Physiology of Skin Disorders Erin Madigan - Fleck

Physiology of Skin Disorders
Erin Madigan - Fleck l.c.e., c.n.h.p., b.s., m.s., n.d.
(C)
THE ACUTE ASSESSMENT OF THE SKIN IS IMPERATIVE IN THE
PRACTICE OF CORRECTIVE SKIN CARE WHETHER IN THE SPA OR
CLINICAL SETTING. THE OBSERVATIONS MADE BY AESTHETICIANS
ARE OF VITAL IMPORTANCE ASSISTING PHYSICIANS IN THE
MANAGEMENT OF SKIN DISORDERS - THROUGH AESTHETIC
TREATMENT, PRODUCT SELECTION & HOME CARE PROTOCOLS.
THIS CD PRESENTATION OFFERS A COMPREHENSIVE VIEW OF
MANY OF THE MOST COMMON SKIN DISORDERS THAT THE
AESTHETICIAN MAY ENCOUNTER WHILE PERFORMING SKIN CARE
SERVICES AT THE SPA OR MEDICAL FACILITY. THE IMAGES ARE
ACCOMPANIED BY PATHOPHYSIOLOGY ASSESSMENT, ETIOLOGY,
STANDARD MEDICAL PROTOCOL PRESCRIBED BY PHYSICIANS,
COMPATABLE AESTHETIC TREATMENT & ALTERNATIVE MEDICINE
VIEWS WITH OVER 200 POWER POINT TILES WITH IMAGES & TEXT.
DISCLAIMER
The information provided in this presentation is for educational
purposes only and to be used strictly by licensed aestheticians and
medical professionals.
This information should not be construed as medical advice, nor
shall the medical protocols mentioned be deemed appropriate for
aestheticians to perform. It is the responsibility of the licensed
professional to adhere to the medical and cosmetology laws in their
particular state in regards to the application of any of the methods or
protocols mentioned herein.
The makers of this presentation shall hold harmless from any liability
whatsoever as a result of faulty procedures, consultations or advice
given or performed by any individual who has viewed this
presentation.
Important Information
The information in this presentation is under strict
copyright protection according to state and federal
laws.
Under no circumstances may any part of this
presentation be copied, transmitted, or duplicated in
any form whatsoever without explicit written
permission from the maker.
Images in this presentation are the property of
Dermnet.com and may not be copied in any form
without consent from the owner(s).
About Alternative Medicine
The information in this presentation regarding alternative medicine
protocols provide a general overview of treatment in the natural health
community known to assist in the management of common skin
disorders.
These protocols are not a substitute for medical care in the treatment of
serious skin conditions, and should not be recommended by the
aesthetician in the place of medical care.
They are presented as an adjunct to treatment, and do not represent
the actual program that a alternative medicine practitioner would
prescribe for an individual.
If your client desires to treat their condition with holistic protocols,
please refer them to a certified and qualified natural health practitioner
in your area.
Please be aware of the laws and liabilities in your state with regard to
recommending vitamin supplements to clients without certification as a
nutritional counselor, nutritionist, dietician, practitioner or medical
professional.
SKIN CARE & PRESCRIPTION DRUGS
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ESTIMATED THAT 50% OF PEOPLE IN THE U.S. USE
PRESCRIPTION AND OTC DRUGS
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THIS COULD POSSIBLY EQUATE TO ABOUT 1/2 YOUR CLIENTS
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MODERN SKIN CARE PRODUCTS HAVE ENHANCED
INGREDIENT ACTIVITY POTENTIAL - POSSIBLE VOLITALE
INTERACTIONS WITH RX’S
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RE-ASSESSMENT OF YOUR CLIENT’S MEDICATIONS AND
HEALTH STATUS SHOULD BE DONE AT EACH VISIT
SKIN CARE & PRESCRIPTION DRUGS
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SYNERGISTIC REACTIONS - INCREASE IN POTENCY OF THE
DRUG
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CANCELLATION REACTIONS - DRUGS OR INGREDIENTS MAY
CANCELL OUT THE ACTIVITY OF EACH OTHER
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ANTAGONISTIC REACTIONS - EACH DRUG MAY DECREASE THE
INTENDED POTENCY
PATHOLOGY PRIMER
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INFLAMMATION IS CONSIDERED A DISEASE PROCESS
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INFLAMMATION IS A PROTECTIVE PROCESS RESPONDING TO
AN INJURY OR DESTRUCTION OF TISSUE WHEREBY THE
RESPONSE REPRESENTS AN ATTEMPT TO DESTROY BOTH THE
ANTAGONIST & INJURED TISSUE
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INFLAMMATION AFFECTS THE EPIDERMIS, DERMIS &
SUBCUTANEOUS TISSUE IN TANDEM
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CHARACTERISTICS OF INFLAMMATION : REDNESS, SWELLING,
HEAT & PAIN
PATHOLOGY PRIMER
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ACUTE: SUDDEN ONSET OF THE CONDITION / SUB ACUTE
CHRONIC : LASTS FOR MONTHS / SUBCHRONIC
STAGE ONE = VASCULAR EFFECT / VASODIALATION -ACCOUNTS
FOR THE REDNESS OF INJURED SKIN
STAGE TWO = LEUKOCYTIC INFFILTRATION - PASSAGE OF WHITE
BLOOD CELLS INTO INJURED TISSUE
STAGE THREE = PHAGOCYTOSIS - WHITE BLOOD CELLS DESTROY
THE INVADERS
PEARLS OF WISDOM
WHEN TO REFER MEDICAL CARE
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CYSTIC & PUSTULOUS ACNE
UNIDENTIFIABLE PIGMENTED LESIONS
RHINOPHYMA
WHEALS, NODULES, CYSTS, EROSION,ULCER, FISSURE
SEBORRHEIC DERMATITIS
SEVERE TELANGECTASIA
SEVERE CONTACT DERMATITIS, ECZEMA
PSORIASIS, IMPETIGO, HERPES, SEBORRHEIC KERATOSES,
SHINGLES, RINGWORM
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IF YOU DON’T KNOW - DON’T GO!
ACNE VULGARIS
&
SOLAR
COMEDONES
ACNE VULGARIS
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ACNE VULGARIS
PATHOPHYSIOLOGY
DEVELOPMENT OF ACNE LESION
1.
FOLLICULAR EPIDERMAL HYPERPROLIFERATION
2.
SUBSEQUENT PLUGGING OF THE FOLLICE & EXCESSIVE
SEBUM
3. PROPIONIBACTERIUM INFILTRATION
4. INFLAMMATION
ACNE VULGARIS
PATHOLOGY & ETIOLOGY
• INFLAMMATORY DISORDER OF THE PILO SEBACEOUS GLAND
• MANIFESTS WHERE THERE IS A HIGH CONCENTRATION OF
SEBACEOUS GLANDS
• PRESENTS SEBUM RETENTION PAPULES
• RETENTION HYPERKERATINIZATION
• INFLAMMATORY CYSTS & PUSTULES
• OPEN & CLOSED COMEDONES
• CYSTIC NODULES
• HYPERTROPIC SCARRING
ACNE VULGARIS
PATHOLOGY & ETIOLOGY
• PROPIONI BACTERIUM
• GENETIC PRE-DISPOSITION
• ENDOCINE & ADRENAL INFLUENCES
• ANDROGEN IMBALANCES
• DIHYROTESTOSTERONE
• EMOTIONAL STRESS TRIGGERS
ACNE VULGARIS
PATHOLOGY & ETIOLOGY
• AUTOINTOXICATION
• LYMPHATIC STAGNATION
• TOXIC LIVER / OVERLOAD
• POLYCYSTIC OVARY SYNDROME
• LITHIUM, ORAL CONTRACEPTIVES, GLUCOCORTICOIDS
• INDUSTRIAL POLLUTANTS - OILS, COAL TAR DERIVITATIVES,
TOBACCO SMOKE, CHLORINATED HYDROCARBONS
ACNE VULGARIS
PATHOLOGY & ETIOLOGY
• CIRCULATING HORMONE - DHEA- S SULFATE & COMEDONAL
ACNE
• INCREASE IN IGF-1 INSULIN HORMONE / HIGH GLYCEMIC LOAD
• DIMINISHED LEVELS OF LINOLEIC ACID
• INTERLEUKIN -1-ALPHA = PRO INFLAMMATORY CYTOKINE & THE
DEVELOPMENT OF COMEDONES
• 85-100% OF INDIVIDUALS IN THE U.S. AT SOME POINT DURING
THEIR LIVES
ACNE VULGARIS
ANTIBIOTICS & ACNE
• ANTIBIOTICS DESTROY THE BACTERIA THAT PRODUCES AN
ENZYME THAT CHANGES SEBUM INTO FREE FATTY ACIDS
• FREE FATTY ACIDS ARE IRRITANTS AND CAN TRIGGER
INFLAMMATION AND RUPTURING OF THE SEBACEOUS GLANDS FORMING A PAPULE
• ANTIBIOTICS INHIBIT THE ENZYME THAT BREAKS DOWN SEBUM
INTO FREE FATTY ACIDS
• DISADVANTAGES OF CONTINUAL ANTIBIOTIC USE INCLUDE:
SUPRESSION OF THE IMMUNE SYSTEM AND INTESTINAL
DYSBIOSIS
ACNE VULGARIS
MEDICAL INTERVENTION
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KEY PRODUCTS - MILD CLEANSER AND ANTISEPTIC WASH
GLYCOLIC ACID - WASH / LOTION
SALICYLIC ACID - WASH / LOTION
BENZOL PEROXIDE
RETIN -A , RENOVA ,AVITA
TAZAROTENE GEL
MILD ACNE
AZELAIC ACID CREAM
CLINDAMYCIN
RETINOIDS
ISOTRETINION
ADAPALENE - DIFFERIN
PHOTODYNAMIC THERAPY
OMNILUX BLUE LED
DERMAL PLANNING
ACNE VULGARIS
MEDICAL INTERVENTION
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TOPICAL & ORAL MEDICATIONS USUALLY FOR AT LEAST 6 MONTHS
TETRACYCLINE
MINOCYCLINE
DOXYCYCLINE
ERYTHROMYCIN
ANTI - ANDROGENS
MODERATE TO
SPIRONOLACTONE
SEVERE ACNE
ISOTRETINION
CRYOTHERAPY
INTRALESIONAL INJECTIONS - STEROIDS
DIATHERMY
DERMAL PLANNING
DERMABRASION, MICRODERMABRASION
BLUE & RED LIGHT PHOTOTHERAPY/ LED
CANDELA SMOOTHBEAM DIODE LASER
TOPICAL MEDICIMENTS
Topical Medications Chart - PDR Physicians Desk Reference
ERYTHROMYCIN
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Benzamycin
Erycette
Erygel
Erymax
T-Stat
Emgel
Erythra - Derm
SULFUR
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Klaron
TRETINOIN
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Altinac
• Sulfacet R
• Avita
• Sulfoxyl Lotion
• Retin - A
• Novacet
• Retin - A micro
• Plexion
• Renova
• Tretinion (generic)
TOPICAL MEDICIMENTS
Topical Medications Chart - PDR Physicians Desk Reference
CLINDAMYCIN
BENZOYLPEROXIDE
HYDROQUINONE
• BenzaClin
• BenzaClin
• Cleocin T
• Clindets
• Clindagel
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Benzac
Benzac AC
Benzac W
W Wash
Benzac 5 & 10
Benzashave
Benzamycin
Benzamycin Pak
Brevoxyl
Clinac BPO
Desquam E
Desquam X
Pan Oxyl
Triaz
• Alphaquin
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Claripel
Melaquin
Melanex
Eldopaque Forte
Eldoquin Forte
Solaqin Forte
Glyquin
Lustra - AF
Alustra
TOPICAL MEDICIMENTS
Topical Medications Chart
PDR Physicians Desk Reference
HYDROCORTISONE &
BENZOL PEROXIDE
METRONIDAZOLE
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Metrocream
Vanoxide
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AZELAIC ACID
Azelex
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ADAPALENE
Differin
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TAZAROTENE
Tazorac
• Metrogel
• Metrolotion
• Noritate
All medications listed are
the registered trademarks
of one of the following
companies:
ICN Pharmaceuticals
Neutragena Corp.
Straus Pharmaceuticals
Ferndale Laboratories
Bertek Pharmaceuticals
Upsher-Smith
Paddock Laboratories
Galxo Wellcome
Westwood Squibb
Allergan
Ortho Dermatological
Medicis Dermatologics
Galderma Laboratories
Stiefel Labs
Pharmacia & Upjohn
Dermick Laboratories
Galxo Smith Kline
Novartis Pharmaceuticals
ACNE VULGARIS
AESTHETIC TREATMENT
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ABOVE GRADE 2 - REFER TO M.D.FOR MEDICAL TREATMENT
NO MICRODERMABRASION, IPL, OR CHEMICAL PEELING IF
PATIENT IS ON: Differin, Accutane, Metro Gel, Tazarotene, Retin- A
MICRODERMABRASION
GALVANIC DESINCRUSTATION
ULTRASOUND
LED DIODE
MANUAL LYMPHATIC DRAINAGE
ZENO ACNE CLEARING DEVICE
EXTRACTION, EXPRESSION
IPL - FOR RESIDUAL SCARRING
ACNE VULGARIS
AESTHETIC TREATMENT
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KNEIPP THERAPY
RETINOIDS
ZINC
AZELAIC ACID
SALICYLIC ACID
LACTIC ACID
ENZYMES
VITAMIN C
SEA BUCKTHORN EXTRACT
BENZOL PEROXIDE 5 % < PROPIANI BACTERIUM
ACNE VULGARIS
ALTERNATIVE MEDICINE
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INFRARED SAUNA
ACUPUNCTURE
HERBOLOGY & BOTANICALS
INCREASE EXERCISE
COLON HYDROTHERAPY
HYPERBARIC OXYGEN
APPROPRIATE CELLULAR HYDRATION
HOMEOPATHIC DRAINAGE
LIVER & GALL BLADDER DETOX
ACNE VULGARIS
ALTERNATIVE MEDICINE
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R/O LEAKY GUT SYNDROME
R/O POLYCYSTIC OVARY SYNDROME
< REFINED CARBS, INORGANIC IRON, DAIRY, RED MEAT
< SULFITES & SODA POP
WHOLE FOODS >FIBER & DIGESTIVE ENZYMES
AVOID FOODS WITH IODINE (SHELLFISH)
AVOID MILK & DAIRY PRODUCTS- HORMONES, SOMATIC CELLS
( PUS )
• AVOID HIGH FAT FOODS
• > FOODS WITH ZINC - 50 MG. PER DAY
• > FOODS WITH B6 - AIDS IN METABOLISM OF HORMONES, PMS
AND ACNE - 50 MG. PER DAY
ACNE VULGARIS
ALTERNATIVE MEDICINE
• HIGH PROTIEN DIET - LESS 5-ALPHA REDUCTION OF
TESTOSTERONE & MORE CYTOCHROME P-45- HYDROXILATION
OF ESTRADIOL - (HORMONE BALANCE)
• ZINC INHIBITS 5-ALPHA REDUCTASE & PROLACTIN - PROLACTIN
INCREASES ANDROGENS
• VIT B6 REDUCES PREMENSTRUAL ACNE & PLAYS A ROLE IN THE
NORMAL METABOLISM OF STERIOD HORMONES
ACNE VULGARIS
ALTERNATIVE MEDICINE
IMPORTANT NUTRIENTS
VIT A - BETA CAROTENE - VIT C - CALCIUM - SELENIUM - SILICA
B VITAMINS - B6 - BIOTIN - EFA’S - OLIVE OIL - COD LIVER OIL
FLAX OIL - OMEGA 3 EPA - GAMMA LINOLENIC ACID (GLA)
L- CYSTEINE - L-PROLINE & ALL AMINO ACIDS
SOLAR COMEDONES
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SOLAR COMEDONES
ETIOLOGY & PATHOLOGY
• MULTIPLE OPEN & CLOSED COMEDONES ON ACTINICALLY
DAMAGED SKIN IN THE PERIORBITAL & TEMPORAL REGION
• COMMON IN MIDDLE AGE TO ELDERLY MALES
• ALSO KNOWN AS FAVRE RACOUCHET SYNDROME
• ASSOCIATION WITH CIGARETTE SMOKING
SOLAR COMEDONES
MEDICAL INTERVENTION
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RETINOIDS
SPF
DERMABRASION
CURETTAGE
LASER
CHEMICAL EXCISION
C02 LASER
SOLAR COMEDONES
AESTHETIC TREATMENT
• MICRODERMABRASION
• DESINCRUSTATION
• ENZYMES
• LACTIC ACID
• GLYCOLIC ACID
• MANUAL & INSTRUMENT EXTRACTION
ROSACEA
ROSACEA
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ROSACEA
PATHOLOGY & ETIOLOGY
• PROGRESSIVE VASCULAR DISORDER EXHIBITING WEAKNESS
AND FRAGILITY OF BLOOD VESSELS OF THE FACE
• CHRONIC HISTORY OF EPISODIC REDDENING
• HYPERMIA (EXCESSIVE BLOOD FLOW)
• ERYTHEMA (CONGESTED CAPILLARIES)
• PERSISITANT ERYHTEMA & SYMETRICAL PATTERN
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REACTIVITY OF THE CAPILLARIES TO HEAT & STIMULI
ROSACEA
PATHOLOGY & ETIOLOGY
• 2-3 MM PAPULES, SCATTERED LESIONS, TELANGECTASIA, NO
COMEDONES
• MAY EFFECT THE OCCULAR REGION
• MAY CO-EXHIST WITH ACNE - BUT UNREALATED TO ACNE
ITSELF
• ACNE MAY PRECEED THE ONSET OF ROSACEA, BUT
NOT AN INDICATOR
• AGE OF ONSET 30-50
ROSACEA
PATHOLOGY & ETIOLOGY
• DIFFERENTIAL DIAGNOSIS - ACNE, PERI ORAL DERMATITIS,
SEBORRHEIC DERMATITIS, PROLONGED USE OF
GLUCOCORTICOIDS
• 1 IN 20 PEOPLE ON THE U.S. HAVE ROSACEA - EFFECTS
WOMEN 3X’S MORE
• EARLY INTERVENTION AT ONSET IMPORTANT TO
DISCOURAGE PROGRESSION
ROSACEA
PATHOLOGY & ETIOLOGY
• PREVELANT CELTIC, NORDIC DECENT - 8-10 MILLION IN THE
BRITISH ISLES ARE EFFECTED
• HISTORY OF THE DISORDER DATES BACK TO MID 1300’S
• DEMODEX FOLLICULORUM MITE POSTULATED
• CHRONIC INFLAMMATION & DELAYED FOOD ALLERGIES
• MINERAL DEFICIENCIES - HYPERACIDITY
FLUSHING MECHANISM & NITRIC OXIDE
• PRE ROSACEA FLUSHING IS AN EARLY SIGN OF THE
DISORDER
• EARLIEST DETECTION IN CHILDHOOD - THE “HEALTY GLOW”
MAY ACTUALLY BE A SIGNAL OF DEVELOPMENT
• ROSEACA BLOOD VESSELS HAVE GENETIC BASED
STRUCTURE ABNORMALITY IN THE INNER LINING AND WALLS
OF THE BLOOD VESSELS - OFFERING LESS PROTECTION AND
REPAIR MECHANISMS
• REPEATED FLUSHING CAUSES VASCUALR HYPERRESPONSIVENESS & ENHANCES DIALATION & STRUCTURAL
CHANGES TO BLOOD VESSELS
FLUSHING MECHANISM & NITRIC OXIDE
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FLUSHING IS LOCALIZED TO THE FACE BECAUSE:
1. GREATER BLOOD FLOW TO THE FACE
2, FLOW IS 20-30 TIMES GREATER THAN REQUIRED
3. GREATER WIDTH OF VESSELS & SUPERFICIAL VESSELS
4. RESPONDS TO MORE STIMULI - THINNER SKIN
5. THERMOREGULATORY BLOOD VESSELS AID IN
REDUCING HEAT FROM FLUSHING
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AS ROSACEA PROGRESSES - SENSITIVITY INCREASES
NERVOUSNESS, ANXIETY, ANGER CONTRIBUTE TO
EPISODIC FLUSHING
FLUSHING MECHANISM & NITRIC OXIDE
• NITRIC OXIDE IS PRODUCED AND RELEASED AT EACH
INCIDENCE OF INCREASED BLOOD FLOW OR FLUSHING
• NITRIC OXIDE IS PRODUCED BY ENZYMES LOCATED IN AND
AROUND THE BLOOD VESSELS & SKIN (NITRIC OXIDE
SYNTHASE ENZYMES)
• NITRIC ACID IS FORMED ON THE INNER WALL OF BLOOD
VESSELS, EPIDERMAL & DERMAL CELLS & DIALATOR
NERVES AROUND BLOOD VESSELS
• IT EFFECTS NEARBY BLOOD VESSELS AND BINDS TO
RECEPTOR CELLS ON VASCULAR SMOOTH MUSCLE CELLS
DISORDERS THAT MAY PROVOKE FLUSHING
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HIGH BLOOD PRESSURE
CARCINOID SYNDROME - TUMORS
PHEOCHROMOCYTOMA - TUMORS SECRETING ADRENALINE
HYPERTHYROIDISM - OVER ACTIVE THYROID
MASTOCYTOSIS - INCREASE IN MAST CELLS
LUPUS - AUTOIMMUNE DISEASE
SEASONAL ALLERGIES
PERIMENOPAUSE, MENOPAUSE
GASTROINTESTINAL DISORDERS
LEAKY GUT SYNDROME
CANDIDA ALBICANS
VITAMIN SUPPLEMENTS OR PRESCRIPTION DRUGS
SYNTHETIC HORMONE REPLACEMENT
ROSACEA SYMPTOMOLOGY
1. FACIAL REDNESS / ERYTHEMA
2. TELANGIECTASIA
3. INFLAMMED SKIN & HYPER - REACTIVITY
4. UNEVEN TEXTURE - SURFACE FEEL
5. SMALL - MEDIUM PAPULES
6. SMALL PUSTULES
7. FACIAL BURNING , STINGING SENSATIONS
8. FACIAL PUFFINESS, EDEMA
9. RHINOPHYMA - KERATINOUS HYPERPLASIA
PLEWING & KLINGMAN CLASSIFICATION
STAGE 1 - ERYTHEMA & TELANGIECTASIAS
STAGE 2 - ERYTHEMA, TELANGIECTASIAS, PAPULES
& SMALL PUSTULES
STAGE 3 - DEEP ERYTHEMA, PAPULES, PUSTULES, NODULES
DENSE TELANGIECTASISAS. MAY EXHIBIT A
PERSISTANT “SOLID’ EDEMA OF THE CENTRAL PART
OF THE FACE.
STAGE 4- RHINOPHYMA = LOBULAR SEBACEOUS HYPERPLASIA &
CONNECTIVE TISSUE FORMATION
ROSACEA
MEDICAL INTERVENTION
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ANTIBIOTIC COURSE 6-12 WEEKS
METRONIDAZOLE (METROGEL) NORITATE
SODIUM SULFACETAMIDE
AZELAIC ACID
CLONIDINE
TETRACYCLINE, MINOCYCLINE, DOXYCYCLINE
ISOTRETINION
ELECTRODESSICATION
SCLEROTHERAPY (SALINE)
IPL
PEELS
ROSACEA
MEDICAL INTERVENTION
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CLARITHROMYCIN
MOXONODINE
AZITHROMYCIN
BETA BLOCKERS
CLONIDINE
PULSED DYE LASER- THIN BLOOD VESSELS
PHOTODERM- INTENSE PULSED LIGHT
VASCULIGHT LASER - THIN & THICK VESSELS
VERSAPULSE LASER - LONG PULSE, LESS SIDE EFFECTS
V-BEAM LASER - LONG PULSE, GOOD FOR TELANGECTASIA
ENDOSCOPIC TRANSTHORACIC SURGERY - CLAMPS
SYMPATHETIC NERVES - RESTRICTS FLUSHING
ROSACEA
DRUG INGREDIENTS- ANTAGONISTS
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AMINOBENZIOC ACID (PABA)
AVOBENZENE (PARSOL 1789)
(METHOXYDIBENZOYLMETHANE)
BENZOCAINE
BENZOYL PEROXIDE
BENZYL NICOTINATE
CAPSAICIN
CORTICOSTERIODS
DIETHANOLAMINE P - METHOXYCINNAMATE
DIOXYBENZONE
ETHYLHEXYL P - METHOXYCINNAMATE
ETHYL SALICYLATE
GLYCOL SALICYLATE
HYDROCORTIZONE
HYDROGEN PEROXIDE
HYDROQUINONE
METHYL NICOTINATE
IBUPROFEN
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METHYL SALICYLATE
OCTINOXATE (OCTYLMETHOXYCINNAMATE)
OXYBENZONE
RESORCINOL
RETINOIDS
SALICYLIC ACID
SULISOBENZONE
TOPICAL ANTI HISTAMINES
TRICHLORACETIC ACID
TRICLOSAN
ALCOHOL (ETHANOL OR SPIRITS)
AMINOPHYLLIN
ANABOLIC STEROIDS
ANGIOTENSIN (ACE INHIBITORS)
ASPARTAME ( NUTRISWEET)
ASPIRIN
CALCITONON
CALCIUM CHANNEL BLOCKERS
COCAINE
CORTICOTROPIN - HORMONE
ROSACEA
DRUG INGREDIENTS- ANTAGONISTS
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LOVASTATIN
MARIJUANA
NAPROXEN (NAPROSYN)
NIACIN (VIT B3)
NICOTINE
NIFEDIPINE
NITRATES
NITROGLYCERIN
OPIOID NARCOTICS (MORPHINE,ETC;)
PROGESTERONE
SIMVASTATIN (ZOCOR)
SODIUM MONOGLUTAMATE
THEOPHYLLINE
VANCOMYCIN
VASODIALATORS
VIAGRA
ROSACEA
COSMETIC INGREDIENTS- ANTAGONISTS
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2- BROMO 2- NITROPROPANE -1,3 DIOL
ACETONE
ALBUMIN (EGG WHITES)
ALCOHOL - ETHANOL, ETHYL, ISOPROPYL,
ISOPROPANOL
SD ALCOHOL
ALGAE
ALPHA HYDROXY ACIDS & SALTS:
GLYCOLIC, LACTIC, MALIC, CITRIC,
TARTARIC, SODIUM GLYCOLATE,
AMMONIUM LACTATE
AMMONIA
ARACHIDONIC ACID
ARNICA OIL
ASCORBIC ACID
BALSAM PERU
BARLEY
BAY LAUREL OIL
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BAYBERRY OIL
BENTONITE CLAY
BENZALKONIUM CHLORIDE
BENZOPHENONES
BERGAMONT OIL
BITTER ORANGE OIL
BLACK PEPPER OIL
BROMELAIN
CAFFEINE
CAMPHOR OIL
CAPSICUM
CAYENNE
CETRIMONIUM BROMIDE
CHAMOMILE OIL
CINNAMIC ALDEHYDE
CINNAMON OIL
CLOVE OIL
COCOA BUTTER
CORAINDER OIL
ROSACEA
COSMETIC INGREDIENTS- ANTAGONISTS
•
•
•
•
•
•
•
•
•
•
•
•
•
CORN EXTRACT
CORNSTARCH
DIAZOLINDINYL UREA
DMAE
DMDM HYDANTOIN
EUCALYPTUS OIL
FENNEL OIL / EXTRACT
FIR NEEDLE OIL
FRAGRANCES
GERANOIL (CHEMICAL CONSTITUIENT)
FOUND IN:
PALMAROSA, GERANIUM,
JASMINE,LAVANDER, CITRONELLA,
& ROSE ESSENTIAL OILS
GINGER
GINSENG
GRANULAR EXFOLIANTS: OATMEAL,
WALNUT, KERNALS, SALT, SAND,
PUMICE, BEADS, CORUNDUM
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
GRAPEFRUIT OIL OR EXTRACT
IMIDAZOLIDINYL UREA
IODINE
LANOLIN
LECITHIN
LEMON OIL
LEMONGRASS OIL
LIME OIL
MANNAN
MENTHOL
MICA
MONTMORILLONITE
MUSTARD
MYRRH OIL
NETTLE, STINGING NETTLE
NIACIN ( B3)
NICOTINIC ACID
NUTMEG OIL
OAK MOSS EXTRACT
ORANGE OIL
PABA
ROSACEA
COSMETIC INGREDIENTS- ANTAGONISTS
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
PAPAIN
PABA
PAPAYA EXTRACT
PEANUT OIL
PENNYROYAL OIL
PEPPERMINT OIL
PHENOL
PHENOXYETHANOL
PHOSPHATIDYLCHOLINE
PINE OIL
PROPYLENE GLYCOL
QUATERNIUM - 15
RETINOL (VIT A)
ROSEMARY OIL, RUE OIL
SACCHAROMYCES (YEAST)
SACCHAROMYCES LYSATE - TRF
SAGE ESSENTIAL OIL
SALICYLIC ACID
SANDALWOOD ESSENTIAL OIL
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
SEAWEED
SESAME OIL
SODIUM C14-16 OLEFIN SULFATE
SODIUM LAURETH SULFATE
SODIUM LAURYL SULFATE
SOY PROTIEN
SPEARMINT OIL
STEARIC ACID
STEARALKONIUM CHLORIDE
SULFUR
TANGERINE OIL
TEA - LAURYL SULFATE
TEA TREE OIL
THYME ESSENTIAL OIL
TOCOPHEROL
TOCOPHERYL NICOTINATE
TUMERIC OIL
VANILLA OIL, EXTRACT
WINTERGREEN
WITCH HAZEL
YLANG - YLANG OIL
ROSACEA
AESTHETIC TREATMENT
• INGREDIENT KNOWLEDGE IMPERITATIVE IN SELECTION OF
PRODUCTS & TREATMENT
• EXTENT OF TREATMENT IS CORRELATED TO THE DEGREE OF
INFLAMMATION
• DO NOT PERFORM TREATMENTS DURING EPISODIC
INFLAMMATION OR EXTRACT PAPULES
• LED / IPL
• ULTRASOUND
• PROBIOTIC PRODUCTS
• MANUAL LYMPHATIC DRAINAGE
• OXYGEN THERAPY
• TELANGECTASIA ELECTRODESSICATION
ROSACEA
AESTHETIC TREATMENT
• NO BRUSHING OR AGGRESSIVE MICRODERMABRASION
• DO NOT USE ENZYMES CONTAINING LIPASE - LEAVES THE
SURFACE OF THE SKIN SUBJECT TO BACTERIAL INFECTION
• AVOID SUNSCREENS WITH OCTYL METHOXYCINNAMATE,
AVOBENZENE (PARSOL1789), BENZOPHENONES
• AVOID TRIGGERS = ALCOHOL, SPICES, CAFFEINE, SUNLIGHT,
NUTS, STIMULANTS, SUGAR, MUSHROOMS
ROSACEA
TOPICAL INGREDIENT DECK
•
•
•
•
•
•
•
•
•
•
•
•
CHAMOMILE
AZULENE
HYPERICUM (ST. JOHNS WORT)
HORSE CHESTNUT EXTRACT
CITRUS BIOFLAVINIODS
SEA BUCKTHORN EXTRACT
ALOE VERA
GREEN TEA
GRAPESEED EXTRACT
HYALURONIC ACID
ZINC OXIDE
ZINC SALICYLATE
VITAMIN E
VITAMIN C
ZINC
ARNICA
CALENDULA
DIMETHICONE
DMAE
LICORICE
AZELAIC ACID
ROSACEA
ALTERNATIVE MEDICINE
•
•
•
•
•
•
•
•
•
LUNG AND LIVER IMBALANCES
DETOXIFICATION
CHECK HYDROCHLORIC ACID LEVELS
PANCREATIN / AFTER MEALS
AVOID YEAST AND MUCUS FORMING FOODS
AVOID SPICY FOODS, LAMB, CHOCOLATE, ALCOHOL
HERBOLOGY & BOTANICALS
ACUPUNCTURE
HOMEOPATHIC DRAINAGE
ROSACEA
ALTERNATIVE MEDICINE
•
•
•
•
•
OLIGIOMERICPROANTHOCYANIDINS - “OPC’S”
FLAX SEED OIL
BORAGE OIL
ESTER-C
GRAPE SEED EXTRACT
AUTO IMMUNE
& NUTRITIONAL
DISORDERS
LUPUS ERYTHEMATOSUS
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LUPUS ERYTHEMATOSUS
PATHOLOGY & ETIOLOGY
• AUTOIMMUNE DISEASE THAT CAUSES INFLAMMATION IN
VARIOUS PARTS OF THE BODY, ESPECIALLY THE SKIN, JOINTS,
& KIDNEYS
• TISSUE INJURY TO THE EPIDERMAL - DERMAL JUNCTION
• IMMUNE MEDIATED ATTACKS ON NORMAL CELLS OF THE BODY
• ATROPHY OF THE EPIDERMIS, SLIGHT EDEMA
LUPUS ERYTHEMATOSUS
PATHOLOGY & ETIOLOGY
• BUTTERFLY RASH, SHARPLY DEFINED WITH FINE SCALING
• SIGNATURE BUTTERFLY MARKING IS A RESULT OF DAMAGED
BLOOD VESSELS
• RED SCALY PATCHES THAT LEAVE WHITE SCARS
• SCALY PAPULES AND PLAQUES MAY APPEAR ON THE BODY
LUPUS ERYTHEMATOSUS
PATHOLOGY & ETIOLOGY
•
DISEASE ORIGINATES FROM POLYCLONAL B
CELL IMMUNITY THAT INVOLVES CONNECTIVE TISSUE AND
BLOOD VESSELS
• 90% OF CASES HAVE SKIN INVOLVEMENT- SEVERE CASES MAY
HAVE RENAL, CARDIAC, PULMONARY DISEASE
• GENETIC & ENVIORNMENTAL FACTORS
• DISCOID LUPUS - LIMITED TO THE SKIN
• SYSTEMIC FORMS & DRUG INDUCED CAN EFFECT ANY ORGAN
OF THE BODY
LUPUS ERYTHEMATOSUS
PATHOLOGY & ETIOLOGY
VARIATIONS OF LUPUS
•
•
•
•
•
•
•
•
SYSTEMIC LUPUS ERYTHEMATOSUS
DISCOID LUPUS ERYTEMATOSUS
SUBACUTE LUPUS ERYTHEMATOSUS
LUPUS PROFUNDUS
NEONATAL LUPUS ERYTHEMATOSUS
CUTANEOUS LUPUS MUCINOSIS
CHILBALIN LUPUS
DRUG INDUCED LUPUS - LITHIUM, SULPHONAMIDES,
MINOCYCLINE
LUPUS ERYTHEMATOSUS
MEDICAL INTERVENTION
•
•
•
•
•
•
•
•
•
NO SUN EXPOSURE
PREDNISONE / ORAL STERIODS
REST
STEROIDS, CORTICOSTERIODS
IMMUNOSUPPRESSIVE RX’S
ANTI-MALARIALS
RETINOIDS, ISOTRETINION
ERYTHROMYCIN
IMMUNOGLOBULIN IV’S
LUPUS ERYTHEMATOSUS
AESTHETIC TREATMENT
•
•
AESTHETIC TREATMENT
CAMOUFLAGE MAKEUP ON RESIDUAL SCARRING
DIABETIC SKIN
DIABETES
PATHOLOGY & ETIOLOGY
• CHRONIC DISEASE OF THE PANCREAS- TYPE 1 & 11
• TYPE 11 - 90% OF CASES IN THE U.S.
• CAUSED BY INEFFICENT AMMOUNT OF INSULIN CIRCULATING
IN THE BLOOD
DIABETES
PATHOLOGY & ETIOLOGY
TYPE 11 MEDICATIONS: SULFONYLUREAS (SULFA)
DIABINESE
MICRONSE
GLIPIZIDE
PRECOSE
TOLINASE
ORINASE
DIABETA
GLIMEPRIIDE
GLYSET
AMARYL
GLYBURIDE
AVANDIA
GLUCOPAGE
DIABETIC SKIN
PATHOLOGY & ETIOLOGY
• LACK OF CIRCULATION RESULTS IN SKIN ASPHIXIATION &
HYPERKERATINIZATION, ULCERS, CELLULITIS AND
HIGH RISK OF SKIN INFECTIONS
• DIABETES REDUCES NERVE SENSITIVITY - NEUROPATHY
UNDETECTED SENSITIVITY
• MEDICATIONS CAN CAUSE DEHYDRATED SKIN
DIABETIC SKIN
PATHOLOGY & ETIOLOGY
• BLOOD SUGAR LEVELS POORLY CONTROLLED - BODY
PRODUCES EXCESS URINE TO RID ITSELF OF EXCESS BLOOD
GLUCOSE- RESULTS IN SKIN DEHYDRATION
• MAY HAVE ALOPECIA MAY EFFECT HAIR FOLLICLE AND
PRODUCE SPORADIC HAIR LOSS
• HBP, HEART DISEASE ARTHRITIS, GLAUCOMA MAY CO EXISTRX’S MAY POTENTIATE SIDE EFFECTS FROM AESTHETIC
TREATMENTS
DIABETIC SKIN
AESTHETIC TREATMENT
AHA’S - BHA’S - JESSNERS - IPL
MICRODERMABRASION -ACIDS - SALTS - SCRUBS
• NO SALICYLIC ACID - CAN POTENTIATE SULFONYLUREAS &
CAUSE HYPOGLYCEMIA.
• NIACIN, CORTICOSTERIODS & ESTROGEN CAN INCREASE
SUGAR LEVELS IN THE BLOOD CAUSING HYPOGLYCEMIA
DIABETIC SKIN
AESTHETIC TREATMENT
• TREAT AS SENSITIVE SKIN
• MILDER CRÈME PASTE ENZYMES / PAPAYA
• FOCUS ON IMPROVING TEXTURE AND PERIPHERAL
CIRCULATION
• MANUAL LYMPHATIC DRAINAGE W MD / RX
XANTHELASMA
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XANTHELASMA
PATHOLOGY & ETIOLOGY
• MULTIPLE, LONGITUDAL CREAMY ORANGE, SLIGHTLY
ELEVATED PAPULES
• INDICATIVE OF LOCAL METABOLIC DISEASE AND CELLULAR
DYSFUNCTION
• CAUSED BY ACCUMULATION OF FAT IN MACROPAGE IMMUNE
CELLS
• MAY SIGNAL CARDIO VASCULAR DISEASE OR HYPERLIPIDAEMIA
(HIGH BLOOD FATS)
XANTHELASMA
PATHOLOGY & ETIOLOGY
• MAY ALSO BE SECONDARY HYPERLIPIDEMIA ASSOCIATED
WITH:
DIABETES CHIRRHOSIS RENAL FAILURE ALCOHOLISM
HYPERTHYRIODISM
PANCREATITIS
• AGE OF ONSET 50 Y.O.
XANTHELASMA
MEDICAL INTERVENTION & AESTHETIC TREATMENT
•
•
•
•
•
•
LASER
EXCISION
ELECTRODESSICATION
TRICHLORACETIC ACID
DISEASE MANAGEMENT
AESTHETIC TREATMENT
ACANTHOSIS NIGRACANS
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ACANTHOSIS NIGRACANS
PATHOLOGY & ETIOLOGY
• DIFFUSED VELVETY THICKENING OF PRIMARILY THE NECK,
BODY FOLDS, GENITALS, KNUCKLES, UNDER BREASTS
• REPRESENTS AN UNDERLYING HEALTH CONDITION RATHER
THAN A SKIN DISEASE
• MAY BE CAUSED BY HYPERSECRETION OF THE PITUITARY
PEPTIDE, OR NON SPECIFIC GROWTH PROMOTING THE EFFECTS
OF HYPERINSULINEMIA
ACANTHOSIS NIGRACANS
PATHOLOGY & ETIOLOGY
•
ENDOCRINE INFLUENCES - OBESITY
•
TYPE 2 DIABETES
•
CUSHINGS DISEASE, ADDISONS DISEASE
• HYPOTHYRIODISM
• MAY ALSO REPRESENT AN INTERNAL MALIGNANCY OF THE
GASTROINTESTINAL TRACT IN RARE CASES
ACANTHOSIS NIGRICANS
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• CORRECT UNDERLYING DISEASE PROCESS
•
•
•
•
•
•
•
•
•
INSULIN MANAGEMENT
GLUCOCORTICOID THERAPY
LASER
TOPICAL RETINIODS
NICOTONIC ACID
ISOTRETINION, METFORMIN
FISH OILS
ENZYME TREATMENT
NO PIGMENTATION THERAPY
BENIGN
NEOPLASMS
& CYSTS
SEBACEOUS HYPERPLASIA
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SEBACEOUS HYPERPLASIA
PATHOLOGY & ETIOLOGY
• SMALL ELEVATED TUMORS - BENIGN CONDTION OF THE
SEBACOUS GLANDS
• SINGLE OR MULTIPLE, PALE YELLOW, SLIGHTLY ELEVATED
PAPULE
• FOUND ON THE FOREHEAD,CHEEKS, LOWER LID, NOSE
• DEVELOP FROM SEBOCYTE CELLS & INCREASED LIPIDS AT
CENTRAL EXCRETORY DUCT, AND A DECREASED EPIDERMAL
CELL TURNOVER
SEBACEOUS HYPERPLASIA
PATHOLOGY & ETIOLOGY
• APPEAR AFTER 30 Y.O. IN 25% OF POPULATION
• GENETIC PREDISPOSITION POSSIBLE
• MAY COINCIDE WITH LONGTERM IMMUNOSUPPRESSION WITH
CYCLOSPORIN
• POSSIBLE INVOLVEMENT OF A DECREASE IN CIRCULATING
ANDROGENS AS WITH OCCURS WITH AGING
SEBACEOUS HYPERPLASIA
MEDICAL INTERVENTION
•
•
•
•
•
•
•
•
EXCISION BIOPSY - TO R/O BASAL CELL
CRYOSURGERY
EXCISION, SHAVE EXCISION
AMINOLEVULINIC ACID & UV
TRICHLORACETIC ACID
ELECTRODESSICATION
LASER- ARGON, PULSE DYE & CO2
RETIN - A
SEBACEOUS HYPERPLASIA
AESTHETIC TREATMENT
• RETINOIDS
• LACTIC, GLYCOLIC ACID
• AZELAIC ACID
• L ASCORBIC ACID
• ENZYMES
• MICRODERMABRASION
SKIN TAGS
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SKIN TAGS
PATHOLOGY / ETIOLOGY
• ALSO CALLED ACROCHORDONS
• COMMON SOFT NEOPLASM CONSTRUCTED OF COLLAGEN
FIBER & BLOOD VESSELS
• SKIN COLORED OR PIGMENTED, AND RANGE IN SIZE FROM1
MM TO 5 CM
• APPEAR IN SKIN FOLDS, NECK, ARMPITS
SKIN TAGS
PATHOLOGY / ETIOLOGY
• MAY DEVELOP AS A RESULT OF CHAFFING & IRRITATION OR
HUMAN PAPILLOMA VIRUS (WART VIRUS)
• PEDUNCULATED - LESION WITH STALK LIKE ATTACHMENT TO
THE SKIN
• FILIFORM - LESION THAT APPEARS TO BE THREAD LIKE
• TEND TO BE MORE NUMEROUS IN TYPE 11 DIABETES &
OBESITY
SKIN TAGS
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• CURVED OR SERRATED SCISSOR BLADE EXCISION
• SIMPLE BLADE EXCISION
• ELECTRODESSICATION
• CYROSURGERY
• LIGATION (SUTURE OR COPPER WIRE TENSION)
• COPPER BROMIDE LASER
DERMATOSIS PAPULOSA
NIGRA
PATHOLOGY / ETIOLOGY
• BENIGN CUTANEOUS CONDITION PREVELANT IN DARKER
SKIN TYPES AND ASIANS
• EFFECTS FEMALES MORE THAN MALES
• MULTIPLE, SMALL, HYPERPIGMENTED, FLAT TO SEMI FLAT
PAPULES APPROX. 1 - 5 MM - GENETIC PREDISPOSITION 4045%
• FOUND PRIMARILY ON THE MALAR AREA OF THE FACE &
FOREHEAD, MAY PRESENT ON THE NECK, UPPER BACK,
CHEST
DERMATOSIS PAPULOSA
NIGRA
PATHOLOGY / ETIOLOGY
• BELIEVED TO BE A NEVIOD DEVELOPMENTAL DEFECT OF THE
PILOSEBACEOUS FOLLICLE
• INCIDENCE, SIZE AND QUANTITY OF THE LESIONS INCREASE
WITH AGE
DERMATOSIS PAPULOSA NIGRA
MEDICAL INTERVENTION& AESTHETIC TREATMENT
• TREATMENT IS NOT GENERAL, UNLESS LESIONS ARE
UNDESIRABLE
• AGGRESSIVE THERAPIES MAY PRESENT PIH AND KELOID
SCARRING
• SUPERFICAL LIQUID NITROGEN THERAPY
• CURETTAGE
• ELECTRODESICATION
• COPPER BROMIDE LASER
• NO SPECIALIZED AESTHETIC TREATMENT FOR THIS DISORDER
REFER CLIENT TO PHYSICIAN ONLY
NEVI
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DOME
BLUE
DOME
COBBLESTONE
A -TYPICAL
A - TYPICAL
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NEVI
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NEVUS SPILLUS
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COBBLESTONE
DOME
A TYPICAL
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DOME
NEVI
PATHOLOGY & ETILOGY
• ACQUIRED MELANOCYTIC NEVOCELLULAR ARE BENIGN
TUMORS
• DUE TO PROLIFERATION OF PIGMENT CELLS & MELANOCYTES
• VARY IN TONE FROM FLESH, TO PINK TO BLACK OR BROWN
• NUMBER OF MOLES IS DEPENDANT ON GENETICS AND
AMMOUNT OF SUN EXPOSURE
NEVI
PATHOLOGY & ETILOGY
• MELANOCYTIC MAY BE CONGENITAL OR DEVELOP OVER
YEARS
• MOLES MAY DARKEN FOLLOWING SUN EXPOSURE OR
PREGNANCY
• CONVENTIONAL ACQUIRED NEVI ARE ARE < THAN 1 CM
• EXCISION REMOVAL PERMITS HISTOLOGY / SCREENING
NEVI
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• SHAVE BIOPSY
• EXCISION BIOPSY
• PUNCH BIOPSY
• ELECTRODESSICATION
• CYROTHERAPY
KERATOSES & PRE
CANCEROUS
LESIONS
ACTINIC- SOLAR
KERATOSES
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ACTINIC-SOLAR KERATOSES
PATHOLOGY & ETIOLOGY
• SUN INDUCED PRE MALIGNANT LESIONS THAT INCREASE
WITH AGE - ABNORMAL CELL DEVELOPMENT
• ACQUIRED WITH YEARS OF HABITUAL SUN EXPOSURE
• MULTIPLE, DISCRETE, FLAT OR THICKENED, SCALY, SKIN
COLOR LESIONS
• TYPICALLY HAVE A ERYTHEMATOUS BASE AND ARE ABOUT
3-10 MM & MAY ENLARGE INTO MORE ELEVATED LESIONS
ACTINIC-SOLAR KERATOSES
PATHOLOGY & ETIOLOGY
• MAY PRESENT YELLOW CRUSTS & FLAKING, PEELING &
OBVIOUS INFLAMMATION
• THE DEVELOPMENT OF THESE LESIONS MAY BEGIN AS
EARLY AS 20 YEARS OLD IN INDVIDUALS WHO RECEIVE HIGH
SUN EXPOSURE AND DO NOT USE SUN PROTECTION.
• WHEN THE BODY EXHIBITS DEPRESSED IMMUNITY, THE
LESIONS WILL OFTEN PRESENT INCREASED ERYTHEMA
• PRE DISPOSITION IS GENERALLY PRESENT - ESPECIALLY
WITH FAIR SKINNED & LIGHT HAIR INDIVIDUALS.
ACTINIC-SOLAR KERATOSES
PATHOLOGY & ETIOLOGY
• COMMON ON FACE, NOSE, CHEEK, UPPER LIP AND
FOREHEAD
• MAY ALSO APPEAR ON AREAS CONTINUALLY EXPOSED TO
THE SUN - HANDS, CHEST, EARS
• MAY DEVELOP INTO SQUAMOUS CELL
• OZZING SUGGESTS DEGENARATION INTO MALIGNANCY
ACTINIC-SOLAR KERATOSES
MEDICAL INTERVENTION
•
•
•
•
•
•
•
•
CYROSURGERY
CURETTAGE
DIATHERMY
SURGICAL EXCISION
RETIN - A
5 - FLUOROURACIL CREAM
IMIQUIMOD
PHOTODYNAMIC THERAPY -CHEMICAL / LIGHT THERAPY
WITH AMINOLEVULINIC ACID
ACTINIC-SOLAR KERATOSES
MEDICAL INTERVENTION
•
•
•
•
•
•
•
•
FLASHLAMP
Q SWITCHED YAG LASER
COPPER BROMIDE LASER
IPL PHOTODERM
Q SWITCHED ALEXANDRITE
Q SWITCHED RUBYSUNSCREEN
CHEMICAL PEELING
DICLOFENAC GEL
ACTINIC-SOLAR
KERATOSES
AESTHETIC TREATMENT
•
•
•
•
•
•
AHA’S
VITAMIN C
RETINOIDS
AZELAIC ACID
IPL
LED
SEBHORREIC KERATOSES
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SEBHORREIC KERATOSES
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SEBHORREIC KERATOSES
ETIOLOGY & PATHOLOGY
• MOST COMMON BENIGN NEOPLASMS
• HAVE NO MALIGANT POTENTIAL
• DEVELOP FROM PROLIFERATION OF EPIDERMAL CELL &
PRESENT DRY, ROUGH IRREGULAR LESIONS
• THE LESIONS DEVELOP A VELVETY FINISH WITH
MATURATION AND MAY FEEL GREASY TO THE TOUCH
SEBHORREIC KERATOSES
ETIOLOGY & PATHOLOGY
• EPIDERMAL GROWTH FACTORS & RECEPTORS HAVE BEEN
IMPLICATED IN THE DEVELOPMENT OF SEBORRHEIC
KERATOSES
• SOME CASES ARE INHERITED FROM AN AUTOSOMAL
DOMINANT MODE OF GENETICS
SEBHORREIC KERATOSES
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• AMMONIUM LACTATE
• ALPHA HYDROXY ACIDS
• TRICHLORACETIC ACID
• ELECTRODESSICATION
• COPPER BROMIDE LASER
• SHAVE EXCISION
• DERMABRASION
• SHAVE BIOPSY
• CRYOSURGERY
• CURETTAGE
AESTHETIC TREATMENT
CARCINOMA
A B C D’S
OF
CANCER
ASYMMETRICAL SHAPE
UNEVEN BORDER
MULTIPLE COLORS
DIAMETER
BASAL CELL CARCINOMA
MALIGNANT B. CELL
MALIGNANT B. CELL
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BASAL CELL
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PIGMENT B. CELL
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MALIGNANT B. CELL
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BASAL CELL
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BASAL CELL CARCINOMA
• MOST COMMON MALIGNANT CUTANEOUS NEOPLASM
• TYPICALLY APPEARS ON FAIR SKIN WITH PREVIOUS
SUNBURNS
• BLEEDING OR SCABBING SORE THAT HEALS AND REOCCURS
• MAY PRESENT A SMALL TRANSLUCENT GROWTH WITH
ROLLED EDGES
• 85% APPEAR ON HEAD & NECK - 25% OCCUR ON NOSE
BASAL CELL CARCINOMA
• USUALLY NOT LIFE THREATENING
• MAY ALSO APPEAR AT THE SITE OF PREVIOUS TRAUMASCARS, THERMAL BURNS
• THERE IS A TENDANCY FOR BCC INHERITANCE
• SUN EXPOSURE, TANNING BEDS INCREASE RISK
• NODULAR, SUPERFICIAL, SCLEROSING, ULCERATED,
PIGMENTATED, MULTIPLE SUPERFICIAL
BASAL CELL CARCINOMA
• CURETTAGE
• ELECTRODESSICATION
• EXCISION SURGERY
• MOH’S SURGERY
• CRYOSURGERY
• PHOTODYNAMIC THERAPY - CHEMICAL
• IMIQUIMOD CREAM
• RADIOTHERAPY ( X- RAY, SMALL DOSES)
• SUNSCREENS
SQUAMOUS CELL
CARCINOMA
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SQUAMOUS CELL
CARCINOMA
• OCCUR IN MIDDLE AGE AND ELDERLY POPULATION
• FOUND IN OUTER LAYERS OF EPIDERMIS & IS A FORM OF
KERATINOCYTE
• OFTEN PRESENT A RED, SCALY LESION THAT WILL NOT
HEAL
• LESIONS THAT DO NOT HEAL WITHIN 3 WEEKS SHOULD BE
EVALUATED
• LESIONS ON THE LIP OR EAR TEND TO METASTASIZE IF
UNCHECKED
SQUAMOUS CELL
CARCINOMA
• MOST EVASIVE SCC’S DEVELOP FROM SOLAR KERATOSES
OR MAY DEVELOP FROM LEG ULCERS
• PRIOR RADIATION, CHEMICAL BURNS, CHRONIC ULCERS
MAY PRESENT HIGH FREQUENCY OF HIGH METASTASIS
• MAY MEASURE FROM A FEW MILLIMETERS TO CENTIMETERS
SQUAMOUS CELL
CARCINOMA
•
•
•
•
•
•
•
•
•
ELECTRODESSICATION
EXCISION SURGERY
CURETTAGE
CYROSURGERY
MOH’S SURGERY
5 - FLUOROURACIL CREAM
IMIQUIMOD CREAM
RADIATION
SUNSCREENS
MALIGNANT MELANOMA
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MALIGNANT MELANOMA
•
MOST DANGEROUS / MAY METASTASIZE INTO ORGANS
• ORIGINATES IN THE MELANOCYTIC SYSTEM & DEVELOPS
FROM AN EXHISTING LESION (MOLE)
• DETERMING FACTORS INCLUDE: DEGREE OF PIGMENTATION,
GENETICS, EXTENT OF SUN EXPOSURE, ANATOMIC POSITION &
IMMUNOLOGIC STATUS
MALIGNANT MELANOMA
• CLINICAL MELANOMA
• SUPERFICIAL SPREADING MELANOMA
• LENTIGO MALIGNA MELANOMA
• NODULAR MELANOMA
• ACRALENTIGINOUS MELANOMA
CANDIASIS
& TINEA
FACIALIS
CANDIASIS & TINEA
TINEA
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CANDIASIS &TINEA
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CANDIASIS
PATHOLOGY & ETIOLOGY
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INFLAMMATORY REACTION OF THE SKIN DUE TO CANDIDA
ALBICANS YEAST
• COLONIZE IN THE GASTROINTESTINAL TRACT
• MAY EFFECT MOUTH, FACE, GENITALS & SKIN FOLDS
• OVAL SHAPED, RED, INFLAMMED PATCHES, SMALL PAPULES,
MARGINAL SCALING WITH PALE WHITE EDGES
• MAY MANIFEST ON MOIST OCCLUDED SKIN
CANDIASIS
PATHOLOGY & ETIOLOGY
DIABETICS
HOST FACTORS:
IMMUNO COMPRISED
OBESITY
SYSTEMIC & TOPICAL GLUCOCORTICOIDS
EXCESSIVE ANTIBIOTIC USE EXCESS SUGAR IN DIET
ORAL CONTRACEPTIVES IUD DEVICE
LACK OF HYDROCHLORIC ACID
*BARTENDERS, FLORISTS, HEALTH CARE WORKERS
CANDIASIS
AESTHETIC TREATMENT
AHA’S, BHA’S MICRODERM, MICROCURRENT, BRUSHING
GOMMAGE, ALCOHOL, ESSENTIAL OILS
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MAY NOT TREAT THE SKIN UNTILL MOIST
LESIONS ARE DRY - TREAT AS SENSITIVE SKIN
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> LYMPHATIC DRAINAGE / W M.D. / RX
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OXYGEN THERAPY
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AZULENE, ST. JOHNS WORT, PROBIOTICS, COMFREY
ALOE, YOGURT, LICORICE
CANDIASIS
ALTERNATIVE MEDICINE
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AVOID SUGAR & SIMPLE CARBS
COMFREY, ROSEMARY & CALENDULA OINTMENT
AVOID MUCOUS & FUNGUS FORMING FOODS
PROBIOTICS
CANDIDA DIET
EFA’S
INCREASE PROTIEN
MAGNESIUM
L- CARNITINE
CHROMIUM GTF
TINEA FACIALIS
PATHOLOGY & ETIOLOGY
• WELL CIRCUMSCRIBED MACULE - PLAQUE
• ELEVATED BORDER, CENTRAL REGRESSION - PINK TO RED
IN COLOR
• MAY PRESENT ASYMETRY
• ANIMAL EXPOSURE, CHRONIC TOPICAL APPLICATION OF
GLUCOCORTIODS
• DIFFERENTIAL - SEBORRHEIC DERMATITIS, CONTACT
DERMATITIS, LUPUS, PHOTOTOXIC DRUG ERRUPTION
TINEA FACIALIS
MEDICAL INTERVENTION
TOPICAL & SYSTEMIC
ANTIFUNGALS
LOTRIMIN MICATIN
NIZORAL
LOPROX
NAFTIN
LAMISIL
FLUCONAZOLE
KETOCONAZOLE
TERBINAFINE
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TINEA FACIALIS
AESTHETIC TREATMENT
AESTHETIC TREATMENT
ATOPIC
DERMATITIS
(ECZEMA)
ATOPIC DERMATITISECZEMA
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ATOPIC DERMATITIS ECZEMA
PATHOLOGY
& ETIOLOGY
• PRURITIC DISEASE THAT USUALLY BEGINS IN INFANCY
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MAY LEAD TO LICHENIFICATION & HYPERPLASIA
DUE TO RUBBING & SCRATCHING
• POORLY DEFINED PATCHES, ERYTHEMA - WITH OR W/O
SCALES - MAY PRESENT EDEMA & VESICLES
• MAY OOZE SERUM & FORM DRY CRUSTS
ATOPIC DERMATITIS ECZEMA
PATHOLOGY
& ETIOLOGY
• ACUTE, SUB ACUTE OR CHRONIC RELAPSING DISORDER INTERNAL & EXTERNAL FACTORS
• SERUM & CELLULAR HISTAMINE RELEASE TRIGGERING
ANTIGEN - ANTIBODY REACTIONS
• REPETATIVE CYCLES OF DRYNESS & ITCHING
• MAY INDICATE ZINC OR VITAMIN A DEFCIIENCY
ATOPIC DERMATITIS ECZEMA
PATHOLOGY
& ETIOLOGY
• EFFECTS FACE, FOREHEAD, EYES,NECK, CHEST, HANDS, FEET
• THE CHRONIC FORM PRESENTS LICHENIFICATION / LESS
ERYTHEMA & MORE ITCHING
• LIPID ABNORMALITIES INCREASE TRANSPIDERMAL WATER
LOSS
• CONTACT ALLERGAN TRIGGER
• CANDIDIA ALBICANS, HYDROCHLORIC ACID DEFICIENCY
ATOPIC DERMATITIS ECZEMA
PATHOLOGY
& ETIOLOGY
• GENETICS - ASTHMA, ALLERGIC RHINITIS, FOOD ALLERGIES
• ELICITING FACTORS: WHEAT EGGS, MILK, PEANUTS, FISH &
SOY & AREOALLERGANS - DUST MITES
• RECURRENT STAPHYLOCOCCAL INFECTIONS
PATHOPHYSIOLOGY GUIDELINES
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CLIENT WILL PRESENT AN ITCHY SKIN CONDITION
HISTORY OF INVOLVEMENT IN THE SKIN CREASE & FOLDS
CHRONIC DRYNESS, DISCOMFORT ITCHING
PERSONAL HISTORY OF ASTHMA, HAY FEVER OR ATOPIC
DISEASE
HISTORY OF DRY SKIN WITHIN THE LAST YEAR
DERMATITIS ON THE CHEEK OR FOREHEAD
POSSIBLE LATERAL THINNING OF THE EYEBROWS
EXTRA CREASE OF TISSUE UNDER THE EYES
ATOPIC DERMATITISECZEMA
MEDICAL INTERVENTION
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EMOLLIENTS
COOL ROOMS
DUST REDUCTION
OIL BATHS
HYDROCORTIZONE
WET DRESSINGS
BENADRYL- TOPICAL & SYSTEMIC
NEOMYCIN SULFATE
CALADRYL LOTION
KERAMYCIN
ANTIHISTAMINES
“HYPOALLERGENIC” SOAPS & LAUNDRY DETERGENTS
ATOPIC DERMATITISECZEMA
MEDICAL INTERVENTION
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ORAL & TOPICAL ANTIBIOTICS
ORAL & TOPICAL STERIODS
ORAL CORTICOSTERIODS
IMMUNOMODULATORS
CICOSPORIN
PHOTOTHERAPY
AVOID HYDRAZINE DYES - FD&C YELLOW # 5
ATOPIC DERMATITISECZEMA
AESTHETIC TREATMENT
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HYDRATING, SOOTHING TREATMENT
LED DIODE
OXYGEN THERAPY
HYPERICUM
CALENDULA
SEA BUCKTHORN EXTRACT
CHAMOMILE
AZULENE
PARAFFIN TREATMENT WITH EFA’S
ATOPIC DERMATITISECZEMA
ALTERNATIVE MEDICINE
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INFLAMMATORY SIGN OF INTERNAL TOXINS
EXPEL TOXINS FROM THE INSIDE 1ST
R/O FOOD SENSITIVITES
AVOID AMINAL FATS ) ARACHADONIC ACID
> HYDROCHLORIC ACID / DRINK VINEGAR & H20
DEAD SEA SALT BATH
> OMEGA 3&6
> QUERCETIN
B COMPLEX, B12, FOLIC ACID, BIOTIN, ZINC
AVOID ORAL CONTRACEPTIVES, EXCESSIVE PROTIEN INTAKE
ATOPIC DERMATITISECZEMA
ALTERNATIVE MEDICINE
• > FOODS WITH VITAMIN A, C, E , B’S, ZINC, COPPER, SELENIUM
• AVOID IODINE & BROMIDES
• AVOID FOODS THAT PROVOKE ALLERGIC REACTIONS PEANUTS SEAFOOD EGGS MILK
SOY
WHEAT CHOCOLATE ALCOHOL SPICY FOOD
TROPICAL FRUIT
RED MEATS
DERMATITIS
ALLERGIC CONTACT
DERMATITIS
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ALLERGIC CONTACT
DERMATITIS
PATHOLOGY & ETIOLOGY
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IRRITANT CONTACT DERMATITIS - EXPOSURE TO CHEMICAL OR
OTHER ANTIGEN THAT ELLICITS A HYPERSENSITIVTY REACTION
• CONTACT ALLERGIC DERMATITIS - ACUTE OR CHRONIC
INFLAMMATORY REACTION TO SUBSATNCED THAT COME IN
CONTACT WITH THE SKIN
• C.A.D. REACTION OCCURS SOME HOURS AFTER CONTACT, AND
DIMINISHES PROVIDING THE SKIN HAS NO FURTHER CONTACT
• ACUTE-WELL DEMARCATED PLAQUES OF ERYTHEMA AND
EDEMA WHICH ARE SUPERIMPOSED AND CLOSELY SPACED
ALLERGIC CONTACT
DERMATITIS
PATHOLOGY & ETIOLOGY
• SUBACUTE - PLAQUES OF MILD ERYTHEMA, SMALL DRY SCALES
OR SUPERFICIAL DESQUIMATION
• CHRONIC- THICKENING OF THE EPIDERMIS, SCALING,
PAPULES,EXCORIATIONS, PIGMENTATION, MILD ERYTHEMA
ALLERGIC CONTACT
DERMATITIS
PATHOLOGY & ETIOLOGY
ALLERGANS
LOTIONS
DYES
CREAMS
JEWELRY
PERFUME
ESSENTIAL OILS
ANIMAL ENZYMES PRINTERS INK
OXIDIZING AGENTS TOPICAL MEDICATIONS
PLASTICS
METALS
LAUNDRY DETERGENT
INDUSTRIAL OILS
AGRICULTURAL EMISSIONS
RUBBER
DISENFECTANTS
COSMETICS
GASES
SKIN & HAIR PRODUCTS
ALLERGIC CONTACT
DERMATITIS
MEDICAL INTERVENTION
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PREVENTION - REMOVE SOURCE OF ALLERGAN
WET DRESSINGS - BURROWS SOLUTON
PREDNISONE
TOPICAL CORTICOSTERIODS
SYSTEMIC CORTICOSTERIODS
EMOLLIENT CREAMS
CICLOSPORIN
AZATHIOPRINE
OATMEAL THERAPY - HOME BATHS, COMPRESSES, MASKS &
CREAMS
ALLERGIC CONTACT
DERMATITIS
AESTHETIC TREATMENT
AESTHETIC TREATMENT
PERI - ORAL DERMATITIS
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PERI ORAL DERMATITIS
PATHOLOGY & ETILOGY
• IRREGULARLY GROUPED PAPULOPUSTULES
• ERYTHEMA, NO COMEDONES
• INITIAL LESIONS ARE PERIORAL, SPARING VERMILLION OF LIPS
• SENSATION OF BURNING AND TIGHTNESS
• PERIORAL AREA, NASO LABIAL FOLD - PERIORBITAL (EYES)
• EFFECTS MOSTLY WOMEN - 20 - 45 Y.O.
PERI ORAL DERMATITIS
PATHOLOGY & ETILOGY
• UV LIGHT, HEAT & WIND INCREASE SYMPTOMOLOGY
• EXCESSIVE USE OF TOPICAL STERIODS MAY PRECIPITATE
• FUSIFORM SPIRILLA BACTERIA & CANDIDIA SPECIES
• GASTROINTESTINAL DISTURBANCES, MALABSORPTION,
HORMONAL DISTURBANCES
• MAY INDICATE DENTAL INFECTIONS
PERI ORAL DERMATITIS
PATHOLOGY & ETILOGY
• FLUORINATED TOOTHPASTE
• CINNAMON, ANISE, PEPPERMINTTOOTHPASTE
• RED & YELLOW - FOOD & COSMETIC DYES
• PETROLATUM OR PARAFFIN BASED COSMETICS
• ISOPROPRYL MYRISTATE
PERI ORAL DERMATITIS
PATHOLOGY & ETILOGY
• DIFFERENTIAL DIAGNOSIS:
ROSACEA, ECZEMA OR SEBACEOUS DERMATITIS
• TOPICAL GLUCORTICOID ‘S / MAY AGGRAVATE CONDITION
• RULE OUT STAPHYLOCOCCUS INFECTION
• MAY LAST WEEK TO MONTHS
PERI-ORAL DERMATITIS
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• ANTI INFLAMMATORY - TOPICAL & SYSTEMIC
• LOW POTENCY CORTICOSTEROIDS
• AVOID TRIGGER STIMUALANTS ( ALCOHOL, SPICY FOODS)
• NYDRAZID
• ISOTRETINOIN (ACCUTANE)
• METRONIDAZOLE
• ERYTHROMYCIN
• MINOCYCLINE
• DOXYCYCLINE
AESTHETIC TREATMENT
• TETRACYCLINE
FACTITIAL DERMATITIS
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FACTITIAL DERMATITIS
PATHOLOGY & ETIOLOGY
• ONSET DUE TO CHRONIC STRESS OR PSYCHIATRIC ORIGIN
• VARIOUS ERRATIC PLACEMENT OF EXCORIATIONS
• CAUSED BY HABITUAL PICKING, SCRATCHING OR GOUGING
WITH THE FINGERNAILS
• MAY PRESENT HYPERPIGMENTATED MACULES
• LESIONS ARE LOCATED ONLY AT AREAS WHERE THE HANDS
CAN REACH
FACTITIAL DERMATITIS
MEDICAL INTERVENTION
• INTRALESIONAL TRIAMCINOLONE
• PIMOZIDE
• PSYCHIATRIC COUNSELING
FACTITIAL DERMATITIS
AESTHETIC TREATMENT
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RX FROM MD / INFORMED CONSENT
CAUTIOUS APPROACH & MONITOR BEHAVIOR
BASIC SKIN CARE PROTOCOLS / FREQUENT VISITS
NO MICRODERM , PEELS OF ANY KIND UNTIL MD APPROVES
DO NOT TREAT OPEN LESIONS
DEMONSTATE & REVIEW PRODUCT APPLICATION / MOA
SHEETS FOR HOME CARE
• ENCOURAGE INTERACTION / PARTICIPATION
• IF BEHAVIOR PRESISTS, REFER BACK TO MD & DISCONTINUE
SERVICES
• Be positive - not condescending!
SEBORRHEIC DERMATITIS
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SEBORRHEIC DERMATITIS
PATHOLOGY& ETILOGY
• EFFECTS 2-5 % OF POPULATION
• PINK, OILY EDEMA- YELLOW & BROWN CRUSTS- FACE, EARS,
HAIR & UPPER TRUNK
• DRY SCALING PAPULES 5 - 20 MM, STICKY CRUSTS, SCALING
• APPEARS WHERE SEBACOUS GLAND MOST ACTIVE
• GRADULA ONSET- MAY BE WORSE IN DRY WINTER
• ZINC DEFICIENCY
SEBORRHEIC DERMATITIS
PATHOLOGY& ETILOGY
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STAPHYLOCOCCUS AUREUS
CORNEOBACTERIUM ACNE
CANDIDA ALBICANS
MALASSEZIA (PITYROSPORUM ORBICULARE) YEAST
COLONIZATION
• THE INTENSITY OF THE DERMATITIS IS IN PROPORTION TO
THE FUNGUS
• EMOTIONAL & PHYSICAL STRESS TRIGGER
SEBORRHEIC DERMATITIS
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• GLUTOCORTICOIDS (MAY CAUSE ERYTHEMA,
TELANGECTASIA, PERIORAL DERMATITIS OR ROSACEA)
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COAL TAR, SALICYLIC ACID - SCALP
LACTIC ACID
MICRONAZOLE CREAM
KETOCONAZOLE
AESTHETIC TREATMENT
CICLOPIROX
HYDROCORTISONE
SEBORRHEIC DERMATITIS
ALTERNATIVE MEDICINE
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INTERNAL DETOXIFICATION
DEAD SEA SALT BATHS
AVOID FOOD TRIGGERS
> FOODS WITH BETA CAROTENE, VITC, B12, FOLATE, ZINC,
BIOTIN
> OMEGA 3&6
CALENDULLA
LICORICE
CHAMOMILE
HYPERPIGMENTATION
and
PIGMENTATION
DISORDERS
MELASMA
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MELASMA
PATHOLOGY & ETILOGY
• ACQUIRED BLOTCHY, BROWN MASK LIKE
HYPERPIGMENTATION USUALLY FOUND IN GENETICALLY
PRESDISPOSED WOMEN
• COMMON IN WOMEN 20-40 & TYPICALLY OCCURS DURING
PREGNANCY OR IN CONJUNCTION WITH ORAL
CONTRACEPTIVES
• HORMONAL IMBALANCES & OVARIAN DISORDERS
MELASMA
PATHOLOGY & ETILOGY
• THYROID DYSFUNCTION
• MAY ALSO BE TRIGGERED BY RX DILANTIN
• INHERITED BASELINE SKIN TONES OF LIGHT OLIVE TO DEEP
OLIVE ARE MORE SUSCEPTABLE
• ESTROGEN & UVA - UVB DETERMINING FACTOR IN A PREDISPOSED INDIVIDUAL
MELASMA
MEDICAL INTERVENTION
• FRAXEL LASER
• HYDROQUINONE
• CYROSURGERY
• ALPHA HYDROXY ACIDS
• TRETINION CREAM
• AZELAIC , GLYCOLIC ACID
MELASMA
MEDICAL INTERVENTION
• RETIN -A
• JESSNER PEEL
• TCA PEEL
• TRI LUMA (HYDROQUININE & RETIN A)
• FLUOCINOLONE ACETONIDE
• SOLAGE (TRETINOIN & MEQUINOL INHIBITOR)
MELASMA
AESTHETIC TREATMENT
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LIGHT MICRODERMABRASION
LED DIODE
LASER
GALVANIC / WITH SUPRESSORS
ENZYMES
MODIFIED JESSNER
IPL
ULTRASOUND
CYROSURGERY
AHA’S LESS THAN 30%
MELASMA
SKIN LIGHTENERS & TYROSINASE INHIBITORS
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AHA’S
BHA’S
MELANOSTAT
SCUTELLARIA
RUMEX CRISPUS (YELLOW DOCK)
GRAPEFRUIT SEED EXTRACT
ORYZA SATIVA (RICE)
ASPERGILLUS FERMENT
SOPHORIA ANGUSTIFOLIA
SODIUM ASCORBYL PHOSPHATE
MAGNESIUM ASCORBYL PHOSPHATE
NASTURTIUM OFFICINALE
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LICORICE
ARBUTIN
MULBERRY
GREEN TEA
RETINOL
LACTIC ACID
KOJIC ACID
BEARBERRY
BURNER ROOT
ASCORBIC ACID
VITILIGO
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VITILIGO
PATHOLOGY & ETIOLOGY
• AUTO IMMUNE INFLUENCE IN WHICH MELANOCYTE CELLS ARE
DESTROYED -RESULTING IN IRREGULARLY SHAPED WHITE
PATCHES
• FACE, NECK, EYES, BODY FOLDS, GENITALS
• HAIR MAY GREY AT AN EARLY AGE
• PIGMENTATION LOSS MAY BEGIN BEFORE AGE 20
• MAY BE IN GOOD GENERAL HEALTH, BUT MAY BE MORE
SUSCEPTABLE TO DIABETES, THYRIOD DISEASE, PERNICIOUS
ANEMIA (B12 DEFICIENCY), ADDISONS DISEASE (ADRENAL)
VITILIGO
PATHOLOGY & ETIOLOGY
• GENETIC PRESDISPOSITION - 30% OF CASES
• OXIDATIVE STRESS (EXCESS HYDROGEN PEROXIDE) DUE TO
VIRUSES OR BACTERIA
• THYROID DISORDERS
• PERNICIOUS ANEMIA
• ADRENOCORTICAL INSUFFICIENCY
• NEUROTROPIC ( NERVOUS SYSTEM & MELANOCYTES)
• TOXINS EFFECTING MELANOGENESIS
• TRAUMA
• NUTRIENT DEFICIENCIES AT BIRTH
• 2-5 MILLION PEOPLE IN U.S. HAVE VITILIGO
VITILIGO
MEDICAL INTERVENTION & AESTHETIC TREATMENT
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SUN PROTECTION
DIHYDROXYACETONE (SUNLESS TAN)
TOPICAL STERIOD CREAM
PROTOPIC OINTMENT (JAPAN) SOIL BACTERIUM
PUVA LIGHT THERAPY- PSORALEN RX & UVA
NARROWBAND UVB PHOTOTHERAPY
MICROPIGMENTATION
DEPIGMENTATION - MONOBENZYL ETHER OF HYDROQUINONE
CAMOUFLAGE MAKEUP
VITILIGO
MEDICAL INTERVENTION & AESTHETIC TREATMENT
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ELIDEL (IMMUNOMODULATOR)
ALDARA (IMMUNOMODULATOR)
IMIQUIMOD (IMMUNOMODULATOR)
PSEUDOCATALASE (PCAT) H2O2 REDUCTION CREAM
RATOKERM NARROW UVB BEAM LASER (ITALY)
EXCIMER NARROW UV LASER
V-TAR (COAL TAR)
AUTOLOGOUS MELANOCYTE TRANSPLANT
MELAGENINA CREAM (CUBA)
NOVITIL /SINVITIL / DERMABEST - NATURAL TOPICAL
LENTIGO
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LENTIGO
PATHOLOGY & ETIOLOGY
• SMALL SHARPLY CIRCUMSIZED PIGMENTED MACULE
• MAY EVOLVE OVER YEARS , OR APPEAR SUDDENLY
• PIGMENT MAY BE SOLID, VARIGATED WITH COLOR RANGING
FROM BROWN TO BLACK
• MAY BE A SOLIATARY LESION OR MULTIPLE
LENTIGO
PATHOLOGY & ETIOLOGY
• LENTIGO SIMPLEX - MOST COMMON FORM - NOT INDUCED BY
SUN EXPOSURE
• SOLAR LENTIGO / LIVER SPOTS- DEVELOP FROM SUN
EXPOSURE - COMMON IN CELTIC TYPES
• PUVA LENTIGO - DEVELOP WITH 5 YEARS OR MORE OF PUVA
LIGHT THERAPY
• SUN BED LENTIGO - OCCUR WITH HISTORY OF TANNING BED
USE
LENTIGO
MEDICAL INTERVENTION
• CYROSURGERY
• Q SWITCHED ND YAG LASER
• HGM K1 KRYPTON LASER
• 532 NM DIODE VANADATE LASER
• COPPER BROMIDE LASER
• TRETINION CREAM
• HYDROQUINONE CREAM
SOLAR LENTIGO
AESTHETIC TREATMENT
• LED DIODE
• TRADITIONAL LIGHTENING PRODUCTS
• CYROSURGERY
• KOJIC ACID
• IPL
DRUG INDUCED PHOTOSENSITIVITY
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DRUG INDUCED PHOTOSENSITIVTY
PATHOLOGY & ETILOGY
• ADVERSE PHOTOSENSITIVTY & SIMULTANEOUS EXPOSURE
TO CERTAIN DRUGS
• REACTION MAY BE FROM INGESTION,INJECTION,OR TOPICAL
OF DRUGS AND CONTACT WITH UV LIGHT
• CHEMICAL MAY BE THERAPEUTIC, COSMETIC, INDUSTRIAL
OR AGRICULTURAL
DRUG INDUCED PHOTOSENSITIVTY
PATHOLOGY & ETILOGY
• PHOTOTOXIC = INCREASED REACTION FROM EXPOSURE TO
SUN - EDEMA, VESICLES, ERYTHEMA
• PHOTOALLERGIC = IMMUNOLOGICAL RESPONSE ERRUPTION IS PAPULAR, VESICULAR, ECZEMA LIKE &
OCCURS ONLY IN PEOPLE WHO ARE PREVIOUSLY
SENSITIZED
• STAGE 1- IMMEDIATE ERYTHEMA & URTICARIA
• STAGE 2- DEVELOP SUNBURN PATTERN - 16-24 HR,48-72 HR
• STAGE 3- DELAYED HYPERPIGMENTATION - 72-96 HR
DRUG INDUCED PHOTOSENSITIVTY
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• DIFFICULT TO TREAT
• ABNORMAL REACTIONS EXCLUDE THE USE OF IMPORTANT
DRUGS
• PHOTOTOXIC REACTION DISSAPEARS AFTER THE CESSATION
OF THE DRUG
• IN SEVERE CASES IMMUNOSUPPRESSIVE DRUGS ARE
PRESCRIBED
• GLUCOCORTICIODS
• ORAL CYCLOSPORINE
AESTHETIC TREATMENT
PHYTOPHOTO DERMATITIS
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PHYTOPHOTO DERMATITIS
ETILOGY & PATHOLOGY
• INFLAMMATION CAUSED BY CONTACT WITH CERTAIN PLANTS
DURING RECREATIONAL OR OCCUPATIONAL EXPOSURE TO
SUNLIGHT
• ALSO CALLED BERLOQUE DERMATITIS- NECKLACE AREA
• MAY DEVELOP ON ANY SKIN
• ACUTE VESICLES, ERYTHEMA
• RESIDUAL HYPERPIGMENTAION IN UNUSUAL STREAKS
• WOODS LAMP INDICATES INCREASED PIGMENTARY STAINING
• MAY PRESENT PRURITIS
PHYTOPHOTO DERMATITIS
ETILOGY & PATHOLOGY
PHOTOACTIVE CHEMICALS
LIME
LEMON WILD PARSLEY CELERY
PARSNIPS
CARROT
GREENS
FIGS
PERFUME OILS - OIL OF BERGAMONT
( BERGAPTEN - 5 - METHOXYPSORALEN)
PHYTOPHOTO DERMATITIS
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• WET DRESSINGS
• GLUCOCORTICOIDS
• TREAT ONLY RESIDUAL PIGMENTATION AFTER INFLAMMATION
HAS SUBSIDED
• LED & TYROSINAISE INHIBITORS
• KOJIC ACID
• ENZYMES
• LACTIC ACID
• NO MICRODERMABRASION - AGGRESSIVE PEELING
PSORIASIS
KERATOSIS PILARIS
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KERATOSIS PILARIS
PATHOLOGY & ETIOLOGY
• HEREDITARY DISORDER - ABNORMAL FORMATION OF
KERATIN
• INCREASED CELLULAR HYPERPLASIA- OFTEN ASSOCIATED
WITH ATOPIC DERMATITIS, ASTHMA
• SMALL SPINY FOLLICULAR PAPULES ON THE FACE AND
EXTREMETIES
• THE SMALL CELLS IN THE FOLLICLE FORM A HORNY PLUG
INSTEAD OF EXFOLIATING - WIDENING THE PORES
KERATOSIS PILARIS
PATHOLOGY & ETIOLOGY
• COMMON IN CELTIC & OVERWEIGHT INDIVIDUALS
• WORSE IN THE DRY, COLD WINTER - IMPROVES IN WARM
WEATHER
• MAY REPRESENT CONVERSION DIFFICULTIES WITH BETA
CAROTENE
• CONDITION RESPONDS WELL WITH EFA’S AND VITAMIN A
TOPICALLY
KERATOSIS PILARIS
MEDICAL INTERVENTION
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PROPYLENE GLYCOL/GLYCOLIC - LACTIC ACID MIXTURES
ISOTRETINION
SALICYLIC ACID
GLYCOLIC ACID
LACTIC ACID
TOPICAL RETINOIDS
PULSE DYE LASER
PREPARATIONS CONTAINING UREA
KERATOSIS PILARIS
AESTHETIC TREATMENT
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SALT & SEAWEED BODY TREATMENTS
HYDRATION & SEMI OCCLUSIVE AGENTS
LIPID BASED PARAFFIN TREATMENT
TOPICAL VITAMIN A
KERATOLYTIC AGENTS - ENZYMES
GLYCOLIC ACID - PEELS, LOTIONS
LACTIC ACID - PEELS, LOTIONS
SALICYLIC ACID - PEELS, LOTIONS
LOOFAH EXFOLIATION
PSORIASIS VULGARIS
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PSORIASIS VULGARIS
PATHOLOGICAL PRESENTATIONS
• PLAQUE PSORIASIS - HEAVILY KEATINIZED SILVERY WHITE
PLAQUES
• INVERSE - CHRONIC AND INTENSE INFLAMMATION
• ERYTHRODERMIC- EXCESSIVE SHEDDING, ERYTHEMA
• PUSTULAR- WEEPING & LICHENIFICATION (SCALING)
PSORIASIS VULGARIS
PATHOLOGY & ETIOLOGY
• GLUTTATE- SMALL , ROUND LESIONS
• PSORIATIC ARTHRITIS - MAY DEVELOP FROM CHRONIC &
SEVERE CASES OF THE DISEASE - JOINT PAIN,
INFLAMMATION & STRUCTURAL JOINT DEFORMITIES
• PSORIATIC ARHTHRITIS SIGNS: FEVER, PITTED, CHIPPING
YELLOW FINGERNAILS - INFLAMMED NAIL BED
• EFFECTS 5-8% OF PATIENTS WITH PSORIASIS
PSORIASIS VULGARIS
PATHOLOGY & ETIOLOGY
• CHRONIC RECURRING SCALING PAPULES & PLAQUES ROUND & SERPIGINOUS PATTERNS
• LESIONS ARE PEACHY - PINK PAPULES WITH MARKED
“MICA” SILVERY SCALE
• SCALES MAY OFTEN BE REMOVED BY SCRATCHING
• CELLULAR PROLIFERATION IS 28 TIMES GREATER THAN
NORMAL PRODUCTION OF CELLS - 3-4 DAYS RATHER THAN
28 TO 30 DAYS FOR SKIN CELL MATURATION
PSORIASIS VULGARIS
PATHOLOGY & ETIOLOGY
• IMMUNE MEDIATED - CHRONIC INFLAMMATION
• GROWTH DISTURBANCES ARE SECOND TO AN IMMUNE CELL
INFILTRATION OF THE SKIN AND THE RELEASE OF
CYTOKINES ( IMMUNE MEDIATORS) PROMOTES CELL
GROWTH & INFLAMMTATION AT THE SAME TIME
• EVIDENCE INDICATES THAT LYMPHOCYTES LEAD THE
ATTACK ON THE SKIN
• PSORATIC PLAQUES EXAMPLIFY BREEDING GROUNDS FOR
BACTERIA
PSORIASIS VULGARIS
PATHOLOGY & ETIOLOGY
• MAY LAST FOR YEARS OR DECADES WITH ERRATIC COURSE
OF FLAREUPS
• EFFECTS 1.5% - 2.0% OF THE POPULATION
• ANTIGENS MAY BE THE CAUSE THROUGH DELAYED
HYPERSENSITIVTY MECHANISMS
• FOOD ANTIGENS APPEAR AS IMMUNE COMPLEXES, ATTACH
TO SKIN CELLS & TRIGGER LYMPHOCYTIC ACTIVITY
PSORIASIS VULGARIS
PATHOLOGY & ETIOLOGY
• ONE PARENT HOSTS - 8% OF OFFSPRING ACQUIRE
• BOTH PARENTS HOST - 41% OF OFFSPRING ACQUIRE
• MAY PRESENT STREPTOCOCCAL BACTERIA
• STRESS = GREATEST INFLAMMATION TRIGGER
• ITCHING, RUBBING, SCRATCHING - STIMULATE
PROFLIERATIVE PROCESS
PSORIASIS VULGARIS
PATHOLOGY & ETIOLOGY
• MAY BE LOCALIZED OR SPAN ENTIRE BODY WITH PUSTULAR
& NON PUSTULAR FORMATION
• SYSTEMIC INFECTIONS MAY PROVOKE PSORIASIS
• ENZYMATIC, CYCLIC, NUCLEOTIDE & IMMUNOLOGIC
INFLUENCES
• OTHER FACTORS: SEVERE SUNBURN, TOPICAL DRUGS,
ANTIMALARIAL THERAPY, BETA BLOCKERS, WITHDRAWAL
OF CORTICOSTERIODS
PSORIASIS VULGARIS
MEDICAL INTERVENTION
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PSORALEN / PUVA LIGHT THERAPY (CARCINOGENIC?)
FLUORINATED CORTICOSTERIODS
INTRALESIONAL INJECTIONS
GLUCOCORTICOIDS , TRIAMCINOLONE
TAZAROTENE GEL
METHOTREXATE
CYCLOSPORINE
RETINOIDS, SALICYLIC ACID
COAL TAR / ANTHRALIN
VITAMIN D , VIT A ANALOGUES
NARROW BAND UVB LIGHT - 308 NM
PSORIASIS VULGARIS
AESTHETIC TREATMENT
• APPROACH WITH CAUTION - MD CARE URGED
• NO PEELING, MICRODERMABRASION - CAN TRIGGER
FORMATION OF PLAQUES OR DEVELOP BACTERIAL
INFECTION - DEVELOP SCARRING
• SEA BUCKTHORN EXTRACT
• MINERAL INFUSIONS
PSORIASIS VULGARIS
AESTHETIC TREATMENT
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SALICYLIC ACID CREAM OR LOTION
SQUALENE, SORBITOL
COPPER PEPTIDES
TOPICAL VITAMIN C
TOPICAL VITAMIN A, D & E
GREEN TEA
LED THERAPY
SALINE, SALT WATER
NO WAXING
PSORIASIS VULGARIS
ALTERNATIVE MEDICINE
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R/O FOOD SENSITIVIES
AVOID AMINAL FATS ( ARACHODINIC ACID )
DEAD SEA SALT BATHS
LIMIT SIMPLE CARBOHYDRATES
AVOID ALCOHOL, SPICY FOOD, SEAFOOD, RED MEATS
> FIBER, GARLIC, EFA’S
> FOODS WITH VITAMIN A, E, FOLATE, ZINC, SELENIUM,
TOPICAL VITAMIN D
VIT A,D,
STRESS REDUCTION
VASCULAR
DISORDERS
ANGIOMAS
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ANGIOMAS
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ANGIOMAS
PATHOLOGY & ETILOGY
• BRIGHT RED VASCULAR LESIONS FOUND PRINCIPALLY ON THE
TRUNK
• OFTEN REFERRED TO AS CHERRY OR STRAWBERRY
HEMANGIOMAS
• NUMEROUS MODERATELY DIALTED CAPILLARIES LINED WITH
FLATTEN ENDOTHELIAL CELLS
• FIRST APPEAR ABOUT AGE THIRTY AND INCREASE WITH AGE
ANGIOMAS
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• SURGICAL EXCISION
• COPPER BROMIDE LASER COAGULATION
• IPL
• ELECTRODESSICATION
• CAMOUFLAGE MAKEUP
SPIDER ANGIOMA
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SPIDER ANGIOMA
PATHOLOGY & ETILOGY
• SMALL ,VASCULAR PAPULAR FORMATION - “STARBURST”
PATTERN RADIATING TO FINE ENDINGS
• APPEARS ON FACE, FOREARMS & HANDS
• MAY APPEAR IN CHILDREN WITHOUT ANY SIGNIFICANCE
• PREGNANCY, SYNTHETIC ESTROGEN THERAPY, ORAL
CONTRACEPTIVES
• RARE CASES - VIRAL HEPATITIS , ALCOHOLIC CIRRHOSIS
SPIDER ANGIOMA
MEDICAL INTERVENTION & AESTHETIC TREATMENT
• ELECTRODESSICATION
• COPPER BROMIDE LASER
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IPL
• LED DIODE
• CAMOUFLAGE MAKEUP
NEVUS FLAMMEUS
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NEVUS FLAMMEUS
PATHOLOGY & ETILOGY
• PORT WINE STAIN - CONGENITIAL
• USUALLY PENETRATE TO DERMIS
• IRREGULAR SHAPED RED-VIOLET VASCULAR
MALFORMATION OF DERMAL BLOOD VESSELS
• MOST COMMONLY APPEAR ON THE FACE
• “STORK BITE” VIOLET - PINK PATCH AT NAPE OF THE NECK
NEVUS FLAMMEUS
MEDICIAL INTERVENTION & AESTHETIC TREATMENT
• TUNABLE DYE LASER
• COPPER VAPOR LASER
• CAMOUFLAGE MAKEUP
DERMATOLOGICAL
PROCEDURES
CRYOTHERAPY
• SKIN LESIONS ARE FROZEN FOR REMOVAL WARTS, MOLES, SKIN TAGS, SOLAR KERATOSES, SEBORRHEIC
KERATOSES, SUPERFICIAL BASAL CELLS
• LIQUID NITROGEN SPRAY OR LIQUID CARBON DIOXIDE SNOW
• APPLIED TO THE SKIN FOR A FEW SECONDS TO FREEZE THE
LESION
• CARBON DIOXIDE SNOW IS SOMETIMES MIXED WITH ACETONE
TO FORM A SLUSH MIXTURE
CRYOTHERAPY
• STINGS AND MAY BE PAINFUL
• IMMEDIATE REDNESS, INFLAMMATION AND SWELLING
• TREATMENT AREA WILL BLISTER WITHIN A FEW HOURS
• WITHIN A FEW DAYS A SCAB WILL FORM AND EVENTUALLY
FALL OFF
• TREATMENT MAY RESULT IN SECONDARY
HYPOPIGMENTATION
CURETTAGE & DIATHERMY
• SURGICAL SCRAPING OF A LESION FOR REMOVAL & BIOPSY
• “CURETTE” SPOON SHAPED INSTRUMENT WITH SHARP EDGES
IS USED FOR THE SCRAPING
• THE WOUND SITE IS THEN CAUTERISED WITH A HOT WIRE
BEADED TIP / ELECTROSURGICAL UNIT ( DIATHERMY)
• THE PROCEDURE HELPS TO STOP ANY BLEEDING & AIDS IN
THE DESTRUCTION OF ANY REMAINING TUMOR CELLS
• THIS PROCEDURE WILL ALWAYS LEAVE SOME DEGREE OF
SCARRING, WHICH IS USUALLY FLAT AND ROUND
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THANK YOU FOR PURCHASING
PHYSIOLOGY OF SKIN DISORDERS
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