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Thread: Parathyroid Panoramic 4 picture - Endocrine Histology Atlas

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    Default Parathyroid Panoramic 4 picture - Endocrine Histology Atlas

    Addison’s disease is an uncommon autoimmune disease, characterized by chronic and insufficient functioning of the outer layer of the adrenal gland. The adrenal glands are located atop each kidney and produce vital glucocorticoid hormones. Because of this chronic under-functioning of the adrenal glands, persons with Addison’s disease have a deficiency in the production of glucocorticoid hormones. Glucocorticoid hormones are involved in how the body utilizes and stores carbohydrates, protein, fat and blood sugar.

    The adrenal gland also plays a role in the immune response. A deficiency in glucocorticoid hormones causes an increase in the release of sodium and a decreased release of potassium in the urine, sweat, saliva, stomach and intestines. These changes can cause low blood pressure and increased water excretion that can in some cases lead to severe dehydration.

    Although there are many underlying factors in the development of adrenal insufficiencies, including destruction of the adrenal cortex due to diseases such as tuberculosis, the growth of tumors, non-autoimmune diseases amyloidosis and adrenoleukodystrophy, and atrophy of the gland due to prolonged use of cortical steroids used in the treatment of other conditions and illnesses, most cases of Addison’s disease are thought to be autoimmune in nature.

    Agammaglobulinemia is an immune disorder related to antibody deficiency (hypogammaglobulinemia) and is manifested in a variety of immune deficiency disorders in which the immune system is compromised. This group of immune deficiencies may be the consequence of an inherited condition, an impaired immune system from known or unknown cause, a relation to autoimmune diseases, or a malignancy.

    Immunoglobulin deficiencies may be referred to by many different names, as there are several variables within the separate but related immune disorders; and there are also many subgroups. Antibody deficiency, immunoglobulin deficiency, and gamma globulin deficiency are all synonyms for hypogammaglobulinemia.

    Alopecia areata is an autoimmune disorder which is characterized by hair loss. Alopecia areata is found equally in both men and women. The disease can occur at any age, including childhood.

    The hair loss may result in round bald patches on the scalp (alopecia areata) or involve the loss of all facial and scalp hair (alopecia totalis). The loss of all body hair is called alopecia universalis. Alopecia postpartum is characterized by loss of significant hair following pregnancy and is usually temporary. When a patient is diagnosed with alopecia, the first question is usually about whether or not the hair will regrow. The answer is usually vague as each case is different. Regrowth of hair may occur in some patients; and in other, the hair loss is permanent.

    Amyloidosis is a disorder in which abnormal proteins build up in tissues and organs. The cause of primary amyloidosis is unknown. The condition is related to abnormal and excess production of antibodies by a type of immune cell called plasma cells. Clumps of abnormal proteins build up in certain organs. This reduces their ability to work correctly. Symptoms depend on the organs affected. This disease can affect the tongue, intestines, skeletal and smooth muscles, nerves, skin, ligaments, heart, liver, spleen, and kidneys. Symptoms include: abnormal heart rhythm, fatigue, numbness of hands or feet, shortness of breath, hoarseness or changing voice, and joint pain.

    Ankylosing spondylitis is an autoimmune disease and is a type of arthritis of the spine. It causes swelling between your vertebrae, which are the disks that make up your spine, and in the joints between your spine and pelvis. The disease is more common and more severe in men. It often runs in families. Early symptoms include back pain and stiffness. These problems often start in late adolescence or early adulthood. Over time, ankylosing spondylitis can fuse your vertebrae together, limiting movement. Symptoms can worsen or improve or stop altogether. The disease has no cure, but medicines can relieve the pain, swelling and other symptoms. Exercise can also help.
    Parathyroid Panoramic picture Endocrine Histology attachment.php?s=d74946946107e2281ea7aa5f445e1bd2&attachmentid=1315&d=1439060772

    Anti-GBM/Anti-TBM nephritis: Anti–glomerular basement membrane (anti-GBM) antibody disease is a rare autoimmune disorder caused by autoantibodies that attack the walls of small blood vessels (capillaries) in the kidney. Anti-GBM disease that only affects the kidneys is called anti-GBM glomerulonephritis. This is a form of inflammation (-itis), which is injury to tissue caused by white blood cells (leukocytes). Glomerulonephritis due to Anti-GBM antibody disease is rare. It occurs in less than 1 case per million persons. It affects mostly young, white men aged 15-35. After age 50, women are more likely to be affected. The sexes overall are affected approximately at a male-female ratio of 3:2. It is seen very rarely in children. Some evidence suggests that genetics may play an important role in this disease. 60-70% of patients have both lung and kidney involvement. This is called Goodpasture’s Syndrome. 20-40% have only kidney involvement, which is called “renal limited” anti-GBM disease. Symptoms may include: chills and fever, nausea and vomiting, weight loss, chest pain, bleeding may cause anemia, respiratory failure, and kidney failure. Treatment of anti-GBM disease is focused on removing the anti-GBM antibody from the blood.

    Antiphospholipid syndrome (APS) is an autoimmune syndrome caused by antiphospholipid antibodies. These antibodies are often referred to by different terms, including anticardiolipin antibody, lupus anticoagulant, and antiphospholipid antibody. APS can be primary or secondary, and also can be referred to by the name Hughes syndrome or “sticky blood”.

    Various manifestations of antiphospholipid antibody syndrome include: recurrent fetal loss; thrombocytopenia; large vessel occlusive syndromes (deep venous thromboses and pulmonary embolism); cardiac disease, skin manifestations (livedo reticularis, digital ischemia, cutaneous necrosis); ocular disease (visual disturbances, episcleritis (inflammation of the sclera) and keratitis (inflammation of the cornea); central nervous system syndromes as cerebral ischemia, stroke, transient ischemic attack (TIA) or venous thrombosis) and other cns presentations including dementia, migraine and seizure; Disorders of mentation (forgetfulness and confusion). A patient with these varied neurologic symptoms may be misdiagnosed wit multiple sclerosis.

    There is a strong familial association which has been demonstrated. APS is of utmost importance to the clinician interested in women’s health issues. The disease occurs more frequently in women, plays a major role in fetal loss, and is associated with numerous serious and predominantly female disease states.

    Autoimmune hepatitis is a chronic inflammatory autoimmune disease of the liver. It usually occurs by itself, but it can coexist with other autoimmune diseases. The male/female ratio is 8:1, and it most often occurs in persons of Northern European extraction. It is usually classified as Type I or Type II. Type I is the most common and occurs at any age, most commonly in women. Type II is less common, affecting mostly girls between the ages of two to fourteen, although adults can have it too.

    Fatigue is the most common symptom and other symptoms include an enlarged liver, jaundice, itching skin rashes, joint pain, and abdominal pain. These symptoms range from mild to severe and can lead to cirrhosis (scarring and hardening) of the liver and may eventually lead to liver failure. Many people with autoimmune hepatitis experience remission within two years of starting treatment. Sometimes the disease will return so periodic treatment may be necessary.

    Autoimmune inner ear disease (AIED) is an unusual form of progressive non-age-related sensorineural hearing loss and sometimes vertigo. It occurs in both ears with cochlear and vestibular symptoms that progress over a period of weeks to months and affects hearing, and often balance function, in both ears. The classic presentation is with bilateral fluctuating but progressive sensorineural hearing loss leading on to severe deafness. Tinnitus (ringing, tinkling, buzzing, or other sounds in the ear) and intra-aural pressure may occur, as well as dizziness or vertigo.

    References:
    http://www.aarda.org/descriptions-of...n'sdisease











    Last edited by Medical Photos; 08-08-2015 at 07:06 PM.

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