiotics (e.g., erythromycin gel).

Acne

Rosacea
ONSET
ADOLESCENCE
THIRTIEs TO FIFTIES
2.SEX
MALE>.F
FEMALES.>MALES
3.SITE
FACE,UPPER TUNCK, UPPER ARMS
FACE
4.FLUSHING&TELEANGECTASIa
_
+
5.Comedons
+
_
6.Eye complecations
_-----
+
7.Rhinophyma
_
+
8.Responce to treatment
slow
rapid

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