18 Acne Vulgaris & Melasma
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Transcript of 18 Acne Vulgaris & Melasma
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Acne vulgarisa chronic
inflammatory disease of
the pilo-sebaceous follicles
characterized by:comedones (opencomedo or blackhead,closed comedone orwhitehead),papules, pustules,nodules, and often scars
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Pathogenesis
Acne is follicular disease with comedo formation
Comedones reveal:
thinned epithelium,dilated follicularcanal filled withlamelar lipid-
impregnatedkeratinous material.
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Four key element of pathogenesis :
1. Follicular epidermal hyperproliferation
2. Excess sebum production3. Inflamation
4. The presence and activity of
Propionibacterium acnes
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primarily affect:face, neck, uppertrunk and upper
arms
begins atpuberty
disease of theadolescent(85% of allteenagers)
Neonatal acnedevelops few days
after birth
Infantile acne :cases that
persist after thefirst 4 weeks of
life
the first sign ofincreased sex
hormone
production
ACNE
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Predisposing factors
- comedogenic greasy or occlusive products
acne cosmetica
- mechanical or frictional forces
- overexuberant washing
- chin straps, violins, hats,
surgical tape
- acne venenata
- drug-induced acne
- endocrinologic disorder
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- woman and children
- irregular menses and hirsutism- acne resistant to conventional
therapy
- relapse quickly after a course
of isotretinoin- sudden onset of severe acne
Hyperandrogenic state
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- serum dehydro
epiandrosterone
sulfate (DHEAS)
-testosterone
Screening test for virilizing tumor(adrenal tumors, congenital adrenalhyperplasia, ovarian tumor)
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Polycystic ovarian syndrome (PCOS)
- serum testosteron
- LH/ FSH ratio (>2-3)
- ovulation < 9 periods per year
or period >40 days apart
- sign of hyperandrogenism
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Gradation of acne
Comedonal acne
Papulopustular acne
Conglobate acne
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ACNE CLASIFICATION
KOMEDO PAPUL/PUSTUL NODUL
MILD < 20 50 >5
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Acne
neonatorum
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Differential diagnosis
1.1. Acneiform eruption- Characterized by papules and pustules- No comedone- Associated to certain drugs glucocorticoid,
isoniazid, high dose of vit B complex,phenobarbital, tetracycline, iodides,bromides
- Sudden onset
- Different distribution to acne vulgaris(Appear on wide distribution)
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2. 2.Rosacea- Chronic eruption of the
central face
- Burning or stingingsensation
- Characterized by :
persistenterytheme, flushing,telangiectasis,papule,pustule, cyste,progressive hyperplasiaof sebaceous glands
- No comedones
- Thickened skin of nose(rhynophyma)
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3. Perioral dermatitis
- Confined inflammation of perioral &perinasal regions
- Predominant in child-bearing woman
- No exact etiology (sensitivity of sun
exposure, acne, rosacea, infection ofcandida or demodex folliculorum,misuse of potent topical steroid )
-Clinnical findings : persistenterytheme, scale with small papule andpustules in the perioral and nasolabial
regions
-There is five millimeter clear zone atthe vermilion edge
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TRE TMENT
- Avoidance of
specific foods is not
necessary
- Scrubbing of theface worsen acne
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Medical therapy
2.Systemic & topical retinoids
1.Systemic & topical antimicrobials
3.hormonal therapy
4.intralesional corticosteroids
5.physical modalities
- comedo extractor- photodynamic therapy- Laser- Dermabrasi
- Bedah Skalpel
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pitted
scars
keloids
wide-moutheddepressions
Complications
Scarring
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MELASMA
(CHLOASMA FACIEI)
dr. IGA SUMEDHA PINDHA, Sp.KK(K)dr. IGAA ELIS INDIRA, SpKK
dr. NLP.RATIH V KARNA, SPKK
Lab/SMF Ilmu Kesehatan Kulit dan Kelamin
FK UNUD/RS Sanglah Denpasar
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amount of melanin
type of melamin (eumelanin =
brown, pheomelanin = yellow orred)
degree of vascularity
presence of carotene
thickness of the stratum corneum
Visible pigmentation of the skin or hair is acombination of
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Melanin is formed from
tyrosine, via the actionof tyrosinase, in the
melanosomes ofmelanocyte Pigmentation require
the adequate manufacture
of melanin appropriate transport of
melanosomes within themelanocyte
The melanosomes aretransferred from a
melanocyte to a group
of 36 keratinocytescalled the epidermalmelanin unit
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MELASMA
Affect darker-complexioned individuals
(Fitzpatrick skin types IV and V)
Most frequently in young women, men 10%
Melasma is
characterized
by
brownpatchestypically on
the malar
prominences
and foreheadquite sharply
demarcated
Clinical
patterns:
centrofacialmalar
mandibular
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PREDISPOSING
FACTORS
Use of dilantin
Pregnancy
Endocrinologic
disorders
hormonal : ingestionof estrogen (oralcontraceptives or
hormonereplacementtherapy [HRT] at
menopause)
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Epidermalbased :
Dermalbased :
Mixed :
woods light lesion
woods light lesion
epidermal anddermal
Melasma classified as
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Pathology
1. Epidermal type
Increasing of melanin disposition on basal, suprabasaland epidermal layers. Vacuolar degeneration in basalcells.
2. Dermal typePerivascular melanin contained macrophag onsuperfisial dermis and middermis layers
3. Mixed type
Both of histologic findingsElectron mic. : scattered melanosomes in keratinosit.
Dopa staining : increasing of melanocytes count.
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Differential diagnosis
Drug induced hyperpigmentation
Hyperpigmentation post inflamation
Ochronosis exogen Mercury deposition on the skin
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Treatment
Avoid exposure to sunlight
Use sunblock with broad-spectrum UV
Treatment
Gold standard bleaching cream withhydroquinone 2% - 4%
Tretinoin cream increase efficacy
Treatment
Kligmansformula : combination of
hydroquinone, tretinoin and topical steroid Glycolic acid added to hydroquinone to
enhance efficacy
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Complication from use high concentration of
hydroquinone
satellite pigmentation local ochronosis
Other topical therapy
azelaic acid, kojic acid
N-acetyl-4-cysteaminyphenol, licorice extract,arbutil
Surgical procedures
peels laser treatment
pretreatment with hydroquinone result
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