5. 15.4.Keloids and hypertrophic scars
15.5.Keratoacanthoma
15.6.Epidermal cyst
15.7.Sebaceous hyperplasia
15.8.Syringoma
16. PREMALIGNANT AND MALIGNANT NON-MELANOMA SKIN TUMORS
16.1.Actinic keratosis
16.2.Bowen’s disease
16.3.Leukoplakia
16.4.Paget’s disease of the breast
16.5.Extramammary Paget’s disease
16.6.Cutaneous T-cell lymphoma
16.7.Squamous cell carcinoma
16.8.Basal cell carcinoma
16.9.Cutaneous metastasis
6. 17. NEVI AND MALIGNANT MELANOMA
17.1.Nevi, melanocytic nevi, moles
17.2.Dysplastic nevi
17.3.Malignant melanoma
18. VASCULAR TUMORS
18.1.Hemangiomas of infancy
18.2.Cherry angiomas
18.3.Pyogenic granuloma
18.4.Telangiectasias
18.5.Spider angiomas
Dr. Noemie Ramos: Topics 1 – 6
Dr. Robert Manlapig : Topics 7 – 12
Dr. Diana del Rio: Topics 13 – 18
7. ECZEMA
Definition
- a non-contagious, pruritic, inflammatory skin disorder
- often regarded as synonymous with “dermatitis”
- may be acute, subacute, chronic
Classification
Extrinsic
• Irritant contact dermatitis
• Allergic contact dermatitis
• Photodermatitis
Intrinsic
• Seborrheic dermatitis
• Nummular dermatitis
• Dyshidrotic eczema
• Atopic dermatitis
• Lichen simplex chronicus
• Stasis dermatitis
• Xerotic eczema
IRRITANT CONTACT DERMATITIS
Occurs when strong chemicals or substances insult the integrity of the
epidermis
Non-allergenic in nature – no previous sensitization necessary
Common causes: alkalis and acids
ALLERGIC CONTACT DERMATITIS
Delayed or cell- mediated type hypersensitivity
Caused by an allergen: a substance to which the patient’s skin is specifically
and often highly sensitive
Not all chemicals are allergenic to same degree, nor can any one allergen
sensitize all people.
The range of possible substances which may produce ACD is extremely wide
and innumerable.
PHOTODERMATITIS
Irradiation by ultraviolet light results in the transformation of certain
substances into allergens (photoallergic) or irritants (phototoxic).
Many plant families are known to cause a phototoxic response – citrus and
mulberry.
Medications (particularly sulfa drugs, thiazides, tetracycline) have also been
implicated in photodermatitis
8. Treatment of Contact Dermatitis
Prevention & avoidance of contact with irritant or allergen
Barrier creams, non-alkaline cleansers
Topical steroids
Oral antihistamines
Oral antibiotics
Oral steroids, in severe cases
SEBORRHEIC DERMATITIS
A chronic, inflammatory papulosquamous skin disorder
Related to high load of Pityrosporum yeast on the skin
More severe among patients with neurologic disease and HIV infection
Greasy and scaly confluent papules on erythematous base
Common sites: scalp, eyebrows, eyelashes, nasolabial folds, paranasal skin,
external skin canal and presternal area
Treatment:
Facial lesions
• Topical antifungal creams (azoles)
• Antidandruff shampoo or soap with zinc pyrithione or selenium
sulfide (as facial wash)
• Mild steroid creams/lotions
• Topical immune modulators
Scalp lesions
• Antifungal/antidandruff shampoos: ketoconazole, ciclopirox, tar,
salicylic acid, selenium sulfide, zinc pyrithione
• Topical steroid lotion
• Severe cases: oral antifungal (azoles)
.
NUMMULAR DERMATITIS
Annular coin-shaped pruritic plaques
Often associated with atopy
Treatment: topical steroid or intralesional triamcinolone acetonide
DYSHIDROTIC ECZEMA
Papulovesicular dermatitis of hands and feet
Misnomer: pathophysiology is NOT related to sweating
Treatment: topical or intralesional steroid
Oral prednisone – if severe
ATOPIC DERMATITIS
A chronic and recurrent inflammatory dermatologic condition marked by
severe pruritus causing excoriations, lichenification and susceptibility to skin
infections.
Generally begins early in life and characterized by periods of remission and
exacerbation.
The distribution of affected skin varies with age.
9. No sex predilection; however, males have an earlier onset while females
have a worse prognosis.
Genetic factors are likely responsible for a variety of dermatologic and/or
immunologic abnormalities which underlie AD.
Immunologic abnormalities include hypersensitivity reactions, impaired
immunoregulation of IgE and increased mast cell releasability
Triggers:
• Irritants: wool and acrylic in clothing, perfumes, cosmetics, soaps,
cleaning agents, alcohol containing products
• Infections
• Allergens
• Sweating
• Changes in temperature
• Physical and emotional stresses
Diagnostic Criteria: Clinical
Must have 3 or more major features
• Pruritus
• Typical morphology and distribution:
o Flexural lichenification or linearity in adults
o Facial and extensor involvement in infant and children
• Chronic or chronically relapsing dermatitis
• Personal or family history of atopy (asthma, allergic rhinitis, AD)
Plus 3 or more minor features
• Xerosis
• Ichthyosis/ Palmar hyperlinearity/ Keratosis pilaris
• Immediate (type I) skin test reactivity
• Elevated serum IgE
• Early age of onset
• Tendency toward cutaneous infection/ impaired cell-mediated
immunity
• Tendency toward nonspecific hand or foot dermatitis
• Nipple eczema
• Cheilitis
• Recurrent conjunctivitis
• Dennie-Morgan infraorbital fold
• Keratoconus
• Anterior subcapsular cataracts
• Orbital darkening
• Facial pallor / facial erythema
• Pityriasis alba
• Anterior neck folds
• Itch when sweating
• Intolerance to wool and lipid solvents
• Perifollicular accentuation
10. • Food allergy
• Course influenced by environmental / emotional factors
• White dermatographism / delayed blanch
Treatment:
• Patient education
• Avoidance of triggers
• Emollients
• Topical corticosteroids
• Topical immune modulators
• Antihistamines
• Antibiotics – for secondary bacterial infection
• Phototherapy
LICHEN SIMPLEX CHRONICUS
A localized plaque of chronic eczematous inflammation resulting from
habitual rubbing and scratching
Common sites: wrists, ankles, anogenital area (anus, vulva, scrotum),
posterior neck, upper eyelids
Treatment:
Stress management
Oral antihistamines
Topical steroid ointment
Intralesional steroid injection
STASIS/GRAVITATIONAL DERMATITIS
An eczematous dermatitis of the legs, associated with edema, varicosed/
dilated veins and hyperpigmentation
Treatment
Leg elevation
Leg compression – stockings, ext. pneumatic compression devices
Wet compress for 10-20 mins BID for acute exudative inflammation –
KMnO4, Burrow’s, normal saline
Topical steroids
Oral antihistamines
Oral antibiotics, if indicated
Pentoxyfilline 400 mg BID-TID
Bland emollient
Sclerotherapy
Vein stripping
11. ASTEATOTIC/XEROTIC ECZEMA
Eczema due to dryness of the skin
Related to altered lipid composition of the stratum corneum and to other
subtle changes in epidermal differentiation
Common sites: lower legs, forearms, and hands
Worse during low humidity/cold season
Treatment:
Increase water intake.
Bathe only once daily with tepid water.
Avoid drying agents: rubbing alcohol, harsh soaps, detergents.
Limit exposure to cold temperature and wind.
Apply unscented emollients after bath and whenever necessary –
petroleum jelly, urea- containing cream/lotion, lactic acid.
Apply low-potency steroid ointment.
12. ACNE AND RELATED DISORDERS OF PILOSEBACEOUS GLANDS
Acne vulgaris
Rosacea
Perioral dermatitis
ACNE VULGARIS (Common Acne)
A common inflammatory pilosebaceous disease characterized by comedones,
papules, pustules, nodules and cysts, with occasional scarring.
Predilection sites: face, neck, chest, upper back
More severe in males
Pathogenesis
Androgens stimulate sebum production
Hyperkertinization of follicle lining à plugging à comedones
Sebum is converted to free fatty acids by microbial lipases made by
Propionibacterium acnes
FFA + bacteria à inflammation
Exacerbating Factors
Comedogenic topical agents
Steroids
Menstruation
Drugs: OC pills, lithium, iodides
Stress
Note: FOOD is not an aggravating factor
Acne Severity Grading
I- Comedonal, few lesions, no scarring
II- Papular, moderate number, +/- scarring
III- Pustular, >25 lesions, moderate scarring
IV- Nodulocystic, severe scarring
Treatment
Topical
• Benzoyl peroxide
• Clindamycin/Erythromycin
• Retinoic acid, isotretinoin
• Adapalene, azelaic acid
13. Oral
• Antibiotics
Tetracycline, minocycline, doxycycline, lymecycline
Erythromycin
Co-trimoxazole
• Hormones (anti-androgen)
Cyproterone acetate
High estrogen OCP
• Isotretinoin
Adjunctive procedures
• Intralesional steroids
• Acne surgery
• Chemical peeling: AHA, TCA
ROSACEA
A chronic and recurrent inflammatory disorder of the pilosebaceous units
and vasculature of the face
Telangiectases, flushing, papules and pustules
No comedones
F>M, 30-50 years old
Sites: forehead, cheeks, nose, chin, eyes
Unknown pathogenesis
Exacerbating factors: heat, cold, wind, sun, stress, drinking hot liquids,
alcohol, caffeine, spices
Treatment
Topical
– Metronidazole gel/cream
– Clindamycin, erythromycin
Systemic
– Tetracycline, erythromycin
– Oral isotretinoin
PERIORAL DERMATITIS
Discrete erythematous papules and/or pustules that often become confluent
on perioral and periorbital skin
Initial lesions on nasolabial folds with rim of sparing around the vermillion
border of the lips
F>M, 15-40 y/o
Aggravated by potent topical steroids and toothpaste
Treatment
Topical: Metronidazole gel/cream
Systemic: Tetracycline
14. URTICARIA
Circumscribed areas of raised erythema and edema of the superficial dermis
May be acute (<6 wks) or chronic (>6 wks)
Cause can be difficult or even impossible to determine
Affects 15-20% of the general population, in the U.S. and internationally
Acute urticaria: men = women
Chronic urticaria: men < women
Can occur in any age group; chronic urticaria is more common in the fourth
and fifth decades
Pathophysiology
Occurs following release of histamine, bradykinin, kallikrein, or acetylcholine
à intradermal edema from capillary and venous vasodilation and occasional
leukocyte infiltration.
Clinical Appearance
Wheals ± angio-oedema
– Wheal
central swelling of variable size, surrounded by a reflex
erythema
associated itching or sometimes burning
transient, resolution within 1-24 h
– Angio-edema
sudden, pronounced swelling of the lower dermis and subcutis
sometimes pain, rather than itching
frequent involvement of mucous membranes
resolution within 72 h
New classification of urticaria based on its duration, frequency and cause
Spontaneous urticaria
Physical urticaria
Special types of urticaria
Disorders related to urticaria
New guidelines for routine diagnosis of urticaria
Thorough history
– including all possible trigger factors as well as the key characteristics
of the type of urticaria
Physical examination
– including a test for dermographism
Specific challenge and laboratory tests
– on the basis of the suspected cause
15. Key questions
Time of onset of disease
Frequency and duration of whealing
Associated angio-oedema
Associated subjective symptoms (e.g. pain)
Family history (urticaria, atopy)
Previous or current allergies, infections, internal diseases
Induction by physical agents or exercise
Use of drugs (NSAIDs, injections, immunisations, hormones, laxatives)
Food, smoking habits
Occupation, hobbies
Pharmacotherapy
H1 Antihistamines
– act by competitive inhibition of histamine at the H1 receptor, which
mediates wheal and flare reactions, bronchial constriction, mucus
secretion, smooth muscle contraction, edema, hypotension, CNS
depression, and cardiac arrhythmias
First generation antihistamines
– Hydroxyzine hydrochloride: 50-100 mg PO/IM bid-qid
– Diphenhydramine: 25-50 mg PO q6-8h prn; 10-50 mg IV/IM
q6-8h prn; not to exceed 400 mg/d
– May cause drowsiness
Second generation antihistamines
– Less or non-sedating
– Loratadine, cetirizine: 10 mg OD
– Desloratadine, levocetirizine: 5 mg OD
– Fexofenadine 180 mg OD
H2 Antihistamines
– Reversible, competitive blockers of histamine at H2 receptors,
particularly those in gastric parietal cells.
– Highly selective, do not affect H1 receptors, and are not
anticholinergic agents
– may have a role when used in combination with H1 antihistamines in
selected instances of urticaria
– Cimetidine 300-800 mg PO q6-8h
– Ranitidine 150 mg PO bid
– Famotidine 20-40 mg/d PO bid
Glucocorticoids
– stabilize mast cell membranes and inhibit further histamine release &
reduce the inflammatory effect of histamine and other mediators
– use in urticaria remains controversial; generally recommended in
more severe and refractory cases
16. – Adults: 40 mg prednisone in a short burst children: 1 mg/kg/d for 5
days
Epinephrine
– may be used in conjunction with antihistamines when deemed
appropriate
– alpha-adrenergic effects result in vasoconstriction of the superficial
cutaneous vessels and directly oppose the vasodilatory effect of
histamine
– has no effect on pruritus
17. PAPULOSQUAMOUS DISORDERS
• PSORIASIS
• LICHEN PLANUS
• PITYRIASIS ROSEA
PSORIASIS
A chronic inflammatory papulo-squamous disease of unknown etiology
characterized by sharply demarcated, dull red scaly papules and plaques,
particularly on the extensor prominences and in the scalp.
Epidemiology & Etiology
• Prevalence estimated at 1-3% of the population
• Etiology is multifactorial and poorly understood.
• There are known inherited genetic factors with several documented
environmental triggers.
• Men and women are equally affected, siblings and offspring are at increased
risk of developing psoriasis.
• Onset at any age, though early onset implies a less stable, more severe
clinical course.
• Age of onset peaks during 20s and again in 50s.
• Once expressed, psoriasis is likely to follow a relentless, waxing and waning
course.
• Extent and severity of the disease varies widely.
• Environmental factors influence the course and severity.
• The degree of pruritus varies.
• The psychosocial impact can be severe.
• One-third of patients have nail involvement.
• Psoriatic arthritis is found in 5-8% of patients.
Factors which may exacerbate psoriasis:
• Physical trauma (Koebner phenomenon)
• Infections (Streptococcus, Candida)
• Drugs (lithium, beta-blockers, antimalarials, steroid withdrawal)
• Low humidity/winter season
• Immunodeficiency
Clinical Types of Psoriasis
Plaque psoriasis
Guttate psoriasis
Localized pustular psoriasis
Inverse or intertriginous psoriasis
Generalized pustular psoriasis
Erythrodermic psoriasis
18. Nail Findings
Pitting
Onycholysis
Subungual thickening
Oil drop sign
Nail dystrophy
Psoriatic Arthritis
Most common form: asymmetric oligoarticular (70%)
Rheumatoid factor negative
Treatment
Topical therapy
Topical steroids
Tar
Anthralin
Vit. A analogue – Tazarotene
Vit. D3 analogue – Calcipotriol, Calcitriol
Phototherapy
PUVA
Selective UVB therapy (Narrowband UVB)
Systemic therapy
Methotrexate
Cyclosporine
Retinoids
LICHEN PLANUS
Acute or chronic inflammation of mucous membranes or skin characterized
by violaceous, shiny, pruritic papules topped with fine white lines (Wickham’s
striae)
Sites: flexor surface of wrists, lumbar region, shins, eyelids, scalp, buccal
mucosa, tongue, lips, nails
Scalp lesions associated with alopecia
Mnemonic 6P’s: pruritic, purple, polygonal, peripheral, papules, penis
Precipitating factor: severe emotional stress
Associated with hepatitis C
Treatment
Topical or intralesional corticosteroids
Short courses of oral prednisone (rarely)
PUVA for generalized or resistant cases
Oral retinoids for erosive lichen planus in the mouth
19. PITYRIASIS ROSEA
Acute self-limiting erythematous eruption characterized by red, oval patches
and papules with marginal collarette of scales
Sites: trunk, proximal aspect of arms and legs
Etiology: probably viral
Long axis of lesions follow lines of cleavage producing “Christmas tree”
pattern on the back
Starts with a “herald patch” which precedes other lesions by 1-2 weeks
Varied degree of pruritus
Clears spontaneously in 6-12 weeks
Treatment
No treatment needed unless itchy or widespread
Topical steroids
Emollients
UVB
Antihistamines as needed
20. HYPERSENSITIVITY SYNDROMES & VASCULITIS
Erythema multiforme (EM)
– EM minor
– EM major
Stevens-Johnson syndrome (SJS)
Toxic epidermal necrolysis (TEN)
Spectrum of disorders with varying presence of characteristic skin lesions,
blistering and mucous membrane involvement.
----------------------------------------------------------à
EM minor EM major SJS TEN
CLINICAL FEATURES
ERYTHEMA MULTIFORME
• Macules/papules with central vesicles
• Classic bull’s eye pattern of concentric light and dark rings (target lesions)
• EM minor: no mucosal lesions, bullae or systemic symptoms
• EM major: (+) mucosal lesions, bullae and systemic symptoms
S.J.S
• EM with more mucous membrane involvement and blistering
• “atypical lesions” – red circular patch with dark purple center
• More “sick” (high fever)
• Sheet like epidermal detachment in <10%
T.E.N.
• Severe mucous membrane involvement
• 50% have no target lesions
• Diffuse erythema and necrosis
• Sheet like epidermal detachment in >30%
SITES INVOLVED
EM: mucous membrane ; extremities & face, palms and soles
SJS: generalized with prominent face and trunk involvement
TEN: generalized, nails may also shed
COMPLICATIONS
Corneal ulcers, keratitis, anterior uveitis, stomatitis, vulvitis, balanitis
Corneal scarring, blindness, phymosis, vaginal synechiae
Tubular necrosis and acute renal failure
21. ETIOLOGY
Drugs: sulfonamides, NSAIDs, anticonvulsants, penicillin, allopurinol
– SJS: 50% drug-related
– TEN: 80% definitely drug-related
Infection: herpes, mycoplasma
Idiopathic: >50%
COURSE & PROGNOSIS
EM: lesions last 2 weeks
SJS: <5% mortality, regrowth of epidermis by 3 weeks
TEN: 30% mortality due to fluid loss, secondary infection
TREATMENT
Withdraw suspected drug
Symptomatic treatment
Steroids in severely ill patients (controversial)
Infection prophylaxis
TEN: admit to burn unit
ERYTHEMA NODOSUM
Acute or chronic inflammation of venules in the subcutaneous fat
characterized by round, red, tender nodules
15-30 y/o; F>M
Sites: asymmetrically located on bilateral lower legs, knees, arms
Associated with fever, arthralgia, malaise
Associations:
• Infections: PTB, Group A Strep, leprosy
• Drugs: sulfonamides, oral contraceptives
• Autoimmune disorders
• Malignancy
• 40%: idiopathic
Investigations:
– Chest x-ray
– Throat culture
– ASO titer
– PPD
Treatment:
– NSAIDs
– Treat underlying cause
22. HYPERSENSITIVITY VASCULITIS
Also known as leukocytoclastic vasculitis
Inflammation of the blood vessels
Due to a hypersensitivity reaction to a known drugs, auto-antigens, or
infectious agents such as bacteria.
Immune complexes lodge in the vessel wall, attracting polymorphonuclear
leukocytes which, in turn, release tissue-degrading substances leading to an
inflammatory process.
Clinical presentation: palpable, usually painful , petechiae or purpura arising
in crops
Sites of predilection: legs and forearms
May affect the nerves, kidneys (common), heart and joints
Diagnostic Criteria: At least 3 out of 5 of the following:
1. Age >16
2. Use of possible triggering drug
3. Palpable painful purpura (3 Ps)
4. Maculopapular rash
5. Skin biopsy showing neutrophil infiltration around blood vessel
Treatment
Eliminate the cause.
Antihistamines
Oral steroids – in severe cases
23. HAIR & SCALP DISORDERS
Important Points in History Taking
Family history of baldness or other scalp/hair conditions
Use of medications
Pregnancies and other stressful situations
Hair manipulations and styles
Use of coloring dyes, hairpieces and wig
Past/present illnesses
Dietary history
Examination of the Scalp and Hair
1. Examine the entire scalp.
2. Examine individual lesions.
3. Palpate the cervical region in search of enlarged lymph nodes.
4. Observe: structure and color of skin
erythema or telangiectasia
scales – color, consistency, degree of greasiness
atrophy and scarring
5. Establish the pattern of hair loss: localized or diffuse.
6. Examine hairs and follicular openings in alopecic patches.
7. Determine state of hair on other body parts.
8. A complete physical examination and blood chemistry tests may be indicated.
Presenting Scalp Problem
Hair Loss (Alopecia)
Erythema/Scaling (Erythematosquamous)
Infestation
Tumor
ALOPECIA
NON-SCARRING ALOPECIA
Localized
• Alopecia areata
• Traumatic alopecia: trichotillomania, cosmetic
• Tinea capitis
• Secondary syphilis
Generalized
• Androgenetic alopecia
• Telogen defluvium
• Hypervitaminosis alopecia
• Metabolic & nutritional deficiency alopecia
• Drug-induced alopecia
24. SCARRING ALOPECIA
Chemical & thermal burns
Radiodermatitis
Viral: trigeminal herpes zoster, varicella
Bacterial: folliculitis, furuncle, TB, HD
Treponemal: SY, yaws
Dermatoses of unknown causes: LE, pseudopelade, LP,
foll. decalvans, morphea
Developmental defects
Hereditary disorders
ALOPECIA AREATA
Autoimmune disorder characterized by patches of localized hair loss in scalp,
eyebrows, eyelashes etc.
“Exclamation mark” pattern – hairs fractured and have tapered shafts
Associated with dystrophic nail changes – fine stippling
May be associated with other autoimmune diseases like vitiligo, thyroid
disease
Spontaneously resolves, but worse prognosis if young age of onset and
extensive involvement
Recurrence often precipitated by emotional distress
Treatment:
• Intralesional triamcinolone acetonide
• Topical steroid (lotion, solution)
• Immune modulators (tacrolimus)
TRICHOTILLOMANIA
Impulse control disorder characterized by compulsive hair pulling
Nervous children under stress and adults with emotional disorders
Presents with Ill-defined, irregularly shaped alopecic patches with normal and
broken hairs; variable distribution
Course: Chronic unless treated
Treatment: Counseling, psychiatric referral
TINEA CAPITIS
Incidence & Etiology
– Fairly common in children before puberty
– Affects boys more often than girls
– Caused by Microsporum & Trichophyton
– May be acquired by contact with other patients, contaminated
objects like combs and caps, or through infected animals like dogs &
cats
25. Clinical features
– Microsporum: large, round, scaly patches with stumps of broken hairs;
kerion-painful inflamed mass, heals with scarring
– Trichophyton: small, angular patches with black dots; favus- yellowish
crusts, lusterless hairs, atrophy
Course
– Chronic, may resolve spontaneously
– Microsporum infections heal at puberty; Trichophyton infections tend
to persist into adulthood.
Diagnosis
– KOH examination and culture
– Wood’s light examination:
Microsporum – green fluorescence
Treatment
– Griseofulvin
– Ketoconazole
– Itraconazole
– Terbinafine
– Fluconazole
SYPHILITIC ALOPECIA
Incidence & Etiology
– Common in patients with secondary syphilis
– Sexually transmitted
Clinical Features
– Small (“moth-eaten”) alopecic patches, more on temporal regions;
with other signs of syphilis
Course
– Hair regrowth after treatment
Diagnosis
– Serologic tests for syphilis
VDRL, RPR
TPHA, FTA-Abs
Treatment
– Benzathine penicillin G
2.4 million units IM single dose
– Pencillin allergy
Doxycycline 100 mg BID x 14 days
Tetracycline 500 mg QID x 14 days
Erythromycin 500 mg QID x 14 days
– Children: Benzathine pen G 50,000 u/kg IM, single dose
26. ANDROGENIC (MALE-PATTERN) ALOPECIA
Incidence & etiology
– Extremely common; occurs in genetically predisposed individuals,
usually males
– Usually begins in middle or late 20’s or early 30’s but may develop at
any time after puberty
– Due to postpubertal replacement of terminal hairs by vellus hairs
which are eventually lost
– Androgen dependent
Clinical features
– Males: bitemporal recession, replacement of terminal hairs by vellus
hairs à patches of thinning and alopecia on the vertex à alopecic
areas join at the center of the scalp
– Females: diffuse alopecia at top of scalp
– Asymptomatic
Course
– Chronic and progressive. Alopecia is most noticeable in the 3rd and
4th decades; thereafter, the process is slowly progressive.
Treatment
– Topical minoxidil
– Males: Finasteride 1 mg/day
– Females: Antiandrogen drugs
– Hair transplants, wigs, scalp reduction
TELOGEN EFFLUVIUM
Incidence & etiology
– Relatively common
– Occurs most often in postpartum women
– Also seen:
After high fevers associated with infections
When patients cease taking OC pills
Following use of high dose systemic steroids
With sudden physical & emotional stress
After surgery, blood loss or shock
In patients on “crash diet”
Clinical features
– Diffuse hair loss/thinning of hair
– Occurs about 2-4 months after the stressful event
– No inflammation or other symptoms like scaling, pruritus or atrophy
– Patients often complain that their hair is lost in “handfuls” after
shampooing, brushing or combing
27. Course
– Self-limited; regrowth of hair usually begins within 2-6 months
– In severe cases, regrowth may be only partial
Treatment
– Elimination of stress, when possible
– Use mild shampoo and avoid vigorous brushing of hair
SCALP INFESTATIONS
Pediculosis capitis
Scabies*
PEDICULOSIS CAPITIS
Incidence & etiology
– Relatively common condition in children
– Females > males
– Caused by Pediculosis humanus var capitis
– Lice may be transmitted by direct contact or by fomites such as
combs, caps and beddings
Clinical features
– Pruritus: first and most prominent feature
– Presence of nits attached to hair or lice on the scalp
– Secondary eczematization and impetiginization of the scalp are
common
– Cervical adenitis
– Matted hair with pustules and purulent or hemorrhagic crusts in
advanced stages
Treatment
– Permethrin
– Lindane
– Crotamiton
ERYTHEMASQUAMOUS DISORDER OF THE SCALP*
Psoriasis
Seborrheic dermatitis
Discoid lupus erythematosus
Tinea capitis
28. TUMORS OF THE SCALP*
Benign
Seborrheic keratosis
Trichilemmal cyst
Premalignant
Actinic keratosis
Malignant
Basal cell carcinoma
Squamous cell carcinoma
Melanoma
NAIL DISEASES*
Onychomycosis/tinea unguium
Paronychia
Psoriasis
Ingrown toenail
* To be discussed in detail under specific disease entities.