1. Dermatology Maculopapular and Plaque DermatitisBy
Stacey Singer-Leshinsky R-PAC

2. Maculopapular Description
A Maculopapular rash is usually a large erythematous area with confluent bumps.
Plaque

3. Allergic and Hypersensitivity Dematoses
Inflammatory response
Epidermal edema and separation of epidermal cells.
Includes: Atopic dermatitis, Nummular eczema, Dyshidrotic eczema, Contact dermatitis, stasis dermatitis, Diaper dermatitis, perioral dermatitis, seborrheic dermatitis, lichen simplex chronicus, Psoriasis, lichen planus, seborrheic keratosis, Actinic keratosis

4. Atopic Dermatitis (Eczema)
Type I (IgE) hypersensitivity inflammatory reaction
Risk factors: Family history of atopy. Exacerbated by scratching, stress

5. Atopic Dermatitis (Eczema)
Epidemiology: Usually begins prior to 6m of age.
(FACE): flexor surfaces get adults, children extensor)

6. Atopic Dermatitis Clinical Manifestations
Acute form
Pruritus.
Appear erythematous, edematous with papules/plaques.
Scaling, weeping, and crusting

7. Atopic Dermatitis Clinical Manifestations
Chronic form
Lichenification
painful fissures
                              
                                                                                  

8. Atopic Dermatitis Clinical Manifestations
Infantile eczema
Weeping inflammatory patches and crusted plaques on:

9. Atopic Dermatitis Clinical Manifestations
Juvenile/adult
Affects flexural areas
Appear as dry, lichenified pruritic plaques

10. Atopic Dermatitis Diagnosis/ Complications
History
Serum IgE
Differentiate from viral HSV
Complications:

11. Atopic Dermatitis Management
Avoidance of triggers. Avoid scratching
Lubricants.
Oral antihistamines
Topical corticosteroids

12. Atopic Dermatitis Management
Topical antibiotics for staphylococcus aureus infection
Non-glucocorticoid anti-inflammatory agents now available such as pimecrolimus.
Avoid oral steroids

13. Nummular Eczema Inflammatory response. Etiology:
Risk factors: young and old. Fall and winter. Xerosis.
Clinical manifestations
Round coin like sharply demarcated erythematous papulovesicular patches/ plaques
Intense pruritus,
Lichenification

14. Nummular Eczema Diagnosis /Differentials
History and physical exam
Rule out secondary infection, allergy
Differential diagnosis to include seborrheic dermatitis, psoriasis, contact dermatitis, tinea

15. Nummular Eczema Management
Avoid scratching
Lubricants
Oral antihistamines
Topical corticosteroids
Intralesional triamcinolone
Systemic antibiotics
Phototherapy
Complications:

16. Dyshidrotic Eczema
Recurrent chronic relapsing form of vesicular hand and foot dermatitis
No evidence of eccrine gland dysfunction dyshidrotic
Intraepidermal vesicles
Etiology/risks: Unknown etiology
Epidemiology: Prior to age 40.

17. Dyshidrotic Eczema Clinical Manifestations
Pruritus and burning
Begins on lateral fingers and progress to palms and soles.
Vesicles: 1-2mm with clear fluid resembling tapioca
Later: desquamation and Lichenification

18. Dyshidrotic Eczema Diagnosis/Differentials
Clinical
Rule out secondary infection, allergy
Differential diagnosis to include contact dermatitis, drug reaction
Complications:

19. Dyshidrotic Eczema Management
Burrow wet dressings
High potency glucocorticoids and occlusive dressings
Topical antipruritics.
Severe need systemic steroids
Intralesional Triamcinolone
Systemic antibiotics

20. Contact Dermatitis
Cell mediated reaction involving sensitized T lymphocytes.
Etiology
Irritant form: Chemical insult to skin. No previous sensitizing event.
Allergic form is delayed-hypersensitivity reaction. Skin sensitized from initial exposure. During next exposure patient has reaction.

21. Contact Dermatitis Clinical manifestations
Develop 24-96h post exposure
Pruritus
Acute present as vesicles with clear fluid on erythematous edematous skin.
Sub-acute is edema and papules
Chronic-

22. Contact dermatitis Diagnosis/Differential Diagnosis
Clinical
Rule out secondary infection.
Patch testing
Differential diagnosis to include seborrheic dermatitis, atopic eczema

23. Contact Dermatitis Treatment
Remove etiologic agent
Wet dressings with gauze soaked in Burow’s solution changed every 2-3 hours.
Topical corticosteroids
Systemic corticosteroids

24. Stasis Dermatitis
Inflammatory skin disease that occurs on lower extremities
Extravasation of plasma proteins and RBC into subcutaneous tissues. Becomes brown in color due to hemosiderin deposits
Results in interstitial fluid accumulation . Leads to reduced capillary blood flow

25. Stasis Dermatitis Can progress to venous stasis ulcers and fibrosis
Found in 6-7% of elderly population

26. Stasis Dermatitis Acute form: Initially medial aspect of ankle.
Inflammation
Weeping lesions
Plaques/ Erythema
Crusting/ Exudate

27. Stasis Dermatitis Chronic form
Thin, shiny bluish brown irregularly pigmented scaling skin.

28. Stasis Dermatitis Diagnosis/Differentials
Clinical
Doppler
Differential diagnosis to include contact dermatitis, Atopic dermatitis, cellulitis

29. Stasis Dermatitis Management
Mid potency topical corticosteroids.
Control chronic edema
For ulcers:
Unna venous boot changed every week.
Wound care
Advise patient to elevate legs and wear compression stockings
Avoid standing or sitting for long time

30. Diaper Dermatitis Irritant dermatitis
Cutaneous Candidiasis infection (C. Albicans )
Risks: areas where warmth and moisture lead to maceration of skin or mucous membranes

31. Diaper Dermatitis History and Physical Exam
Pruritus, pain
Erythematous papules/vesicles, edema
Satellite lesions to Peri-genital, peri-anal, inner thigh, buttocks

32. Diaper Dermatitis Diagnosis/Differentials
Diagnosis- KOH examination
Differential diagnosis to include contact dermatitis, child abuse

33. Diaper Dermatitis Management
Topical antifungal agents such as Nystatin, miconazole, or clotrimatzole
Topical corticosteroids
Complications
Educate care givers

34. Perioral Dermatitis
Facial dermatosis with confluent papulopustular lesions. Lead to inflammatory plaques.
Unknown etiology.
Risks: young women, prolonged use of topical steroids or steroid sprays

35. Perioral Dermatitis History and Physical Exam
Lesions resemble rosacea
Burning
Follicular papules, vesicles and pustules on an erythematous base
Grouped    

36. Perioral Dermatitis Diagnosis/ Differentials
Clinical.
Rule out secondary causes.
Differentials
Acne Vulgaris
Contact dermatitis
Rosacea
seborrheic dermatitis

37. Perioral Dermatitis Management
AVOID topical corticosteroids.
Antibiotics
Metronidazole, erythromycin topical
Systemic antibiotics: Monocycline, Doxycycline, or tetracycline
Wash with mild soap, use nonfluorinated toothpaste.
Avoid oral contraceptives

38. Seborrheic Dermatitis Seborrhea
Skin rash that occurs in areas of high sebaceous gland concentration
Cutaneous inflammation to dermis
Etiology: Immune response to endogenous yeast Pityrosporum
Triggered by seasonal changes, scratching, emotional stress, medications.

39. Seborrheic Dermatitis
Infants
Affects scalp, flexural area and perioral
Erythematous plaques
Fine white scales
Thick yellow brown greasy scaling

40. Seborrheic Dermatitis
Adults
Pruritus
Burning
Erythematous plaques with scaling

41. Seborrheic Dermatitis Diagnosis/Differentials
History/Physical
Differential diagnosis to include atopic dermatitis, candidiasis, lupus

42. Seborrheic Dermatitis Management
Selenium sulfide shampoos, 2% ketoconazole shampoo, ketoconazole cream.
Salicylic acid
Corticosteroids
Cradle cap-
Treat for secondary infection

43. Lichen Simplex Chronicus
End stage of pruritic and eczematous disorders.
Skin responds to physical trauma by epidermal hyperplasia.
Common areas
Risk factors:

44. Lichen Simplex Chronicus History and Physical Exam
Well circumscribed plaques with lichenified or thickened skin
Pruritus-
Hyperpigmentation
Excoriation

45. Lichen Simplex Chronicus Diagnosis/Differentials
Differential diagnosis to include psoriasis Vulgaris, contact dermatitis, fungal infection
Diagnosis
Clinical
Biopsy shows hyperplasia acanthosis, hyperkeratosis
KOH examination

46. Lichen Simplex Chronicus Management
High potency topical glucocorticoids
Oral antihistamines-
Hydration
Complications:

47. Psoriasis
Increased epidermal cell proliferation due to a shortened epithelial cell cycle. Leads to hyperkeratosis.
This results in keratinization defects, forming thick adherent scales .
Patients have exacerbations and remissions.
Can be triggered by stress, class I topical corticosteroids, or Koebner reaction.
Etiology: Genetic abnormalities in the immune system

48. Psoriasis History and Physical Exam
Plaque lesions most common
Erythematous or salmon colored plaques with distinct borders covered with silvery white scales
Extensor >flexor.
Nails

49. Psoriasis History and Physical Exam
Pustular psoriasis:
Painful
Deep sterile yellow pustules
Pustules evolve into red macules

50. Psoriasis History and Physical Exam
Guttate Psoriasis
Could be immune
Slight pruritus
Small erythematous papules with fine scale
Can be discrete or confluent

51. Psoriasis Diagnosis/Differentials
Skin biopsy shows increased mitosis in keratinocytes
Auspitz phenomenon
Differential diagnosis to include lichen planus, eczema

52. Psoriasis Management Supportive care Hydrating creams
Mid-potency topical glucocorticoids
Retinoids such as tazarotene
UV light combined with coal tar, salicylic acid, and anthralin
Systemic immunosuppressive – Moderate, severe or disabling psoriasis

53. Lichen Planus
Cell mediated immunologic reaction targeting keratinocytes.
Etiology: Unknown, possibly genetic, liver disease.
Involves skin and/or mucous membranes.
Risks: age, HLA associated gene

54. Lichen Planus History and Physical Exam
Pruritic, polygonal, purple, flat topped papules covered with fine scales
Lesions
Found on flexor areas, shins, and mucous membranes.
Lesions resolve with post inflammatory hyperpigmentation.

55. Oral Lichen Planus Oral lesions involve the tongue and buccal mucosa
Present with wickham’s striae
Can then erode

56. Lichen Planus Diagnosis/Differentials
Clinical inspection
Skin biopsy
Look for associated disorders
Differential diagnosis to include chemical exposure, psoriasis, candidiasis, scabies
Complications to include squamous cell carcinoma, alopecia

57. Lichen Planus Management
Antihistamines
Topical corticosteroids
Systemic corticosteroids
Topical and systemic retinoids Retinoids normalize epidermal differentiation and are anti inflammatory
Immunosuppressant -Cyclosporine.

58. Seborrheic Keratosis
Due to proliferation of Keratinocytes and melanocytes
Etiology: Genetics
Usually asymptomatic
Benign, however must rule out malignant melanoma
Spontaneous resolution rare

59. Seborrheic Keratosis Begin as sharply define light brown flat macules
Then develop velvety to a warty surface with multiple plugged follicles
Pasted on plaque
Color from brown to black
Size up to several centimeters.

60. Seborrheic Keratosis Diagnosis/Differentials
Skin Biopsy
Differentials
Actinic Keratosis
Carcinoma
Warts

61. Seborrheic Keratosis Management
Keratolytic agents-leads to desquamation of hornified epithelium- Ammonium Lactate lotion
Trichloroacetic acid- cauterizes skin, keratin and tissues.

62. Actinic Keratosis Found in those with fair skin
Sun exposure leads to damage to keratinocytes by UV radiation
Hyperkeratotic form more prominent and palpable.

63. Actinic Keratosis Multiple, discrete flat or elevated
Skin colored, yellow-brown or brown.
Dry, rough, adherent scaly lesion
3-10mm

64. Actinic Keratosis Diagnosis/Differentials
Diagnosis:Biopsy will show epidermal changes
Differentials
Squamous cell carcinoma
Lupus
Seborrheic keratosis

65. Actinic Keratosis Management
Topical 5-fluorouracil:
Surgical curettage or cryosurgery
Retinoids
Dermabrasion
Avoid sun exposure.

66. Urticaria
IgE or complement mediated edema of dermis or subcutaneous tissue
Etiology: antigens
Pathology: Mast cell stimulated to degranulate by IgE.

67. Urticaria Clinical: Pink Edematous Papules or plaques
Vary in appearance
Resolve within 24 hours
Angioedema: Painless, deeper urticaria

68. Urticaria
Diagnostics:
Management:
Eliminate cause
Oral antihistamines

69. Review 1
In infants this lesion is found on extensor surfaces while in adults it is found on flexor surfaces.
Pt presents with pruritic lesions that are erythematous
What is this?

70. Review #2 Pruritus and burning prior to eruption
Vesicles resemble tapioca
No erythema
What is this?
Where is it found?
How is it treated?

71. Review #3 This is the result of chronic venous insufficiency
What is it?
How is it managed?

72. Review #4
This rash occurs in areas with high sebaceous gland concentration.
What is it?
Describe this lesion
What is the management?

73. Review #5 T-cell mediated autoimmune disease
Abnormal growth of keratinocytes
Erythematous plaques with distinct borders and silvery white scales
What is this?
Where is it found?
How is it treated?

74. Review #6 What is the pathophysiology behind this? Describe this
What are management options?

75. Review #7
What is this?
What is the management of this?

76. Review #8 What is this? What causes this?
What is the treatment for this?

77. Review #9 What is this? What is the cause of this?
How is this treated?

78. Review #10 What is this? What is the cause of this?
How is this managed?