Sarcoidosis Ppt Free !EXCLUSIVE! Download

The cause of sarcoidosis is unknown, but experts think it results from the body's immune system responding to an unknown substance. Some research suggests that infectious agents, chemicals, dust and a potential abnormal reaction to the body's own proteins (self-proteins) could be responsible for the formation of granulomas in people who are genetically predisposed.

There is no cure for sarcoidosis, but most people do very well with no treatment or only modest treatment. In some cases, sarcoidosis goes away on its own. However, sarcoidosis may last for years and may cause organ damage.

Sarcoidosis Ppt Free Download

Download 🔥 https://blltly.com/2y7Yuu 🔥

Signs and symptoms of sarcoidosis vary depending on which organs are affected. Sarcoidosis sometimes develops gradually and produces symptoms that last for years. Other times, symptoms appear suddenly and then disappear just as quickly. Many people with sarcoidosis have no symptoms, so the disease may be discovered only when a chest X-ray is done for another reason.

Leslie Cooper, M.D., Mayo Clinic Cardiology: He had rapid re-narrowing to the arteries to his heart after they had placed stents. In his case, they were related to an autoimmune disease, sarcoidosis.

Sarcoidosis can affect any organ. Most often it affects the lungs and lymph nodes in the chest. You may feel extremely tired or have a fever. You may also have other symptoms depending on what organ is affected. Your doctor will diagnose sarcoidosis in part by ruling out other diseases that have similar symptoms.

The cause of sarcoidosis is unknown.[2] Some believe it may be due to an immune reaction to a trigger such as an infection or chemicals in those who are genetically predisposed.[12][13] Those with affected family members are at greater risk.[4] Diagnosis is partly based on signs and symptoms, which may be supported by biopsy.[6] Findings that make it likely include large lymph nodes at the root of the lung on both sides, high blood calcium with a normal parathyroid hormone level, or elevated levels of angiotensin-converting enzyme in the blood.[6] The diagnosis should be made only after excluding other possible causes of similar symptoms such as tuberculosis.[6]

In 2015, pulmonary sarcoidosis and interstitial lung disease affected 1.9 million people globally and they resulted in 122,000 deaths.[10][11] It is most common in Scandinavians, but occurs in all parts of the world.[14] In the United States, risk is greater among black people as opposed to white people.[14] It usually begins between the ages of 20 and 50.[4] It occurs more often in women than men.[4] Sarcoidosis was first described in 1877 by the English doctor Jonathan Hutchinson as a non-painful skin disease.[15]

Localization to the lungs is by far the most common manifestation of sarcoidosis.[27] At least 90% of those affected experience lung involvement.[28] Overall, about 50% develop permanent pulmonary abnormalities, and 5 to 15% have progressive fibrosis of the lung parenchyma. Sarcoidosis of the lung is primarily an interstitial lung disease in which the inflammatory process involves the alveoli, small bronchi, and small blood vessels.[29] In acute and subacute cases, physical examination usually reveals dry crackles.[28] At least 5% of cases include pulmonary arterial hypertension.[28][30] The upper respiratory tract (including the larynx, pharynx, and sinuses) may be affected, which occurs in between 5 and 10% of cases.[31]

Histologically, sarcoidosis of the heart is an active granulomatous inflammation surrounded by reactive oedema. The distribution of affected areas is patchy with localised enlargement of heart muscles. This causes scarring and remodelling of the heart, which leads to dilatation of heart cavities and thinning of heart muscles. As the situation progresses, it leads to aneurysm of heart chambers. When the distribution is diffuse, there would be dilatation of both ventricles of the heart, causing heart failure and arrhythmia. When the conduction system in the intraventricular septum is affected, it would lead to heart block, ventricular tachycardia and ventricular arrhythmia, causing sudden death. Nevertheless, the involvement of pericardium and heart valves are uncommon.[38]

Conduction abnormalities are the most common cardiac manifestations of sarcoidosis in humans and can include complete heart block.[41] Second to conduction abnormalities, in frequency, are ventricular arrhythmias, which occurs in about 23% of cases with cardiac involvement.[41] Sudden cardiac death, either due to ventricular arrhythmias or complete heart block is a rare complication of cardiac sarcoidosis.[42][43] Cardiac sarcoidosis can cause fibrosis, granuloma formation, or the accumulation of fluid in the interstitium of the heart, or a combination of the former two.[44][45] Cardiac sarcoidosis may also cause congestive heart failure when granulomas cause myocardial fibrosis and scarring.[46] Congestive heart failure affects 25-75% of those with cardiac sarcoidosis. Diabetes mellitus and sarcoidosis-related arrhythmias are believed to be strong risk factors of heart failure in sarcoidosis.[47] A small (20-40%) increased risk of acute myocardial infarction has also been described.[48] Pulmonary arterial hypertension occurs by two mechanisms in cardiac sarcoidosis: reduced left heart function due to granulomas weakening the heart muscle or from impaired blood flow.[49]

Prolactin is frequently increased in sarcoidosis, between 3 and 32% of cases have hyperprolactinemia[60] this frequently leads to amenorrhea, galactorrhea, or nonpuerperal mastitis in women. It also frequently causes an increase in 1,25-dihydroxy vitamin D, the active metabolite of vitamin D, which is usually hydroxylated within the kidney, but in sarcoidosis patients, hydroxylation of vitamin D can occur outside the kidneys, namely inside the immune cells found in the granulomas the condition produces. 1,25-dihydroxy vitamin D is the main cause for hypercalcemia in sarcoidosis and is overproduced by sarcoid granulomata. Gamma-interferon produced by activated lymphocytes and macrophages plays a major role in the synthesis of 1 alpha, 25(OH)2D3.[61] Hypercalciuria (excessive secretion of calcium in one's urine) and hypercalcemia (an excessively high amount of calcium in the blood) are seen in

Abnormal blood tests are frequent, accounting for over 50% of cases, but are not diagnostic.[28][31] Lymphopenia is the most common blood anomaly in sarcoidosis.[28] Anemia occurs in about 20% of people with sarcoidosis.[28] Leukopenia is less common and occurs in even fewer cases but is rarely severe.[28] Thrombocytopenia and hemolytic anemia are fairly rare.[19] In the absence of splenomegaly, leukopenia may reflect bone marrow involvement, but the most common mechanism is a redistribution of blood T cells to sites of disease.[70] Other nonspecific findings include monocytosis, occurring in the majority of sarcoidosis cases,[71] increased hepatic enzymes or alkaline phosphatase. People with sarcoidosis often have immunologic anomalies like allergies to test antigens such as Candida or purified protein derivative.[65] Polyclonal hypergammaglobulinemia is also a fairly common immunologic anomaly seen in sarcoidosis.[65]

The exact cause of sarcoidosis is not known.[2] The current working hypothesis is, in genetically susceptible individuals, sarcoidosis is caused through alteration to the immune response after exposure to an environmental, occupational, or infectious agent.[76] Some cases may be caused by treatment with tumor necrosis factor (TNF) inhibitors like etanercept.[77]

The heritability of sarcoidosis varies according to ethnicity. About 20% of African Americans with sarcoidosis have a family member with the condition, whereas the same figure for European Americans is about 5%. Additionally, in African Americans, who seem to experience more severe and chronic disease, siblings and parents of sarcoidosis cases have about a 2.5-fold increased risk for developing the disease.[26] In Swedish individuals heritability was found to be 39%.[78] In this group, if a first-degree family member was affected, a person has a four-fold greater risk of being affected.[78]

Investigations of genetic susceptibility yielded many candidate genes, but only few were confirmed by further investigations and no reliable genetic markers are known. Currently, the most interesting candidate gene is BTNL2; several HLA-DR risk alleles are also being investigated.[79][80] In persistent sarcoidosis, the HLA haplotype HLA-B7-DR15 is either cooperating in disease or another gene between these two loci is associated. In nonpersistent disease, a strong genetic association exists with HLA DR3-DQ2.[81][82] Cardiac sarcoid has been connected to tumor necrosis factor alpha (TNFA) variants.[83]

Several infectious agents appear to be significantly associated with sarcoidosis, but none of the known associations is specific enough to suggest a direct causative role.[84] The major implicated infectious agents include: mycobacteria, fungi, borrelia, and rickettsia.[85] A meta-analysis investigating the role of mycobacteria in sarcoidosis found it was present in 26.4% of cases, but they also detected a possible publication bias, so the results need further confirmation.[86][87] Mycobacterium tuberculosis catalase-peroxidase has been identified as a possible antigen catalyst of sarcoidosis.[88] The disease has also been reported by transmission via organ transplants.[89] A large epidemiological study found little evidence that infectious diseases spanning years before sarcoidosis diagnosis could confer measurable risks for sarcoidosis diagnosis in the future.[90]

While TNF is widely believed to play an important role in the formation of granulomas (this is further supported by the finding that in animal models of mycobacterial granuloma formation inhibition of either TNF or IFN- production inhibits granuloma formation), sarcoidosis can and does still develop in those being treated with TNF antagonists like etanercept.[95]B cells also likely play a role in the pathophysiology of sarcoidosis.[26] Serum levels of soluble human leukocyte antigen (HLA) class I antigens and angiotensin converting enzyme (ACE) are higher in people with sarcoidosis.[26] Likewise the ratio of CD4/CD8 T cells in bronchoalveolar lavage is usually higher in people with pulmonary sarcoidosis (usually >3.5), although it can be normal or even abnormally low in some cases.[26] Serum ACE levels have been found to usually correlate with total granuloma load.[85] 006ab0faaa