Integumentary - Psoriasis Midterm Notes PDF

2 1 INTEGUMENTARY – Psoriasis Psoriasis Psoriasis is a chronic, non-contagious, autoimmune, relapsing skin disorder that affects the skin, nails, and some4mes the joints (in psoria4c arthri4s). It is ch...

2 1 INTEGUMENTARY – Psoriasis Psoriasis Psoriasis is a chronic, non-contagious, autoimmune, relapsing skin disorder that affects the skin, nails, and some4mes the joints (in psoria4c arthri4s). It is characterized by scaly, thick, silver plaques that typically appear on the scalp, elbows, and knees. 1. Most Likely Cause The most likely cause of psoriasis includes gene@c and immune system dysfunc@on. Psoriasis is an autoimmune condi@on in which T-cells mistakenly aCack healthy kera@nocytes, resul4ng in rapid skin cell turnover. Cause: o Autoimmune Disease: T-cells become ac4vated and release cytokines, which promote the rapid produc4on of kera4nocytes and cause inflamma4on. o Gene@c Factors: A family history of psoriasis increases the risk of developing the condi4on. o Environmental Triggers: External triggers like stress, infec@ons (like strep throat), injury to the skin (Koebner phenomenon), and medica@ons (e.g., lithium, beta-blockers) can trigger or exacerbate the disease. 2. Pathophysiology The pathophysiology of psoriasis is mul@factorial, involving the immune system, gene@c predisposi@on, and environmental triggers. The main processes include the ac@va@on of dendri@c cells (DCs), T-cells, and the release of cytokines (IL-12, IL-23, IL-17, TNF-α), which lead to increased kera4nocyte prolifera4on and inflamma4on. 1. An@gen Presenta@on and T-cell Ac@va@on: o Unknown an@gens are taken up by dendri@c cells (DCs), which ac4vate naive T cells into Th1 and Th17 cells via the produc4on of IL-12 and IL-23. o Ac4vated T cells produce cytokines (TNF-α, IL-17, and IL-23), which recruit more immune cells to the skin and ac4vate kera4nocytes. 2. Kera@nocyte Hyperprolifera@on: o The release of cytokines promotes kera@nocyte prolifera@on and reduces the 4me for kera4nocytes to fully mature (normal matura4on takes 26-30 days, but in psoriasis, it takes only 3-4 days). o The accelerated rate of mitosis leads to thickening of the epidermis and accumula4on of immature kera@nocytes on the surface, which form the scaly, silvery plaques characteris4c of psoriasis. 3. Inflamma@on and Immune Cell Infiltra@on: o T cells, neutrophils, and other immune cells infiltrate the skin, producing cytokines and chemokines that increase local inflamma4on and aPract more immune cells. o Hyperplasia of kera@nocytes causes thickened skin, forming the visible plaques and scales seen in psoriasis. 4. Chronic Inflamma@on and Psoria@c Arthri@s:  2 o If the inflamma4on extends to the joints, it results in psoria@c arthri@s, characterized by joint pain, s@ffness, and swelling. 3. Disease Transmission Transmission: o Not transmissible. Psoriasis is not contagious and cannot be spread from person to person through physical contact. o The disease is an autoimmune disorder driven by an overac4ve immune system, not an infec4on. 4. Risk Factors The risk factors for psoriasis include both gene@c predisposi@ons and environmental triggers. Non-Modifiable Risk Factors Gene@cs: Family history of psoriasis increases the risk of developing the condi4on【. Age: Psoriasis can develop at any age but is most commonly seen in two age groups: early-onset (16-22 years) and late-onset (57-60 years). Modifiable Risk Factors Environmental Triggers: o Stress: Psychological stress triggers the release of cor4sol, which can exacerbate psoriasis. o Infec@ons: Strep throat (GuPate Psoriasis) can trigger an outbreak. o Skin Injury (Koebner Phenomenon): Trauma, cuts, scrapes, or burns on the skin can trigger plaque development at the injury site. o Certain Medica@ons: Beta-blockers, an@malarials, and lithium are known to worsen psoriasis. Lifestyle Factors: o Smoking: Smoking is associated with increased severity and risk of psoriasis. o Alcohol Consump@on: Excessive alcohol use is a risk factor for increased psoriasis severity. o Obesity: Increased adipose 4ssue produces inflammatory cytokines that worsen psoriasis. Summary Table Criteria Psoriasis Most Likely Autoimmune disease (T-cell ac4va4on), gene@c predisposi@on, external Cause triggers (injury, infec4on, medica4ons). T-cell ac@va@on → cytokine release (TNF-α, IL-17, IL-23) → kera@nocyte Pathophysiology hyperprolifera@on → plaque forma@on. Transmission Not transmissible. Psoriasis is an autoimmune disorder, not an infec4on. Modifiable: Smoking, alcohol consump4on, stress, infec4ons (strep), skin Risk Factors injury, and certain medica4ons. Non-Modifiable: Gene4cs, family history, age.  3 Clinical Manifesta@ons Plaques: Well-demarcated, erythematous plaques with a silvery-white scale are seen on the scalp, elbows, knees, and extensor surfaces. Pruritus (itching): Common symptom in individuals with psoriasis. Koebner Phenomenon: New psoriasis plaques develop at sites of skin trauma (e.g., cuts, burns, or scratches). Nail Changes: Psoriasis can cause picng, discolora@on, and onycholysis (separa4on of the nail from the nail bed). Psoria@c Arthri@s: Occurs in 30% of people with psoriasis and presents with joint pain, swelling, and s@ffness.