hyper & hypo- pigmentation DISORDERS

Slides:



Advertisements
Similar presentations
An Illustration for the students who aspire for medical studies. a power. presentation from T. MADHAVAN, M. Sc., M.L.I.S., M. Ed., M. Phil., P.G.D.C.A.,
Advertisements

Pityriasis rosea. pityriasis rosea is an acute,self- limited skin disease.It is characterized by the presence of rosy-coloured,round to oval macular lesions.
Where to Buy How Neutriderm Works Professionals HyperpigmentationHyperpigmentation Pigmentary Disorders Home Customers Voice Buy Now Contact Home >> Pigmentary.
SQUAMOUS CELL CARCINOMA
Melasma.
Pharmacology-4 PHL 425 First Lecture By Abdelkader Ashour, Ph.D. Phone:
Therapeutic approaches to hypopigmentation disorder Dr. Oussama Al Haj-Hussein, Syria.
Pharmacology-4 PHL 425 Third Lecture By Abdelkader Ashour, Ph.D. Phone:
Ozone Loss and Skin Cancer. Problem Susan Solomon found the correlation between the disappearance of ozone and increased concentration of chloroflurocarbons.
Skin Cancer Carlos Garcia MD Dermatology at OUHSC No conflicts of interest to disclose.
Casey Bower. What is Melanoma? Melanoma is the most common cancer in the United States and the most dangerous form of skin cancer, melanoma begins in.
Skin Cancer BY: Taylor Lawrence. Description Skin Cancer- cancer that forms in the tissues of the skin Actinic Keratosis- This cancer is one of the most.
Basal Cell Carcinoma By: Linsey Morris. Description Most common form of skin cancer. Least deadly. The risk is related to the amount of sun exposure to.
Skin Problems – infections, allergies, or damages Ch 4 Integument System Warning: Graphic Pictures.
WARM UP 11/18 1. Name the 4 layers of the epidermis in order. 2. What do melanocytes do? 3. What is found in the stratum spinosum? 4. What does keratin.
Pathologies of the Integumentary System
SKIN CANCER Senior Health-Bauberger. SKIN CANCER Skin cancer is the most common form of cancer in the United States The two most common types of skin.
Pigmentation Disorders Fahad Al Sudairy, M.D.. NB : Hypo : decrease color Hyper : increase color Depigmentation : totally disappearance of the color.
Skin Cancer Colleen M., Anna C., Page B. The black ribbon is the symbol for Melanoma/Skin Cancer Awareness.
Pharmacology-4 PHL 425 First Lecture By Abdelkader Ashour, Ph.D. Phone:
FOH Presents… Skin Cancer
(Slide 1: Title Slide: Nu Skin University)
Alegre. almora. alonzo. amaro. amolenda. anacta. andal. ang. ang. ang. Dermatology Case 2:
Juliane Williams Anatomy and Physiology Block 4. What is Vitiligo? It is a pigmentation disorder in which melanocytes in the skin are destroyed.
SKIN CANCER PREVENTION & IDENTIFICATION. Why is skin cancer important?  the most common type of cancer in the United States  about 40 to 50 % of Americans.
Tanning. Avae Marcello.
Scaly Dermatoses. Dandruff, seborrheic dermatitis, and psoriasis are chronic scaly dermatosis Dandruff inflammatory form and it has a substantial cosmetic.
Disorders of skin color Dr. Kejian Zhu Sir Run Run Shaw Hospital
MELASMA.
Melanoma. Remember: melanoma ≠ myeloma 1. What, in general, is a melanoma? A tumor of melanin-forming cells (melanocytes from the basal layer of the.
Cancer Invasive cellular neoplasm that has the capability of spreading throughout the body or body parts; uncontrolled cell growth.
Pharmacology-4 PHL 425 Second Lecture By Abdelkader Ashour, Ph.D. Phone:
 Skin Cancer In Young Adults Kerry Phifer Maddie Walsh.
 “Mask of Pregnancy” is a tan or dark skin discoloration.  Mostly in women who are taking oral or patch contraceptives or hormone replacement therapy.
Skin Hazards from Sun Exposure Resource: cancer/ss/slideshow-sun-damaged-skin.
Disorders of pigmentation. Hypopigmentation. Hyperpigmentation.
SKIN CANCER PREVENTION May Background Information PART ONE.
Melanoma Raising Awareness. Quick Facts About 68,720 people were diagnosed with melanoma in ,650 died of melanoma Melanoma accounts for 3% of skin.
Disorder of Skin Pigmentation
Melasma. Biology of melanocyte Dendritic cell at basal layer of epidermis Dendritic cell at basal layer of epidermis Produce melanin and send to surrounding.
黄褐斑 chloasma melasma. Definiton Melasma (also known as Chloasma faciei, or the mask of pregnancy when present in pregnant women) is a tan or dark skin.
白 癜 风 vitiligo. Definition Vitiligo is a condition that causes depigmentation of parts of the skin. It occurs when skin pigment cells die or are unable.
VITILIGO.
MALIGNANT MELANOMA. Outline Introduction Aetiology Types Invasion and Metastasis Risk Factors Diagnosis and Staging Treatment and Prevention.
LIGHT RELATED AND PIGMENTATION DISORDERS. DR DE-KAA NIONGUN.L.PAUL MBBS(JOS), FWACP,Grdt. Cert.in Derm(BKK),PGDE, MNIM, JP.
TAKE OUT SWEAT GLAND LAB TO TURN IN TAKE OUT INTEGUMENTARY DISEASES CHART Do Now 9/10/14.
HCS 1100 SLOs: 5 and 6.  Protection from the sun – avoiding times of high sun intensity and wearing protective clothing or sun screen.  Good nutrition-
Pigmentation Diseases
Vitiligo.
Integumentary System Diseases and Abnormal Conditions
The Integumentary System
Sun induced skin diseases
Diseases/Disorders of the Integumentary System
Diseases/Disorders of the Integumentary System
Dr. Qassim Al-chalabi M.B.Ch.B F.A.B.H.S (Dermatology & Venereology)
Pigmentary disorders Mohammed A. AlShahwan MD
INFECTIONS Allergies, Fungal, Bacterial, Viral, Infection, Inflammation, and Genetic.
Pharmacology-4 PHL 425 First Lecture By Abdelkader Ashour, Ph.D. Phone:
Skin Cancer A Colorado Concern.
Too Early for an Itchy Rash Small Group Teaching Problem Based Learning Department of Dermatology College of Medicine King Saud University Riyadh.
Melasma.
VITILIGO Pharmacology IV (PHL 425)
Mary Collier, FCSE, MS Texas AgriLIFE Extension Service, Terry County
Melasma & Ephelis Pharmacology IV (PHL 425)
8th & 7th Grade Objective 1.2.
Pityriasis rosea Lianjun Chen Huashan Hospital.
Diseases/Disorders of the Integumentary System
Lesson 2: Diseases and Disorders
Presentation transcript:

hyper & hypo- pigmentation DISORDERS Kenneth M. caranguian md

subtopics Melasma Lentigo Freckles Juvenile lentigens Solar lentigens PIH Nevus of ota Idiopatic gutate hypomelanosis pytiriasis alba vitiligo

MELASMA Acquired in genetically predisposed women. light-brown to gray-brown macules and patches on sun- exposed areas. Chloasma- synonymous term, aka “mask of pregnancy” 2nd or 3rd trimester, OCP or exogenous estrogens Fades slowly after pregnancy or discontinuation of OCP

DISTRIBUTION: sides of the face, forehead, upper lip, chin, malar eminences and sides of the neck. PATHOPHYSIOLOGY: Unknown or uncertain Study - high expression of MSH in keratinocytes that plays a key role in hyperpigmentation Most common in women during reproductive years, 90% Family history of >30%

PHYSICAL FINDINGS: symmetric, intensity of pigmentation varies color- uniform but may be blotchy, edges- irregular, well defined, (-) inflammation

DIFFERENTIAL DIAGNOSIS: 1. Exogenous ochronosis associated with bleaching agent hydroquinone. It is caused by the deposition of polymerised homogentisic acid in the skin. 2. PIH dx is clinical Skin that was previously inflamed due to dermatitis. Hx: erythema, pruritus, and dermatitis 3. Phototoxic reaction Dx is clinical exposed to systemic or topical medicines or cosmetics, and UV radiation. Begins abruptly, in contrast to melasma, which develops gradually.

TREATMENT NOTE: The patient should not be promised great therapeutic results.

Topical Bleaching Agents A. HYDROQUINONE 2%- 5% cream or lotion b.i.d. for 2 months. Compete with tyrosine oxidation by acting as an alternate substrate for tyrosinase, the enzyme that converts tyrosine to melanin and selective damage to melanosomes and melanocytes

m/c side effects: irritation and contact dermatitis - treated with topical steroids Common side effect among abusers is exogenous ochronosis- extended use of HQ Alternating HQ in 4-month cycles with other depigmenting agents can prevent or reduce side effects.

B.MONOBENZYL ETHER OF HYDROQUINONE (MBEH/Benoquin) melanocidal Selectively taken up by melanocytes and metabolized into free radicals that can destroy melanocytes permanently, leading to irreversible depigmentation Reserved for generalized depigmentation with extensive vitiligo Requires 9-12 months of continuous daily application to achieve complete depigmentation effect

C. KLIGMAN’S formula 5% HQ , 0.1% TRETINOIN, and 0.1% DEXAMETHASONE - in hydrophilic ointment

D. AZELAIC ACID a naturally occurring dicarboxylic acid derived from Pityrosporum ovale 15- 20% Applied BID x 3-12 months, well tolerated tx of acne- decreases comedo formation Unlike HQ, it targets only hyperactive melanocytes and thus will not lighten skin with normally functioning melanocytes

glycolic acid (topical or peels 30-70%) Jessner's solution F. OTHER TREATMENTS – kojic acid glycolic acid (topical or peels 30-70%) Jessner's solution microdermabrasion Alternative agents with potential therapeutic effects include aloesin (aloe vera), arbutin (bearberry fruits), licorice extract (Glabridin), soy, and vitamin C.

SUNSCREENS/ SUNBLOCKS Because the ability of the sun to darken lesions is much greater than HQ to bleach the pigment, strict avoidance of sunlight is imperative. Broad-spectrum with SPF 30 or > Preferably containing, mexoryl, avobenzone or physical blockers- titanium dioxide or zinc oxide that blocks both UVA and UVB IPL and Fractional CO2 laser may have additional benefits but results are variable

LENTIGO Common, benign, circumscribed, 1-3 cm light yellow or light brown macules from a localized proliferation of melanocytes due to acute or chronic sun exposure Histologically - increased number of melanocytes in the basal layer of the epidermis affects 30 yrs old and above May arise after sunburn or after PUVA overdosage It is a localized hyperpigmentation in 3 patterns : 1. Freckles (Ephelides) 2. Juvenile Lentigo 3. Solar lentigo

FRECKLES HISTORY: childhood, 5-7 yrs old AD M/c in redheads, blondes and fair skinned Paradoxically, there are fewer melanocytes in a freckle than in normal surrounding skin, but those that are present are large and able to form more melanin than usual Darkens during summertime and fade almost completely during winter Usually confined to face, arms, upper trunk

PHYSICAL FINDINGS: Appears as 1-2 cm, sharply defined, red or tan to light brown macules with uniform color

2. JUVENILE LENTIGENS HISTORY: childhood Lesions do not increase in number or size, or darken in response to sunlight characteristic feature of certain hereditary conditions May persist year round or may spontaneously resolve

PHYSICAL FINDINGS: appears as round to oval macules, 2 to 10 mm in diameter Darker than freckles Uniformly tan, or brown or black

Common in sun exposed skin 3. SOLAR LENTIGENS HISTORY: Common in sun exposed skin Increased in number and size in advancing years 75% of white people over 60 yrs have one or more lesions Aka- liver age spots Usually in association with other changes from sun damage, including wrinkling, dryness, and actinic keratoses

PHYSICAL FINDINGS: Tend to be larger (2- 20mm) Oval to geometric macules uniform in color, appear as fine grains, blotchy, with borders that are sharply defined

TREATMENT Monitor existing lesions for interval change Stable lesions do not require tx HQ solutions, tretinoin, azelaic acid cream, glycolic acid peels and creams are all valuable in reducing hyperpigmenation over weeks to months

POST INFAMMATORY HYPERPIGMENTATION (PIH) Results from any skin injury excessive irritation from cosmetic products and procedures, pimples, scratching or any kind of trauma Gradual darkening several weeks after the original injury More common in darker skin and sun exposed Some are more prone to PIH than others resolve after several months or years

NEVUS OF OTA bluish gray spots (forehead, temples, upper cheeks, around the eye, and eyebrow and nose, mucosa, conjunctivae, and tympanic membranes) With shades of blue, black, purple or brown More common in Asians in 1- 2 % of the population can cause facial disfigurement - emotional and psychologic distress Females > males (4x) Both dermal and epidermal components may co exist Creams- ineffective Can be effectively lightened with pigment lasers (ND-YAG, Q switched) but multiple treatment sessions (about 7 to 10) are required

IDIOPATHIC GUTATE HYPOMELANOSIS DESCRIPTION: Common assymptomatic dermatosis of unknown etiology Consists of white small macules in sun exposed upper and lower extremities HISTORY: middle aged and older people 50- 70 % over the age of 50 F>M Genetic predisposition Although asymptomatic, it is cosmetically distressing Lesions are stable in size but the number increases with age

PHYSNICAL FINDINGS: Macules are white and hypopigmented, 2 to 5 mm, Borders regular and smooth to slight xerotic scaling

Encourage sun protection with clothing Sunscreens are less effective TREATMENT: Encourage sun protection with clothing Sunscreens are less effective Can be camouflaged with tinted make up Self tanning creams that contains dihydroacetone darkens the lesions, but the appearance is not pleasing A light spray with liquid nitrogen may partially fade the lesions although there is a potential to worsen the dyspigmentation Reassurance is all that is required

PITYRIASIS ALBA hypopigmented, slightly elevated, fine scaling patches with indistinct borders typically on the lateral cheeks, lateral upper arms and thighs young children, resolves in early adulthood Asymptomatic No history of prior rash, trauma or inflammation Loss of pigment is often more noticeable and distressing in darkly pigmented people

Specific cause is unknown Hypopigmentation due to both reduced activity of melanocytes with fewer and smaller melanosomes Often seen in children between the ages 3 and 16 years males > females Occurs more frequently in those of light skinned, but is more apparent in those with darker complexion

White macules are round to oval, varies in size, usually 2-4 cm in diameter A fine surface scale often seen on close inspection Lesions more common in lateral cheeks, lateral upper arms and thighs Condition more obvious in summer and in darker skin types

DIFFERENTIAL DIAGNOSIS: PIH history of another inflammatory skin disorder; Atopic dermatitis, very itchy symmetrical plaques that respond to topical steroids; Psoriasis- symmetrical scaly plaques in typical sites including scalp; Pityriasis versicolor- affects upper trunk of adolescents and adults and has positive microscopy; Tinea corporis - has positive mycology Nummular dermatitis - dry or crusted itchy round patches; Vitiligo - progressive macules with complete pigment loss and no scale

TREATMENT: Treatment is not necessary since it will resolve on its own.  Reassurance- loss of pigment is not permanent and fades with time If the patches are red or itchy, mild topical steroid can be applied. Sometimes these will help make the skin disorder disappear faster, but other times it may have absolutely no effect at all.

PROGNOSIS: very good. no scaring However if forcefully remove with constant washing with skin products it could remain longer than usual. But if the correct treatment is applied it can disappear more quickly

VITILIGO Sex – equally affected but has a predominance to female- reflects greater concern about cosmetic appearance Age – begin at any age 50% (10-35y/o) old age – unusual Incidence – common worldwide Race - all races Inheritance - >30%, family history, thyroid disease and DM

THREE SUBTYPES OF VITILIGO: Localized or focal- <20% body surface area One or more macules in two single area. limited to one or may only a few body areas. Generalized, aka vitiligo vulgaris; and universalis -complete or near complete depigmentation. most common pattern

Segmental vitiligo- much more common in children than adults tends to spread rapidly within the segment of skin. One or more macules in dermatomal or quasidermatomal pattern. It corresponds to one or more dermatomes unilaterally and may meet or slightly pass the midline.

Common sites includes dorsal hands and fingers, face, body folds, axillae, genitalia There is also predilection for orifices including eyes, nostrils, mouth, nipples, umbilicus, anus

PHYSICAL FINDINGS: Consists of white depigmented 0.5 to 5 cm macules and patches with well defined borders

DIFFERENTIAL DIAGNOSIS: 1. Idiopathic guttate hypomelanosis Small, circular macules, slowly progressive accumulation of isolated lesions. 2. Pityriasis alba Asymptomatic, ill-defined small patches with fine scaling in children and adolescents 3. Discoid Lupus Erythematuses

4. Pityriasis versicolor Polycyclic, well-demarcated, typical upper trunk and shoulder distribution. 5. Seborrheic Dermatitis Distribution pattern- (e.g., scalp, forehead, eyebrow, nasolabial fold, periauricular, central chest, and back), greasy scales, dandruff.

TREATMENT: General guide: Psoralen plus ultraviolet A (PUVA) a combination treatment using Psoralen (P) and exposing the skin to Ultraviolet A (UVA)= PUVA General guide: if vitiliginous skin is <6 cm2 (the size of a quarter or half- dollar)- topical psoralens large portion - systemic psoralens and sunlight extremely widespread (>50%),-depigmentation with MBEH may be considered

They radically increase the erythema response of skin to long-wave ultraviolet light (UVA) after either topical application or systemic administration. 75% will have partial repigmentation when treated twice a week for > 1 year. Thus therapy be initiated gradually and monitored carefully.

Successful therapy requires 9-18 months. 2 Successful therapy requires 9-18 months. 2. Narrowband UVB (NB-UVB)- also use as monotherapy 3. Depigmenting the surrounding skin to blur the margins or removing all remaining pigmentation in extensive cases may lead to cosmetic improvement. Blurring of the margins may be attempted with HQ compounds. 4. Oil of Bergamot- contains psoralen as photosensitizer making skin sensitive to the tanning effect of sunlight

5. Broad spectrum sunscreens - at least spf 30 6 5. Broad spectrum sunscreens - at least spf 30 6. Concealing and Camouflaging agents 7. Topical immunomodulators- induce repigmentation up to 90%. 0.1% tacrolimus ointment BIDx2 months, nearly as effective as superpotent topical corticosteroids and does not carry risk of adverse effects.

8. Surgical techniques- transplant of autologous melanocytes or cultured epidermal autografts to nonpigmenting areas has promising effect with stable vitiligo that fails to respond to topical or phototherapies The surgical technique include tissue and cellular grafting

Thank you!