Gout is caused by high levels of uric acid in the blood that form needle-shaped urate crystals in the joints, causing inflammation and pain. It is characterized by episodes of acute inflammatory arthritis. Diagnosis involves examining synovial fluid for urate crystals or measuring uric acid levels in the blood. Treatment involves medications to relieve pain and inflammation during attacks and reduce uric acid levels long-term to prevent future attacks. Lifestyle changes like diet modification and weight control can also help lower uric acid levels.
Gouty Arthritis/Gout is a type of crystal arthropathy characterized by recurrent attacks of acute arthritis.
Pathophysiology, clinical features, investigations, treatments modalities and complications
Gout is a crystal deposition disease caused by monosodium urate crystals in the joints and tissues due to hyperuricemia. It ranges from asymptomatic hyperuricemia to acute gouty arthritis with severe pain, to chronic tophaceous gout with joint damage. Diagnosis involves identifying urate crystals in synovial fluid or tophi. Treatment goals include rapid relief of acute flares, prevention of future flares, and reducing uric acid levels long-term through lifestyle changes and urate-lowering therapy such as allopurinol.
Gout is caused by deposition of urate crystals in the joints due to elevated levels of uric acid (hyperuricemia) in the blood. It typically presents as sudden, severe pain and swelling in one joint, often the big toe. Diagnosis is confirmed by identifying needle-shaped urate crystals in joint fluid under polarized light microscopy. Treatment involves lifestyle modifications, medications like colchicine and allopurinol to prevent attacks and lower uric acid levels long-term.
This document discusses hyperuricemia and gout. It defines hyperuricemia as an elevated level of uric acid in the blood. It then covers the etiology, epidemiology, diagnosis, risk factors, complications, prevention and treatment of both hyperuricemia and gout. Gout is described as a form of inflammatory arthritis that results from excess uric acid in the blood, causing sudden, severe pain and swelling in the joints. Common treatments include NSAIDs, colchicine, steroids, and allopurinol or febuxostat to reduce uric acid levels.
Gout is a metabolic disorder resulting from elevated uric acid levels and deposition of urate crystals in the joints. It involves a spectrum of conditions including hyperuricemia, acute inflammatory arthritis attacks, tophaceous deposits of urate crystals in and around joints, renal disease, and kidney stones. Gout typically involves recurrent attacks of severe pain and swelling in joints like the first metatarsophalangeal joint. Chronic untreated gout can cause permanent joint damage and deformity from urate tophi. Diagnosis involves identifying urate crystals in joint fluid or tissues.
Gout is caused by deposition of uric acid crystals in the joints, which leads to acute inflammation. It typically presents as sudden severe pain, swelling and redness in one joint, most commonly the big toe. Diagnosis is made based on symptoms and identification of crystals in joint fluid under polarized microscopy. Treatment involves medications to reduce symptoms during acute attacks as well as long-term drugs like allopurinol or probenecid to lower uric acid levels and prevent future episodes. Without treatment, gout can progress to a chronic stage with multiple joint involvement and growth of tophi deposits in the tissues.
The document discusses hyperuricemia and gout. It defines hyperuricemia as a plasma urate concentration greater than 7.0 mg/dl and can result from increased urate production, decreased urate excretion, or a combination. Gout is caused by the deposition of monosodium urate crystals in the joints and other tissues, which can cause acute inflammatory arthritis. The first metatarsophalangeal joint is commonly affected. Treatment involves medications like colchicine, NSAIDs, or glucocorticoids for acute attacks and urate-lowering therapies for long-term management.
Gouty Arthritis/Gout is a type of crystal arthropathy characterized by recurrent attacks of acute arthritis.
Pathophysiology, clinical features, investigations, treatments modalities and complications
Gout is a crystal deposition disease caused by monosodium urate crystals in the joints and tissues due to hyperuricemia. It ranges from asymptomatic hyperuricemia to acute gouty arthritis with severe pain, to chronic tophaceous gout with joint damage. Diagnosis involves identifying urate crystals in synovial fluid or tophi. Treatment goals include rapid relief of acute flares, prevention of future flares, and reducing uric acid levels long-term through lifestyle changes and urate-lowering therapy such as allopurinol.
Gout is caused by deposition of urate crystals in the joints due to elevated levels of uric acid (hyperuricemia) in the blood. It typically presents as sudden, severe pain and swelling in one joint, often the big toe. Diagnosis is confirmed by identifying needle-shaped urate crystals in joint fluid under polarized light microscopy. Treatment involves lifestyle modifications, medications like colchicine and allopurinol to prevent attacks and lower uric acid levels long-term.
This document discusses hyperuricemia and gout. It defines hyperuricemia as an elevated level of uric acid in the blood. It then covers the etiology, epidemiology, diagnosis, risk factors, complications, prevention and treatment of both hyperuricemia and gout. Gout is described as a form of inflammatory arthritis that results from excess uric acid in the blood, causing sudden, severe pain and swelling in the joints. Common treatments include NSAIDs, colchicine, steroids, and allopurinol or febuxostat to reduce uric acid levels.
Gout is a metabolic disorder resulting from elevated uric acid levels and deposition of urate crystals in the joints. It involves a spectrum of conditions including hyperuricemia, acute inflammatory arthritis attacks, tophaceous deposits of urate crystals in and around joints, renal disease, and kidney stones. Gout typically involves recurrent attacks of severe pain and swelling in joints like the first metatarsophalangeal joint. Chronic untreated gout can cause permanent joint damage and deformity from urate tophi. Diagnosis involves identifying urate crystals in joint fluid or tissues.
Gout is caused by deposition of uric acid crystals in the joints, which leads to acute inflammation. It typically presents as sudden severe pain, swelling and redness in one joint, most commonly the big toe. Diagnosis is made based on symptoms and identification of crystals in joint fluid under polarized microscopy. Treatment involves medications to reduce symptoms during acute attacks as well as long-term drugs like allopurinol or probenecid to lower uric acid levels and prevent future episodes. Without treatment, gout can progress to a chronic stage with multiple joint involvement and growth of tophi deposits in the tissues.
The document discusses hyperuricemia and gout. It defines hyperuricemia as a plasma urate concentration greater than 7.0 mg/dl and can result from increased urate production, decreased urate excretion, or a combination. Gout is caused by the deposition of monosodium urate crystals in the joints and other tissues, which can cause acute inflammatory arthritis. The first metatarsophalangeal joint is commonly affected. Treatment involves medications like colchicine, NSAIDs, or glucocorticoids for acute attacks and urate-lowering therapies for long-term management.
Gout is a medical condition characterized by recurrent attacks of acute inflammatory arthritis, usually in the joints of the big toe. It is caused by high levels of uric acid in the blood which form needle-like crystals that accumulate in the joints, tendons and surrounding tissue, causing pain, inflammation and swelling. Symptoms include severe joint pain, redness and swelling of the affected area. Treatment focuses on reducing uric acid levels through lifestyle changes like diet modification and medications.
This document discusses gout and pseudogout. It provides details on the epidemiology, pathogenesis, clinical features, investigations, imaging, diagnosis and treatment of both conditions. For gout, it describes the stages from asymptomatic hyperuricemia to acute gouty arthritis to chronic tophaceous gout. It outlines treatment approaches for the different stages, including medications like colchicine, NSAIDs and allopurinol. For pseudogout, it briefly covers pathogenesis, clinical features, diagnosis and treatment.
Pathophysiology and clinical management of gouty arthritisSoujanya Pharm.D
Gout is the most common inflammatory joint disorder caused by deposition of urate crystals in joints. It affects around 1-2% of adults and is more common in men. Risk factors include genetics, diet high in purines, alcohol, obesity, and medications. Gout progresses through acute inflammatory attacks, intercritical periods, and chronic tophaceous stages if urate levels remain elevated. Treatment involves NSAIDs to rapidly alleviate acute attacks and urate-lowering drugs like allopurinol or febuxostat long-term to prevent future attacks and reduce urate levels. Lifestyle modifications and diet control are also important for gout management.
Gout is a rheumatic disease caused by elevated levels of uric acid (hyperuricemia) which leads to the deposition of urate crystals in the joints. It predominantly affects males between 30-60 years of age and females after menopause. The prevalence is higher in developed countries and Oceanic populations. Hyperuricemia occurs due to increased production or decreased excretion of uric acid and causes an imbalance that results in crystal formation and inflammation in the joints.
This document summarizes information about crystal arthritis, specifically gout. It provides a history of gout, describing it as one of the oldest diseases documented. It discusses the pathophysiology and risk factors of gout, and describes the typical stages and presentations of both acute and chronic gout, including joint destruction and extra-articular manifestations. The document also discusses treatment options and targets for gout, including lowering uric acid levels.
Gout is caused by high levels of uric acid in the blood that form crystals in the joints, causing inflammation and pain. It was once thought to be a disease of kings due to its association with rich foods and alcohol. Symptoms include sudden, severe pain and swelling in joints like the big toe. Diagnosis involves testing blood and urine uric acid levels and examining joint fluid. Treatment focuses on relieving pain and reducing uric acid through medications like NSAIDs, colchicine, corticosteroids, allopurinol, and febuxostat. Lifestyle changes around diet, weight, and alcohol intake can help prevent future gout attacks.
This document provides an overview of gout and hyperuricemia. It discusses the pathophysiology, clinical presentations, diagnosis and treatment. Key points include: Gout is caused by elevated uric acid leading to monosodium urate crystal formation in joints; the most common presentation is acute inflammatory arthritis, often in the great toe; diagnosis involves identifying crystals in synovial fluid or tophi and measuring uric acid levels; treatment focuses on lifestyle modifications and medications to reduce uric acid production or enhance excretion.
Gout is a type of inflammatory arthritis caused by deposition of urate crystals in the joints due to persistent hyperuricemia. It manifests as recurrent acute flares typically involving the great toe, as well as chronic tophaceous gout with subcutaneous urate deposits. The pathophysiology involves urate crystal formation triggering inflammation through activation of the NLRP3 inflammasome and recruitment of leukocytes. Acute gout flares are usually self-limiting due to feedback mechanisms that limit inflammation, though chronic tophaceous gout can develop if hyperuricemia is untreated.
The document discusses gout, a type of arthritis caused by uric acid crystals in the joints. It defines gout, lists its symptoms such as sudden severe pain in joints like the big toe, and describes its typical progression from asymptomatic to acute attacks to a chronic condition if left untreated. Risk factors include being male, obesity, diet high in purines, and certain medications. Diagnosis involves examining synovial fluid for uric acid crystals. Treatment focuses on relieving acute attacks, preventing future attacks by reducing uric acid levels in the blood long-term through medications and diet changes, and managing chronic complications through continued medical care.
This document discusses gout and pseudogout (calcium pyrophosphate deposition disease or CPPD). It provides a historical overview and describes the crystals involved in gout (monosodium urate) and pseudogout (calcium pyrophosphate dihydrate). It discusses the clinical presentation, risk factors, diagnosis, treatment and long term outcomes of gout and pseudogout. Radiographic findings and fluid analysis findings that can help differentiate gout from pseudogout are also summarized.
Gout is a metabolic disease caused by high levels of uric acid in the bloodstream, which can accumulate and crystallize in the joints, causing inflammation. It occurs when there is either overproduction of uric acid by the body or inadequate excretion by the kidneys. Common symptoms include sudden, severe pain and swelling in joints like the big toe. Treatment focuses on reducing uric acid levels through medications and dietary changes like limiting purine-rich foods and alcohol.
Here are the key points I would suggest to the aircrew:
- Lose weight through diet and exercise to achieve a healthy BMI, as obesity is a risk factor for hyperuricemia and gout.
- Limit alcohol intake, especially beer which is strongly associated with hyperuricemia.
- Follow a low-purine diet by reducing intake of organ meats, red meat, seafood etc. which are high in purines.
- Stay well hydrated by drinking plenty of water as uric acid is more soluble in urine produced in larger volumes.
- Start on allopurinol 100mg once daily which is a xanthine oxidase inhibitor to lower uric acid production
The document provides biographical information about Dr. Manoj R. Kandoi, the author of the book "The Basics of Arthritis". It states that Dr. Kandoi founded the Institute of Arthritis Care & Prevention non-profit organization focused on arthritis patient education and support. He has published several papers on arthritis and written the book to guide arthritis patients and healthcare professionals. Contact information for Dr. Kandoi and the Institute is provided.
1. Gout and pseudogout are types of crystal arthritis caused by sodium urate crystals or calcium pyrophosphate crystals respectively.
2. Gout prevalence is increasing, especially in developed countries, and affects men more than women. Risk factors include diet, medications, age, gender and medical conditions.
3. Pseudogout usually affects the knees and wrists of elderly women, causing painful flare ups that are treated similarly to gout.
Gout is a common, painful form of arthritis.
It causes swollen, red, hot and stiff joints. Gout occurs when uric acid builds
up in your blood. This happens if your body produces extra acid or does not
eliminate enough, or if you eat too many foods with purines, such as liver and
dried beans. Pseudogout has similar symptoms and is sometimes confused with
gout. However, it is caused by calcium phosphate, not uric acid.
Often, gout first attacks your big toe. It
can also attack ankles, heels, knees, wrists, fingers and elbows.
You are more likely to get gout if you:
Are a man
Have family
member with gout
Drink
alcohol
At first, gout attacks usually get better in
days. Eventually, attacks last longer and occur more often. Uric acid buildup
can lead to kidney stones.
Untreated gout can cause permanent joint and kidney damage. You can treat gout
with medicines.
Gout - Clinical features , diagnosis and managementRohit Rajeevan
Gout is a metabolic disease resulting from deposition of urate crystals in the joints and tissues. It was first identified by Egyptians in 2640 BC and described by Hippocrates. It predominantly affects men over age 40 and is associated with purine-rich foods and comorbidities like diabetes. Symptoms include recurrent acute inflammatory arthritis attacks, tophi formation, and chronic arthritis. Diagnosis involves synovial fluid analysis demonstrating urate crystals. Treatment includes NSAIDs, colchicine, urate-lowering drugs like allopurinol, and lifestyle modifications like diet and exercise. Pseudogout is caused by calcium pyrophosphate crystals and presents similarly but is diagnosed by demonstrating different crystals on syn
Gout is caused by high levels of uric acid in the blood that lead to painful inflammation in joints. It occurs when uric acid crystals deposit in joints, especially those in the big toe. Risk factors include diet high in purines, obesity, kidney disease, genetics, and certain medications. Symptoms range from joint pain and swelling to tophi formation and arthritis. Treatment focuses on lifestyle changes like diet modification and medication to reduce uric acid levels and relieve pain.
The Science of Software Testing - Experiments, Evolution & Emergence (2011)Neil Thompson
The document discusses the history and evolution of software testing from the early days of debugging programs to the current conceptions of testing as both an engineering discipline and a scientific field of study. It traces the development of software testing from initial methods focused on demonstration and destruction to more modern prevention-oriented and quality-focused approaches. The document also examines perspectives on treating software testing as a science through use of the scientific method, experiments, and evolving theories and models of both development and testing.
Gout is a medical condition characterized by recurrent attacks of acute inflammatory arthritis, usually in the joints of the big toe. It is caused by high levels of uric acid in the blood which form needle-like crystals that accumulate in the joints, tendons and surrounding tissue, causing pain, inflammation and swelling. Symptoms include severe joint pain, redness and swelling of the affected area. Treatment focuses on reducing uric acid levels through lifestyle changes like diet modification and medications.
This document discusses gout and pseudogout. It provides details on the epidemiology, pathogenesis, clinical features, investigations, imaging, diagnosis and treatment of both conditions. For gout, it describes the stages from asymptomatic hyperuricemia to acute gouty arthritis to chronic tophaceous gout. It outlines treatment approaches for the different stages, including medications like colchicine, NSAIDs and allopurinol. For pseudogout, it briefly covers pathogenesis, clinical features, diagnosis and treatment.
Pathophysiology and clinical management of gouty arthritisSoujanya Pharm.D
Gout is the most common inflammatory joint disorder caused by deposition of urate crystals in joints. It affects around 1-2% of adults and is more common in men. Risk factors include genetics, diet high in purines, alcohol, obesity, and medications. Gout progresses through acute inflammatory attacks, intercritical periods, and chronic tophaceous stages if urate levels remain elevated. Treatment involves NSAIDs to rapidly alleviate acute attacks and urate-lowering drugs like allopurinol or febuxostat long-term to prevent future attacks and reduce urate levels. Lifestyle modifications and diet control are also important for gout management.
Gout is a rheumatic disease caused by elevated levels of uric acid (hyperuricemia) which leads to the deposition of urate crystals in the joints. It predominantly affects males between 30-60 years of age and females after menopause. The prevalence is higher in developed countries and Oceanic populations. Hyperuricemia occurs due to increased production or decreased excretion of uric acid and causes an imbalance that results in crystal formation and inflammation in the joints.
This document summarizes information about crystal arthritis, specifically gout. It provides a history of gout, describing it as one of the oldest diseases documented. It discusses the pathophysiology and risk factors of gout, and describes the typical stages and presentations of both acute and chronic gout, including joint destruction and extra-articular manifestations. The document also discusses treatment options and targets for gout, including lowering uric acid levels.
Gout is caused by high levels of uric acid in the blood that form crystals in the joints, causing inflammation and pain. It was once thought to be a disease of kings due to its association with rich foods and alcohol. Symptoms include sudden, severe pain and swelling in joints like the big toe. Diagnosis involves testing blood and urine uric acid levels and examining joint fluid. Treatment focuses on relieving pain and reducing uric acid through medications like NSAIDs, colchicine, corticosteroids, allopurinol, and febuxostat. Lifestyle changes around diet, weight, and alcohol intake can help prevent future gout attacks.
This document provides an overview of gout and hyperuricemia. It discusses the pathophysiology, clinical presentations, diagnosis and treatment. Key points include: Gout is caused by elevated uric acid leading to monosodium urate crystal formation in joints; the most common presentation is acute inflammatory arthritis, often in the great toe; diagnosis involves identifying crystals in synovial fluid or tophi and measuring uric acid levels; treatment focuses on lifestyle modifications and medications to reduce uric acid production or enhance excretion.
Gout is a type of inflammatory arthritis caused by deposition of urate crystals in the joints due to persistent hyperuricemia. It manifests as recurrent acute flares typically involving the great toe, as well as chronic tophaceous gout with subcutaneous urate deposits. The pathophysiology involves urate crystal formation triggering inflammation through activation of the NLRP3 inflammasome and recruitment of leukocytes. Acute gout flares are usually self-limiting due to feedback mechanisms that limit inflammation, though chronic tophaceous gout can develop if hyperuricemia is untreated.
The document discusses gout, a type of arthritis caused by uric acid crystals in the joints. It defines gout, lists its symptoms such as sudden severe pain in joints like the big toe, and describes its typical progression from asymptomatic to acute attacks to a chronic condition if left untreated. Risk factors include being male, obesity, diet high in purines, and certain medications. Diagnosis involves examining synovial fluid for uric acid crystals. Treatment focuses on relieving acute attacks, preventing future attacks by reducing uric acid levels in the blood long-term through medications and diet changes, and managing chronic complications through continued medical care.
This document discusses gout and pseudogout (calcium pyrophosphate deposition disease or CPPD). It provides a historical overview and describes the crystals involved in gout (monosodium urate) and pseudogout (calcium pyrophosphate dihydrate). It discusses the clinical presentation, risk factors, diagnosis, treatment and long term outcomes of gout and pseudogout. Radiographic findings and fluid analysis findings that can help differentiate gout from pseudogout are also summarized.
Gout is a metabolic disease caused by high levels of uric acid in the bloodstream, which can accumulate and crystallize in the joints, causing inflammation. It occurs when there is either overproduction of uric acid by the body or inadequate excretion by the kidneys. Common symptoms include sudden, severe pain and swelling in joints like the big toe. Treatment focuses on reducing uric acid levels through medications and dietary changes like limiting purine-rich foods and alcohol.
Here are the key points I would suggest to the aircrew:
- Lose weight through diet and exercise to achieve a healthy BMI, as obesity is a risk factor for hyperuricemia and gout.
- Limit alcohol intake, especially beer which is strongly associated with hyperuricemia.
- Follow a low-purine diet by reducing intake of organ meats, red meat, seafood etc. which are high in purines.
- Stay well hydrated by drinking plenty of water as uric acid is more soluble in urine produced in larger volumes.
- Start on allopurinol 100mg once daily which is a xanthine oxidase inhibitor to lower uric acid production
The document provides biographical information about Dr. Manoj R. Kandoi, the author of the book "The Basics of Arthritis". It states that Dr. Kandoi founded the Institute of Arthritis Care & Prevention non-profit organization focused on arthritis patient education and support. He has published several papers on arthritis and written the book to guide arthritis patients and healthcare professionals. Contact information for Dr. Kandoi and the Institute is provided.
1. Gout and pseudogout are types of crystal arthritis caused by sodium urate crystals or calcium pyrophosphate crystals respectively.
2. Gout prevalence is increasing, especially in developed countries, and affects men more than women. Risk factors include diet, medications, age, gender and medical conditions.
3. Pseudogout usually affects the knees and wrists of elderly women, causing painful flare ups that are treated similarly to gout.
Gout is a common, painful form of arthritis.
It causes swollen, red, hot and stiff joints. Gout occurs when uric acid builds
up in your blood. This happens if your body produces extra acid or does not
eliminate enough, or if you eat too many foods with purines, such as liver and
dried beans. Pseudogout has similar symptoms and is sometimes confused with
gout. However, it is caused by calcium phosphate, not uric acid.
Often, gout first attacks your big toe. It
can also attack ankles, heels, knees, wrists, fingers and elbows.
You are more likely to get gout if you:
Are a man
Have family
member with gout
Drink
alcohol
At first, gout attacks usually get better in
days. Eventually, attacks last longer and occur more often. Uric acid buildup
can lead to kidney stones.
Untreated gout can cause permanent joint and kidney damage. You can treat gout
with medicines.
Gout - Clinical features , diagnosis and managementRohit Rajeevan
Gout is a metabolic disease resulting from deposition of urate crystals in the joints and tissues. It was first identified by Egyptians in 2640 BC and described by Hippocrates. It predominantly affects men over age 40 and is associated with purine-rich foods and comorbidities like diabetes. Symptoms include recurrent acute inflammatory arthritis attacks, tophi formation, and chronic arthritis. Diagnosis involves synovial fluid analysis demonstrating urate crystals. Treatment includes NSAIDs, colchicine, urate-lowering drugs like allopurinol, and lifestyle modifications like diet and exercise. Pseudogout is caused by calcium pyrophosphate crystals and presents similarly but is diagnosed by demonstrating different crystals on syn
Gout is caused by high levels of uric acid in the blood that lead to painful inflammation in joints. It occurs when uric acid crystals deposit in joints, especially those in the big toe. Risk factors include diet high in purines, obesity, kidney disease, genetics, and certain medications. Symptoms range from joint pain and swelling to tophi formation and arthritis. Treatment focuses on lifestyle changes like diet modification and medication to reduce uric acid levels and relieve pain.
The Science of Software Testing - Experiments, Evolution & Emergence (2011)Neil Thompson
The document discusses the history and evolution of software testing from the early days of debugging programs to the current conceptions of testing as both an engineering discipline and a scientific field of study. It traces the development of software testing from initial methods focused on demonstration and destruction to more modern prevention-oriented and quality-focused approaches. The document also examines perspectives on treating software testing as a science through use of the scientific method, experiments, and evolving theories and models of both development and testing.
This presentation is about our paper which was presented at the Hypertext conference 2008.
Abstract: In recent literature, several models were proposed for reproducing and understanding the tagging behavior of users. They all assume that the tagging behavior is influenced by the previous tag assignments of other users. But they are only partially successful in reproducing characteristic properties found in tag streams. We argue that this inadequacy of existing models results from their inability to include user’s background knowledge into their model of tagging behavior. This paper presents a generative tagging model that integrates both components, the background knowledge and the influence of previous tag assignments. Our model successfully reproduces characteristic properties of
tag streams. It even explains effects of the user interface on the tag stream.
Links to the paper:
http://dx.doi.org/10.1145/1379092.1379109
http://www.uni-koblenz.de/~staab/Research/Publications/2008/DellschaftStaabHypertext08.pdf
Presentation made by Shalini Srivatastava of K V Cantt Mathura in the stage 3 of Mathura Genius Award 2009 (Junior Level) organized by Paarth Educational Foundation (www.paarth.in)
Eventtypes allow you to categorize events at search time based on search definitions. For example, defining an eventtype called "problem" that includes terms like "error", would tag any events containing those terms as eventtype="problem". This provides a dynamic way to tag events without modifying the raw data. Reports in Splunk display search results in a formatted view like a table or chart and can be placed on dashboards. Apps are collections of Splunk configurations and code that allow you to customize your Splunk environment for specific use cases.
La Unión Europea ha propuesto un nuevo paquete de sanciones contra Rusia que incluye un embargo al petróleo. El embargo se aplicaría gradualmente durante seis meses para el petróleo crudo y ocho meses para los productos refinados. Este paquete de sanciones requiere la aprobación unánime de los 27 estados miembros de la UE.
Measuring the Influence of Tag Recommenders on the Indexing Quality in Taggin...Klaas Dellschaft
This presentation is about our paper which was presented at the Hypertext conference 2012. In this paper, we investigate a methodology for measuring the influence of tag recommenders on the indexing quality in collaborative tagging systems. We propose to use the inter-resource consistency as an indicator of indexing quality. The inter-resource consistency measures the degree to which the tag vectors of indexed resources reflect how the users understand the resources. We use this methodology for evaluating how tag recommendations coming from (1) the popular tags at a resource or from (2) the user's own vocabulary influence the indexing quality. We show that recommending popular tags decreases the indexing quality and that recommending the user's own vocabulary increases the indexing quality.
Links to the paper:
http://dx.doi.org/10.1145/2309996.2310009
http://www.west.uni-koblenz.de/files/publications/dellschaft2012mti.pdf
The document provides information on the site and building located at 40 Panditya Road in Kolkata, India. It describes the site's orientation, layout, and surrounding context. It also summarizes the building's architectural style, construction materials, zoning, climate response strategies, and area program breakdown by level. Diagrams are included showing plans, sections, elevations, and solar studies of the building.
This document does not contain any text to summarize. It appears to be blank or contain only formatting characters. In 3 sentences or less, a summary cannot be generated since there is no information presented in the document to summarize.
The document discusses the demolition and construction of a new upper school at Colorado Academy. It took less than a week to demolish the old upper school. The construction of the new upper school is underway, with the foundation sealed and waterproofed, brick ledge in place, and electrical and mechanical work beginning inside the structure. Crews are also backfilling around the foundation.
The knight Huldbrand comes upon a fisherman's cottage near a lake and forest. Inside he meets the fisherman, his wife, and their ward Undine, a beautiful 18-year-old girl. Undine takes a liking to Huldbrand but gets in trouble for misbehaving. She storms off into the dark night in a rage. Huldbrand and the fisherman call out for her to return, worried for her safety, but to no avail. Undine remains missing in the night.
Presentation given by Siddharth Saxena of Sacred Heart Convent School in the Stage 3 of Mathura Genius Award 2009 (Senior Level) organized by Paarth Educational Foundation (www.paarth.in)
Box SA licious is a gourmet gift basket company that exclusively supports South Australian food and wine producers. They offer a variety of gift baskets for different occasions, including large hampers, children's hampers, baby hampers, and smaller gift options. Their gift baskets highlight specific SA producers like Knappstein wines, Lyndoch Lavender farm, and Coopers beers. Customers can order items online at www.boxsalicious.com.au.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms for those who already suffer from conditions like anxiety and depression.
Roland Kelly LinkedIn Profile 2012 v4.4Roland Kelly
This document provides a summary of Roland Kelly's professional experience and qualifications. Roland has over 25 years of experience in strategic leadership roles managing global teams across various industries including automotive, aerospace, defense, consumer products, semiconductors, and high technology. He has a proven track record of driving growth and operational excellence. Currently, Roland works as an advisor to the board of a UK company and resides in Menlo Park, California.
Presentation given by Vasundhara Agarwal of St. Dominics School in the Stage 3 of Mathura Genius Award 2009 (Senior Level) organized by Paarth Educational Foundation (www.paarth.in)
The document discusses the history and development of several professional soccer leagues, including the English Premier League established in 1863, the Japanese J-League founded in 1993 to replace the Japan Soccer League, and the Thai Premier League which was established in 1996 and is a member of the Asian Football Confederation. The document also includes a table comparing the sources of revenue for Manchester United in 1997 and 2005, with commercial revenue becoming a larger source of income over time.
This document provides information about the BUS 370 course including the course website, materials, and class conferences. It also outlines the main topics that will be covered in the course such as communication skills, interpersonal applications, and business applications. The document discusses why communication skills are important and defines key communication concepts like the communication process, filters, sensory modalities, and strategies.
Xanthinuria
Xanthinuria, also known as xanthine oxidase deficiency, is a rare genetic disorder causing the accumulation of xanthine. It is caused by a deficiency of the enzyme xanthine oxidase.
Orotic aciduria
Orotic aciduria is a disease caused by an enzyme deficiency resulting in a decreased ability to synthesize pyrimidines. It is the only known enzyme deficiency of the de novo pyrimidine synthesis pathway.
Gout
Gout is caused by a condition known as hyperuricemia, where there is too much uric acid in the body.
Gout is a metabolic disease caused by elevated levels of uric acid in the blood that leads to painful inflammation in joints. It was first identified by Egyptians and was known as the "Disease of Kings" due to its association with rich diets and alcohol consumption. Gout occurs when uric acid crystallizes and deposits in joints, tendons and surrounding tissues, causing sudden and severe attacks of pain, swelling and redness in the joints. Diagnosis involves physical examination of affected joints along with laboratory tests of serum uric acid levels and microscopic examination of synovial fluid to detect urate crystals. Treatment focuses on reducing uric acid production through medications and dietary changes to limit purine intake and prevent future gout
Gout is caused by elevated levels of uric acid in the blood which can crystallize and deposit in the joints, causing inflammation and pain. It is usually characterized by recurrent attacks of inflammatory arthritis in the joint at the base of the big toe. Treatment involves medications like NSAIDs to reduce inflammation during acute attacks and allopurinol or probenecid for long-term prevention by lowering uric acid levels through inhibition of uric acid synthesis or reabsorption. Lifestyle changes and a diet low in purine-rich foods can also help prevent gout attacks.
The synovium lines joints and produces synovial fluid. It contains two cell types - type A macrophages and type B fibroblasts. Synovial fluid contains hyaluronic acid and lubricates joints. Crystal synovitis occurs when urate or calcium pyrophosphate crystals deposit in the synovium, causing inflammation. Gout is caused by monosodium urate crystals and often affects the big toe joint. Pseudogout is caused by calcium pyrophosphate crystals and commonly affects large joints like the knee. Both present with sudden onset severe pain and swelling that usually resolves within 1-2 weeks. Diagnosis involves identifying the characteristic crystals in synovial fluid under polarized microscopy.
The synovium lines joints and produces synovial fluid. It contains two cell types and secretes hyaluronic acid. Synovial fluid contains water, proteins, and nutrients. The two main types of crystal synovitis are gout caused by monosodium urate crystals typically in the big toe, and pseudogout caused by calcium pyrophosphate crystals usually in large joints like the knee. Both involve crystal deposition in the synovium and similar acute inflammatory attacks. Risk factors, investigations, and treatments aim to reduce crystal levels and attack frequency or progression. Complications can include joint damage and renal problems if untreated.
This document discusses crystal deposition diseases, specifically gout. It begins by defining gout as the deposition of monosodium urate crystals in joints and tissues, resulting from hyperuricaemia. It then covers the etiology and pathogenesis of hyperuricaemia and gout, clinical manifestations including acute arthritis, tophi, and nephropathy. It concludes with discussing investigations, differential diagnosis, and treatment approaches for both acute gout flares and long-term management.
Gout is a type of arthritis caused by high levels of uric acid in the blood. Uric acid crystallizes and deposits in joints, causing sudden, severe attacks of pain, swelling and tenderness. Gout typically affects the big toe joint initially and can progress through stages from asymptomatic hyperuricemia to acute attacks of gouty arthritis, periods of intercritical gout, and finally chronic tophaceous gout if left untreated. Risk factors include genetics, diet high in purines, obesity, medications and other medical conditions.
Gout is a form of arthritis caused by high levels of uric acid in the blood (hyperuricemia) which can form crystals that deposit in joints, causing sudden and severe pain. It occurs more commonly in males and risk increases with age, obesity, diet high in purines, alcohol consumption, medical conditions like diabetes, and certain medications. An acute gout attack causes intense pain, inflammation, and redness in joints like the big toe. Long term management involves medications, dietary changes, and lifestyle modifications to prevent recurrent attacks.
This document discusses four types of arthritis: gouty arthritis, alkaptonuric arthritis, haemophilic arthritis, and moderating the discussion. It provides details on the definition, etiology, clinical features, pathology, diagnosis and treatment of each type of arthritis. Gouty arthritis is caused by deposition of urate crystals in the joints. Haemophilic arthritis results from bleeding into joints in those with haemophilia. Alkaptonuric arthritis is caused by a genetic defect affecting phenylalanine and tyrosine metabolism.
it is brief introduction on Gout disease in humans its causes, prevention, treatment and management of this disease, risk factors in previous medical history etc.
HYPERURICAEMIA + all related brand training material.pptxPabitra Thapa
Uric acid is produced when the body breaks down purines. Febuxostat is a new drug for treating hyperuricemia and gout that works by selectively inhibiting the enzyme xanthine oxidase, unlike allopurinol which non-selectively inhibits several enzymes. Febuxostat has been shown to effectively lower uric acid levels at recommended doses without needing dose adjustments for mild to moderate kidney or liver dysfunction, as opposed to allopurinol which requires dosage adjustments for renal impairment. Management of gout focuses on long-term urate-lowering therapy to maintain uric acid levels below target thresholds to prevent further crystal formation and promote crystal dissolution.
This document discusses uric acid and hyperuricemia. It summarizes that uric acid is the final product of purine breakdown in humans. Hyperuricemia can result from increased uric acid production, decreased excretion, or a combination. Complications of long-term hyperuricemia include gouty arthritis, kidney stones, and kidney damage. The diagnosis of gout involves identifying urate crystals in joint fluid. Treatment aims to resolve acute gout attacks and lower uric acid levels to prevent future attacks through medications and lifestyle changes.
Gout is a metabolic disorder caused by hyperuricemia, or high levels of uric acid in the blood. It most commonly affects middle-aged men and causes sudden, severe pain and inflammation in joints like the big toe. Acute gout occurs when uric acid crystals form in a joint, while chronic gout results in long-term joint damage. Treatment involves medications like NSAIDs, colchicine, corticosteroids, and allopurinol to reduce pain and prevent further attacks by lowering uric acid levels. Lifestyle changes like diet modification and exercise can also help prevent gout flares.
Gout is a metabolic disorder caused by elevated levels of uric acid in the blood (hyperuricemia). Uric acid crystallizes and deposits in joints, causing sudden and severe attacks of arthritis. Gout can be primary, due to overproduction of uric acid, or secondary, due to other conditions that reduce excretion or increase production of uric acid. Treatment involves medications to reduce uric acid levels such as allopurinol and probenecid, as well as lifestyle changes like a low-purine diet and increased fluid intake. Nonsteroidal anti-inflammatory drugs and corticosteroids are used to treat acute gout attacks and bring down joint inflammation.
NSAIDs are used to treat pain, fever, and inflammation. They work by blocking cyclooxygenase and lipoxygenase pathways, which inhibits the formation of prostaglandins and reduces inflammation. Common NSAIDs include aspirin, ibuprofen, and naproxen. While effective, they can cause side effects like gastric irritation, bleeding risks, and kidney issues. Gout is a type of arthritis caused by uric acid crystals in the joints. It is treated by addressing acute attacks with NSAIDs and colchicine while also managing uric acid levels long-term with drugs like allopurinol to prevent future attacks.
Nephrotic syndrome is a kidney disorder characterized by heavy protein in the urine, low blood protein levels, fluid retention causing edema, and high cholesterol. It is caused by damage to the glomeruli in the kidneys, which allows protein to pass into the urine. Common causes include infections, cancers, autoimmune diseases, medications, and genetic factors. Symptoms include generalized edema, fatigue, loss of appetite, and shortness of breath. Diagnosis involves blood and urine tests to detect low protein and high protein in the urine. Treatment focuses on reducing edema with diuretics, lowering blood pressure and proteinuria with ACE inhibitors, and using steroids to reduce inflammation in some cases.
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
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How to Build a Module in Odoo 17 Using the Scaffold MethodCeline George
Odoo provides an option for creating a module by using a single line command. By using this command the user can make a whole structure of a module. It is very easy for a beginner to make a module. There is no need to make each file manually. This slide will show how to create a module using the scaffold method.
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
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2. What is Gout?
Gout is defined as a peripheral arthritis, resulting
from the deposition of MSU crystals at one or more
joints.
Characterized by Hyperuricemia
Known as:
o Rich man’s Disease / Disease of Kings
o Poor man’s Gout
3. Uric acid Product of purine catabolism
Ionized forms of uric acid readily form salt.
98% of Uric acid forms monosodium salts
MSU crystals form in synovial fluid when solubility
limit are exceeded.
These crystals provoke an inflammatory reaction.
6. Research has shown that risk factors for development of
gout can be attributed to the increasing longevity, dietary
and lifestyle changes and a history of comorbidities.
There is an increased incidence of gout among:
•Males between the ages of 20 – 40.
•Men have higher serum urate levels.
•Post menopausal women
•Patients on diuretics.
•Such medication increase reabsorption of uric acid in
kidneys hence increasing the risk of developing gout.
•Patients with hypertension, diabetes, hyperlipidemia,
chronic kidney disease, or the metabolic syndrome.
•Studies show that more than 60% of patients with gout have
the metabolic syndrome.
7. Diet :
Beer drinking, High red meat and seafood consumption
increases risk.
Purine-rich vegetable consumption does not notably
increase risk of hyperuricemia and development of
gout.
Both incidence and Prevalence of Gout is increasing.
For example, Data from US managed care reflected an
increase in gout prevalence from 2.9 cases per 1000
persons in 1990 to 5.2 cases per 1000 in 1999.
Societies such as New Zealand, Taiwan and USA show
increasing prevalence.
More prevalent among African American Males than
European American males.
8.
9.
10.
11. Causes of Gout (Etiology)
High levels of uric acid circulating in the blood, which
can cause needle-shaped urate crystals to settle in the
tissues of the joints as well as the kidneys.
These crystals are sodium urate crystals which are the
end products of purine matabolism.
this deposition first causes acute then chronic gouty
arthritis.
12. Causes of Gout (Etiology)
Inheritance of certain genes
This inherited gene causes an abnormality in the
enzyme of purine metabolism (primary gout).
Several X-linked mutations have been identified in the
PRPP synthetase gene which results in the enzyme
having either:
Increased Vmax for the production of PRPP
A lower Km for ribose 5-phosphate
Decreased sensitivity to its purine nucleotide inhibitors
The overall result is increased purine production
resulting in high levels of plasma uric acid.
14. Causes of Gout (Etiology)
Secondary Gout may be caused from cancer, chronic renal
failure or any of the following:
From being overweight and eating a rich diet.
Lymphoma: a usually malignant tumour of lymphoid
tissue
Leukemia: an acute or chronic disease characterized by an
abnormal increase in the number of white blood cells in
bodily tissues
hemolytic anemia: anemia caused by excessive destruction
of red blood cells.
The latter three may be the underlying cause of the uric
acid buildup that results in gout.
15. Causes of Gout (Etiology)
Chronic exposure to high levels of lead decreases the
body’s excretion of urates, allowing uric acid to
accumulate in the blood.
16. Any metabolic aberration which reduces the rate of synthesis of AMP or
GMP from IMP, or from purine bases by the salvage mechanism, or which
accelerates the removal of nueleotides into macromolecules or through
increased catabolism, may in theory result in reduced intracellular
concentrations of regulatory nucleotides and release of the
amidotransferase from inhibition. This would permit excessive synthesis of
phosphoribosylamine and ultimately of uric acid.
The turnover of nucleic acids and coenzymes ultimately results
in production of free purine bases, chiefly adenine, hypoxanthine and
guanine, which are largely recycled into purine ribonucleotides and nucleic
acid once again, by reactions sometimes referred to as salvage
pathways. A fraction of hypoxanthine and guanine is further oxidized
to uric acid, which is a biologically inert end product excreted largely
in the urine.
17. tudies of the rates of production of uric acid in subjects
with primary gout have disclosed evidence of excessive
synthesis of purines in a large percentage of patients.
On a diet very low in purines, 24 per cent excreted
quantities of urate in urine in excess of 590 mg per day,
the upper limit of the normal range.
ric acid is produced by xanthine oxidase from xanthine
and hypoxanthine, which in turn are produced from
purine. Uric acid is more toxic to tissues than either
xanthine or hypoxanthine.
18. n human blood plasma, the reference range of uric acid
is between 3.6 mg/dL and 8.3 mg/dL
urines are found in high amounts in animal internal
organ food products, such as liver. A moderate amount
of purine is also contained in beef, pork, poultry, fish
and seafood, asparagus, cauliflower, spinach,
mushrooms, green peas, lentils, dried peas, beans,
oatmeal, wheat bran and wheat germ.
xamples of high purine sources include: sweetbreads,
anchovies, sardines, liver, beef kidneys, brains, meat
extracts (e.g Oxo, Bovril), herring, mackerel, scallops,
game meats, and gravy.
19. 1. Turnover of nucleic acid and coenzymes results in
the production of free purine bases (Adenine,
hypoxantine and guanine). These bases go to the
salvage pathways.
2. Decreased activity of HGPRT which catalyzes a
reaction of hypoxantine, guanine and adenosine
with PRPP to give IMP, GMP and AMP results in the
buildup of PRPP and reduced levels of IMP,GMP
and AMP.
3. Hence hypoxanthine, guanine and adenine would
go towards the production of xanthine which is
oxidixed to uric acid – leading to hyperuricemia.
4. N.B. InVon Geirke Disease, G6P is shunted to the
HMP pathway – lead to the increased production of
R5P – leading to the increased production of PRPP.
20.
21.
22.
23. Signs & Symptoms
Acute gout attacks: a rapid onset of pain in the
affected joint followed by warmth, swelling, reddish
discoloration, and marked tenderness.
Bursitis
The small joint at the base of the big toe is the most
common site of an acute gout attack. Other joints
that can be affected include the ankles, knees, wrists,
fingers, and elbows.
Intense tenderness: even a blanket touching the skin
over the affected joint can be unbearable
24. These painful attacks usually subside in hours to days,
with or without medication
Symptoms related to Chronic Gout
Chronic (tophaceous) gout: nodular masses of uric
acid crystals (tophi) deposit in different soft tissue
areas of the body
Such as: fingers, at the tips of the elbows, and around
the big toe;
Rarely in ears, vocal cords and around the spinal cord
25.
26.
27.
28. *Physical examination and medical history
*Measuring blood uric acid levels
*Examination and analysis of synovial fluid
*Radiography
29. DIAGNOSIS
Physical examination and medical history
patient’s description of symptoms
Gout is more likely if:
- Arthritis first appears in the big toe than if it first appears
elsewhere
- Onset of symptoms (pain and swelling) takes days or
weeks .symptoms which take hours to develop probably
indicate a disorder other than gout.
- Abnormal enlargements in joints that had been affected by
previous injury or osteoarthritis are possible signs of gout
30. DIAGNOSIS
Measuring blood uric acid levels
A blood test is usually given for measuring uric acid and
detecting hyperuricemia. A low level of uric acid in the
blood makes a diagnosis of gout much less probable, and a
very high level increases the likelihood of gout.
• Uric acid levels in the blood during an attack of gout can lie
within or below the normal range
• or
• Hyperuricemia may be prevalent in population and doesn’t
necessarily indicate gout.
31. DIAGNOSIS
Examination of synovial fluid
Examination of synovial fluid is the most accurate method for
diagnosing gout.
Synovial fluid analysis
The sample is examined through a microscope under polarized
light. This special light will reveal the presence of monosodium
urate (MSU) crystals, which will nearly always confirm a
diagnosis of gout.
Examination of aspirated joint fluid can rule out other disorders
that mimic gout, such as septic arthritis and pseudogout.
32. DIAGNOSIS
Uric acid crystals under polarized light
33. DIAGNOSIS
Occasionally, patients with gout may present without
uric acid crystals in the synovial fluid aspirate.
However, aspiration repeated five hours to one day
later shows crystals in the synovial fluid of most of
these patients
34. DIAGNOSIS
Radiography
is not very useful in diagnosing initial attacks of acute
gouty arthritis. The radiographic findings are
generally nonspecific, consisting of soft tissue
swelling around a joint.
Bony abnormalities indicate the presence of chronic
gout.
In general, gout must be untreated or inadequately
treated for approximately 12 years before chronic
arthritis and bony erosions are seen on radiographs.
37. There are two essential concepts behind the
treatment of Gout:
1. Its is critical in stopping the inflammation caused by
the gouty arthritis.
2. It is vital in addressing the long term management of
the disease in order to prevent further attacks and
shrink crystal deposits.
38. There are basically three ways of treating Gout:
1. Self Care
3. Medications
5. Surgery
39. Self Care
Take medications as prescribed.
While a joint is hot and swollen, aggravation should
be prevented to so as to reduce further discomfort.
The following would be helpful:
Using of a cane or similar support to keep your weight
off that joint.
Keep the swollen joint elevated above your chest as
much as possible.
Ice packs can be helpful in relieving pain and reducing
inflammation.
Maintaining adequate hydration is key for minimizing
attacks and decreasing the formation of kidney
stones.
40. Reduce the consumption of alcohol since:
It is known to have a diuretic effects and can contribute
to dehydration and precipitate the acute gout attack.
Affects uric acid metabolism resulting in
hyperuricemia.
Dietary changes can help reduce the amount of uric
acid in the blood;
Purine rich food should be avoided (shellfish and organ
meats such as liver, brains, kidneys, and sweetbreads)
41. Medication
There are three aspects/lines of treatment of
gout with medication:
Pain relievers such as acetaminophen (Tylenol) or
other more potent analgesics are used to manage
pain.
The exact mechanism of action of acetaminophen is
not known. Acetaminophen relieves pain by elevating
the pain threshold, that is, by requiring a greater
amount of pain to develop before a person feels it.
42. Anti-inflammatory agents such as NSAIDS,
colchicine, and corticosteroids, used to decrease
joint inflammation.
NSAIDS such as:diclofenac, etoricoxib,
indomethacin, ketoprofen and naproxen.
Most of these drugs function by inhibiting the
COX-2 resulting in the reduction of prostaglandins
production.
43. Colchicine is useful in suppressing the inflammation.
The exact mechanism of action of colchicine is not
known but is speculated that it impairs the motility of
granulocytes and hence prevent the inflammatory
phenomena that initiate an attack or it may involve
reduction in uric acid deposition leading to a
reduction in the inflammatory response. Colchicine is
not an analgesic (pain killer), but it reduces pain in
acute gouty arthritis.
44. Corticosteroids such as prednisone a synthetic
corticosteroids mimic the action of cortisol
(hydrocortisone), the naturally-occurring corticosteroid
produced in the body by the adrenal glands.
Corticosteroids are potent anti-inflammatory effectors.
Prednisone is inactive in the body and, in order to be
effective, first must be converted to prednisolone by
enzymes in the liver. Therefore, prednisone may not work
as effectively in people with liver disease whose ability to
convert prednisone to prednisolone is impaired.
They function by inhibiting phospholipase A2 the enzyme
responsible for the release of Archidonic acid from
membrane phospholipids – the precursor for
prostaglandins.
45. • Medications for managing the chronic underlying
metabolic derangement that causes hyperuricemia and
gout. That is, medications that reduce the elevated levels
of uric acid in the blood.
• These medication are taken over prolonged periods to
lower blood uric acid level.
• Medicines used to lower blood uric acid level work either
by increasing the kidney's excretion of uric acid or by
decreasing the body's production of uric acid from the
purines in foods.
• These medicines are generally not started until after the
inflammation from acute gouty arthritis has subsided
because they can worsen the attack. If they are already
being taken prior to the attack, they are continued and
only adjusted after the attack has resolved.
46. Allopurinol lowers the blood uric acid level by
preventing uric acid production. It acts by blocks the
metabolic conversion from purines by inhibiting
xanthine oxidase, the enzyme responsible for the
conversion of xanthine to uric acid.
Probenecid (Benemid) and sulfinpyrazone
(Anturane) are medications that are commonly used
to decrease uric acid blood levels by increasing the
excretion of uric acid into the urine.
These act by preventing the reabsorption of uric acid
by the kidney and hence increasing its excretion from
the body in the urine
47. Surgery
Surgery is rarely needed for gout unless significant
joint damage has occurred from lack of effective
treatment
48. Prevention
The key to prevent gout is to maintain the
concentration of uric acid within the normal
range (7.0 mg/dL),this can be achieved by:
Avoiding excessive intake of purine rich food such as
those high in proteins and fats e.g. seafood, beef,
poultry
Maintain a healthy body weight via proper diet and
exercise.
49. Avoid foods rich in fructose, sucrose (glucose and
fructose) especially high fructose corn syrup (a
common sweetener in soft drinks which results in
hyperuricemia), and diuretic foods or drugs( increases
urination).
Restrict your intake of alcohol, especially beer(high in
guanosine), on the basis that brewer’s yeast are very
rich in purine, beer also can inhibit the elimination of
uric acid and can cause dehydration which may lead
to gout.
50. Avoid diet low in potassium(good sources: tomatoes,
potatoes,bananas,soybeans,brown rice) since a
deficiency increases urate in blood.
Avoid consuming too much acid containing
substances
Drink plenty of liquids, especially water, to dilute and
assist excretion of urates
51. Maintain an adequate intake of Vitamin C since it has
been demonstrated to increase excretion on uric acid
and in turn lower serum urate levels by dissolving the
needle-like crystals that deposit themselves between
the joints and connective tissue.
Aviod prolonged exposure to low temperature.
52. Prognosis/Outlook
It is excellent is you are properly diagnosed and
treated.
The optimal regimens for the treatment of acute
gout attacks and chronic gout conditions still
require further long-term studies. Research
scientists will continue to develop less toxic and
more effective medications to battle this
"scourge of the ages”.
53. Primary Gout is almost exclusively a disease of adult
men because their kidneys excrete uric acid less well,
and return more to blood, than do the kidneys of
women and children.
In adult men urate already circulates at levels close to
the maximum before crystals will form