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.
Dr. Ashutosh Kumar presented on gout. Gout is a disorder caused by excess uric acid in the body that leads to painful inflammation in joints. It ranges from asymptomatic hyperuricemia to acute gout attacks to chronic gout with tophi formation. Diagnosis involves examining crystals in joint fluid or tophi. Treatment goals are to rapidly resolve flares, prevent future flares, reduce inflammation, and lower uric acid levels long-term to prevent progression. Medications include NSAIDs, colchicine, corticosteroids for flares and allopurinol or febuxostat for urate-lowering. Lifestyle changes like diet modification and weight control can also help manage the
Gout is a type of arthritis caused by high levels of uric acid in the blood. It most commonly affects the big toe joint. Gout occurs when uric acid crystallizes and the crystals deposit in joints, tendons and surrounding tissues. Long-term untreated gout can lead to chronic arthritis and joint damage. Gout is diagnosed through blood tests to measure uric acid levels and examination of joint fluid under a microscope to detect urate crystals. Treatment involves medications to reduce uric acid levels and relieve pain and inflammation. Lifestyle changes like diet modification and exercise are also important for managing gout.
Gout is caused by high levels of uric acid in the bloodstream, which results in painful inflammation in joints like the big toe. It is more common in men and can be caused by diet, obesity, kidney problems, or other medical conditions. The most reliable way to diagnose gout is through microscopic examination of joint fluid to check for uric acid crystals or high uric acid levels in blood tests. Treatment focuses on reducing uric acid through medication and lifestyle changes.
Gout is a type of arthritis caused by high levels of uric acid in the blood. It most commonly affects the big toe joint, causing sudden and severe pain. There are different types of gout including acute gout, chronic gout, and pseudogout. Risk factors include being overweight, drinking alcohol, eating red meat, and using diuretics. Treatment involves medications to reduce uric acid levels and prevent attacks, as well as lifestyle changes like losing weight, staying hydrated, and following a diet low in purines and high in fruits and vegetables.
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.
This document provides an overview of gout, including defining it as a medical condition characterized by recurrent attacks of acute inflammatory arthritis. Key points discussed include the signs and symptoms of pain, swelling and redness in affected joints; causes such as high uric acid levels in the blood which can be due to genetics, diet or medications; risk factors and complications; diagnosis through tests of synovial fluid, blood and x-rays; management through medications, diet changes and nursing care focused on pain management, mobility and anxiety reduction.
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.
Dr. Ashutosh Kumar presented on gout. Gout is a disorder caused by excess uric acid in the body that leads to painful inflammation in joints. It ranges from asymptomatic hyperuricemia to acute gout attacks to chronic gout with tophi formation. Diagnosis involves examining crystals in joint fluid or tophi. Treatment goals are to rapidly resolve flares, prevent future flares, reduce inflammation, and lower uric acid levels long-term to prevent progression. Medications include NSAIDs, colchicine, corticosteroids for flares and allopurinol or febuxostat for urate-lowering. Lifestyle changes like diet modification and weight control can also help manage the
Gout is a type of arthritis caused by high levels of uric acid in the blood. It most commonly affects the big toe joint. Gout occurs when uric acid crystallizes and the crystals deposit in joints, tendons and surrounding tissues. Long-term untreated gout can lead to chronic arthritis and joint damage. Gout is diagnosed through blood tests to measure uric acid levels and examination of joint fluid under a microscope to detect urate crystals. Treatment involves medications to reduce uric acid levels and relieve pain and inflammation. Lifestyle changes like diet modification and exercise are also important for managing gout.
Gout is caused by high levels of uric acid in the bloodstream, which results in painful inflammation in joints like the big toe. It is more common in men and can be caused by diet, obesity, kidney problems, or other medical conditions. The most reliable way to diagnose gout is through microscopic examination of joint fluid to check for uric acid crystals or high uric acid levels in blood tests. Treatment focuses on reducing uric acid through medication and lifestyle changes.
Gout is a type of arthritis caused by high levels of uric acid in the blood. It most commonly affects the big toe joint, causing sudden and severe pain. There are different types of gout including acute gout, chronic gout, and pseudogout. Risk factors include being overweight, drinking alcohol, eating red meat, and using diuretics. Treatment involves medications to reduce uric acid levels and prevent attacks, as well as lifestyle changes like losing weight, staying hydrated, and following a diet low in purines and high in fruits and vegetables.
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.
This document provides an overview of gout, including defining it as a medical condition characterized by recurrent attacks of acute inflammatory arthritis. Key points discussed include the signs and symptoms of pain, swelling and redness in affected joints; causes such as high uric acid levels in the blood which can be due to genetics, diet or medications; risk factors and complications; diagnosis through tests of synovial fluid, blood and x-rays; management through medications, diet changes and nursing care focused on pain management, mobility and anxiety reduction.
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.
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.
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 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.
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.
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.
Gout is a type of arthritis caused by uric acid crystals accumulating in the joints. It usually affects the big toe but can impact other joints as well. Treatment for gout involves medications to relieve pain and swelling during attacks and prevent future attacks. Common drugs used include colchicine, NSAIDs, corticosteroids, and allopurinol. Colchicine is particularly effective for treating acute gout flares and preventing recurrent attacks by reducing inflammation and inhibiting uric acid crystal deposition. However, it can cause side effects like gastrointestinal upset if taken in high doses or for a long period of time.
The document provides information about the physical examination of a patient with gout. It describes the typical history of gout including risk factors like being male over 30, family history, hypertension, alcohol use, and diuretic use. Acute gout causes sudden severe joint pain lasting 1-2 weeks, while chronic gout causes recurrent attacks leading to joint damage. On examination, the patient may appear obese and red-skinned with swelling in common sites like the big toe. Tophi may form around joints and ulcers can develop. The affected joint will feel hot, tender and have reduced range of motion.
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.
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 is a form of arthritis caused by urate crystals depositing in joints due to high uric acid levels. It exists in primary and secondary forms. Primary gout is caused by inborn errors in purine metabolism and usually affects older men. Secondary gout is caused by other conditions like renal insufficiency that decrease uric acid excretion. Gout progresses through asymptomatic, acute, and chronic stages and is characterized by painful joint inflammation and tophi formations. Treatment involves medications like allopurinol to reduce uric acid production as well as a low purine diet and increased fluid intake.
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 elevated uric acid levels in the blood (hyperuricemia) which can lead to the deposition of urate crystals in the joints, causing inflammation and pain.
- There are different treatments for the acute attacks and long-term management. For acute attacks, NSAIDs or corticosteroids can be used to reduce pain and inflammation. Colchicine may also be used.
- For long-term management and prevention of recurrent attacks, allopurinol is commonly prescribed to lower uric acid levels by inhibiting its production. Probenecid or other uricosuric
Gout is caused by deposits of sodium urate crystals in joints and tissues. It can be primary, due to a hereditary purine metabolism disorder, or secondary to drugs or other conditions that inhibit uric acid excretion. The document discusses the incidence, risk factors, pathophysiology, clinical manifestations, complications, diagnosis, and collaborative care of gout including treatments for acute attacks and chronic management. Tests like serum uric acid levels and synovial fluid analysis are used to monitor therapy for this metabolic disorder characterized by hyperuricemia and acute or chronic arthritis.
This document discusses gout, a metabolic disease characterized by recurrent attacks of acute inflammatory arthritis caused by elevated uric acid levels in the blood. It defines gout and discusses its pathogenesis, stages, risk factors, clinical features, differential diagnosis, investigations, and treatment. The document outlines that gout results from uric acid crystallizing and depositing in joints due to either overproduction or under excretion of uric acid. It can be diagnosed through testing of synovial fluid, blood, or urine and is treated with medications, diet modification, exercise, and surgery if needed.
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.
This document discusses the treatment of a patient presenting with acute gout in their big toe. Key points include:
1) The patient's uric acid levels were elevated at 325 umol/L and further testing showed signs of inflammation.
2) Treatment for the acute attack involves NSAIDs, colchicine, steroids and aspirating the joint if needed.
3) For long-term management the patient was started on allopurinol 300mg daily with recommendations to slowly increase the dose up to 800mg as needed to maintain uric acid levels below 300 umol/L.
4) Lifestyle factors like diet, alcohol intake and weight management can also help control gout symptoms
I was asked by the organizers to review updates on the management of gout. I compared guideline recommendations from the 2008 Philippine CPG to the 2012 ACR Recommendations and the 2014 3E Initiative.
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.
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.
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 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.
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.
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.
Gout is a type of arthritis caused by uric acid crystals accumulating in the joints. It usually affects the big toe but can impact other joints as well. Treatment for gout involves medications to relieve pain and swelling during attacks and prevent future attacks. Common drugs used include colchicine, NSAIDs, corticosteroids, and allopurinol. Colchicine is particularly effective for treating acute gout flares and preventing recurrent attacks by reducing inflammation and inhibiting uric acid crystal deposition. However, it can cause side effects like gastrointestinal upset if taken in high doses or for a long period of time.
The document provides information about the physical examination of a patient with gout. It describes the typical history of gout including risk factors like being male over 30, family history, hypertension, alcohol use, and diuretic use. Acute gout causes sudden severe joint pain lasting 1-2 weeks, while chronic gout causes recurrent attacks leading to joint damage. On examination, the patient may appear obese and red-skinned with swelling in common sites like the big toe. Tophi may form around joints and ulcers can develop. The affected joint will feel hot, tender and have reduced range of motion.
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.
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 is a form of arthritis caused by urate crystals depositing in joints due to high uric acid levels. It exists in primary and secondary forms. Primary gout is caused by inborn errors in purine metabolism and usually affects older men. Secondary gout is caused by other conditions like renal insufficiency that decrease uric acid excretion. Gout progresses through asymptomatic, acute, and chronic stages and is characterized by painful joint inflammation and tophi formations. Treatment involves medications like allopurinol to reduce uric acid production as well as a low purine diet and increased fluid intake.
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 elevated uric acid levels in the blood (hyperuricemia) which can lead to the deposition of urate crystals in the joints, causing inflammation and pain.
- There are different treatments for the acute attacks and long-term management. For acute attacks, NSAIDs or corticosteroids can be used to reduce pain and inflammation. Colchicine may also be used.
- For long-term management and prevention of recurrent attacks, allopurinol is commonly prescribed to lower uric acid levels by inhibiting its production. Probenecid or other uricosuric
Gout is caused by deposits of sodium urate crystals in joints and tissues. It can be primary, due to a hereditary purine metabolism disorder, or secondary to drugs or other conditions that inhibit uric acid excretion. The document discusses the incidence, risk factors, pathophysiology, clinical manifestations, complications, diagnosis, and collaborative care of gout including treatments for acute attacks and chronic management. Tests like serum uric acid levels and synovial fluid analysis are used to monitor therapy for this metabolic disorder characterized by hyperuricemia and acute or chronic arthritis.
This document discusses gout, a metabolic disease characterized by recurrent attacks of acute inflammatory arthritis caused by elevated uric acid levels in the blood. It defines gout and discusses its pathogenesis, stages, risk factors, clinical features, differential diagnosis, investigations, and treatment. The document outlines that gout results from uric acid crystallizing and depositing in joints due to either overproduction or under excretion of uric acid. It can be diagnosed through testing of synovial fluid, blood, or urine and is treated with medications, diet modification, exercise, and surgery if needed.
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.
This document discusses the treatment of a patient presenting with acute gout in their big toe. Key points include:
1) The patient's uric acid levels were elevated at 325 umol/L and further testing showed signs of inflammation.
2) Treatment for the acute attack involves NSAIDs, colchicine, steroids and aspirating the joint if needed.
3) For long-term management the patient was started on allopurinol 300mg daily with recommendations to slowly increase the dose up to 800mg as needed to maintain uric acid levels below 300 umol/L.
4) Lifestyle factors like diet, alcohol intake and weight management can also help control gout symptoms
I was asked by the organizers to review updates on the management of gout. I compared guideline recommendations from the 2008 Philippine CPG to the 2012 ACR Recommendations and the 2014 3E Initiative.
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.
This is a short presentation on gout and gouty arthritis. This also gives a brief idea about the causes of gout, its clinical features and investigations. This also provides basic information regarding management and prevention of gout and its associated complications
Dr.A.Mohan krishna
Consultant orthopedic surgeon
Apollo hospitals,
Hyderabad
Appointments: 9247258989
9441184590
www.drmohankrishna.com
www.bonesandjointsclinic.com
www.healthyjointclub.com
Gout is a type of arthritis caused by a buildup of uric acid crystals in the joints. It occurs when uric acid builds up in the blood and causes joint inflammation. Risk factors include age, sex, family history, certain medical conditions, dietary and lifestyle habits such as excessive alcohol consumption and being overweight. Diagnosis involves medical history, physical exam, and tests to measure uric acid levels in the blood and urine. Treatment includes medications to reduce uric acid levels like colchicine, allopurinol, and probenecid. Surgical removal of urate crystals may be required in severe cases. Nursing care focuses on pain management, maintaining activity levels, and monitoring for hyperthermia and other
Cure For The Gout An Overview June-2012Keith Heeres
http://www.cureforthegout.net
Gout affects more than 8.3 million people in the United States.
Prevalence of gout increases with age, and gout affects more men than women.
The rising incidence and prevalence of gout may be related to:
Aging population
Increasing obesity levels
Dietary changes
Gout is most commonly seen and treated by primary care physicians.
It can be misdiagnosed and, perhaps more importantly, undertreated.
Gout can damage the kidneys by depositing uric acid crystals. The kidneys concentrate uric acid from the blood and create an acidic environment, which promotes crystal formation. Repeated gout attacks can lead to uric acid crystal deposits called tophi in the kidneys, which could previously cause kidney failure. While medications now treat high uric acid levels, natural prevention of gout by diet control is also important for protecting kidney health.
This document discusses asymptomatic hyperuricemia and whether or not it should be treated. It covers the physiology of uric acid production and excretion by the kidneys. While acute hyperuricemia nephropathy, uric acid nephrolithiasis, and hyperuricemia after renal transplantation are clear reasons to treat, the evidence for treating asymptomatic hyperuricemia to prevent chronic gouty nephropathy, cardiovascular issues, insulin resistance, hypertension, and inflammation is unclear. Treatment may be warranted if uric acid levels are very high (≥ 8) or if the patient is symptomatic, but otherwise the decision to treat asymptomatic hyperuricemia remains uncertain based on current evidence.
Relationship between Adiposity, inulin resistance and gout.Jack Kwemboi
This document discusses the relationship between adiposity, insulin resistance, and gout. It states that obesity leads to chronic low-grade inflammation in adipose tissue, contributing to insulin resistance. Insulin resistance then causes hyperinsulinemia, inhibiting urate excretion by the kidneys and leading to hyperuricemia and gout. Metabolic syndrome, which includes insulin resistance, is also linked to higher uric acid levels and prevalence of gout. The conclusion is that adiposity can lead to insulin resistance, hyperinsulinemia, hyperuricemia due to inhibited urate excretion, and ultimately gout.
- The document discusses the treatment and management of gout. It provides guidelines on drug dosing for allopurinol and colchicine based on kidney function.
- The target for serum uric acid levels with treatment is provided, with lower targets for those with tophaceous gout.
- Treat-to-target therapy is recommended to keep serum uric acid levels below the recommended targets in order to prevent gout flares and reduce tophi formation. Regular monitoring of serum uric acid levels is important.
The document discusses the role of uric acid in the body and debates whether or not hyperuricemia should be treated. It presents evidence that uric acid has both antioxidant and pro-oxidant properties. Higher levels of uric acid may protect against cancer and neurodegenerative diseases but can also lead to gout and kidney problems if levels are too high. The document reviews several studies looking at the relationship between uric acid levels, bone mineral density, and cardiovascular risks.
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.
The Management of Gout and Hyperuricemiadbmstrategy6
This document provides recommendations for diagnosing and managing gout and hyperuricemia based on an updated review of evidence and guidelines. It describes gout as a progressive disease involving four stages from asymptomatic hyperuricemia to chronic arthropathy. The recommendations are meant to help physicians and other healthcare providers properly diagnose and treat patients with gout and hyperuricemia.
The document discusses purine and pyrimidine metabolism and their role in genetic material replication, transcription, protein synthesis and cellular metabolism. It then focuses on hyperuricemia and gout, explaining that this results from increased uric acid production or impaired excretion. The key biochemical pathways of purine degradation to uric acid are described, as well as the factors influencing uric acid solubility and excretion by the kidneys through specific transporters. The causes, clinical manifestations and approach to treatment of hyperuricemia are summarized.
Gout is a clinical disease caused by the deposition of monosodium urate crystals in tissues, which can cause acute gouty arthritis, tophaceous gout, gouty nephropathy, or uric acid stones. The aims of gout treatment are to improve outcomes by suppressing flares, eliminating gout permanently, resolving tophi, and managing comorbidities. First-line treatment for hyperuricemia involves xanthine oxidase inhibitors or uricosuric agents to lower uric acid levels. Diuretics can cause hyperuricemia and gout by increasing urate reabsorption, and treatment may involve changing medications or adding allopurinol.
This document defines and describes different types of bladder stones. Primary stones develop in sterile urine, while secondary stones occur due to infection, outflow obstruction, or impaired bladder emptying. The most common type is mixed stones. Diagnosis involves urinalysis, ultrasound, and radiography. Treatment depends on the cause but may include lithotripsy, percutaneous litholapaxy, or catheter removal to break up the stones. Various modalities like lithotrites, lasers, and evacuators are used for fragmentation and removal of stones and stone fragments from the bladder.
Hyperuricemia in chronic kidney disease: Do we treat or not?
The document discusses the relationship between hyperuricemia, chronic kidney disease, and cardiovascular disease. It reviews evidence that higher uric acid levels increase the risk of chronic kidney disease in the general population. However, in patients with chronic kidney disease, hyperuricemia itself was not associated with progression to end-stage renal disease. It was associated with increased risk of cardiovascular events. Treating hyperuricemic chronic kidney disease patients with allopurinol for 9-24 months helped preserve renal function and reduced cardiovascular events.
Gout is the most common cause of inflammatory arthritis in the US. Treatment of acute gout flares includes nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or colchicine. A randomized controlled trial found that oral prednisolone and naproxen provided equivalent pain relief for acute gout attacks. Colchicine is also effective for treating flares and preventing future attacks by interfering with neutrophil and monocyte activation. Management of gout focuses on both acute flare treatment and long-term urate-lowering therapy to reduce uric acid levels and prevent future attacks.
Hyperuricemia is caused by high levels of uric acid in the blood and can be due to underexcretion of uric acid by the kidneys, overproduction of uric acid, or a combination of both. Underexcretion is the most common cause and can result from reduced kidney function or medications that impact excretion. Overproduction occurs when there is excessive breakdown of purines from foods or the body. Certain genetic disorders, tumors, or diets high in purines can lead to overproduction. Conditions like alcohol use, fructose intake, or rapid weight loss may cause both overproduction and underexcretion of uric acid.
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.
This document provides an overview of osteoarthritis (OA), including its etiology, diagnosis, and treatment options. It discusses how OA is the breakdown of articular cartilage in a joint. Risk factors include mechanical damage from injury or excess weight, genetics, and residual effects from other arthritic conditions. Diagnosis involves assessing symptoms, physical exam findings, and imaging like x-rays. Conservative treatment includes weight loss, physical therapy, bracing, topical NSAIDs, nutraceuticals like glucosamine and chondroitin, and injections. Surgery is not usually recommended when OA is the sole diagnosis.
Diuretics are substances that promote urine formation and loss of salt from the body. They are prescribed to treat high blood pressure, fluid retention due to conditions like heart failure or kidney disease, and edema. There are three types of diuretic medications that work by lowering salt and water levels in the body. Diuretics can interact with other medications a person is taking, so patients should inform their doctor about all medicines and supplements. Common side effects include weakness, cramps, rashes, and gastrointestinal issues.
Gout is a type of arthritis characterized by sudden, severe attacks of pain and inflammation in joints, often affecting the joint at the base of the big toe. It occurs when urate crystals accumulate in joints, causing inflammation. Risk factors include lifestyle choices, certain medical conditions, family history, and age. Treatment involves medications to treat acute attacks and prevent future attacks and complications like recurrent gout, advanced gout, or kidney stones. Lifestyle changes like maintaining hydration and a balanced diet can also help prevent gout.
Module: Pharmacotherapy III
Module Coordinator: Dr. Arwa M. Amin Mostafa
Academic Level: Postgraduate, Master of Pharmacy in Clinical Pharmacy
School: Dubai Pharmacy College
Year of first presented in Class: 2018
This presentation is for Educational purpose. It has no commercial value associated with it.
End-stage renal disease is a condition in which the kidneys no longer function normally and required excellent medical and nursing care for the managing this condition.
Nonsteroidal anti-inflammatory drugs (NSAIDs) work by blocking cyclooxygenase (COX) enzymes, which reduces prostaglandin production and consequently decreases inflammation, pain, and fever. NSAIDs are used to treat conditions like arthritis, gout, and postoperative pain but can cause side effects like gastrointestinal ulceration and bleeding by inhibiting protective prostaglandins in the stomach. They may also increase risks of cardiovascular and renal issues. Care must be taken with NSAID combinations or when used with other drugs that impact renal function.
Arthritis is inflammation of the joints that causes pain, stiffness, and swelling. There are over 100 types but the most common are osteoarthritis, rheumatoid arthritis, and gout. Osteoarthritis involves wear and tear of cartilage between bones. Rheumatoid arthritis is an autoimmune disorder where the immune system attacks joint lining. Gout is caused by high uric acid levels forming crystals in the joints. Lifestyle changes like diet, exercise, and stress management can help manage arthritis symptoms.
This document provides biographical information about Dr. Rachmat Gunadi Wachjudi and discusses the pathophysiology and treatment of rheumatic pain. It notes that Dr. Wachjudi is the head of the Department of Internal Medicine at Dr. Hasan Sadikin Hospital Bandung. The document then discusses topics like acute pain in hospitals, prevalence of chronic pain, knee osteoarthritis, approaches to assessing and treating rheumatic pain, pharmacologic and non-pharmacologic pain management strategies, considerations for NSAID therapy, and providing a practical approach to managing rheumatic pain.
Gout is a form of arthritis caused by high levels of uric acid in the bloodstream. It most commonly affects the big toe joint, causing sudden and severe pain. Gout is caused by an excess production or impaired excretion of uric acid by the kidneys. Uric acid crystallizes and forms needle-like deposits in the joints, triggering inflammation and pain. Treatment involves medications to reduce uric acid levels, relieve pain and inflammation during gout attacks, and prevent future attacks and joint damage from long-term gout. Lifestyle changes like diet modification and exercise can also help lower uric acid levels and prevent gout complications.
DrRic Yoga for Hypertension Presented at Integrative Sports and Wellness (sli...DrRic Saguil
This document discusses how yoga can help lower blood pressure and manage hypertension. It explains that hypertension is caused by an overactive stress response that increases sympathetic nervous system activity. This floods the body with stress hormones and increases blood pressure. Yoga helps activate the relaxation response and parasympathetic nervous system to decrease stress hormones and lower blood pressure. The document covers yoga concepts like nadis, chakras and pranayama that work to unblock energy flow in the body and reduce stress levels.
A 55-year-old male presented with jaundice, decreased urination, and swelling of the body for 1 month. He has a history of alcoholism and smoking for 3 years. Laboratory tests revealed elevated bilirubin, liver enzymes, and signs of portal hypertension. He was diagnosed with alcoholic liver disease. Treatment included medications to protect the liver, manage complications, and lifestyle changes like abstaining from alcohol. Due to his condition, consultation with nutrition, gastroenterology, nephrology, neurology, and infectious disease services was recommended. Immunization against common liver pathogens and lifestyle modifications were also advised to prevent further damage and support recovery.
This document discusses constipation and provides information on its causes, symptoms, diagnosis, and treatment options. It notes that constipation can be caused by medications, diseases, or irritable bowel syndrome. Lifestyle changes and over-the-counter medications are recommended for self-treatment, including bulk forming, emollient, lubricant, saline, and stimulant laxatives. Different types of laxatives are described based on their mechanisms of action and appropriate usage. Referral is advised if symptoms persist longer than 2 weeks.
Osteoporosis is a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to increased bone fragility and a consequent increase in fracture risk. It is a major public health threat. Key factors in the development of osteoporosis include peak bone mass attainment, bone loss, and bone quality. Dual energy X-ray absorptiometry is the gold standard test used to diagnose osteoporosis. Lifestyle modifications and pharmacological therapies including bisphosphonates, parathyroid hormone, and monoclonal antibodies are used for fracture prevention and treatment.
This document summarizes the key aspects of drug therapy for gout. It begins with an overview and case presentation of a patient experiencing an acute gout attack. It then discusses the role of uric acid in gout and how hyperuricemia can lead to crystal deposition and inflammation. The main drugs for treating gout are reviewed, including colchicine, NSAIDs, and steroids for acute gout attacks, as well as allopurinol and probenecid for long-term uric acid lowering to prevent future attacks. Allopurinol works by inhibiting uric acid production while probenecid enhances uric acid excretion from the kidneys. Important considerations and potential adverse effects are
This document discusses various health issues like heart disease, cancer, arthritis, blood pressure, kidney stones, and diabetes. It introduces supplements and herbal medicines to treat these conditions, including B.P. Cure for blood pressure, Stone Killer for kidney stones, and SugarNil to fight diabetes. The document also discusses the herb Arjun and how its capsules can benefit heart health.
Osteoarthritis is a highly prevalent joint disease that causes breakdown of cartilage. Non-surgical treatment includes weight loss, physical therapy, bracing, acetaminophen, topical or oral NSAIDs, nutraceuticals like glucosamine sulfate and chondroitin sulfate, and injectables like steroids or hyaluronic acid. Glucosamine sulfate has been shown to reduce symptoms and possibly prevent further joint space narrowing, making it a potential disease-modifying treatment for osteoarthritis.
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 UPDATE AHMED YEHIA 2024, case based approach with application of the latest guidelines ACR and EULAR, Ahmed Yehia Ismaeel, MD Beni-Suef University
ACR EULAR CLASSIFICATION CRITERIA FOR GOUT
EULAR 2023 Guidelines on gout imaging
ACR guideline recommendations for gout management
How to Control Your Asthma Tips by gokuldas hospital.Gokuldas Hospital
Respiratory issues like asthma are the most sensitive issue that is affecting millions worldwide. It hampers the daily activities leaving the body tired and breathless.
The key to a good grip on asthma is proper knowledge and management strategies. Understanding the patient-specific symptoms and carving out an effective treatment likewise is the best way to keep asthma under control.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
Giloy in Ayurveda - Classical Categorization and SynonymsPlanet Ayurveda
Giloy, also known as Guduchi or Amrita in classical Ayurvedic texts, is a revered herb renowned for its myriad health benefits. It is categorized as a Rasayana, meaning it has rejuvenating properties that enhance vitality and longevity. Giloy is celebrated for its ability to boost the immune system, detoxify the body, and promote overall wellness. Its anti-inflammatory, antipyretic, and antioxidant properties make it a staple in managing conditions like fever, diabetes, and stress. The versatility and efficacy of Giloy in supporting health naturally highlight its importance in Ayurveda. At Planet Ayurveda, we provide a comprehensive range of health services and 100% herbal supplements that harness the power of natural ingredients like Giloy. Our products are globally available and affordable, ensuring that everyone can benefit from the ancient wisdom of Ayurveda. If you or your loved ones are dealing with health issues, contact Planet Ayurveda at 01725214040 to book an online video consultation with our professional doctors. Let us help you achieve optimal health and wellness naturally.
“Psychiatry and the Humanities”: An Innovative Course at the University of Mo...Université de Montréal
“Psychiatry and the Humanities”: An Innovative Course at the University of Montreal Expanding the medical model to embrace the humanities. Link: https://www.psychiatrictimes.com/view/-psychiatry-and-the-humanities-an-innovative-course-at-the-university-of-montreal
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7shruti jagirdar
Unit 4: MRA 103T Regulatory affairs
This guideline is directed principally toward new Molecular Entities that are
likely to have significant use in the elderly, either because the disease intended
to be treated is characteristically a disease of aging ( e.g., Alzheimer's disease) or
because the population to be treated is known to include substantial numbers of
geriatric patients (e.g., hypertension).
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
PGx Analysis in VarSeq: A User’s PerspectiveGolden Helix
Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
The purpose of this webcast is to:
Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
Following genotyping, explore alternative tertiary workflow concepts in VarSeq to handle PGx reporting.
Moreover, we will include insights users will need to consider when validating their PGx workflow for all possible star alleles and options you have for automating your PGx analysis for large number of samples. Please join us for a session dedicated to the application of star allele genotyping and subsequent PGx workflows in our VarSeq software.
Pictorial and detailed description of patellar instability with sign and symptoms and how to diagnose , what investigations you should go with and how to approach with treatment options . I have presented this slide in my 2nd year junior residency in orthopedics at LLRM medical college Meerut and got good reviews for it
After getting it read you will definitely understand the topic.
1. WHEN IN GOUT
Amit Gir, MD
NOON CONFERENCE
March 4, 2011
BLUE TEAM
Mark Gennis, M.D.
Olha Norman, M.D.
Matt Mauck, M.D.
Mostafa Ahmed, M3
Note: The following lecture contains only 0.3% of your recommended daily educational value.
6. If you’re not supposed
to have lots of acid in
your blood, then what
is GOUT?
7. If you’re not supposed
to have lots of acid in
your blood, then what
is GOUT?
An inflammatory response to elevated
crystalized uric acid levels depositing
into joint spaces leading to destruction
and pain
29. WHAT CAUSES GOUT?
Increased uric acid levels usually asymptomatic
Gouty Attacks:
•Increased urate crystals released
•Form de novo in the joint space
•Trauma
•Surgeries
•Medications (allopurinol, diuretics, cyclosporine)
35. WHO GETS GOUT?
•2x Men vs. Women
•Estrogen has mild uricosuric effect
•(i.e. gout rare in pre-menopausal)
36. WHO GETS GOUT?
•2x Men vs. Women
•Estrogen has mild uricosuric effect
•(i.e. gout rare in pre-menopausal)
•Rare < age 30: unless genetic defect
37. WHO GETS GOUT?
•2x Men vs. Women
•Estrogen has mild uricosuric effect
•(i.e. gout rare in pre-menopausal)
•Rare < age 30: unless genetic defect
•(HGPRT ↓, ↑ PRP synthetase activity)
38. WHO GETS GOUT?
•2x Men vs. Women
•Estrogen has mild uricosuric effect
•(i.e. gout rare in pre-menopausal)
•Rare < age 30: unless genetic defect
•(HGPRT ↓, ↑ PRP synthetase activity)
High in elderly because:
39. WHO GETS GOUT?
•2x Men vs. Women
•Estrogen has mild uricosuric effect
•(i.e. gout rare in pre-menopausal)
•Rare < age 30: unless genetic defect
•(HGPRT ↓, ↑ PRP synthetase activity)
High in elderly because:
•Prevalence of Metabolic Syndrome
40. WHO GETS GOUT?
•2x Men vs. Women
•Estrogen has mild uricosuric effect
•(i.e. gout rare in pre-menopausal)
•Rare < age 30: unless genetic defect
•(HGPRT ↓, ↑ PRP synthetase activity)
High in elderly because:
•Prevalence of Metabolic Syndrome
•Diuretic Use
41. WHO GETS GOUT?
•2x Men vs. Women
•Estrogen has mild uricosuric effect
•(i.e. gout rare in pre-menopausal)
•Rare < age 30: unless genetic defect
•(HGPRT ↓, ↑ PRP synthetase activity)
High in elderly because:
•Prevalence of Metabolic Syndrome
•Diuretic Use
•Low dose ASA Use
42. WHO GETS GOUT?
•2x Men vs. Women
•Estrogen has mild uricosuric effect
•(i.e. gout rare in pre-menopausal)
•Rare < age 30: unless genetic defect
•(HGPRT ↓, ↑ PRP synthetase activity)
High in elderly because:
•Prevalence of Metabolic Syndrome
•Diuretic Use
•Low dose ASA Use
(Our pt had iatrogenic menopause)
50. CLINICAL PRESENTATION
•Redness, swelling, intense pain
•Fever/Chills
•Usually at night
•Monoarticular
•Commonly 1st metatarsophalangeal (Greek for “Big Toe”) joint
•Lasts 5-7 days (severe up to 2 weeks)
51. CLINICAL PRESENTATION
•Redness, swelling, intense pain
•Fever/Chills
•Usually at night
•Monoarticular
•Commonly 1st metatarsophalangeal (Greek for “Big Toe”) joint
•Lasts 5-7 days (severe up to 2 weeks)
•Can be self-limited
52. CLINICAL PRESENTATION
•Redness, swelling, intense pain
•Fever/Chills
•Usually at night
•Monoarticular
•Commonly 1st metatarsophalangeal (Greek for “Big Toe”) joint
•Lasts 5-7 days (severe up to 2 weeks)
•Can be self-limited
•Chronic ➝ polyarticular/UE
64. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
65. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
66. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
67. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
Redness of Joint
68. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
Redness of Joint
1st toe pain/swelling
69. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
Redness of Joint
1st toe pain/swelling
Unilateral tarsal joint
70. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
Redness of Joint
1st toe pain/swelling
Unilateral tarsal joint
Suspected Tophus
71. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
Redness of Joint
1st toe pain/swelling
Unilateral tarsal joint
Suspected Tophus
Hyperuricemia
72. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
Redness of Joint
1st toe pain/swelling
Unilateral tarsal joint
Suspected Tophus
Hyperuricemia
Asymmetric joint swelling on PE or XR
73. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
Redness of Joint
1st toe pain/swelling
Unilateral tarsal joint
Suspected Tophus
Hyperuricemia
Asymmetric joint swelling on PE or XR
Cysts w/o Erosions on XR
74. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
Redness of Joint
1st toe pain/swelling
Unilateral tarsal joint
Suspected Tophus
Hyperuricemia
Asymmetric joint swelling on PE or XR
Cysts w/o Erosions on XR
Negative Joint Fluid Cx
75. DIAGNOSIS
Clinical Dx (any 6 of the following)
>1 acute arthritis attack
> Max inflammation developed within a day
One joint
Redness of Joint
1st toe pain/swelling
Unilateral tarsal joint
Suspected Tophus
Hyperuricemia
Asymmetric joint swelling on PE or XR
Cysts w/o Erosions on XR
Negative Joint Fluid Cx
Urate microcystals in joint fluid during attack
83. TREATMENT
NOT Required to determine if under-
excretor or over-producer
Under or Over excreters respond to allopurinol
84. TREATMENT
NOT Required to determine if under-
excretor or over-producer
Under or Over excreters respond to allopurinol
Allopurinol Intolerance ➝ verify no Hx
of Nephrolithasis and an under-excretor
91. TREATMENT
Gouty Arthritis
NSAIDS (caution: renal disease, bleeding, ulcers, elderly)
Corticosteroids - 40 mg/day (caution: DM)
-Intra-articular Steroid Injection (Once infection R/O)
Colchicine
Most effective: one joint, <24 hrs
Normal renal function ➝ 2 or 3 six mg doses a day until
relief
92. TREATMENT
Gouty Arthritis
NSAIDS (caution: renal disease, bleeding, ulcers, elderly)
Corticosteroids - 40 mg/day (caution: DM)
-Intra-articular Steroid Injection (Once infection R/O)
Colchicine
Most effective: one joint, <24 hrs
Normal renal function ➝ 2 or 3 six mg doses a day until
relief
Avoid IV form ➝ bone marrow/neuromuscular tox