Psoriasis Lecture 37 - Part 3 PDF

Summary

This document provides a comprehensive overview of psoriasis, encompassing its predisposition, symptoms, pathophysiology, diagnosis, and treatment methods. It covers the prevalence, potential triggers, and important aspects of managing this condition.

Full Transcript

Psoriasis Recall: Psoriatic Arthritis (Some Progress from Psoriasis to PSA) Predisposition to Psoriasis • Prevalence: 1-8.5% of the population • Positive family history in 30% of patients • Inheritance is considered “multifactorial” • Can develop at any time in life, but usually at puberty or meno...

Psoriasis Recall: Psoriatic Arthritis (Some Progress from Psoriasis to PSA) Predisposition to Psoriasis • Prevalence: 1-8.5% of the population • Positive family history in 30% of patients • Inheritance is considered “multifactorial” • Can develop at any time in life, but usually at puberty or menopause • Can be aggravated by environmental factors – Infections – group A strep, HIV infection – Stress – Alcohol and drugs – prednisone, beta blockers, lithium • Strong MHC association – HLA-Cw602, HLA-DR7 Symptoms of Psoriasis https://post.healthline.com/wp-content/uploads/2020/02/Psoriasison-trunk-1296x728-gallery_slide4.jpg Five cardinal morphologic features 1. Red plaques (raised) 2. Well circumscribed margins 3. Bright salmon-red color 4. Silvery micaceous scale 5. Symmetric distribution Clinical course of disease • Commonly on scalp, retroauricular, ears, umbilicus, and extensor surfaces over bony prominences • Relapsing and remitting course of… • …Pruritus, fissuring, and bleeding of lesions • 5% of patients with psoriasis also have psoriatic arthritis https://ijdvl.com/content/126/2006/72/2/Images/ijdvl_2006_72_2_161_25653_1.jpg Pathophysiology of Psoriasis • Chronic immunologic disease of skin characterized by profound cutaneous inflammation and epidermal hyperproliferation • Skin Autoantigen is unknown but melanocyte ADAMTSL5 & cathelicidin peptides can be involved • Believed to be caused by an environmental trigger that damages keratinocytes, causing inflammatory response • Process ‒ Stressed/damaged keratinocytes release DNA and antimicrobial peptides that activate local DCs ‒ CD4 Th1 and Th17 cells activated o Th1 production of IL-2 and IFN-γ → T cell proliferation and differentiation and mac activation o Th17 production of IL-2, IL-17, and IL-22 → T cell proliferation, PMN recruitment, keratinocyte hyperproliferation • Result – dysregulated keratinocyte proliferation and inflammatory response https://www.frontiersin.org/articles/10.3389/fimmu.2019.01764/full The Pathogenesis of Psoriasis v v Diagnosis of Psoriasis Diagnosis based on: • Medical history – recent skin damage or infection • Physical exam • Biopsy Histopathologic findings: • CMI – CD4 T cells with Th1 and Th17 • Intense cutaneous inflammation – many PMNs, maybe some macs • Keratinocyte hyperproliferation psoriasis normal Histology of Psoriasis https://www.jacionline.org/article/S0091-67491400181-X/fulltext https://www.cell.com/trends/genetics/fulltext/S0168-9525(10)00129-0 Treating Psoriasis Topical creams, ointments, gels, lotions containing: • Glucocorticoids • Tars • Calcipotriol (vitamin D derivative) • Anthralin • Tazarotene (retinoid – vitamin A derivative) • Salicylic acid Elbow psoriasis, pre- and post treatment UV-B or UV-A + psoralens (PUVA) Systemic therapies • Methotrexate • Acitretin (oral retinoid) • Cyclosporine • Biologics – targeting TNF, IL-17, IL-12/IL-23, and PDE4 (see suppl. slides) https://qtxasset.com/quartz/qcloud5/media/image/2017-07/Cyndi.jpg?VersionId=S8z3C6XozszHuaTM5Y0zOK0X7n61DIez

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