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NR 507NP Week 8 Dermatology Conditions

Chamberlain University Nursing NR 507 Advanced Pathophysiology Aaron Boone 6 pages
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e. Thickened, pitted, or ridged nails f. Psychological impact (self-conscious) 5. Psoriatic Arthritis CMs a. Joint pain/stiffness (especially in AM) b. Swelling/warmth c. Joint inflammation d. Nail changes e. Enthesitis (inflammation where tendons/ligaments attach to bones) f. Dactylitis (sausage digits) g. Fatigue h. Eye inflammation 6. Diagnosis/Tx of Psoriasis a. Topicals—Corticosteroids, Vit D analogs, retinoids, and calcineurin inhibitors. b. Phototherapy c. Systemic meds—Retinoids, methotrexate, cyclosporine, and biologics d. Avoid triggers ROSACEA 1. Normal Physiology of Skin a. Barrier to prevent pathogens from entering b. Inflammation that attracts other immune cells to the site of injury and to eliminate pathogen. c. Adaptive immune response: dendritic cells in skin capture pathogen and present to T cells to trigger immune response. 2. Pathophys of Rosacea: a chronic inflammatory skin disease that primarily affects the face. a. Genetic predisposition b. Immune dysfunction (particularly innate immune system) c. Vascular abnormalities: Dilation and increased permeability d. Inflammatory mediators: Cytokine and chemokines promote inflammation. e. Microbial factors: Demodex mites and certain bacteria have been shown to dev’t rosacea through triggering immune response in skin. f. Trigger factors: Sun, heat, spicy food, alcohol, and meds. 3. Risk factors ACNE 1. Normal Physiology of Sebaceous Glands and Hair Follicles a. Sebaceous Glands : On all skin except palms and soles. i. Role is to secrete sebum (to hydrate skin) ii. Sebum occurs when lipid-filled sebocytes release substance that travels up toward pore. 1. Testosterone and insulin can modulate gland size and activity level. b. Hair Follicles Assist in thermoregulation (goosebumps = piloerection) 2. Pathophys of Acne a. Hyperkeratinization of hair follicle: rapid shedding of skin cells in the upper portion of the hair follicle, causing excessive cellular material to partially or completely block the follicular pore. b. Abnormal secretion of sebum: may lead to excessive sebum being trapped in the follicular canal or in the sebaceous gland. c. Shift of bacteria from symbiotic to pathogenic: occurs when anaerobic bacteria Cutibacterium multiply in a warm, dark, and inviting environment  This activates the body’s immune and inflammatory response. d. Rupture of follicle: due to increased pressure inside the canal; trapped sebum and keratinized hair cells collect and grow, causing raised lesions (papules) above the skin surface that are at risk of rupture and spreading material underneath the skin. 3. Acne Risk Factors a. Genetics b. Environmental (high temps, high humidity, pollution) c. Improper skin care d. Hormones e. Meds (corticosteroids, androgens, topical creams) f. Diet (high sugar, high dairy) 4. CMs of Acne a. Open comedone (blackhead): Sebum and keratin block the open follicle leading to oxidation b. Closed comedone (whitehead): Sebum and keratin accumulate deep within a blocked or closed follicle c. Papule: Small, raised lesions usually less than 1 cm in size with no observable debris inside. i. Lighter skin coloring and multiple moles. c. Age/Geographic i. Older ii. Higher elevation/Closer to equator d. Family/Personal Skin Cancer Hx e. Medication or Toxic exposure i. Chemo ii. Biologic response modifiers and Disease- modifying antirheumatic drugs f. Genetics and Immune

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