Transcript Black spot - Universitas Hasanuddin

BLACK SPOT
GROUP B2
SCENARIO
A 35 years old woman came to the hospital
with complaint of black spots on both of her
cheeks. She has been having the problems
since 4 months ago. No family history of
similar diseases has ever recorded previously.
Lab assessments reveal normal findings.
KEYWORDS
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35 years old woman
black spots on both of her cheeks
since 4 months ago
No family history
Lab assessments reveal normal findings
QUESTIONS
1. What is the anatomy of the skin?
2. What is the physiology of the skin?
3. What is the pathomechanism of black spots
on the skin?
4. What is the differential diagnosis related to
the case?
ANSWERS
What is the anatomy of the skin?
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Epidermis
– Stratum corneum
– Stratum Lucidum
– Stratum granulosum
– Stratum spinosum
– Stratum basale
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Dermis
– Pars papilare
– Pars retikulare
Hypodermis (subcutis)
– elastin and loose connective tissue
– panikulus adipose
– nerve endings, blood vessel, and lymph
– fibroblasts, macrophages and adipocytes
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Skin gland
– Gland. Sudorifera
• Ekrin gland all over the skin (palm, soles, aksila)
• Apokrin gland aksila, pubis, labia mayora, ear
canal
– Gland. Sebacea
• Except palm and soles. Besides the hair follicle
Hair
– Lanugo baby
– Terminal hair adult
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Ungues
– Thickening of terminal part stratum
corneum.
• Eponikium : skin that cover the
nail at the proximal
• Hiponikium : skin that covered
by the nail
What is the physiology of the skin?
FUNCTIONS
DESCRIPTION
ABSORPTION
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Protects against physical or mechanical damage
Impermeability of Stratum Corneum
Sweat and sebum excretion  ph 5-6.5
Heat sensation: Ruffini body
Cold sensation: Krause body
Touch: tactile Meissner, Merkel Ranvier
Pressure: Paccini body
O2, CO2 & water (steam) transepithelial junction
EXCRETION
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Glands metabolic wastes; NaCl, Urea, Uric Acid, Ammonia
THERMOREGULATION
PIGMENTATION
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Sweat production
Muscle contraction
Melanocyte  produce colour to the skin
KERATINIZATION
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Basal cells – Spinosum – Granulosum – corneum
VITAMIN D PRODUCTION
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7 dehydroxyl cholesterol – sun light  vitamin D production
PROTECTION
PERCEPTION
What is the pathomechanism of black
spots on the skin?
Melanocyte
Chromatophores/
melanophores
Melanin
Brown to black pigment
Exposure to sun rays
photooxidized
Producing more melanin
accumulated
epidermis
As protection for the underlying skin from
sun’s radiation
What is the differential diagnosis
related to the case?
35 YEARS OLD
WOMAN
Yes
BLACK SPOTS ON
BOTH CHEEKS
Yes
NO FAMILY
HISTORY
Yes
MELASMA
Yes
LENTIGO
Yes
Yes
Yes
Yes
POST-INFLAMMATORY
HYPERPIGMENTATION
Yes
Yes
Yes
Yes
MELANOMA
Yes
Females :
males
Depends on
subtypes and
assymetrical
No
(usually with
family history)
EPIDEMIOLOGY
MELASMA - Race: darker skin types > than in
lighter skin types
- Sex: women (90%) > men
- Age: most commonly occurs in
women in reproductive years.
LENTIGO
- Race: fair-skinned whites > darkskinned individuals
- Sex: Women > men
- Age: children – since birth
Adults – acquired
ETIOLOGY
PATHOMECHANISM
- UV light
- Hormone
- Drug
- Genetic
- Race
- cosmetic
Spectrum UV destroys
sulfidril in the epidermis
causes uncontrooled
tyrosinase enzyme which
later lead to melanogenesis
- UV light
Spectrum UV increase
number of melanocyte at
the dermo-epidermal
junction without localized
proliferation
CLINICAL MANIFESTATION
SUPPORTING
EXAMINATION
HISTOPATHOLOGICAL
FINDINGS
MELASMA
Predilection: cheeks and
nose (malar), chin
(mandibular), forehead,
supercilia and upper lip
(centrofacial)
Colour: Light brown or dark
brown
Border: Regular with
irregular edge
- Anamnesis
- Physical examination
- Wood lamp  Epidermal
pigment is enhanced
during examination with a
Wood light, whereas,
dermal pigment is not.
Epidermal melanin is found
in keratinocytes in the basal
and suprabasal area. In
most cases, the number of
melanocytes is not
increased, yet the
melanocytes that are
present are larger, more
dendritic, and more active.
LENTIGO
Predilection: Mucosal
surface of the skin; buccal
mucosa, gums, palatum
durum, lips, nose, mouth,
extremeties
Colour: Brown to black
Shape: Oval shape, irregular
Size: 1-5 mm
- Anamnesis
- Physical examination
-Wood lamp
Increase number of
hyperpigmentated macula
consists of large amount of
melanocyte at the stratum
basale and macrophages
with pigments at the upper
dermis.
Epidermis is covered by
melanin granule.
MELASMA
TREATMENT AND PREVENTION
Treatment
Depigmenting agents – inhibit key enzymes
involved in melanin synthesis. Hydroquinone
USP 4% (Claripel cream with sunscreens)
Retinoids regulate cell growth and
proliferation. Tretinoin (Avita, Retin-A)
Antibiotic agents inhibit DNA synthesis and
mitochondrial enzymes to interrupt
hyperactive melanocytes. Azelaic acid (Azelex)
COMPLICATION
Resistant cases or
recurrences occur often
and are certain if strict
avoidance of sunlight is not
rigidly heeded. It may
return with additional
pregnancies or use of
these medications.
PROGNOSIS
Melasma often fades
over several months
after stopping birth
control pills or HRT,
or after delivering a
child.
In patients in whom
lentigines are associated
with systemic
abnormalities
or complications, the
prognosis may depend on
the severity of the
associated conditions
Good
Prevention
strict avoidance of sunlight
Stop usage of :contraception oral, color
cosmetic and drug can generate melasma
LENTIGO
Treatment
Chemical peels – Removes several layers of sun
damaged skin cells, leaving fresh skin which
has a more even surface and colour
Cryosurgery
Laser; YAG laser
Prevention
The application of sunscreen
Limiting exposure to sun tanning and the use
of artificial sources of UV light
THANK YOU
QUESTIONS?