Dermatology dr.n.ramos

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Dermatology dr.n.ramos

  1. 1. DERMATOLOGY SYLLABUS 1. ECZEMA 1.1. Extrinsic eczema 1.1.1.Allergic contact dermatitis 1.1.2.Irritant contact dermatitis 1.1.3.Photocontact dermatitis 1.2. Intrinsic eczema 1.2.1.Atopic dermatitis 1.2.2.Nummular eczema 1.2.3.Dyshidrotic eczema (pompholyx) 1.2.4.Lichen simplex chronicus 1.2.5.Stasis dermatitis 1.2.6.Asteatotic or xerotic eczema 1.2.7. Seborrheic dermatitis 2. URTICARIA 2.1. Acute urticaria 2.2. Chronic urticaria 2.3. Physical urticaria 2.4. Angioedema 3. ACNE, ROSACEA AND RELATED DISORDERS 3.1. Acne 3.2. Rosacea 3.3. Perioral dermatitis 4. PSORIASIS AND OTHER PAPULOSQUAMOUS DISEASES
  2. 2. 4.1. Psoriasis 4.2. Seborrheic dermatitis 4.3. Pityriasis rosea 4.4. Lichen planus 5. HYPERSENSITIVITY SYNDROMES AND VASCULITIS 5.1. Erythema multiforme 5.2. Stevens-Johnson syndrome 5.3. Toxic epidermal necrolysis 5.4. Erythema nodosum 5.5. Hypersensitivity vasculitis 5.6. Henoch-Schonlein purpura 6. HAIR AND NAIL DISEASES 6.1. Androgenic alopecia 6.2. Telogen effluvium 6.3. Alopecia areata 6.4. Trichotillomania 6.5. Nail diseases 6.5.1.Psoriasis 6.5.2.Paronychia – acute/chronic 6.5.3.Ingrown toenail 6.5.4.Tinea unguium/onychomycosis 7. BACTERIAL INFECTIONS 7.1. Impetigo 7.2. Cellulitis 7.3. Erysipelas
  3. 3. 7.4. Furuncle and carbuncle 7.5. Folliculitis 7.6. Ecthyma 8. VIRAL INFECTIONS 8.1. Warts – common warts, flat warts, plantar warts, genital warts 8.2. Molluscum contagiosum 8.3. Non-genital herpes simplex infection 8.4. Varicella 8.5. Herpes zoster 9. FUNGAL INFECTIONS 9.1. Dermatophyte infections 9.1.1.Tinea capitis 9.1.2.Tinea faciei 9.1.3.Tinea corporis 9.1.4.Tinea manum 9.1.5.Tinea pedis 9.1.6.Tinea cruris 9.1.7.Tinea unguium 9.2. Yeast infections 9.2.1.Pityriasis versicolor 9.2.2.Candidiasis 10. HANSEN’S DISEASE 11. SEXUALLY TRANSMITTED DISEASES 11.1.Syphilis
  4. 4. 11.2.Condyloma acuminata (genital warts) 11.3.Genital herpes simplex 11.4.Pediculosis pubis 11.5.Chancroid 11.6.Molluscum contagiosum 12. INFESTATIONS AND BITES 12.1.Scabies 12.2.Pediculosis 12.3.Flea bites 12.4.Swimmer’s itch 12.5.Cutaneous larva migrans (creeping eruption) 13. CONNECTIVE TISSUE DISEASES 13.1.Lupus erythematosus 13.2.Dermatomyositis 13.3.Scleroderma 13.4.Morphea 14. DISORDERS OF PIGMENTATION 14.1.Vitiligo 14.2.Lentigo 14.3.Melasma 14.4.Idiopathic guttate hypomelanosis 15. BENIGN SKIN TUMORS 15.1.Seborrheic keratosis 15.2.Skin tags 15.3.Dermatofibroma
  5. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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.

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