A C N E 1


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A C N E 1

  1. 1. Dermatology Akmal Abbasi, M.D.
  2. 2. Acne vulgaris (acne) <ul><li>Acne vulgaris (acne)--- is the most common skin disease treated by physicians. </li></ul><ul><li>affects an estimated 17 million people in the United States, including 85% or more of adolescents and young adults. </li></ul><ul><li>chronic condition that may last for years and cause emotional distress and permanent scarring. </li></ul><ul><li>Most adolescents with acne can be managed successfully by their pediatricians. </li></ul>
  3. 3. IMPACT <ul><li>Studies of adolescents and young adults demonstrate a consistent relationship between the presence and severity of acne and anxiety, dissatisfaction with appearance, self-consciousness, & inhibition in social interactions. </li></ul><ul><li>Successful treatment is associated with improved psychological well-being. </li></ul>
  4. 4. WHAT CAUSES ACNE? <ul><li>Acne is a disorder of pilosebaceous follicles, comprised of a follicle or pore, sebaceous gland, and rudimentary, or vellus, hair. </li></ul><ul><li>These specialized follicles are concentrated on the face, chest, and back. </li></ul>
  5. 5. Hormones <ul><li>Androgens have an integral role in causing acne. </li></ul><ul><li>At age 8 or 9 years, before the development of secondary sexual characteristics, the adrenal glands begin to produce increasing amounts of the androgen dehydroepiandrosterone sulfate (DHEAS) in a process called adrenarche. </li></ul><ul><li>Increasing levels of DHEAS cause sebaceous glands to enlarge and produce more sebum. </li></ul><ul><li>In girls, DHEAS levels correlate with the presence of acne in prepuberty and with the future severity of comedonal acne. </li></ul>
  6. 6. Hormones <ul><li>In girls and boys, the prevalence and severity of acne correlate with stage of sexual maturity. </li></ul><ul><li>Despite the importance of androgens in causing acne, most patients with acne have normal hormone levels. </li></ul><ul><li>Measurement of androgens, should be reserved for girls with acne and other evidence of androgen excess (e.g., irregular menses, hirsutism, or clitoromegaly). </li></ul>
  7. 7. Sebum <ul><li>Under the stimulation of adrenal and gonadal androgens, sebum secretion peaks during adolescence and begins to decrease after age 20 years. </li></ul><ul><li>Acne severity typically correlates with rates of sebum secretion. </li></ul><ul><li>Sebum from patients with acne is deficient in linoleic acid, a factor that may cause altered keratinization and follicular obstruction. </li></ul>
  8. 8. Bacteria <ul><li>Propionibacterium acnes is an anaerobic, gram-positive diptheroid that begins to colonize pilosebaceous follicles following increases in sebum production that accompany adrenarche. </li></ul>
  9. 9. Obstruction Within Follicles <ul><li>Pilosebaceous follicles are lined with squamous epithelium that is contiguous with the skin surface. </li></ul><ul><li>In persons with acne, epithelial cells from the follicle lining are not shed properly and become more cohesive. </li></ul><ul><li>The result is a collection of cells that cannot escape the follicle. This process, called comedogenesis , is essential for the development of acne lesions. </li></ul>
  10. 10. Genetics <ul><li>A genetic predisposition to severe acne seems to exist, but other factors modify the disease. </li></ul><ul><li>It is impossible, to predict the severity of disease for an individual based on family history. </li></ul>
  11. 11. CLINICAL MANIFESTATIONS OF ACNE <ul><li>Patients with acne may exhibit </li></ul><ul><ul><li>obstructive or inflammatory lesions </li></ul></ul><ul><ul><li>Scars </li></ul></ul><ul><ul><li>cysts </li></ul></ul>
  12. 12. Obstructive Lesions <ul><li>Initially, obstruction within the follicle is microscopic and cannot be perceived clinically; such lesions are termed microcomedones (singular, microcomedo). </li></ul><ul><li>As comedones enlarge, they become apparent as </li></ul><ul><ul><li>&quot;blackheads&quot; (open comedones) or </li></ul></ul><ul><ul><li>&quot;whiteheads&quot; (closed comedones). </li></ul></ul>
  13. 13. Obstructive Lesions <ul><li>Open comedones represent follicles with a widely dilated orifice. The black color of these lesions is not dirt (it may be the result of the oxidation of melanin, interference in transmission of light through compacted epithelial cells, or the presence of certain lipids in sebum). </li></ul><ul><li>Closed comedones are small, white papules without surrounding erythema. They are follicles that have become dilated with cellular and lipid debris but possess only a microscopic opening to the skin surface. </li></ul>
  14. 14. Multiple, symmetric open comedones
  15. 15. Closed comedones and pustules on cheeks, forehead, nose and chin
  16. 16. Inflammatory Lesions <ul><li>Patients with inflammatory forms of acne manifest erythematous papules, pustules, or nodules. </li></ul><ul><li>Papules and pustules are small, measuring less than 5 mm in diameter, whereas nodules are larger. </li></ul>
  17. 17. Symmetric, follicular, red papules, pustules, and cysts
  18. 18. Symmetric follicular red papules, pustules, and comedones
  19. 19. Multiple red papules and pustules
  20. 20. Scars and Cysts <ul><li>In some patients with acne, scars or cysts develop as inflammatory lesions resolve. </li></ul><ul><li>Most often, and especially on the face, acne scars have the appearance of pits. </li></ul><ul><li>On the trunk, they usually look like small, white spots. </li></ul><ul><li>Rarely, hypertrophic or keloidal scars develop. </li></ul><ul><li>Less common residua of healing acne are cysts, compressible nodules that lack overlying inflammation. </li></ul>
  21. 21. PATIENT EVALUATION <ul><li>History. </li></ul><ul><li>Physical examination. </li></ul><ul><li>To facilitate later comparison, an approximation of the number and types of lesions should be recorded for each region. </li></ul>
  22. 22. TREATMENT Patient Education-- myths <ul><li>Acne is not caused by dirt, and frequent washing does not improve the condition. </li></ul><ul><li>Frequent washing or the use of harsh soaps may irritate the skin and limit a patient's tolerance for topical medications. </li></ul><ul><li>To control oily skin, patients may wash once or twice daily using a mild, nondrying soap. </li></ul><ul><li>For most adolescents, diet plays no role in acne. </li></ul>
  23. 23. Patient Education <ul><ul><li>Picking at, wearing athletic gear over, or otherwise traumatizing acne lesions may increase inflammation, prolong resolution of lesions, and increase the risk for scar formation. </li></ul></ul><ul><ul><li>Cosmetics and moisturizers, especially those containing oils, may worsen acne. </li></ul></ul><ul><ul><li>Adolescents should be advised to take care to select cosmetics that are labeled noncomedogenic or nonacnegenic. </li></ul></ul>
  24. 24. Chronic picking of the papules resulted in erosions, scarring, and postinflammatory hyperpigmentation.
  25. 25. Patient Education <ul><ul><li>A variant of cosmetic acne, known as pomade acne, may occur when greases used to style hair are inadvertently applied to the skin. </li></ul></ul><ul><ul><li>Pomade acne occurs almost exclusively in African Americans and is characterized by the presence of comedones located on the forehead and temporal areas. </li></ul></ul>
  26. 26. Patient Education <ul><ul><li>Young women often experience premenstrual flare-ups of acne that may be caused by the androgenic effects of progesterone that is dominant during the second half of the menstrual cycle. </li></ul></ul><ul><ul><li>Environmental factors may exacerbate acne among young people who come into contact with grease at work (e.g., those employed in auto-repair shops or fast-food restaurants). </li></ul></ul><ul><ul><li>Patients should be advised that acne treatment is a long-term process, requiring 6 to 8 weeks before any therapeutic benefit occurs. </li></ul></ul>
  27. 27. Closed comedones
  28. 28. Medications ( Topical Therapies) Benzoyl Peroxide. <ul><li>BP has an antibacterial effect and is useful in controlling inflammatory acne. </li></ul><ul><li>Benzoyl peroxide is available with or without a prescription in concentrations ranging from 2.5% to 10%. Over-the-counter products include creams, lotions, washes, and gels. Prescription forms typically use a gel vehicle, a factor that enhances efficacy. </li></ul>
  29. 29. Benzoyl Peroxide. <ul><li>A single daily application of a product containing a 5% concentration is adequate for most patients. </li></ul><ul><li>Benzoyl peroxide is usually applied once daily, although twice-daily use may be beneficial for some patients. </li></ul><ul><li>BP is applied as a thin coat to all acne-prone areas, not to individual lesions. </li></ul>
  30. 30. Benzoyl Peroxide. <ul><li>Adverse reactions-- stinging after application and drying, redness, and peeling of the skin. </li></ul><ul><li>Allergic contact dermatitis is an unusual complication characterized by erythema, small papules, and pruritus. </li></ul><ul><li>Patients should be advised that BP may bleach clothing and bedding. </li></ul><ul><li>It is safe for use during pregnancy. </li></ul>
  31. 31. Topical Antibiotics. <ul><li>Topical antibiotics kill P. acnes , reduce concentrations of mediators of inflammation, and may reduce FFAs. </li></ul><ul><li>Products containing clindamycin or erythromycin are available. </li></ul><ul><li>a formulation of BP 5% and erythromycin 3% (e.g., Benzamycin) is more effective than either drug alone. </li></ul><ul><li>formulations of erythromycin and zinc aso available. </li></ul>
  32. 32. Topical Retinoids. <ul><li>For adolescents with many blackheads or whiteheads, topical retinoids are indicated. </li></ul><ul><li>These drugs normalize the keratinization process within follicles, thereby reducing obstruction and the risk for follicular rupture. </li></ul><ul><li>Tretinoin is the best-known topical retinoid and is available in creams (0.025%, 0.05%, and 0.1%), gels (0.01% and 0.025%), and a liquid (0.05%). </li></ul><ul><li>The vehicle affects efficacy; creams are less potent than gels, which are less potent than the liquid. </li></ul>
  33. 33. Topical Retinoids. <ul><li>A new formulation, Retin-A Micro 0.1%, is as effective but less irritating than tretinoin cream 0.1%. </li></ul><ul><li>Tretinoin is also marketed as Avita and Renova and is available in generic form. </li></ul><ul><li>Many adolescents who use tretinoin experience irritation, redness, or dryness. </li></ul><ul><li>For African American patients, this inflammation may result in hypopigmentation that may last several months. To prevent or limit adverse effects, therapy is often begun with the 0.025% cream, the 0.1% micro preparation, or adapalene. </li></ul>
  34. 34. Topical Retinoids. <ul><li>Patients are advised to use the medication every third night, progressing as tolerated over 2 or 3 weeks to a nightly application. </li></ul><ul><li>Approximately half of individuals experience an apparent, temporary worsening of acne 2 or 3 weeks after starting tretinoin therapy usually results from increased photosensitivity caused by irritation. </li></ul><ul><li>Because sensitivity to sunlight is increased, tretinoin should be applied at night, and a sunscreen should be used during the day. </li></ul>
  35. 35. Topical Retinoids. <ul><li>Tretinoin is classified as pregnancy category C (e.g., risk to the fetus cannot be ruled out), so its use is avoided during pregnancy. </li></ul><ul><li>BP inactivates tretinoin, the two drugs should not be applied simultaneously. </li></ul><ul><li>BP may be applied in the morning, and tretinoin at night. </li></ul>
  36. 36. Azelaic Acid. <ul><li>Azelaic acid 20% (Azelex) is antibacterial and anticomedonal. </li></ul><ul><li>It is applied twice daily and seems to be well tolerated, although a few patients experience pruritus, burning, stinging, tingling, or erythema. </li></ul><ul><li>No systemic toxicity has been reported. </li></ul>
  37. 37. Salicylic Acids. <ul><li>Salicylic acid is available in prescription and nonprescription formulations. </li></ul><ul><li>It reduces the formation of obstructive lesions but is less effective than is tretinoin. </li></ul><ul><li>Because it is less irritating, it may be useful for adolescents with obstructive acne who are unable to tolerate topical retinoids. </li></ul>
  38. 38. Systemic Therapies Oral Antibiotics. <ul><li>Possess greater efficacy than topical preparations and are prescribed for patients with more severe or extensive inflammatory acne. </li></ul><ul><li>They exert their anti-inflammatory effect by decreasing bacterial colonization and inhibiting neutrophil chemotaxis & also reduce the concentration of FFAs in sebum. </li></ul><ul><li>Erythromycin and tetracycline are most often prescribed. </li></ul>
  39. 39. Oral Antibiotics. <ul><li>Depending on disease severity, each is initiated at a dose of 250 mg to 500 mg twice daily. </li></ul><ul><li>The primary side effect of erythromycin is gastrointestinal upset, which may be avoided by taking the medication with food. </li></ul><ul><li>Tetracycline is preferred by some clinicians. </li></ul><ul><li>Tetracycline should not be taken with milk; it must be taken on an empty stomach, and, like erythromycin, it may cause gastrointestinal disturbances. </li></ul>
  40. 40. Oral Antibiotics. <ul><li>It should not be used during pregnancy or for patients less than 9 years of age. </li></ul><ul><li>Uncommon adverse effects include photosensitivity and esophageal ulceration. </li></ul><ul><li>Vulvovaginal candidiasis is more likely to develop in female patients taking tetracycline. </li></ul><ul><li>Other alternatives--Doxycycline & Minocycline. </li></ul>
  41. 41. Oral Antibiotics. <ul><li>6 to 8 weeks are required before oral antibiotics produce a significant clinical effect. </li></ul><ul><li>After the development of new lesions has ceased or been satisfactorily reduced, the dose may be tapered gradually or eventually withdrawn. </li></ul>
  42. 42. Oral Antibiotics. <ul><li>Concern often is raised that oral antibiotics may diminish oral contraceptive pill (OCP) efficacy by decreasing enterohepatic recirculation of contraceptive steroids or by enhancing their hepatic degradation or renal or fecal excretion. </li></ul><ul><li>Research fails to support this concern for antibiotics used to treat acne ; however, packaging information provided with some OCPs containing estrogen and progesterone states a &quot;possible&quot; reduction in efficacy during use of ampicillin or tetracyclines. </li></ul>
  43. 43. Isotretinoin. <ul><li>Isotretinoin (13- cis -retinoic acid, Accutane) is an analogue of vitamin A that is highly effective for the treatment of severe or refractory inflammatory acne. </li></ul><ul><li>Isotretinoin therapy may be associated with teratogenicity. </li></ul><ul><li>For this reason, the American Academy of Pediatrics Committee on Drugs has written that isotretinoin and other systemic retinoids should be prescribed &quot;only by those physicians with experience in the therapy ... of severe dermatologic disorders.&quot; Thus, if a pediatrician believes that a patient requires isotretinoin therapy, referral to a dermatologist is indicated. </li></ul>
  44. 44. Hormonal Therapy. <ul><li>Estrogen improves acne by increasing levels of sex hormone-binding globulin, which decreases biologically active free testosterone, and by suppressing gonadotropin secretion, thereby reducing ovarian androgen production. </li></ul><ul><li>The inherent androgenic and antiestrogenic potential of the progestin component of an OCP or other hormonal contraceptive also may influence acne severity. </li></ul>
  45. 45. Hormonal Therapy. <ul><li>Thus, OCPs containing progestins with low androgenic potential (e.g., norethindrone or its acetate, ethynodiol diacetate, or a newer agent, e.g., norgestimate) often are considered to have the most favorable effects on acne. </li></ul><ul><li>Acne is a recognized adverse effect associated with the use of long-acting progestin implants and may occur during the use of depot medroxyprogesterone acetate. </li></ul>
  46. 46. Hormonal Therapy. <ul><li>Adolescents with acne exacerbated by endocrine disorders may require treatment with agents such as spironolactone (an androgen antagonist), low-dose glucocorticoids, or gonadotropin-releasing hormone agonists. </li></ul>
  47. 47. FOLLOW-UP <ul><li>A return visit typically is scheduled for 2 months following the initiation of therapy. </li></ul>
  48. 48. Erisepilas <ul><li>Also known as St. Anthony's fire, usually presents as an intensely erythematous infection with clearly demarcated raised margins, and often with associated lymphatic streaking </li></ul><ul><li>Erysipelas is also more superficial and has margins that are more clearly demarcated from normal skin than does cellulitis. </li></ul><ul><li>The lower legs, face, and ears are most frequently involved. </li></ul>
  49. 49. Erisepilas <ul><li>It may originate in a traumatic or surgical wound, but no portal of entry can be found in most cases. </li></ul><ul><li>In the preantibiotic era, erysipelas was a feared disease with a significant mortality rate, particularly in infants. </li></ul>
  50. 50. Erisepilas
  51. 51. Etiology & Incidence <ul><li>In the majority of cases, group A streptococci are the responsible organisms. </li></ul><ul><li>The second most frequent causative organism is group G streptococci & rarely group C Strep. </li></ul><ul><li>The incidence of erysipelas is rising, especially in young children, the elderly, persons with diabetes, alcoholic persons, and patients with compromised immune systems or lymphedema. </li></ul>
  52. 52. Signs & Symptoms <ul><li>Prodromal symptoms last from 4 to 48 hours. </li></ul><ul><li>They consist of malaise, chills, fever (101° to 104° F), and occasionally anorexia and vomiting. </li></ul><ul><li>Then at the site of infection one or more red, tender, firm spots appear. </li></ul><ul><li>These spots rapidly increase in size, forming a tense, red, hot, uniformly elevated, shining patch with an irregular outline and a sharply defined, raised border. </li></ul>
  53. 53. Signs & Symptoms <ul><li>As the process develops, the color becomes a dark, fiery red and vesicles appear at the advancing border and over the surface. </li></ul><ul><li>Symptoms of itching, burning, tenderness, and pain may be moderate to severe. </li></ul><ul><li>Without treatment, the rash reaches its height in approximately 1 week and subsides slowly over the next 1 or 2 weeks. </li></ul>
  54. 54. Recurrent episodes of infection have resulted in lymphatic obstruction and caused permanent thickening of the skin.
  55. 55. Recurrence. <ul><li>Recurrence after antibiotic treatment occurs in 18% to 30% of cases. </li></ul><ul><li>In particularly susceptible people, erysipelas may recur frequently for a long period and, by obstruction of the lymphatics, cause permanent thickening of the skin (lymphedema). </li></ul><ul><li>Subsequent attacks may be initiated by the slightest trauma or may occur spontaneously to cause further irreversible skin thickening. </li></ul><ul><li>The pinna and lower legs are particularly susceptible to this recurrent pattern. </li></ul>
  56. 56. Treatment <ul><li>Treatment requires the use of parenterally administered penicillin or a first-generation cephalosporin (eg, cefazolin) initially for 24 to 48 hours followed by oral therapy after the patient's condition is clinically improved to prevent complications due to progression of disease and onset of toxic shock. </li></ul><ul><li>Recurrent cases may require long-term prophylactic treatment with low-dose penicillin or erythromycin. </li></ul>
  57. 57. Impetigo <ul><li>*A superficial skin infection due to staphylococci, streptococci or both. </li></ul><ul><li>*Is contagious and autoinoculable </li></ul><ul><li>*Is characterized by spreading red, weeping, and crusting lesions. </li></ul><ul><li>*Two forms are identified. </li></ul><ul><li>*Vesicopustular (lesions are thick and golden-crusted) are caused by group A-Beta hemolytic Strep or staph aureus. </li></ul><ul><li>*Bullous (associated with phage II staph aureus) </li></ul>
  58. 58. Pathophysiology <ul><li>Infection may begin in a trivial cut or abrasion. </li></ul><ul><li>lmpetiginization then follows </li></ul><ul><li>Scratching and poor personal hygiene; particularly among children lead to rapid spread of lesions and often transmission to the house hold contacts, schoo1mates or playmates. </li></ul>
  59. 59. Clinical Manifestations <ul><li>Itching is the only symptom </li></ul><ul><li>The patient will give a history of itching and crusted sores, especially on the face. </li></ul><ul><li>Usually macules, vesicles, bullae, pustules and a copious gummy purulent exudate form honey-colored crusts on an erythematous base. </li></ul><ul><li>Fever in severe infection. </li></ul>
  60. 60. Crusted erosions becoming confluent on nose, cheek, lips & chin (GAS)
  61. 61. Crusted lesions on the arm of a child (Staph Aureus)
  62. 62. <ul><li>D/D: Acute allergic contact dermatitis, Herpes simplex. </li></ul><ul><li>Diagnostic Tests: Smear, Culture--Can identify the causative bacteria-confirm diagnosis </li></ul><ul><li>Complications: Increasing spread without treatment, Systemic effects may occur in children, Ecthyma. </li></ul>
  63. 63. Treatment <ul><li>Attention to personal hygiene </li></ul><ul><li>Isolation may be appropriate </li></ul><ul><li>Systemic antibiotics more effective than topical. </li></ul><ul><li>Mupirocin applied as an ointment is curative for most cases of impetigo. </li></ul><ul><li>Compresses for crusted and weepy lesions </li></ul>
  64. 64. Eczema <ul><li>Freek word meaning to “boil out”. </li></ul><ul><li>Presents with non-specific lesions, such as localized edema, papules & vesicles. </li></ul><ul><li>Eiology—unknown.May be exogenous vs endogenous. </li></ul><ul><li>Itiching is the hallmark of eczema. </li></ul><ul><li>Because of itching, the primary lesion becomes infected which causes secondary changes as scales, crusts & oozing. </li></ul>
  65. 65. Clinical Manifestation <ul><li>Presentation differs at different ages & in different races </li></ul><ul><li>Flexural lichenification in adults </li></ul><ul><li>Facial & extensor involvement in infants </li></ul><ul><li>Tendency towards chronicity or chronically relapsing dermatitis. </li></ul>
  66. 66. PE <ul><li>Patches of redness with weeping areas, scaling or vesiculation.Lesions on neck, face, upper trunk (monk’s cowl) </li></ul><ul><li>Dry leathery skin with lichenification </li></ul><ul><li>Papular eruption & poorly marked hypopigmented patches (pityriasis alba) on the cheeks & extremities of pigmented individuals. </li></ul><ul><li>In the dark skin pt you may not see the pigmentation around the wrist & ankles. </li></ul>
  67. 67. Erythema, papules, scaling & crusting lesions on face & body of an infant
  68. 68. <ul><li>Lab findings: Blinded food challenges for suspected food allergy, RASTs or skin test for dust mite allergy, Eosinophilia &  serum IgE levels. </li></ul><ul><li>D/D: Seborrheic dermatitis (Scalp and Face involvement, Greasy and scaly lesions ), Contact Dermatitis (No Chronicity), Impetigo (no characteristic lesion distribution). </li></ul>
  69. 69. Treatment (General) <ul><li>Avoid anything that irritates the skin, (Low humidity/dry air, Bathing more than once a day, Restrict soap at armpits, groin and feet, Washcloths and brushes) </li></ul><ul><li>Very hot baths (Pat skin to dry after bathing — d o not rub the skin, Cover skin with Vaseline, cream or mineral oil as needed), Eliminate one food at a time, as dairy products are a frequent cause. </li></ul>
  70. 70. Treatment (Local) <ul><li>*Topical application of corticoteroids sparingly. </li></ul><ul><li>*Match potency with severity of dermatitis </li></ul><ul><li>*Begin with hydrocortisone or a slightly stronger Mild steroid. </li></ul><ul><li>*Taper doses to avoid rebound flares. </li></ul><ul><li>*Tacrolimus is used as a first line steroid. </li></ul><ul><li>*Doxepin cream can relieve the pruritus. </li></ul>
  71. 71. Treatment (Specific) <ul><li>Acute Weeping lesions: Saline/aluminum subacetate solution, Apply soothing soaks, baths or wet dressing, Use steroid lotion/cream in preference to ointment, Bandage extremities at night, Apply high-potency corticosteroid after bathing. </li></ul><ul><li>Subacute or scaly lesions: Usually they are dry, but still red and pruritic, Apply mid-high potency steroids in ointment form if tolerated, otherwise use creams. </li></ul><ul><li>Chronic dry, lichenified lesions: High-potency to highest potency steroid ointment for 2-6 weeks, Tar preparation such as LCD are used occasionally. </li></ul>
  72. 72. Systemic and adjuvant therapy <ul><li>Use systemic corticosteroids in extensive and more severe cases </li></ul><ul><li>High oral prednisone dosages. </li></ul><ul><li>Antihistamine for pruritus </li></ul><ul><li>Fissures, crust, erosions or pustules indicate staph infection clinically- Use antistaph antibiotics such as dicloxacillin or first generation cephalosporins. </li></ul><ul><li>Phototherapy — for severly affected patients UVB, UVA, or PUVA </li></ul>
  73. 73. <ul><li>Complications: Eczema herpeticum (generalized herpes simplex infection) treatment for this — Acyclovir. </li></ul><ul><li>Prognosis: Chronicity, Intermittent remissions. </li></ul>
  74. 74. Herpes Zoster ( Shingles ) <ul><li>Acute vesicular eruption due to varicello-zoster virus, usually in adults. </li></ul><ul><li>Caused by reactivation of latent varicello virus in sensory root ganglia in parients previously infected with chicken pox. </li></ul><ul><li>Reactivation is common in the elderly and in immunocompromised patients. </li></ul>
  75. 75. Herpes Zoster in T8-T10 dermatome
  76. 76. Clinical Manifestations <ul><li>Pain- may precede the skin rash </li></ul><ul><li>Prolonged and severe post- herpetic neuralgia in the elderly. </li></ul><ul><li>Lesions are vesicular and deep-seated on an erythematious base. </li></ul><ul><li>Unilateral skin eruption along the line of one or two dematomes. Frequently involved dermatones are T-5 to T-10. </li></ul><ul><li>Sensory loss and motor palsies may accompany the involved dermatomes. </li></ul><ul><li>In Ophthalmic Herpes corneal ulceration and scarring may occur. </li></ul>
  77. 77. D/D <ul><li>Poison Ivy </li></ul><ul><li>Poison Oak </li></ul><ul><li>Allergic contact dermatitis </li></ul><ul><li>Herpes simplex infection </li></ul><ul><li>Myocardial infarction </li></ul><ul><li>Acute abdomen </li></ul>
  78. 78. Complications <ul><li>Bladder and bowel dysfunction </li></ul><ul><li>Persistent neuralgia, anesthesia or scarring following healing </li></ul><ul><li>Facial/other nerve paralysis </li></ul><ul><li>Encephalitis </li></ul><ul><li>Post herpetic neuralgia if trigeminal nerve region is involved. </li></ul>
  79. 79. Treatment <ul><li>General Measures-- In the immunocompetent: </li></ul><ul><li>Early treatment of the elderly to prevent development of post­herpetic neuralgia </li></ul><ul><li>Antiviral therapy for the younger patients </li></ul><ul><li>Adequate hydration, nerve block for severe pain </li></ul><ul><li>Opthalmic consultation, use of systemic steroids </li></ul><ul><li>In the immunocompromised: </li></ul><ul><li>Antiviral Therapy </li></ul>
  80. 80. Treatment <ul><li>Local measures: </li></ul><ul><li>Calamine lotion </li></ul><ul><li>For post-herptic Neuralgia: </li></ul><ul><li>Prevent with an early aggressive antiviral therapy- Capsaicin ointment. </li></ul><ul><li>Regional blocks for chronic post-herpetic neuralgia. </li></ul><ul><li>Amitriptyline- first line oral therapy </li></ul>
  81. 81. Prognosis <ul><li>Motor involvement- temporary palsy </li></ul><ul><li>Otherwise good </li></ul>
  82. 82. Herpes Simplex (Cold/fever Sore, Genital herpes) <ul><li>HS belongs to the group of vesicular dermatoses , caused by a human herpes virus </li></ul><ul><li>Is a local virus infection of the skin or mucous membranes, causing vesicular lesions, typically recurrent. </li></ul><ul><li>HS is a common virus, which frequently causes non-specific illness, often in childhood hence many people have serum antibodies to the organism. </li></ul><ul><li>Several herpes viruses cause infection in man. </li></ul>
  83. 83. <ul><li>Herpesvirus hominis (Herpes Simplex-1): Herpes labialis (cold sores), Keratoconjunctivitis, Finger infections (whitlow), Encephalitis, Primary stomatitis, Genital infection. </li></ul><ul><li>HS 2: Genital infection, neonatal infection (acquired during vaginal delivery). </li></ul><ul><li>CMV: Congenital infection, Infection in immuno –compromised patients (Pneumonitis, Retinitis, </li></ul><ul><li>Generalized infection). </li></ul>
  84. 84. <ul><li>EMV: Infections mononucleosis, Burkitts Lymphoma, Nasopharyngeal carcinoma, Hairy leukoplakia (AIDS patients). </li></ul><ul><li>Varicella Zoster Virus: Chicken pox , Shingles (Herpes Zoster). </li></ul><ul><li>HHV-6: Exanthem subitum, cervical Lymphadenopathy. </li></ul><ul><li>HHV-7: Serologically has association with HHV-6 </li></ul><ul><li>HHV-8: Associated with Kaposis sarcoma </li></ul>
  85. 85. Clinical Manifestations <ul><li>Primary: Burning and stinging, Ulcerative stomatitis (commonest in infants), Keratitis, Finger infection (whitlow), Vulvovaginitis, Balanitis, Encephalitis, Infection disseminated in neonates and the immunocompromised </li></ul><ul><li>Recurrent: Commonest on the lips </li></ul>
  86. 86. HSV-Primary GingivoStomatitis
  87. 87. Herpetic Whitlow
  88. 88. Pathogenesis <ul><li>Lesions start as macules  vesicles  pustules. </li></ul><ul><li>Attacks of herpes labialis may be precipitated by various stimuli including sunlight, menstruation and viral and bacterial infection. </li></ul><ul><li>Genital lesions also commonly occur. </li></ul>
  89. 89. <ul><li>D/D: Chancroid, Syphilis, Pyoderma, Trauma </li></ul><ul><li>Investigations: Direct IFAT — rapid and sensitive, Viral culture -  serum antibody titers, Tzanck smear - Multinucleated cells (least sensitive), HSV-2 Serology by western blot, New ELISA — Determines who is HSV infected and potentially infectious. </li></ul>
  90. 90. Course of Disease <ul><li>Episode of infection typically runs its course in about a week, longer in first infection. </li></ul><ul><li>Secondary bacterial infection  exacerbation of symptoms. </li></ul><ul><li>Intrauterine infection  abortion/fetal damage. </li></ul><ul><li>Disseminated infection in neonates. </li></ul><ul><li>Ocular infection - herpetic (dendritic) keratitis </li></ul>
  91. 91. Treatment <ul><li>Systemic --Acyclovir, Valacyclovir (valine analog of acyclovir), Famciclovir. </li></ul><ul><li>Local --Topical threrapy ineffective, Acyclovir ointment with indications, Penicillin cream for orolabial herpes. </li></ul><ul><li>Prevention: Sunscreens, Prophylactic use of oral acyclovir for recurrences </li></ul><ul><li>Prognosis: good. </li></ul>
  92. 92. Neurodermatitis (Lichen simplex chronicus) <ul><li>*Chronic dermatitis perpetuated by the itch-scratch cycle. </li></ul><ul><li>*Common sites include the arms, neck and lower leg </li></ul><ul><li>*Depression or other psychologic symptoms may be present in patients with chronic stubborn lesions. </li></ul>
  93. 93. Clinical Manifestation <ul><li>Intermittent itching </li></ul><ul><li>Insomnia </li></ul><ul><li>Dry, leathery, hypertrophic, lichenified plaques on the neck, wrists, perineum, or just about anywhere. </li></ul><ul><li>On P/E excessive skin lines are visible, dividing the lesion in rectangular plaques. </li></ul>
  94. 94. Lichen simplex chronicus lesions on posterior neck & occipital Scalp
  95. 95. D/D <ul><li>Plaque-like lesions (psoriasis-lesions redder with whiter scales on elbows, knees, and finger nails) </li></ul><ul><li>Lichen planus (violaceous, usually smaller polygonal papules) </li></ul><ul><li>Nummular dermatitis (coin-shaped) </li></ul>
  96. 96. Treatment <ul><li>Topical corticosteroids (clobetasol, halobetasol, diflorasone and betamethasone dipropionate) </li></ul><ul><li>Flurandrenolide tape (Tx of choice; use with caution; very potent) </li></ul><ul><li>Parenteral triamcinolone acetonide is sometimes curative. </li></ul><ul><li>Tars, eg LCD may also be effective </li></ul><ul><li>Prognosis : Remission during therapy, Recurrence, Development at another site </li></ul>
  97. 97. Scabies Akmal Abbasi, M.D.
  98. 98. Scabies <ul><li>Scabies is a contagious disease caused by the mite Sarcoptes scabiei. </li></ul><ul><li>EPIDEMIOLOGY & DEMOGRAPHICS </li></ul><ul><ul><li>Scabies is generally acquired by sleeping with or in the bedding of infested individuals. </li></ul></ul><ul><ul><li>It is generally associated with poor living conditions and is also common in hospitals and nursing homes. </li></ul></ul>
  99. 99. PHYSICAL FINDINGS & CLINICAL PRESENTATION <ul><ul><li>Primary lesions are caused when the female mite burrows within the stratum corneum, laying eggs within the tract she leaves behind; burrows (linear or serpiginous tracts) end with a minute papule or vesicle. </li></ul></ul><ul><ul><li>Primary lesions are most commonly found in the web spaces of the hands, wrists, buttocks, scrotum, penis, breasts, axillae, and knees. </li></ul></ul><ul><ul><li>Secondary lesions result from scratching or infection. </li></ul></ul><ul><ul><li>Intense pruritus, especially nocturnal, is common; it is caused by an acquired sensitivity to the mite or fecal pellets and is usually noted 1 to 4 wk after the primary infestation. </li></ul></ul><ul><ul><li>Examination of the skin may reveal burrows, tiny vesicles, excoriations, inflammatory papules. </li></ul></ul><ul><ul><li>Widespread and crusted lesions (Norwegian or crusted scabies) may be seen in elderly and immunocompromised patients. </li></ul></ul>
  100. 100. <ul><li>ETIOLOGY </li></ul><ul><li>Human scabies is caused by the mite Sarcoptes scabiei, var. hominis </li></ul><ul><li>WORKUP </li></ul><ul><li>Diagnosis is made on the clinical presentation and on the demonstration of mites, eggs, or mite feces. </li></ul><ul><li>LABORATORY TESTS </li></ul><ul><ul><li>Microscopic demonstration of the organism, feces, or eggs: a drop of mineral oil may be placed over the suspected lesion before removal; the scrapings are transferred directly to a glass slide; a drop of potassium hydroxide is added and a cover slip is applied. </li></ul></ul><ul><ul><li>Skin biopsy is rarely necessary to make the diagnosis. </li></ul></ul>
  101. 101. Scabies organism in a wet mount preparation.
  102. 102. <ul><ul><li>scabies-burrow </li></ul></ul>
  103. 103. Scabies
  104. 104. DIFFERENTIAL DIAGNOSIS <ul><ul><li>Pediculosis </li></ul></ul><ul><ul><li>Atopic dermatitis </li></ul></ul><ul><ul><li>Flea bites </li></ul></ul><ul><ul><li>Seborrheic dermatitis </li></ul></ul><ul><ul><li>Dermatitis herpetiformis </li></ul></ul><ul><ul><li>Contact dermatitis </li></ul></ul><ul><ul><li>Nummular eczema </li></ul></ul><ul><ul><li>Syphilis </li></ul></ul><ul><ul><li>Other insect infestation </li></ul></ul>
  105. 105. TREATMENT <ul><li>Clothing, underwear, and towels used in the 48 hr before treatment must be laundered. </li></ul><ul><li>Following a warm bath or shower, Lindane (Kwell, Scabene) lotion should be applied to all skin surfaces below the neck (can be applied to the face if area is infested); it should be washed off 8 to 12 hr after application. Repeat application 1 wk later is usually sufficient to eradicate infestation. </li></ul><ul><li>Pruritus generally abates 24 to 48 hr after treatment, but it can last up to 2 wk; oral antihistamines are effective in decreasing postscabietic pruritus. </li></ul><ul><li>Topical corticosteroid creams may hasten the resolution of secondary eczematous dermatitis. </li></ul>
  106. 106. TREATMENT <ul><li>If the patient is a resident of an extended care facility, it is important to educate the patients, staff, family, and frequent visitors about scabies and the need to have full cooperation in treatment. Scabicide should be applied to all patients, staff, and frequent visitors, whether symptomatic or not; symptomatic family members of staff and visitors should also receive treatment. </li></ul><ul><li>Permethrin 5% cream (Elimite) is also effective with usually one treatment; it should be massaged into the skin from head to soles of feet; remove 8 to 14 hr later by washing. If living mites are present after 14 days, treat again. </li></ul><ul><li>A single dose (150–200 mg/kg in 6-mg tablets) of ivermectin, an antihelminthic agent, is as effective as topical lindane for the treatment of scabies. It is the best treatment for generalized crusted scabies. </li></ul>
  107. 107. PEARLS & CONSIDERATIONS <ul><ul><li>Lindane is potentially neurotoxic and should not be used for infants and pregnant women (permethrin is safe and effective in these situations). </li></ul></ul><ul><ul><li>Sexual partners should be notified by the pt. and treated. </li></ul></ul>
  108. 108. Pediculosis Akmal Abbasi, M.D.
  109. 109. Pediculosis <ul><li>Pediculosis is lice infestation. </li></ul><ul><li>Humans can be infested with three kinds of lice: Pediculus capitis (head louse), Pediculus corporis (body louse), and Phthirus pubis (pubic, or crab, louse). </li></ul><ul><li>Lice feed on human blood and deposit their eggs (nits) on the hair shafts (head lice and pubic lice) and along the seams of clothing (body lice). </li></ul>
  110. 110. Pediculosis <ul><li>Nits generally hatch within 7 to 10 days. </li></ul><ul><li>Lice are obligate human parasites and cannot survive away from their hosts for longer than 7 to 10 days. </li></ul>
  111. 111. EPIDEMIOLOGY & DEMOGRAPHICS <ul><ul><li>There are 6 million to 12 million cases of head lice in the U.S. yearly. </li></ul></ul><ul><ul><li>Lice infestation of the scalp is most common in children (girls > boys). </li></ul></ul><ul><ul><li>Infestation of the eyelashes is most frequently seen in children and may indicate sexual abuse. </li></ul></ul><ul><ul><li>The chance of acquiring pubic lice from one sexual exposure with an infested partner is >90% (most contagious STD known). </li></ul></ul><ul><ul><li>Body lice is most common in conditions of poor hygiene. </li></ul></ul>
  112. 112. PHYSICAL FINDINGS & CLINICAL PRESENTATION <ul><ul><li>Pruritus with excoriation may be caused by hypersensitivity reaction, inflammation from saliva, and fecal material from the lice. </li></ul></ul><ul><ul><li>Nits can be identified by examining hair shafts. </li></ul></ul><ul><ul><li>The presence of nits on clothes is indicative of body lice. </li></ul></ul><ul><ul><li>Lymphadenopathy may be present (cervical adenopathy with head lice, inguinal lymphadenopathy with pubic lice). </li></ul></ul><ul><ul><li>Head lice is most frequently found in the back of the head and neck, behind the ears. </li></ul></ul><ul><ul><li>Scratching can result in pustules and crusting. </li></ul></ul><ul><ul><li>Pubic lice may affect the hair around the anus. </li></ul></ul>
  113. 113. <ul><li>ETIOLOGY </li></ul><ul><li>Lice are transmitted by close personal contact or use of contaminated objects (e.g., combs, clothing, bed linen, hats). </li></ul><ul><li>DIFFERENTIAL DIAGNOSIS </li></ul><ul><ul><li>Seborrheic dermatitis </li></ul></ul><ul><ul><li>Scabies </li></ul></ul><ul><ul><li>Eczema </li></ul></ul><ul><ul><li>Other: pilar casts, trichonodosis (knotted hair), monilethrix </li></ul></ul>
  114. 114. Diagnosis <ul><li>Diagnosis is made by seeing the lice or their nits. Combing hair with a fine-toothed comb is recommended because visual inspection of the hair and scalp may miss more than 50% of infestations. </li></ul><ul><li>Wood’s light examination is useful to screen a large number of children: live nits fluoresce, empty nits have a gray fluorescence, nits with unborn louse reveal white fluorescence. </li></ul>
  115. 115. Pediculosis
  116. 116. Pediculosis <ul><ul><li>PediculosisPubis </li></ul></ul>
  117. 117. Pediculosis- capitus
  118. 118. TREATMENT <ul><ul><li>Patients with body lice should discard infested clothes and improve their hygiene. </li></ul></ul><ul><ul><li>Combing out nits is a widely recommended but unproven adjunctive therapy. </li></ul></ul><ul><ul><li>Personal items such as combs and brushes should be soaked in hot water for 15 to 30 min. </li></ul></ul><ul><ul><li>Close contacts and household members should also be examined for the presence of lice. </li></ul></ul>
  119. 119. TREATMENT <ul><ul><li>The following products are available for treatment of lice: </li></ul></ul><ul><ul><ul><li>Permethrin: available over the counter (1% permethrin [Nix]) or by prescription (5% permethrin [Elimite]); should be applied to the hair and scalp and rinsed out after 10 min. A repeat application is generally not necessary in patients with head lice. </li></ul></ul></ul><ul><ul><ul><li>Lindane 1% (Kwell), pyrethrin S (Rid): available as shampoos or lotions; they are applied to the affected area and washed off in 5 min; treatment should be repeated in 7 to 10 days to destroy hatching nits. </li></ul></ul></ul><ul><ul><ul><li>Malathion (Ovide) or organophosphate is effective in head lice. It is available by prescription. Use should be avoided in children ≤2 yr. </li></ul></ul></ul>
  120. 120. TREATMENT <ul><li>Eyelash infestation can be treated with the application of petroleum jelly rubbed into the eyelashes three times a day for 5 to 7 days. The application of baby shampoo to the eyelashes and brows three or four times a day for 5 days is also effective. The use of fluorescein drops applied to the lids and eyelashes is also toxic to lice. </li></ul><ul><li>In patients who have previously failed treatment or in whom resistance with 1% permethrin cream rinse occurs, a 10-day course of trimethoprim-sulfamethoxazole (TMP-SMX) 8 mg/kg/day of trimethoprim in divided doses is an effective treatment for head lice infestation. </li></ul><ul><li>Ivermectin (Mectizan), an antiparasitic drug, given in a single oral dose of 200 μg/kg is effective for head lice resistant to other treatments (currently not FDA approved for pediculosis). </li></ul>
  121. 121. PEARLS & CONSIDERATIONS <ul><ul><li>Patients with pubic lice should notify their sexual contacts. Sex partners within the last month should be treated. </li></ul></ul><ul><ul><li>Parents of patients should also be educated that head lice infestation (unlike body lice) does not indicate poor hygiene. </li></ul></ul>