Localised Scleroderma Case Study

The disease progression was discovered, annotated and observed over a several periods. The 1st period, the classical period, described the cutaneous disorder

Like we learned in chapter 1 the job of the integumentary system is to cover and protect the body but what happens if your skin develops a disease like eczema? Eczema is a chronic, common, non-infective inflammatory condition characterized by intense pruritus, redness, and scaling (Eczema, p.1). This condition can appear at any age, but it usually occurs during infancy or early childhood (Eczema, p.1). Eczema or any skin disease are the most common group of occupational health problems leading to absence from work (Eczema, p.1). Several factors play a big role in eczema, both internally and externally, depending on your genetic makeup you may be prone to getting eczema in as early as a few months after you were born or by allergens as a young

Vitiligo is an auto-immune disease where melanocytes, the cells that make pigment in the skin, are destroyed (Vora, Patel, Chaudhary, Mehta & Pilani, 2014). It is characterized clinically by totally white patches of skin, also known as lesions, appearing primarily on visible areas of the body, including face and hands (Osman, Elkordufani & Abdullah, 2009). In very rare cases vitiligo is accompanied by itching or other somatic symptoms but gradual discoloration is generally its only physical symptom (Schmid-Ott et al., 2007). The patches develop unpredictably and while there is a genetic component to vitiligo, race and age do not affect the incidence of the disease (Gupta, Sreenivas, Mehta, Khaitan & Ramam,

Psoriasis is a chronic skin disorder, easily identified by its symptoms of white, scaly skin and red lesions, though not so easily cured or understood. In psoriasis, skin cells mature faster than the body can shed them, causing a buildup. Although there are many theories as to what the cause of such a disease might be – genetics, stress, or other triggers – no one is quite sure why the disease occurs, or what could be a possible way to fully cure it. In this essay we will explore the symptoms, types, and effects of this condition, and also some of the known treatments.

This is a 50 year-old male who required inpatient hospitalization due to dizziness, abdominal pain, headache, and nausea after taking atenolol. Mr. A came to the Emergency Department with complaints of some dizziness two-day prior to admission and collapsed several times. For the past 2 weeks, he had not been taking his blood pressure medications due to financial reasons. He was given clonidine and atenolol from his dialysis center while he was unable to afford his normal hypertension medication. He was dialyzed three times a week through his arteriovenous fistula and had not missed any sessions. He also had increased dyspnea on exertion over the past 3 weeks, orthopnea and usually sleeps on several pillows which worsened between his dialysis. His medical history is significant for hypertension, diabetes mellitus type II, morbid obesity and end stage renal disease on dialysis.

Increased levels of pro-inflammatory cytokines and chemokines result in an infiltration of inflammatory cells forming plexiform lesions consisting of T cells, B cells and macrophages (Savaj et al., 2012). Scleroderma, or systemic sclerosis, is a connective tissue disease characterized by a thickening of the skin. Accumulation of collagen by fibroblasts, platelet adhesion and a type II hypersensitivity reaction lead to endothelial damage. Endothelial damage and decreased vasodilatation result in increased arterial pressure leading to PAH (Mclaughlin, 2009). Patients generally have a poor prognosis unless detected early, as a cure for slceroderma does not exist.

Systemic lupus erythematosus (SLE) is an autoimmune disease that affects multiple tissues and systems and with significant variable clinical features and organ involvement (Cava, 2010). It is characterized by a chronic, relapsing, inflammatory and often febrile multisystemic disorder of connective tissue with wide spectrum of involvement of skin, joints, kidneys and serosal membranes. The exact etiology is noknown, but it represents failure of the regulatory mechanisms of immune system in which body 's own defenses are turned against themselves (Edworthy, 2005##########).

Scleroderma, also called Progressive Systemic Sclerosis, is a chronic connective tissue disease in which excessive amounts of collagen are rapidly deposited into

Thousands of Americans are diagnosed with Scleroderma every year across the nation. Scleroderma, also known as Systematic Sclerosis, is an over production of collagen in body tissues causing patches of skin to tighten and harden and can harm other structures in the body.

Scleroderma literally means “hard skin.” More women than men have the disease. The case can be mild or severe and doctors diagnose it using the patient’s medical history, skin biopsy, lab tests, and a physical exam. Scleroderma is a disease in which the body’s immune system works against itself. With scleroderma the skin sees it’s own tissues as foreign antibodies and actively tries to destroy it, making collagen like it does when there is a present injury. Instead of stopping to produce the collagen after the “injury” is helped, more and more is produced resulting in extra collagen in the cells that can hinder body function. It makes your skin hard or thick and can cause swelling of the joints. The cause is unknown because you are not able to catch it from other people and it is not

Autoimmune diseases, there are cell-mediated immune responses against parts of the body’s own tissues. Many times autoimmune diseases are referred to “body snatchers”. The progressive nonconformity of extra cellular matrix deposition, cutaneous and multi-organ visceral fibrosis, alternations in microvasculature like small arteries and vessels, and body fluid immunological abnormalities are characteristics of progressive systemic sclerosis. Connective tissue involvement of the lungs, skin, heart, kidneys, intestinal tract, muscles, and joints are affected with progressive systemic sclerosis, but not localized scleroderma. This tightening can become nonfunctional for daily activities. Numerous infectious agents (bacterial and viral) have been

LeRoy EC, et al. Scleroderma (systemic sclerosis): classification, subsets and pathogenesis. J. Rheumatol. 1988; 15: 202–205.

|Kaitani, Tokunaga, Matsui and Sanada |Journal of |Quantitative |To identify |606 bed |Prospective |Skin condition|There was no |

According to Yip and Sawatzky (2014), analysis from an earlier research indicated the trigger of MFS was supposed to be chiefly related to the mutation in the fibrillin-1 (FBN-1) gene on chromosome 15 resultant in aberrant fibrillin building that triggers the connective tissue condition, while current research has indicated dysfunctional converting growth factor (TGF)-β cytokine depicts added crucial function in the extracellular matrix homeostasis or makeover.

Due to thickened skin from build- up collagen, motor skills will be greatly affected negatively; such as delay occurs in reaching, moves, walks, flows and paces. Also, weakening of stabilization, grips, lift, walks, transport, endures, calibrates and paces. As well as, malfunction can occur depends on the severity in grip, stabilizes, moves.