9. • UV radiation that reaches
the earth’s surface is
UVA and UVB.
• 95% is in the form of
• link of sun exposure
history (UV) and skin
• UVB absorption by DNA results in a p53 tumor suppressor gene mutation
• UVB exposures over time have been associated with the formation of basal cell
carcinoma and melanoma.
• UVA absorption by DNA results information of oxygen free radicals
• UVA exposure has been linked to the development of melanoma in animal models
11. Sunscreens protect the skin either chemically or physically.
• Chemical sunscreens absorb UV (usually UVB) radiation with
the most common sunscreen ingredient being para-aminobenzoic
acid (PABA), benzophenones, and cinnamates.
• Physical sunscreens work by reflecting UV radiation and
producing a protective barrier. They are usually opaque and
include agents such as zinc oxide and titanium dioxide.
12. SPF (Sun Protection Factor) is a measurement of UVB protection only
SPF 30 blocks 97% for 2 hours
Apply 30 min prior and every 2 hr
13. Chemical Peels
• Application of solution to the skin surface
• Sol improve fine lines, acne scars, Wrinkles,
• Not for loose skin or very wrinkles and
Thirty-one-year-old female with melasma
14. • Superficial peels cause exfoliation of the epidermis without deeper penetration.
• Medium peels affect the epidermis and penetrate into the papillary dermis,
• Deep peels penetrate into the reticular dermis where they cause realignment of
15. • Peels are used for a wide variety of skin conditions ranging from
management of photodamage and melasma to hyperpigmentation,
rosacea, and acne.
• Deeper peels tend to have more profound and longer-lasting effect
compared with superficial peels.
16. • Superficial peels include glycolic acid and salicylic acid,
• Medium peels TCA (20%–35%) and Jessner’s
• Deep peels Phenol and TCA (45%–50%).
• Peels are commonly used in conjunction with other skin resurfacing modalities for improved
17. Laser Resurfacing
• Laser resurfacing relies on the principles of selective thermal destruction
(photothermolysis) to disrupt damaged areas of skin and to induce remodeling
31. • Contact dermatitis is an eczematous
dermatitis caused by exposure to
substances in the environment.
• Those substances act as irritants or
allergens and may cause acute, subacute,
or chronic eczematous inflammation.
1 Contact Dermatitis
33. • Irritant contact dermatitis (ICD)
accounts for 80% of all contact
• The classic picture of contact
dermatitis is a
• well demarcated
• vesicular and/or scaly patch or
plaque with well-defined margins
corresponding to the area of contact
34. Management of Irritant Contact Dermatitis
1. Avoid exposure to irritants by using protective
equipment, such as gloves.
2. Topical steroids are used to initially control
inflammation but there is some evidence that they
may compromise barrier function. Some experts
recommend that the use of topical steroids should be
Bilateral irritant contact
dermatitis of the palms
secondary to repeated contact
with paint solvents.
35. 3. Moisturizers used generously and
frequently increase skin hydration, and
their lipid component improves the
damaged skin barrier. Lipid-rich
moisturizers both prevent and treat irritant
4. Barrier creams containing dimethicone or
perfluoropolyethers, cotton liners, and
softened fabrics prevent irritant contact
Bilateral irritant contact dermatitis of the feet
and ankles due to chronic occlusive
36. 5. Cool compresses are used for acute inflammation. They suppress vesiculation
and decrease inflammation.
6. Hands should be washed in cool or tepid water.
7. Repeated low-level ultraviolet (UV) exposures may be effective for long-term
8. Even after the skin appears normal, it takes approximately 4 months or more for
barrier function to normalize.
37. Nickel allergy
Management of Allergic Contact Dermatitis
1. Minimize products for topical use.
2. Use ointments instead of creams (creams contain
preservatives and are complex mixtures of chemicals).
3. Botanical extracts may be used in “fragrance-free”
4. When patch testing, also test the patient’s consumer
5. Read product labels carefully. Many “dermatologist
recommended” products contain sensitizers (e.g.,
lanolin, fragrance, quaternium-15, parabens,
39. • Irritant Contact Dermatitis and Allergic Contact Dermatitis are not always
discernible clinically, patch testing is required to help identify an allergen
• Patch testing is not useful as a diagnostic test for
irritant contact dermatitis because irritant
dermatitis is a non-immunologically mediated
40. Sites of specific patch tests labelled for
future reference following removal of the
41. 2 Atopic Dermatitis
• Atopic dermatitis is a chronic, pruritic inflammatory
skin condition that typically affects the face (cheeks),
neck, arms, and legs but usually spares the groin and
• AD usually starts in early infancy, but also affects a
substantial number of adults
• AD is commonly associated with elevated levels of
immunoglobulin E (IgE).
42. Clinical Features
• Xerosis (dry skin)
• Lichenification (thickening of the skin and an
increase in skin markings)
• Eczematous lesions (skin inflammation)
• Pruritus Early age of onset IgE reactivity
• Peripheral eosinophilia
• Staphylococcus aureus superinfection
44. • It may be accompanied by other disorders such as allergic rhinitis, asthma, food allergies,
and more rarely eosinophilic esophagitis.
46. 3 Acne
• Acne represents a common dermatologic
condition affecting the pilosebaceous units and
typically presents in adolescence.
• Acne lesions favor the face, neck, upper back,
chest, and upper arms.
• The development of acne involves the interplay of a
variety of factors, including:
• (1) follicular hyperkeratinization;
• (2) hormonal influences on sebum production
• (3) inflammation, in part mediated by P. acnes
• Anatomy and Physiology of the pilosebaceous unit
is essential to understanding the pathogenesis of
acne and designing effective treatment regimens.
49. Clinical Features
• Acne is typically found in sites with well-developed sebaceous glands, most often the face
and upper trunk
• Acne lesions are divided into non-inflammatory and inflammatory groups based upon their
• Incidence and age: predominantly a disorder of
adolescence; affects 85% of individuals between 12 and 24
years of age; may affect all age groups
• Race: lower incidence in African-Americans and Asians
• Sex: more severe forms in males
56. Clinical features
• Facial flushing
• Coarseness of skin
• Inflammatory papulopustular
eruption resembling care
• Nonpitting facial edema with
58. Rosacea was classified into four clinical subtypes
• Pilosebaceous unit abnormalities
• Climate exposures
• Dermal matrix degeneration
• Chemical and ingested agents
• Microbial organisms
• Ferritin expression
• Reactive oxygen species(ROS)
• Increased neoangiogenesis
• Patient education for skin care
• Metronidazole (0. 75%-1 % ) once or twice daily,
• 10% sodium sulfacetamide with 5 % sulfur once daily, and
• azelaic acid once daily
• Oral isotretinoin
61. 5 Psoriasis
Is a chronic, complex, multifactorial, inflammatory disease
that involves hyperproliferation of the keratinocytes in the
epidermis, with an increase in the epidermal cell turnover rate.
62. Clinical finding
• Worsening of a long-term erythematous scaly
• Sudden onset of many small areas of scaly
• Recent streptococcal throat infection, viral
infection, immunization, use of antimalarial
drug, or trauma
• Family history of similar skin condition
• Pain Dystrophic nails Long-term rash with
recent presentation of joint pain
63. • The pathogenesis of this disease is not completely understood
• Environmental, genetic, and immunologic factors appear to play a role.
65. Systemic Treatment
• Retinoids, predominanetly acitretin
• Biologics such as alefacept, etanercept, efaluzimab, and infliximab
Laser and Light Treatments
• Psoralen with Ultraviolet A
• Ultraviolet B (UVB), 311-nm narrowband-UVB (NBUVB)
• 308-nm UVB excimer laser
66. • Nevi are benign tumors composed of nevus cells
that are derived from melanocytes.
• The incidence peaks in the fourth to fifth
• They are present in 1% of newborns
Large congenital hairy nevus.
6 Nevi ( Benign Melanocyte Proliferation )
67. Common acquired melanocytic nevi include:
• Junctional nevi: where there is proliferation of the melanocytes at the dermal-
• Compound nevi: with both intraepidermal and intradermal complexes of
• Intradermal nevi: with the melanocytes being located in the dermis
69. Differentiating these from malignant melanoma can be
• The ABCDE pneumonic
Enlarging or evolving
• Risk assessment and treatment options are considered for each patient.
• Medical and psychosocial concerns need to be discussed.
• Management goals are to decrease the risk for developing melanoma by
surgical removal and to produce good cosmetic results.
• Electrocautery should be avoided
• Most common nevi are small and shave excision is adequate.
72. • Timing of surgery is a consideration.
• The best surgical scars result from surgery performed early in life; however, it may be
best to delay surgery until after age 2 when the full extent of the nevus is evident.
• Very large lesions may require multiple procedures.
• Should be removed down to the fascial layer.
73. 7 Alopecia and Hair Disorder
• The causes of hair loss (alopecia) are numerous.
• Most hair problems seen by the practitioner are due to changes in hair-follicle
• Many inflammatory conditions permanently damage the hair follicle, resulting in
• Alopecia can be the result of hair follicle loss, loss of the hair shaft, or a
combination of both.
75. Generalized Hair loss
A number of events have been documented that prematurely terminate
anagen and cause an abnormally high number of normal hairs to enter the resting, or
• The follicle is not diseased
• Scarring and inflammation are absent.
Resting hairs on the scalp are retained for approximately 100 days before
they are lost; therefore telogen hair loss should occur approximately 3 months after
the event that terminated normal hair growth.
76. CAUSES OF TELOGEN EFFLUVIUM
• Shedding of the newborn (physiologic)
• Postpartum (physiologic)
• Chronic telogen effluvium (no attributable cause or illness)
• Postfebrile (extremely high fevers, e.g. malaria)
• Severe infection
• Severe chronic illness (e.g. HIV disease, systemic lupus erythematosus)
• Severe, prolonged psychological stress
• Postsurgical (implies major surgical procedure)
77. • Hypothyroidism and other endocrinopathies (e.g. hyperparathyroidism, hyperthyroidism)
• Crash or liquid protein diets; starvation/malnutrition
- discontinuation of oral contraceptives
- retinoids (acitretin, isotretinoin) and vitamin A excess
- anticoagulants (especially heparin)
- antithyroid (propylthiouracil, methimazole)
- anticonvulsants (e.g. phenytoin, valproic acid, carbamazepine)
- heavy metals
- β-blockers (e.g. propranolol)
78. • Many physicians test patients with hair loss for iron
deficiency and thyroid abnormalities. Iron deficiency is
commonly found in CTE but treatment for it seldom reverses
the hair loss.
• Treat with 5% minoxidil solution.
79. Localized Hair Loss
Androgenic alopecia (Male Pattern Hair Loss)
• Androgenic alopecia represents one of the
most common acquired forms of hair loss
• Baldness in men is not a disease, but rather a
physiologic reaction induced by androgens in
genetically predisposed men.
• Thinning of the hair begins between the ages
of 12 and 40 years
• Incidence: 30% of males older than 30 years; more than half of males older than
50 years .
• Age: begins after puberty.
• Precipitating factors: polygenetic inherited predisposition .
• No diagnostic tests exist to determine the etiology and natural progression .
• Androgens, in particular testosterone and
dihydrotestosterone (DHT), are required for the
progressive reduction in hair follicle size with each
• Androgenetic alopecia is due to the progressive
shortening of successive anagen cycles.
• There are two populations of scalp follicles: androgen-
sensitive follicles on the top and androgen-independent
follicles on the sides and back of the scalp.
84. Low Level Light Therapy
• In 2007, a low level light
device was approved by the
U. S. Food and Drug
Administration ( FDA) to treat
male pattern hair loss
85. Hair Transplantation Procedure
Trim donor region with moustache trimmer, and tape hair
up so donor suture will not be visible in the postoperative
Donor strip should not be more than 1 cm wide. Strips >1 cm
have an increased risk of creating a hypertrophic scar