Ankylosing spondylitis is a form of chronic inflammation of the spine and the sacroiliac joints. The sacroiliac joints are located in the low back where the sacrum (the bone directly above the tailbone) meets the iliac bones (bones on either side of the upper buttocks). Chronic inflammation in these areas causes pain and stiffness in and around the spine. Over time, chronic spinal inflammation (spondylitis) can lead to a complete cementing together (fusion) of the vertebrae, a process referred to as ankylosis. Ankylosis leads to loss of mobility of the spine. Ankylosing spondylitis is also a systemic rheumatic disease, meaning it can affect other tissues throughout the body. Accordingly, it can cause inflammation in or injury to other joints away from the spine, as well as other organs, such as the eyes, heart, lungs, and kidneys. Ankylosing spondylitis shares many features with several other arthritis conditions, such as psoriatic arthritis, reactive arthritis, and arthritis associated with Crohn s disease and ulcerative colitis. Each of these arthritic conditions can cause disease and inflammation in the spine, other joints, eyes, skin, mouth, and various organs. In view of their similarities and tendency to cause inflammation of the spine, these conditions are collectively referred to as quot;spondyloarthropathies.quot; For more information, please read the following articles; Psoriatic Arthritis, Reactive Arthritis, Crohn s Disease and Ulcerative Colitis. Ankylosing spondylitis is 2-3 times more common in males than in females. In women, joints away from the spine are more frequently affected than in men. Ankylosing spondylitis affects all age groups, including children. The most common age of onset of symptoms is in the second and third decades of life. What causes ankylosing spondylitis? The tendency to develop ankylosing spondylitis is believed to be genetically inherited, and the majority (nearly 90%) of patients with ankylosing spondylitis are born with the HLA-B27 gene. Blood tests have been developed to detect the HLA-B27 gene marker, and have furthered our understanding of the relationship between HLA-B27 and ankylosing spondylitis. The HLA-B27 gene appears only to increase the tendency of developing ankylosing spondylitis, while some additional factor(s), perhaps environmental, are necessary for the disease to appear or become expressed. For example, while 7% of the United States population have the HLA-B27 gene, only 1% of the population actually have the disease ankylosing spondylitis. In Northern Scandinavia (Lapland), 1.8% of the population have ankylosing spondylitis while 24% of the general population have the HLA-B27 gene. Even among HLA-B27 positive individuals, the risk of developing ankylosing spondylitis appears to be further related to heredity. In HLA-B27 positive individuals who have relatives with the disease, their risk of developing ankylosing spondylitis is 12% (6 times greater than for those whose relatives do not have ankylosing spondylitis). Ankylosing spondylitis is a form of chronic inflammation of the spine and the sacroiliac joints. The sacroiliac joints are located in the low back where the sacrum (the bone directly above the tailbone) meets the iliac bones (bones on either side of the upper buttocks). Chronic inflammation in these areas causes pain and stiffness in and around the spine. Over time, chronic spinal inflammation (spondylitis) can lead to a complete cementing together (fusion) of the vertebrae, a process referred to as ankylosis. Ankylosis leads to loss of mobility of the spine. Ankylosing spondylitis is also a systemic rheumatic disease, meaning it can affect other tissues throughout the body. Accordingly, it can cause inflammation in or injury to other joints away from the spine, as well as other organs, such as the eyes, heart, lungs, and kidneys. Ankylosing spondylitis shares many features with several other arthritis conditions, such as psoriatic arthritis, reactive arthritis, and arthritis associated with Crohn s disease and ulcerative colitis. Each of these arthritic conditions can cause disease and inflammation in the spine, other joints, eyes, skin, mouth, and various organs. In view of their similarities and tendency to cause inflammation of the spine, these conditions are collectively referred to as quot;spondyloarthropathies.quot; For more information, please read the following articles; Psoriatic Arthritis, Reactive Arthritis, Crohn s Disease and Ulcerative Colitis. Ankylosing spondylitis is 2-3 times more common in males than in females. In women, joints away from the spine are more frequently affected than in men. Ankylosing spondylitis affects all age groups, including children. The most common age of onset of symptoms is in the second and third decades of life. What causes ankylosing spondylitis? The tendency to develop ankylosing spondylitis is believed to be genetically inherited, and the majority (nearly 90%) of patients with ankylosing spondylitis are born with the HLA-B27 gene. Blood tests have been developed to detect the HLA-B27 gene marker, and have furthered our understanding of the relationship between HLA-B27 and ankylosing spondylitis. The HLA-B27 gene appears only to increase the tendency of developing ankylosing spondylitis, while some additional factor(s), perhaps environmental, are necessary for the disease to appear or become expressed. For example, while 7% of the United States population have the HLA-B27 gene, only 1% of the population actually have the disease ankylosing spondylitis. In Northern Scandinavia (Lapland), 1.8% of the population have ankylosing spondylitis while 24% of the general population have the HLA-B27 gene. Even among HLA-B27 positive individuals, the risk of developing ankylosing spondylitis appears to be further related to heredity. In HLA-B27 positive individuals who have relatives with the disease, their risk of developing ankylosing spondylitis is 12% (6 times greater than for those whose relatives do not have ankylosing spondylitis). Ankylosing spondylitis is a form of chronic inflammation of the spine and the sacroiliac joints. The sacroiliac joints are located in the low back where the sacrum (the bone directly above the tailbone) meets the iliac bones (bones on either side of the upper buttocks). Chronic inflammation in these areas causes pain and stiffness in and around the spine. Over time, chronic spinal inflammation (spondylitis) can lead to a complete cementing together (fusion) of the vertebrae, a process referred to as ankylosis. Ankylosis leads to loss of mobility of the spine. Ankylosing spondylitis is also a systemic rheumatic disease, meaning it can affect other tissues throughout the body. Accordingly, it can cause inflammation in or injury to other joints away from the spine, as well as other organs, such as the eyes, heart, lungs, and kidneys. Ankylosing spondylitis shares many features with several other arthritis conditions, such as psoriatic arthritis, reactive arthritis, and arthritis associated with Crohn s disease and ulcerative colitis. Each of these arthritic conditions can cause disease and inflammation in the spine, other joints, eyes, skin, mouth, and various organs. In view of their similarities and tendency to cause inflammation of the spine, these conditions are collectively referred to as quot;spondyloarthropathies.quot; For more information, please read the following articles; Psoriatic Arthritis, Reactive Arthritis, Crohn s Disease and Ulcerative Colitis. Ankylosing spondylitis is 2-3 times more common in males than in females. In women, joints away from the spine are more frequently affected than in men. Ankylosing spondylitis affects all age groups, including children. The most common age of onset of symptoms is in the second and third decades of life. What causes ankylosing spondylitis? The tendency to develop ankylosing spondylitis is believed to be genetically inherited, and the majority (nearly 90%) of patients with ankylosing spondylitis are born with the HLA-B27 gene. Blood tests have been developed to detect the HLA-B27 gene marker, and have furthered our understanding of the relationship between HLA-B27 and ankylosing spondylitis. The HLA-B27 gene appears only to increase the tendency of developing ankylosing spondylitis, while some additional factor(s), perhaps environmental, are necessary for the disease to appear or become expressed. For example, while 7% of the United States population have the HLA-B27 gene, only 1% of the population actually have the disease ankylosing spondylitis. In Northern Scandinavia (Lapland), 1.8% of the population have ankylosing spondylitis while 24% of the general population have the HLA-B27 gene. Even among HLA-B27 positive individuals, the risk of developing ankylosing spondylitis appears to be further related to heredity. In HLA-B27 positive individuals who have relatives with the disease, their risk of developing ankylosing spondylitis is 12% (6 times greater than for those whose relatives do not have ankylosing spondylitis). The mitral valve (also known as the bicuspid valve or left atrioventricular valve), is a dual flap (bi = 2) valve in the heart that lies between the left atrium (LA) and the left ventricle (LV). In Latin, the term mitral means shaped like a miter, or bishop s cap. The mitral valve and the tricuspid valve are known collectively as the atrioventricular valves because they lie between the atria and the ventricles of the heart and control flow. A normally functioning mitral valve opens to pressure from the superior surface of the valve, allowing blood to flow into the left ventricle during left atria systole (contraction), and closes at the end of atrial contraction to prevent blood from back flowing into the atria during left ventricle systole. In a normal cardiac cycle, the atria contracts first, filling the ventricle. At the end of ventricular diastole, the bicuspid valve shuts, and prevents backflow as the ventricle begins its systolic phase. Backflow may occur if the patient suffers from mitral valve prolapse, causing an audible quot;murmurquot; during auscultation. [edit] Anatomy The mitral valve has two cusps/leaflets (the anteromedial leaflet and the posterolateral leaflet) which guards the opening. The opening is surrounded by a fibrous ring known as the mitral valve annulus. (The orientation of the two leaflets were once thought to resemble a bishop s miter, which is where the valve receives its name.[1]) The anterior cusp protects approximately two-thirds of the valve (imagine a crescent moon within the circle, where the crescent represents the posterior cusp). These valve leaflets are prevented from prolapsing into the left atrium by the action of tendons attached to the posterior surface of the valve, chordae tendinae. The inelastic chordae tendineae are attached at one end to the papillary muscles and the other to the valve cusps. Papillary muscles are finger like projections from the wall of the left ventricle. Chordae tendinae from each muscle are attached to both leaflets of the mitral valve. Thus when the ventricle contracts, the intraventricular pressure forces the valve to close, while the tendons prevent the valve from opening in the wrong direction. [edit] Normal physiology During left ventricular diastole, after the pressure drops in the left ventricle due to relaxation of the ventricular myocardium, the mitral valve opens, and blood travels from the left atrium to the left ventricle. About 70-80% of the blood that travels across the mitral valve occurs during the early filling phase of the left ventricle. This early filling phase is due to active relaxation of the ventricular myocardium, causing a pressure gradient that allows a rapid flow of blood from the left atrium, across the mitral valve. This early filling across the mitral valve is seen on doppler echocardiography of the mitral valve as the E wave. After the E wave, there is a period of slow filling of the ventricle. Left atrial contraction (left atrial systole) (during left ventricular diastole) causes added blood to flow across the mitral valve immediately before left ventricular systole. This late flow across the open mitral valve is seen on doppler echocardiography of the mitral valve as the A wave. The late filling of the LV contributes about 20% to the volume in the left ventricle prior to ventricular systole, and is known as the atrial kick.
sometimes if it is not a problem or causing any systoms they dont do anything about mvp.if it were to start giving problems then meds.of course im no doctor.
Mitral valve prolapse can be treated with surgery. The Mitral Valve is replaced with any one of several options. There are artificial valves as well as valves derived from animal sources. There are advantages to each type and you and your son s Doctor need to discuss the positives and negatives of each type. Your son s Doc needs to be aware of all of his medications for other problems. That said, if his prolapsed Mitral Valve isn t causing him any problems, then there may not be a reason to do anything right now.
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