Posted at 10.15.2018
Connective tissue are being among the most widely distributed and abundant tissue in the body (Volk, 2010). These cells get excited about many functions among which can be providing form and mechanical support of cells, modulation of cell migration, nutritional carry within and between cells, cell expansion and differentiation. The basic components of connective tissue are ground substances, fibrous components and migrating skin cells (Connective Muscle, 2010). The fibrous component comprises of collagenous, reticular and flexible fibers, which are different markedly in their chemical substance and physical constructions and properties. Essentially the most abundant part is collagen which is often found in many cell types. Elastin dietary fiber can be extended and returned to its original shape; it's the major element of skin. Ground chemicals are comprised of glucose and carbohydrate-protein complexes; the more common ground substances being chondroitin sulfate, and hyaluronic acid. The cells of connective tissues can be the migrating type (macrophages, eisonophils, plasma, mast skin cells) or stationary like adipocytes and fibrocytes (Connective Structure, 2010).
Connective tissue are highly diverse but can be categorized to be either loose or thick. The regular thick connective tissues are the tendons and the ligaments. Loose vascular structure gets the synovial membrane which produces synovial substance which functions as a lubricant for the joints. Cartilage is a connective muscle that has a huge amount of ground tissue responsible for its gel-like uniformity and overall flexibility. Other cartilages are made of hyaline and flexible materials. Bone and blood are two other sorts of connective cells. Red blood cells comprise blood cells while calcium phosphate can be an important component of bone tissue (Connective Tissue, 2010).
Connective tissues disorders end result when the tissue are damaged and become dysfunctional. There is a huge and diverse selection of these diseases, however they can be grouped into three main categories (Connective Muscle Disease, 2010). The first type of connective tissue disorder occurs when there is damage and irritation when one's own immune system disorders the connective tissue. These diseases can be seen as a an overproduction of antibodies that can be assessed in the blood. The second kind of connective cells disorders are due to inherited genetic flaws or gene abnormalities. Usually, the inherited disorder also causes tissues abnormalities in other organs like the h eart, lungs, sight, and bones. Some connective muscle disorders also show general symptoms for the first level of the disorders, but the symptoms may or not progress to a complete stage disease. These disorders are categorized as the third and general classification of "undifferentiated connective tissues disorder" or UCTD.
Although there are various kinds of autoimmune connective tissues disorders, this paper is only going to discuss lupus, arthritis rheumatoid and scleroderma. These have a higher prevalence in the population compared to the other diseases. In these diseases, the disease fighting capability attacks the connective tissue resulting in irritation and abnormalities in the arteries. The reason for these autoimmune episodes is the main topic of many studies, but no coherent theory has been forwarded yet.
Lupus or SLE is a long-term infection of the connective cells which can affect the skin, joint parts, lungs, kidneys and other organs of your body (Ginzler, 2008) (Choi & Abueg, 2009). Patients with lupus have arthritis or pain in the bones which could carry on for weeks. They could also present with rashes (butterfly designed rash on the cheeks, and other skin area areas that face the sun). General fatigue, sores, loss of head of hair and seizures. Women that are pregnant may also experience miscarriage. Other symptoms are heartburn, upper body and stomach pain. Because the symptoms develop eventually, lupus is not diagnosed immediately which can result in harm of the kidneys, lungs and brain.
There are eleven essential conditions for diagnosing SLE (Tan, et al. , 1982) (Gill, Quisel, Rocca, & Walters, 2003). With the eleven criteria ser, four must be fulfilled for a identification of SLE. The principal test is the antinuclear antibody titer (ANA), although it has low predictive value in patients who do not have the usual professional medical symptoms. Once the ANA items to a positive bring about these patients, other antibody tests must be performed to verify the examination (Gill, Quisel, Rocca, & Walters, 2003).
Rheumatoid arthritis is a chronic disease where immune system cells episode and inflame membrane around multiple joints resulting in rigidity, swelling, and pain in the joint parts (Ruderman & Tambar, 2008). Arthritis rheumatoid is more prevalent in small joint parts in hands and foot, but additionally, it may affect other much larger joints. This pattern is a attribute of arthritis rheumatoid, though it can also have an effect on other organs apart from the joints. A unique characteristic of the condition is the incident of prolonged rigidity in the morning, which is not seen in other arthritis types. Symptoms of arthritis rheumatoid are lack of appetite and energy, existence of low-grade fevers, dried mouth and sight, and occurrence of rheumatoid nodules, which are hard lumps, within the skin area of hands and elbows.
The synovium has been the focus of studies targeted at understanding the pathogenesis and pathophysiology of arthritis rheumatoid. The synovium is the slim lining encircling the cartilage of the joints and is a major source of nutrients of the cartilage. In normal skin cells, the lining is 1-3 cells thick while it is 5 - 7 cells wider in rheumatoid arthiritis (Bathon, 2010). The synovium is where events leading to infection occur.
The first theory regarding the pathogenesis of arthritis rheumatoid believes the relationship of T cells with up to now unidentified antigen initiates the inflammatory process and pregression of the disease. This belief is dependant on the known increased amounts of course II major histocompatability antigens, Compact disc4+ T skin cells and T cell receptor gene utilization synovium, the thin muscle that lines the cartilage in joints (Bathon, 2010). In the second theory, it is thought that macrophages and fibroblasts cause the perpetuation of the inflammation. This is predicated on the results of studies that show that activated T cells phenotype are relatively absent in serious rheumatoid arthritis, while there is a proliferation of activated macrophages and fibroblasts. The macrophages produce cytokines IL-1 and TNF activate the fibroblasts. These fibroblasts secrete prostaglandins, proteases and other cytokines (IL-6, IL-8) that promote swelling, and erode bone and cartilage (Bathon, 2010) (Maini, et al. , 1999).
Understanding the pathophysiology and the possible causative components of rheumatoid arthritis has resulted in the development of new medications targeted at reducing signals that resultin autoimmune disorders.
Just like lupus, arthritis rheumatoid is difficult to diagnose, especially during the early stages. The original symptoms are simple and act like those seen for aching joints and muscle stiffness that is normally seen in the day (Ruderman & Tambar, 2008). Therefore, a skilled rheumatologist is essential for the correct diagnosis of the clinical symptoms. Physical study of the joints is essential. Certain laboratory testing need to be performed. Red blood cell count up must be performed, since anemia is common in patients with rheumatoid arthritis. In addition lab tests for rheumatoid factor, antibodies to citrullinated peptides, and erythrocytes sedimentation rates (Ruderman & Tambar, 2008). Furthermore, in the overdue stages of the condition, X-rays can be helpful in diagnosing if the disease has progressed. It's important to know that a single test won't confirm a single examination, thus several exams have to be conducted to confirm the problem.
Scleroderma or sclerosis is a uncommon autoimmune disease that impacts the skin characterized by a tightening and thickening of the cells. The activation of immune cells brings about the creation of scar tissue formation in skin, small blood vessels and organs (Merkel, 2008). For a few forms of the disease, scleroderma is not yet curable. A couple of two types: localized scleroderma, which manifests skin damage, and systemic scleroderma, which could lead damage to internal organs. Changes in scleroderma are anticipated to increased and gathered collagen, increasing from the skin to other organs.
It continues to be unclear what can cause scleroderma, though it is known that it is not infectious which is not inherited from parent to child. Exposure to toxins plus some environmental realtors is thought to cause the condition but this must be proven. Additionally it is known that there is tissue damage, swelling and skin bloating. Blood vessels are also destroyed which can cause poor blood circulation, gangrene and ulcers. Each one of these result in scarring, and could be life threatening.
Diagnosis of scleroderma is dependant on physical and medical examinations. Apart from thickening of your skin, blood vessels may be dilated in the face, and other parts of the body. Calcium deposits may also be found in skin area and other organs. Laboratory exams for auto-antibodies are also used, but results might not exactly be conclusive.
The mixed connective-tissue disease (MCTD) features the lifetime and overlapping of varied connective-tissue diseases such as systemic lupus erythematosus, sclerosis, polymyositis and, occasionally, Sj¶gren syndrome. MTCD is usually milder than the other diseases and is also usually considered and intermediate level progressing to either systemic lupus erythematosus or scleroderma.