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Dermatology Lecture Psoriasis ACNE AD
- 3. An immune mediatedpolygenic skin disorder Sharply demarcated erythematous plaque with micaceous scale Localized Vs widespread distribution Comorbidities: • PsoA • metabolic syndrome and CVD • depression
- 4. Worldwide psoriasis prevalence= 2% Seen in all races Although psoriasis can being at any age, there seem to be two peaks in onset: ages 20-30 and ages 50-60.
- 5. Genetic predisposition Environment and behavioral factors Triggers: Infection Trauma Physical or psychological stress Medications beta blockers lithium antimalarias ACE inhibitors rebound with withdraw of steroids.
- 6. Smoking Palmoplantar pustulosisis strongly associated with smoking. Lifestyle factors, • Obesity • Higher BMI • Alcohol consumption Improvement in • Summer months • Ultraviolet radiation • Increased relative humidity.
- 7. + familyhistory ( 35%- 90%) Associated with • HLA-Cw6 • HLA-B27 • HLA-B13 • HLA-DR7 • HLA-B17 • HLA-B57
- 9. Chronic Plaque Pso Guttate Pso Eythrodermic Pso Pustuar Variant Special locatoin Generalized Acrodermatitis continuaof Hallopeau Pustulosis of Plams& Soles Oral mucosa Flexure Pso Scalp Pso Nail Pso
- 10. Chronic Plaque Psoriasis (psoriasisvulgaris) Most common Symmetrically distributed scalp, extensor elbows, knees, and back. The plaques typically are asymptomatic although some pts. complain of pruritis.
- 11. Guttate Psoriasis (= droplike) Commonly seen in children and adolescent Strong association between streptococcal infection (URTI), and guttate psoriasis
- 12. Erythrodermic psoriasis Acute orchronic. Characterized by generalized erythema and scaling from head to toe. Complications: loss of adequate barrier protection (infections and sepsis) and electrolyte abnormalities secondary to fluid loss. Inpatient management.
- 13. Pustular psoriasis Generalizedpustular pso. - Pregnancy ( impetigo herpetiforms) - Rapid tapering of coticosteroids - Hypo ca - Infection Von Zumbusch pattern ( painful) Pustulosis of palms and soles ( sterile) Acrodeermatitis continua of Hallopeau
- 14. Scalp Psoriasis Vsseb. Dermatitis Pityriasis amaintacea
- 15. Inverse psoriasis (Flexural) Shiny pinkto red Less scale Localized dermatophyt, candidal and bacterial infections can be a trigger for flexural pso.
- 16. Nail psoriasis Nail matrixdisease are pitting and leukonychia Nail bed disease are oil drop sign and onycholysis Nail involvement ↑ risk of PsoA
- 17. PsoA 5-30% Hallmarkis erosive changes radiographically Mono and asymmetric oligoartheritis
- 18. History and physicalexamination Skin biopsy is preformed to role out other conditions. No laboratory tests that confirm or exclude the diagnosis.
- 19. • Mild, moderate,and severe replaced with: – Candidates for localized therapy – Candidates for systemic therapy • Candidates for systemic therapy may have one or more of the following features: – BSA greater than 5% – Involvement of vulnerable areas of the body, including palms, soles, face, scalp, and genitals – Significant impact on quality of life – Failure of localized therapy – Concomitant psoriatic arthritis
- 20. Emollients Corticosteroids:mid-high potency for most areas, low potency for face and intertriginous areas Calcipotriene (Dovonex®): works best in combination with topical corticosteroids Tazorotene (Tazorac®): works best in combination with topical corticosteroids Tacrolimus (Protopic®): for face and intertriginous areas Ointments, creams, gels, foams, sprays, shampoos, and medicated tape all available. Topical Therapies for Psoriasis
- 21. Systemic Therapies forPsoriasis • Phototherapy: UVB ( 290-320 nm), narrow-band UVB (311 nm), PUVA ( psoralen, 320-400 nm), Excimer laser (308 nm). • Immunosuppressive drugs: • Methotrexate • Acitretin • Cyclosporine
- 23. Biologics Treatment forPsoriasis • Immunomodultory drugs: • Etanercept (Enbrel®): soluble TNF- receptor • Adalimumab (Humira®): human anti-TNF- mAb • Infliximab (Remicade®): chimeric anti-TNF- mAb • Ustekinumab (Stelara®): human anti-IL-12/IL-23 mAb • Secukinumab (Cosentyx®): human anti-IL-17A
- 24. Monitoring Before andDuring Methotrexate and TNF- Blocker Use • Baseline: PPD, hepatitis profile, CBC with diff, chemistry panel • Every 3 months: clinically monitor progress, CBC with diff and chemistry panel for MTX • Every 6 months: CBC with diff and chemistry panel for TNF- blockers • Every year: PPD for TNF- blockers
- 26. Multifactorial disordersof pilosebaceous unit. Affect all age groups ( Adolesence) ≈ 85% ( B/W 12 and 24 years of age) ↑ risk: XYY karyotype Endocrine disorder: PCOS Hyperandrogenism Hypercortisolism Precocious puberty
- 28. Most oftenin face and upper trunk Non inflammatory acne: • Open and close comedons Inflammatory acne: • Papules, pustules, nodules and cysts PIH and Scarring
- 32. Acne Varients: Postadolescent acne Acne fulminans ( Acne and systemic manifestations) – boys SAPHO syndrome Oral corticosteroid and oral isotretinoin Acne conglobata ( eruptive onset but no systemic manifestations) Part of follicular occlusion tetrad PAPA syndrome
- 34. Acne Mechanica Comedo formation Acneexcoriee des jeunes filles Drug induced acne monomorphic eruption corticosteroid INH Iithium Bromides and Iodides Phenyton Progestins Anabolic Steroid EGFR inhibitors
- 35. Occupational Acne andAcne Cosmetica primarily closed comedones Neonatal Acne ( neonatal cephalic pustulosis) 2 weeks of age Resolves within 3 months of life Not comedones Malasssezia spp. Infentile Acne 3-12 months of age Comedo formation Androgenic production intrinsic to this stage of development Endocrinologic abnormalities
- 40. Introduction • Typically beginsduring infancy or early childhood and its often associated with asthma and allergic rhino- conjunctivitis. • Complex genetic disease with environmental influences. • Intense pruritus and chronically relapsing course. • Infant: ACUTE- cheeks, scalp, and extensor aspects of the extremities. • Children and Adults: Chronic -flexural sites.
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- 49. Epidemiology • Children 10-30%vs. Adult 2-10% • Most in High income countries and some low income countries • Three subsets of AD based on age of onset 1. Early onset type: defined as AD beginning in the first 2 years of life. This is most common type of AD 45% during the first 6 months of life 60% during 1st year of life 85% before 5 years of age 2. Late onset type: defined as AD that starts after puberty 3. Senile onset type: an unusual subset of AD that begins after 60 years of age
- 50. Pathogenesis 1. Genetic 2. Epidermalbarrier dysfunction 3. Immunopathology 4. Role of microbial colonization 5. Role of autoimmunity
- 54. •Systemic therapy (e.g. Cyclo) or UV therapy Step 4 •Mid to high potency TCS Step 3 •Low to mid potenct TCS Step 2 •Basic treatment: skin hydration, avoidence of irritantsStep 1
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Editor's Notes
- #4 From the Greek “psoros” meaning “rough, scabby”. Psoriasis is a common chronic skin disorder typically characterized by erythematous papules and plaques with a silver scale, although other presentation occur. Most cases are not severe enough to affect general health, and treated in the outpatient setting.
- #8 2 parent had pso--- 41% 1 parent had pso--- 14% I sbling had pso--- 6%
- #14 This form can be assoicated with malaise, fever, diarrhea, leukocytosis, and hypocalcemia. Hepatic abnormalities: jaundice, high ALT , AST and ALP, neutrophilic cholangitis
- #17 The presence of nail disease may be important diagnostically, often providing valuable supportive evidence of disease in difficult cases
- #19 Histology finding: epidermal hyperplasia Paraketosis (retention of nuclei in the stratum corneum Neutrophils in the stratum corneum and epidermis Thinned or absentt granular cell layer Microabscesses with neutrophils may be seen
- #21 Tar