1. PAC 03 DERMATOLOGY Vesicular, Bullae, Acneiform Disease By Stacey Singer-Leshinsky R-PAC

2. Terms Vesicle: Bullae: Fluid filled blister greater than 100cm in diameter Acneiform:

3. Vesicular Bullae Bullous Pemphigoid Humoral and cellular response against self-antigens BP 180, 230. These are needed for dermo-epidermal cohesion. Sub epidermal blister formation from cascade of events

4. Vesicular Bullae Bullous Pemphigoid Lesions usually appear on extremities first then trunk. Flexor surfaces of extremities. Exacerbations/remissions.

5. Bullous Pemphigoid History and Physical Exam Non Bullous phase: mild to severe pruritus with excoriated, eczematous, papular, urticarial lesions Bullous phase: Vesicles and bullae on erythematous skin. Filled with clear or blood tinged fluid. Erode and crust.

6. Bullous Pemphigoid Drug Induced Diuretics, analgetics, antibiotics Drug acts as a trigger in patients with genetic susceptibility by modifying immune response

7. Bullous Phemphigoid Diagnosis Clinical confirmed by histopathology/immunopathology Immunofluorescence studies reveal IgG and/or C3 at dermal-epidermal junction IgE in serum Light microscopy of lesions reveals eosinophils, neutrophils, lymphocytes

8. Bullous Phemphigoid Differentials/Complications Differentials include erythema multiforme, drug eruptions, dermatitis herpetiformis Complications

9. Bullous Pemphigoid Treatment Systemic or Topical corticosteroids. Immunosuppressive medications Patients often go into a permanent remission

10. Pemphigus Vulgaris IgG auto antibodies against cell surface of keratinocytes. Results in acantholysis and blister formation. Found in middle age-elderly Can be due to reaction to medications 50-70% of patients have mucosal lesions

11. Pemphigus Vulgaris Clinical manifestations Pain Flaccid blister filled with clear serous fluid Blisters fragile. Blisters rupture Mucosal lesions can precede cutaneous lesions.

12. Pemphigus Vulgaris Diagnosis Nikolsky’s sign positive. Asboe-Hansen sign: gentle pressure on intact bulla forces fluid to spread under the skin away from site of pressure. Immunofluorescence Tzanck smear: acantholytic cells

13. Pemphigus Vulgaris Differentials/complications Differentials: Acute herpetic stomatitis, aphthous stomatitis, erythema multiforme, bullous lichen planus, bullous pemphigoid, Complications Secondary infection Dehydration Often fatal unless treated with immunosuppressive agents Recurrent and relapsing

14. Pemphigus Vulgaris Treatment Treat dehydration Glucocorticoids- Immunosuppressive therapy- Azathioprine, Methotrexate, cyclophosphamide

15. Pilosebaceous Unit Sebaceous gland empties into hair follicle. Pilosebaceous unit opens to surface. Sebaceous gland produces sebum.

16. Pilosebaceous Unit Amount of sebum produced depends on size of gland, rate of sebaceous cell proliferation Large sebaceous glands Sebum production related to androgens Sebaceous glands are rich in staphyloccus epidermidis and Propionibacterium.

17. Acne Vulgaris Primarily disorder of adolescence. Affecting 40-50 million in USA. Psychosocial and economic impact Clinically characterized by comedones and inflammatory lesions Etiology: unknown.

18. Acne Vulgaris Androgens cause sebaceous glands to overproduce sebum. Bacteria secrete lipase which converts lipids to fatty acids. Hyperkeratinization in lining of follicle and follicle plugging. Papules, pustules, scarring result from follicular rupture and inflammatory response

19. Acne Vulgaris Clinical manifestations Non-inflammatory acne: open and closed comedones., open comedones Inflammatory acne: above expands to form papules, pustules, nodules and cysts of varying severity. 1-5mm filled with sterile pus. Found on face, neck, shoulders and upper trunk

20. Acne Vulgaris Diagnosis/Differentials Hormone studies will rule out other etiologies Differential diagnosis to include folliculitis, steroid folliculitis Complications to include abscess formation and severe infection Scarring

21. Acne Vulgaris Management Comedolytics- Sebum suppressive medications- antiandrogens include spironolactone, oral contraceptives Topical/Systemic antibiotics- emycin, clindamycin Benzoyl peroxide- Severe Acne- Isotretinion(Accutane)- inhibits sebaceous gland function and keratinization.

22. Rosacea Peaks in 30-40’s. Associated with Parkinson’s, might be associated with Helicobacter pylori or hair follicle mites (Dermodex folliculorum) Related to vascular hyper-activity- Repeated episodes of dilation lead to release of inflammatory mediators into dermis.

23. Rosacea Involves nose, cheeks, forehead and chin Complain of reddening of face with heat, hot fluids, spicy foods and ETOH Rhinophyma caused by sebaceous hyperplasia M>F Blepharophyma Metrophyma

24. Rosacea Types Vascular Rosacea: Flushing and persistent central facial erythema with or without telangiectasia. Papulopustular rosacea: central facial erythema with transient papules and pustules.

25. Rosacea Types Sebaceous hyperplasia: thickening skin, irregular surface nodularities and enlargement. Ocular rosacea: Foreign body sensation in eyes. Photosensitivity, periorbital edema, telangiectasia of sclera.

26. Rosacea Diagnosis/Differentials Diagnosis: Clinical diagnosis, histopathological features Differential diagnosis: Acne vulgaris- Perioral dermatitis Seborrheic dermatitis Systemic Lupus Erythematosus

27. Rosacea Management Avoid environmental and dietary triggers such as heat/sun exposure, ETOH. Topical Metronidazole- Azelaic acid cream. Tetracycline- treats inflammation. Retinoids- Isotretinoin- Clonidine NO potent topical fluorinated steroids on face

28. Hidradenitis Suppurativa Skin infection that affects apocrine gland bearing skin sites especially the axillae and anogenital areas. Characterized by recurrent boils and draining sinus tracts with scarring.

29. Hidradenitis Suppurativa Risk factors include obesity, apocrine duct obstruction, family history Inflammatory condition originating in the hair follicle. Follicle ruptures spilling contents into surrounding dermis.

30. Hidradenitis Suppurativa Initially inflammatory nodules and sterile abscesses in axillae, groin, perianal areas. Then sinus tracts and hypertrophic scars develop. Pain/foul odor Erythematous abscess up to 2cm Chronic and remitting

31. Hidradenitis Suppurativa Diagnosis/Differentials Diagnosis: Bacterial cultures for antibiotic therapy Differentials: Cellulitis, pilonidal cysts, bacterial folliculitis Complications: Squamous cell carcinoma

32. Hidradenitis Suppurativa Management Might need incision and drainage if large and painful. Antibiotics such as tetracycline, cephalosporin, clindamycin, ciprofloxacin Isotretinoin Corticosteroids Reduce friction and moisture.

33. Hypersensitivity Vasculitis Immune complex mediated inflammation of small vessels such as arterioles, capillaries, venules. Occur as an exaggerated immune response to a drug, infection or autoantibodies This leads to injury to vessel walls, and so decreased function and blood flow.

34. Hypersensitivity Vasculitis Patients might report use of a new drug, history of streptococcal infection or collagen/vascular disease such as lupus, Rheumatoid Arthritis If not isolated then can have systemic vascular involvement of kidneys, muscles, joints, GI tract, peripheral nerves

35. Hypersensitivity Vasculitis Palpable purpura 1-3mm in diameter Usually localized to lower third of legs/ankles Lesions are scattered, discrete, confluent Lesions can form papules and ulcers due to lack of blood supply

36. Diagnosis: confirmed by skin biopsy ( vascular and perivascular infiltration of broken up leukocytes) Look for evidence of systemic disease Hypersensitivity Vasculitis Diagnosis

37. Hypersensitivity Vasculitis Complications/Differentials Complications Systemic vascular involvement Necrosis Irreversible damage to kidneys Differential diagnosis Thrombocytopenia purpura Disseminated intravascular coagulation Rocky Mountain Spotted Fever Steven Johnson Syndrome

38. Hypersensitivity Vasculitis Management Antibiotics If skin involvement use colchicine or Dapsone If visceral involvement then use steroids such as Prednisone combined with Cytotoxic immunosuppressives

39. Folliculitis Common disorder with perifollicular pustules. Etiology: staphylococcus aureus, pseudomonas aeruginosa chemical irritation, friction, perspiration, shaving, skin injury. Follicle infiltrate of lymphocytes, neutrophils, macrophages. Can lead to formation of abscess.

40. Folliculitis Papule or pustule on erythematous base Asymptomatic, mild discomfort or pruritic Favors areas with terminal hair Eye involvement: Healing can lead to keloids

41. Folliculitis Diagnosis/Differentials Diagnosis History and physical exam Cultures, gram stains, KOH Differentials Insect bites Scabies Rosacea Tinea

42. Folliculitis Management Wash area with antibacterial soaps Topical and/or oral antibiotics (s.aureus-often resistant to pcn so use dicloxacillin or cephalosporin or emycin or clindamycin) Pseudomonas Antifungals/Antivirals

43. Xerosis Dry skin Can be a natural occurrence sometimes associated with aging, second to contact dermatitis. Also exogenous causes such as dry climate, excessive exposure to water Etiology:

44. Xerosis Clinical Manifestations Pruritus Involves back, abdomen, extremities Dry rough, scaly skin Cracking, fissuring

45. Xerosis Diagnosis Diagnosis: histological findings Differential Diagnosis: Eczema, contact dermatitis, scabies

46. Xerosis Management Moisturizing agents humectants (alpha hydroxy acids- dry water from deeper layers to skin surface), occlusives which reduce water loss by epidermis

47. Example 1 Prodrome of erythematous skin prior to bullae eruption Pruritus weeks to months prior to blister eruption Extremities first then trunk What is this? What do immunofluorescence studies reveal? Treatment

48. Example 2 Mucosal lesions Flaccid blister on normal or erythematous skin. Blisters rupture leading to erosions What sign is positive? What happens if not treated? Treatment options:

49. Example 3 Follicular comedones with or without inflammatory papules, pustules and nodules What is the cause of this condition? What is the management?

50. Example 4 Blood vessels dilate easily and leakage of inflammatory mediators into dermis Aggravated by what medication Describe the appearance of the lesion Describe the management

51. Example 5 Chronic infection of apocrine sweat glands Inflammatory red hard raised nodules in axilla, groin, perineum What is this? What is the management?

52. Example 6 What is this? What bacteria are involved with this? What is the treatment of this?