pathology & treatment of Gout
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This document provides an overview of gout, a metabolic disease characterized by high blood uric acid levels that can cause painful inflammation in joints. It discusses the production and excretion of uric acid, the pathophysiology of gout, diagnosis methods including blood tests and joint fluid aspiration, and treatment approaches for acute and chronic gout including medications that inhibit uric acid synthesis or increase excretion such as allopurinol, febuxostat, and lesinurad. The mode of action and pharmacokinetics of select medications are also summarized along with references for additional information.
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Gout Presentation
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
Basic information about Gout and Gouty arthritis, Hyperuricemia
For UnderGraduates and Orthopaedic Surgeons
gout
Gout is a metabolic disease characterized by recurrent attacks of inflammatory arthritis caused by elevated levels of uric acid in the blood. It is classified as acute or chronic gout. Risk factors include age, sex, lifestyle, medical conditions, and family history. Treatment involves drugs that inhibit uric acid synthesis like allopurinol, increase uric acid excretion like probenecid, reduce inflammation like NSAIDs, and control symptoms like colchicine. Diet, exercise, medication adherence and surgery are also used to manage gout.
Gout
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 ppt
Gout is a chronic inflammatory disease in which monosodium urate crystal precipitate in joints, soft tissues and cartilage. it is due to increase uric acid level in blood. Gout characterized by red, hot, tender and pain. Presence of MSU crystals (needle shape) in aspirated synovial fluid confirm Gout.
GOUTY ARTHRITIS
Gouty arthritis results from deposition of urate crystals in the joints due to chronic hyperuricaemia. It is most common in middle-aged men and is increasing in prevalence worldwide due to aging populations and obesity. Acute gout causes sudden, severe pain in one or few joints like the toe or ankle. Chronic gout leads to frequent attacks and tophus formation, causing permanent joint damage. Treatment involves NSAIDs to relieve pain, colchicine or uricosuric drugs to prevent attacks, and allopurinol long-term to lower urate levels and prevent complications. Lifestyle changes like weight loss, fluid intake and diet modification also help control gout.
Rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disease characterized by inflammation of the joints, especially in the hands and feet. It affects around 1% of the population and is more common in women. If left untreated, chronic inflammation can lead to joint damage and disability. Management involves reducing inflammation and pain with medications like NSAIDs, corticosteroids, and disease-modifying antirheumatic drugs (DMARDs), with the goal of achieving remission and preventing long-term joint damage and deformity.
RHEUMATOID ARTHRITIS
Rheumatoid arthritis is an autoimmune disease characterized by chronic inflammation of the joints which can lead to joint damage and physical disability. It is a progressive disease affecting the synovial lining of peripheral joints, causing symmetrical inflammation and potentially deforming polyarthritis. Symptoms include tender swollen joints, morning stiffness lasting hours, fatigue, and rheumatoid nodules under the skin. Treatment focuses on relieving pain, reducing inflammation, protecting joints, maintaining function, and controlling systemic effects through use of drugs like NSAIDs, DMARDs, biologics, glucocorticoids, and surgery.
Recommended
Gout Presentation
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
Basic information about Gout and Gouty arthritis, Hyperuricemia
For UnderGraduates and Orthopaedic Surgeons
gout
Gout is a metabolic disease characterized by recurrent attacks of inflammatory arthritis caused by elevated levels of uric acid in the blood. It is classified as acute or chronic gout. Risk factors include age, sex, lifestyle, medical conditions, and family history. Treatment involves drugs that inhibit uric acid synthesis like allopurinol, increase uric acid excretion like probenecid, reduce inflammation like NSAIDs, and control symptoms like colchicine. Diet, exercise, medication adherence and surgery are also used to manage gout.
Gout
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 ppt
Gout is a chronic inflammatory disease in which monosodium urate crystal precipitate in joints, soft tissues and cartilage. it is due to increase uric acid level in blood. Gout characterized by red, hot, tender and pain. Presence of MSU crystals (needle shape) in aspirated synovial fluid confirm Gout.
GOUTY ARTHRITIS
Gouty arthritis results from deposition of urate crystals in the joints due to chronic hyperuricaemia. It is most common in middle-aged men and is increasing in prevalence worldwide due to aging populations and obesity. Acute gout causes sudden, severe pain in one or few joints like the toe or ankle. Chronic gout leads to frequent attacks and tophus formation, causing permanent joint damage. Treatment involves NSAIDs to relieve pain, colchicine or uricosuric drugs to prevent attacks, and allopurinol long-term to lower urate levels and prevent complications. Lifestyle changes like weight loss, fluid intake and diet modification also help control gout.
Rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disease characterized by inflammation of the joints, especially in the hands and feet. It affects around 1% of the population and is more common in women. If left untreated, chronic inflammation can lead to joint damage and disability. Management involves reducing inflammation and pain with medications like NSAIDs, corticosteroids, and disease-modifying antirheumatic drugs (DMARDs), with the goal of achieving remission and preventing long-term joint damage and deformity.
RHEUMATOID ARTHRITIS
Rheumatoid arthritis is an autoimmune disease characterized by chronic inflammation of the joints which can lead to joint damage and physical disability. It is a progressive disease affecting the synovial lining of peripheral joints, causing symmetrical inflammation and potentially deforming polyarthritis. Symptoms include tender swollen joints, morning stiffness lasting hours, fatigue, and rheumatoid nodules under the skin. Treatment focuses on relieving pain, reducing inflammation, protecting joints, maintaining function, and controlling systemic effects through use of drugs like NSAIDs, DMARDs, biologics, glucocorticoids, and surgery.
Gout
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.
Gout management
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.
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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.
Rheumatoid arthritis
Rheumatoid arthritis is a chronic autoimmune disease that causes inflammation and damage to joints. It affects around 1-3% of the global population. While its exact causes are unknown, genetic and environmental factors are believed to play a role. Key symptoms include tender, warm, swollen joints and morning stiffness lasting over an hour. Diagnosis is based on criteria such as the number and location of affected joints, presence of rheumatoid factor or anti-CCP antibodies, and response to treatment. Treatment aims to control symptoms, prevent further joint damage, and improve quality of life using medications such as methotrexate, sulfasalazine, biologics that target cytokines, and newer drugs like tofacitinib. The
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GOUT
Gout is an inflammatory condition of the arthritis-type that results from deposition of monosodium urate crystals in joint spaces or surrounding tissues, leading to an inflammatory reaction that causes intense pain, erythema, and joint swelling.
It is associated with hyperuricemia, defined as a Serum Uric Acid (SUA) level of 6.8 mg/dL (404 μmol/L) or greater, but not all patients with hyperuricemia demonstrate symptoms.
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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.
Rheumatoid arthritis
This document discusses rheumatoid arthritis (RA), an autoimmune disease where the immune system attacks the synovium lining the joints, causing pain, swelling, and inflammation. It covers signs and symptoms of RA like joint stiffness and pain. Risk factors include genetics and gender, with most cases occurring between ages 35-50. Treatment involves NSAIDs, DMARDs, corticosteroids, biologics, and JAK inhibitors to reduce inflammation and slow disease progression. The pathology involves cytokines and immune cells that promote inflammation, and diagnosis is based on symptoms, physical exam, blood tests, and x-rays.
Rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disease that causes inflammation, swelling, and pain in the joints. It affects approximately 1% of the world's population and 0.92% of the adult population in India. There are two main types - seropositive RA, where the body produces immune reactions to normal tissue, and seronegative RA, where tests for rheumatoid factor and anti-CCP antibodies are negative. Risk factors include age 40-60, family history, smoking, obesity, and female sex. Diagnosis involves evaluating symptoms, x-rays of affected joints, and blood tests for rheumatoid factor and anti-CCP antibodies. Treatment includes non-pharmacological therapies as well as drugs like
Gout
introduction , clinical manifestation, diagnosis and treatment of gout ,,,,, differentiation with pseudogout...
Rheumatoid Arthritis
This document provides information about rheumatoid arthritis (RA). It discusses the following key points:
1. RA is a progressive autoimmune disorder characterized by symmetric inflammation of the joints and potential damage to cartilage and bone. It most commonly affects women between ages 35-60.
2. Symptoms include pain, swelling, and stiffness in the small joints of the hands and feet. Left untreated, it can lead to joint deformities and loss of function.
3. Treatment involves relieving pain, reducing inflammation, and slowing disease progression through medications like DMARDs, biologics, steroids, and NSAIDs. Early, aggressive treatment is important to control symptoms and prevent long-term damage.
Rhemutoid arthritis
Rheumatoid arthritis is a chronic autoimmune disease characterized by inflammation of the synovial joints, resulting in joint deformity and immobilization. It has a symmetrical and bilateral effect on joints. Symptoms include morning stiffness lasting over 30 minutes, simultaneous and symmetrical joint swelling not relieved by rest, fever, weight loss, fatigue, and enlarged lymph nodes. Diagnosis involves blood tests to check inflammatory markers and antibodies, along with x-rays, CT/MRI scans, and joint fluid analysis. Treatment focuses on relieving pain and inflammation through NSAIDs, corticosteroids, DMARDs, and biologics to prevent further joint damage.
Pathophysiology and clinical management of gouty arthritis
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.
Rhumatoide arthritis
Rheumatoid arthritis is a chronic inflammatory disorder that causes pain, stiffness, and swelling in the joints. It commonly affects the hands, feet, wrists, elbows, knees, and ankles. The disease course involves periods of exacerbation and remission. Diagnosis is based on symptoms and diagnostic criteria including involvement of specific joints and serological markers. Treatment involves nonsteroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs like methotrexate, biologic medications, and corticosteroids. Without treatment, joint destruction and deformity can occur.
Pathophysiology of Rheumatoid Arthritis
Rheumatoid arthritis is a chronic inflammatory disease that primarily affects the joints, causing swelling, warmth, pain, and stiffness. It results from an autoimmune reaction where the immune system mistakenly attacks healthy joint tissue. This leads to a proliferative synovitis that can cause cartilage and bone destruction over time. RA is characterized by symmetrical inflammation of multiple joints that typically involves the hands, feet, wrists, and knees. It has both articular and extra-articular effects and is associated with an increased risk of comorbidities such as lung or heart disease. The cause is unknown but involves genetic and environmental factors.
Rheumatoid arthritis current diagnosis and treatment
This document provides information on the diagnosis and management of rheumatoid arthritis (RA). It begins with an introduction to RA, noting that it is a chronic inflammatory joint disease affecting approximately 1% of the population. It then discusses the clinical presentation and manifestations of RA, including onset, patterns of joint involvement, and articular and extra-articular symptoms. The document reviews the diagnostic criteria for RA and covers laboratory investigations and radiographic features. It concludes with an overview of the goals and various treatment modalities for RA, including NSAIDs, corticosteroids, disease-modifying antirheumatic drugs (DMARDs), immunosuppressive therapies, and biological therapies.
F1804013742
Male and female rats were exposed to mercury (0.5, 1.0 and 1.5mg/kg) for 12 weeks to investigate the effects on antioxidant enzymes. Mercury exposure inhibited antioxidant enzymes like catalase and superoxide dismutase in a gender-specific manner. In female rats, mercury inhibited catalase and superoxide dismutase in the plasma, erythrocytes, liver and kidneys. In male rats, mercury inhibited superoxide dismutase in the liver and catalase in the kidneys. Mercury levels in tissues correlated negatively with antioxidant enzyme levels, specifically in females. The findings support that mercury exposure affects antioxidant defenses differently between males and females.
Arthritis
Rheumatoid arthritis is a chronic systemic inflammatory arthritis that affects more women than men between ages 35-45. It is characterized by inflammation of the synovium that leads to cartilage degradation and bone damage. Treatment involves non-drug approaches as well as disease-modifying anti-rheumatic drugs (DMARDs) like methotrexate which are started early to slow disease progression. Biologic agents that target cytokines like TNF have also shown effectiveness. The goal of treatment is to reduce pain and inflammation and prevent long-term joint damage.
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Gout
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.
Gout management
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.
Hyperuricemia and Gout
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Presented by Usama Ragab Youssif
For 5th-year medical students - Zagazig University
Gout 13
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.
Rheumatoid arthritis
Rheumatoid arthritis is a chronic autoimmune disease that causes inflammation and damage to joints. It affects around 1-3% of the global population. While its exact causes are unknown, genetic and environmental factors are believed to play a role. Key symptoms include tender, warm, swollen joints and morning stiffness lasting over an hour. Diagnosis is based on criteria such as the number and location of affected joints, presence of rheumatoid factor or anti-CCP antibodies, and response to treatment. Treatment aims to control symptoms, prevent further joint damage, and improve quality of life using medications such as methotrexate, sulfasalazine, biologics that target cytokines, and newer drugs like tofacitinib. The
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Gout and Hyperuricemia
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.
Gout and hyperuricemia
It includes definition, epidemiology, etiology, pathophysiology, management of Gout and Hyperuricemia
Osteoarthritis
Osteoarthritis is a non-inflammatory degenerative condition of the joints characterized by degeneration of articular cartilage and formation of new bone (osteophytes). It commonly affects the hands, knees, hips and spine. Risk factors include age, gender, obesity, injury and genetics. Symptoms include pain, stiffness, swelling and loss of flexibility. Diagnosis is made based on symptoms and confirmed with x-rays or MRI. Treatment involves medications like acetaminophen, NSAIDs, opioids and diacerein as well as complementary therapies and surgery for advanced cases.
GOUT
Gout is an inflammatory condition of the arthritis-type that results from deposition of monosodium urate crystals in joint spaces or surrounding tissues, leading to an inflammatory reaction that causes intense pain, erythema, and joint swelling.
It is associated with hyperuricemia, defined as a Serum Uric Acid (SUA) level of 6.8 mg/dL (404 μmol/L) or greater, but not all patients with hyperuricemia demonstrate symptoms.
Inflammation of arthritis type
Hyperuricemia
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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.
Rheumatoid arthritis
This document discusses rheumatoid arthritis (RA), an autoimmune disease where the immune system attacks the synovium lining the joints, causing pain, swelling, and inflammation. It covers signs and symptoms of RA like joint stiffness and pain. Risk factors include genetics and gender, with most cases occurring between ages 35-50. Treatment involves NSAIDs, DMARDs, corticosteroids, biologics, and JAK inhibitors to reduce inflammation and slow disease progression. The pathology involves cytokines and immune cells that promote inflammation, and diagnosis is based on symptoms, physical exam, blood tests, and x-rays.
Rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disease that causes inflammation, swelling, and pain in the joints. It affects approximately 1% of the world's population and 0.92% of the adult population in India. There are two main types - seropositive RA, where the body produces immune reactions to normal tissue, and seronegative RA, where tests for rheumatoid factor and anti-CCP antibodies are negative. Risk factors include age 40-60, family history, smoking, obesity, and female sex. Diagnosis involves evaluating symptoms, x-rays of affected joints, and blood tests for rheumatoid factor and anti-CCP antibodies. Treatment includes non-pharmacological therapies as well as drugs like
Gout
introduction , clinical manifestation, diagnosis and treatment of gout ,,,,, differentiation with pseudogout...
Rheumatoid Arthritis
This document provides information about rheumatoid arthritis (RA). It discusses the following key points:
1. RA is a progressive autoimmune disorder characterized by symmetric inflammation of the joints and potential damage to cartilage and bone. It most commonly affects women between ages 35-60.
2. Symptoms include pain, swelling, and stiffness in the small joints of the hands and feet. Left untreated, it can lead to joint deformities and loss of function.
3. Treatment involves relieving pain, reducing inflammation, and slowing disease progression through medications like DMARDs, biologics, steroids, and NSAIDs. Early, aggressive treatment is important to control symptoms and prevent long-term damage.
Rhemutoid arthritis
Rheumatoid arthritis is a chronic autoimmune disease characterized by inflammation of the synovial joints, resulting in joint deformity and immobilization. It has a symmetrical and bilateral effect on joints. Symptoms include morning stiffness lasting over 30 minutes, simultaneous and symmetrical joint swelling not relieved by rest, fever, weight loss, fatigue, and enlarged lymph nodes. Diagnosis involves blood tests to check inflammatory markers and antibodies, along with x-rays, CT/MRI scans, and joint fluid analysis. Treatment focuses on relieving pain and inflammation through NSAIDs, corticosteroids, DMARDs, and biologics to prevent further joint damage.
Pathophysiology and clinical management of gouty arthritis
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.
Rhumatoide arthritis
Rheumatoid arthritis is a chronic inflammatory disorder that causes pain, stiffness, and swelling in the joints. It commonly affects the hands, feet, wrists, elbows, knees, and ankles. The disease course involves periods of exacerbation and remission. Diagnosis is based on symptoms and diagnostic criteria including involvement of specific joints and serological markers. Treatment involves nonsteroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs like methotrexate, biologic medications, and corticosteroids. Without treatment, joint destruction and deformity can occur.
Pathophysiology of Rheumatoid Arthritis
Rheumatoid arthritis is a chronic inflammatory disease that primarily affects the joints, causing swelling, warmth, pain, and stiffness. It results from an autoimmune reaction where the immune system mistakenly attacks healthy joint tissue. This leads to a proliferative synovitis that can cause cartilage and bone destruction over time. RA is characterized by symmetrical inflammation of multiple joints that typically involves the hands, feet, wrists, and knees. It has both articular and extra-articular effects and is associated with an increased risk of comorbidities such as lung or heart disease. The cause is unknown but involves genetic and environmental factors.
Rheumatoid arthritis current diagnosis and treatment
This document provides information on the diagnosis and management of rheumatoid arthritis (RA). It begins with an introduction to RA, noting that it is a chronic inflammatory joint disease affecting approximately 1% of the population. It then discusses the clinical presentation and manifestations of RA, including onset, patterns of joint involvement, and articular and extra-articular symptoms. The document reviews the diagnostic criteria for RA and covers laboratory investigations and radiographic features. It concludes with an overview of the goals and various treatment modalities for RA, including NSAIDs, corticosteroids, disease-modifying antirheumatic drugs (DMARDs), immunosuppressive therapies, and biological therapies.
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F1804013742
Male and female rats were exposed to mercury (0.5, 1.0 and 1.5mg/kg) for 12 weeks to investigate the effects on antioxidant enzymes. Mercury exposure inhibited antioxidant enzymes like catalase and superoxide dismutase in a gender-specific manner. In female rats, mercury inhibited catalase and superoxide dismutase in the plasma, erythrocytes, liver and kidneys. In male rats, mercury inhibited superoxide dismutase in the liver and catalase in the kidneys. Mercury levels in tissues correlated negatively with antioxidant enzyme levels, specifically in females. The findings support that mercury exposure affects antioxidant defenses differently between males and females.
Arthritis
Rheumatoid arthritis is a chronic systemic inflammatory arthritis that affects more women than men between ages 35-45. It is characterized by inflammation of the synovium that leads to cartilage degradation and bone damage. Treatment involves non-drug approaches as well as disease-modifying anti-rheumatic drugs (DMARDs) like methotrexate which are started early to slow disease progression. Biologic agents that target cytokines like TNF have also shown effectiveness. The goal of treatment is to reduce pain and inflammation and prevent long-term joint damage.
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Crimson Publishers: Dietary Supplements as a Possible Trigger of Autoimmune H...
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Introduction: Autoimmune hepatitis (AIH) etiology remains unknown, but in genetically predisposed individuals, diverse agents may trigger the disease. Herbal and drug induced AIH have been reported in recent years probable due to the increase in self-medication. More studies are necessary to define if drugs and herbal/dietary supplements unmask and induce AIH or drug-induced hepatitis with autoimmune features.
Purpose: We report an autoimmune hepatitis case possibly induced by herbal/dietary supplements intake.
Case-report: A 55-year-old female presented with a 15-day course of jaundice and increased aminotransferases. Immunologic panel showed antinuclear antibody titer of 1:320 and serum immunoglobulin G (IgG) level approximately 2 times the upper limit of normal. She reported regular daily ingestion of Herbalife® products for 6 months which were discontinued when symptoms began. Laboratory tests worsened despite the fact that patient had stopped supplements usage, and a liver biopsy was performed. Histology was suggestive of both AIH and drug induced liver disease. The patient fulfilled criteria for probable AIH based on the revised criteria for diagnosing autoimmune hepatitis, and improved with prednisolone and azathioprine therapy, with progressive laboratory improvement and symptoms remission.
Discussion: Herbal/dietary supplements induced AIH has been previously reported, but the causality is not yet well established. Worsening of aminotransferases despite supplement suspension, histological findings and favorable response with corticosteroid treatment, supported the hypothesis of AIH induced by the used supplement. This case report aims to demonstrate the possible causality between herbal/dietary supplements and liver injury, including autoimmune hepatitis.pharmacology-gitdrugs.ppt
1. The document discusses various drugs used to treat gastrointestinal disorders such as acid peptic diseases, gastrointestinal motility issues, constipation, diarrhea, and irritable bowel syndrome.
2. It covers classes of drugs including proton pump inhibitors, H2 receptor antagonists, prostaglandin analogs, cytoprotectants, antacids, laxatives, and antidiarrheal agents.
3. The mechanisms of action, pharmacokinetics, side effects and drug-drug interactions of these different drug classes are explained in detail.
Gouty Athritis , Cause of painful joints ,pseudo gout
This document describes the case of a 41-year-old male presenting with bilateral knee swelling and pain for 10 days. His medical history includes a similar illness 7-8 years ago and a history of heavy alcohol consumption. On examination, he has flushed face, icteric eyes, and tender, swollen knees bilaterally. Laboratory tests show elevated uric acid, liver enzymes, and inflammatory markers. X-rays and microscopy confirm chronic tophaceous gout with an acute gout flare. He is treated with anti-inflammatory medications, urate-lowering therapy, and supportive care, and discharged after 8 days with resolution of symptoms.
Hepatoprotective and antioxidant effects of Azolla microphylla based gold nan...
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Abstract
Objective(s):
Our present study sought to evaluate hepatoprotective and antioxidant effects of methanol extract of Azolla microphylla phytochemically synthesized gold nanoparticles (GNaP) in acetaminophen (APAP) - induced hepatotoxicity of fresh water common carp fish.
Materials and Methods:
GNaP were prepared by green synthesis method using methanol extract of Azolla microphylla. Twenty four fishes weighing 146 ± 2.5 g were used in this experiment and these were divided into four experimental groups, each comprising 6 fishes. Group 1 served as control. Group 2 fishes were exposed to APAP (500 mg/kg) for 24 h. Groups 3 and 4 fishes were exposed to APAP (500 mg/kg) + GNaP (2.5 mg/kg) and GNaP (2.5 mg/kg) for 24 h, respectively. The hepatoprotective and antioxidant potentials were assessed by measuring liver damage, biochemical parameters, ions status, and histological alterations.
Results:
APAP exposed fish showed significant elevated levels of metabolic enzymes (LDH, G6PDH and MDH), hepatotoxic markers (GPT, GOT and ALP), reduced hepatic glycogen, lipids, protein, albumin, globulin, increased levels of bilirubin, creatinine, and oxidative stress markers (TBRAS, LHP and protein carbonyl), altered the tissue enzymes (SOD, CAT, GSH-Px and GST) non-enzyme (GSH), cellular sulfhydryl (T-SH, P-SH and NP-SH) levels, reduced hepatic ions (Ca2+, Na+ and K+), and abnormal liver histology. It was observe that GNaP has reversal effects on the levels of above mentioned parameters in APAP hepatotoxicity.
Conclusion:
Azolla microphylla phytochemically synthesized GNaP protects liver against oxidative damage and tissue damaging enzyme activities and could be used as an effective protector against acetaminophen-induced hepatic damage in fresh water common carp fish.04_IJPBA_1841_20.pdf
This document summarizes a study that investigated the effects of administering aqueous extracts of white grub and white grub waste to diabetic rats over two weeks. Key findings include:
1) After the first week, the extract-treated groups showed significant reductions in several liver enzyme and protein levels compared to the untreated diabetic group. Renal parameters were also significantly lower in the extract-treated groups.
2) After the second week, the extract-treated groups continued to show significant reductions in most liver enzymes and proteins compared to the untreated diabetic group. One extract provided more benefits than the other.
3) For renal parameters after two weeks, one extract-treated group showed significantly lower levels of parameters like urea and electroly
Effect of Aqueous Administration of White Grub and Waste Extract on the Level...
Effect of Aqueous Administration of White Grub and Waste Extract on the Level...BRNSS Publication Hub
Introduction: The liver plays a major role in the regulation of carbohydrate metabolism, as it uses glucose as a fuel and kidneys are to excrete metabolic waste products as well as to maintain water, pH, electrolyte balance, production of calcitriol, and hemopoietin. Aim: This study aims to investigate the effect of the administration of white grub and waste on liver and kidney indices on diabetic rats. Materials and Methods: The rats were induced with diabetes by alloxanization and treated with the extracts of white grub and waste for 2 weeks. A total of 25 rats used, were randomly distributed into five groups (G1-G5) each with five rats. G1 served as normal control. G2-G5 served as diabetic control. At the end of the 1st week of extract administration, two animals from each group were randomly selected and sacrificed. At the end of the 2nd week, the remaining three animals from each group were also sacrificed and serum was collected for the determination of liver function indices (serum alkaline phosphatase [ALP], alanine aminotransferase [ALT], aspartate aminotransferase [AST] total bilirubin [TB], direct bilirubin [DB], total protein [TP], albumin [ALB], and globulin [GLB]) and kidney function parameters (urea, creatinine, and electrolyte [sodium “Na,” potassium “K,” bicarbonate “HCO3,” and chloride “Cl”]). Results: After the 1st week, the extract-treated group (G4 and G5) showed significant reductions of ALP, ALT, AST, TP, GLB, and ALB while TB and DB have normal value compared to diabetic untreated group and for renal function (G4 and G5) showed significantly lower levels of urea, Na, K, HCO3, creatinine, and Cl. After the 2nd week, the extract-treated group showed significant reductions of ALP, ALT, AST, DB, TP, ALB, and TB with significant increased levels of GLB and TP compared to diabetic untreated group (G2). G4 (extract treated) showed significantly (P < 0.05) lower levels of urea, Na, Cl, HCO3, and creatinine and with significant increased K levels compared to G2. G5 also extract-treated group indicates significant lower levels of urea, Cl, Na, and HCO3 and higher levels of creatinine and K compared to G2. Conclusion: These results suggest that the administration of aqueous extract of white grub and waste did not have any adverse effect on the liver and kidney functions in diabetic rats. The extracts have positive effect which showed that G4 (treated with whole white grub [WG]) is more effective compared to G5 (treated with WG waste).04_IJPBA_1841_20.pdf
This study investigated the effects of administering aqueous extracts of white grub and its waste on liver and kidney function in diabetic rats. Rats were induced with diabetes and treated with the extracts or a diabetes drug for 2 weeks. After both 1 week and 2 weeks of treatment:
- Liver enzymes and proteins were significantly lower in extract-treated groups compared to untreated diabetic rats, indicating protective effects on the liver.
- Kidney parameters like urea and electrolytes were also significantly lower in extract-treated groups, showing renal protection.
- The whole white grub extract seemed to have slightly better effects than the waste extract alone.
- Both extracts appeared to have positive impacts on liver and kidney function in diabetic rats
4
The document summarizes a study on the effects of cypermethrin pesticide on rabbit biochemistry and liver/kidney histology. Rabbits received low, medium, or high doses of cypermethrin intraperitoneally over 71 days. Blood samples were analyzed for liver and kidney enzymes/proteins. Liver and kidney tissues were examined histologically. Results showed cypermethrin increased liver enzymes and urea/creatinine levels in blood in a dose-dependent manner, indicating liver and kidney damage. Histological examination found corresponding dose-dependent lesions in the liver (degeneration, bile duct hyperplasia) and kidneys (necrosis, cast deposition, increased urinary space), confirming cyper
Liver cirrhosis.2018
55-year-old Abdullah presents with severe gastrointestinal bleeding. He has a history of jaundice and worsening fatigue, appetite, and health over the past 8 years. On examination, he has signs of liver disease including jaundice, edema, enlarged veins in the abdomen, and a small, rough liver. Laboratory tests show abnormal liver function tests, low blood counts, and coagulopathy. Based on the history and examination, Abdullah likely has cirrhosis of the liver complicated by gastrointestinal bleeding. He will need treatment to manage the acute bleeding and long-term management to prevent further complications of his cirrhosis.
Anti-diabetic - 복사본
1) The study characterized the hypoglycemic effects of a glycoprotein purified from the edible brown seaweed Undaria pinnatifida (UPGP).
2) UPGP showed dose-dependent inhibition of yeast and rat intestinal alpha-glucosidase enzymes, with IC50 values of 0.11 and 0.29 mg/mL, respectively.
3) UPGP inhibition of alpha-glucosidase was stable under different temperatures and when exposed to metal ions. UPGP inhibition decreased slightly during gastric digestion but increased during duodenal digestion.
Whey protein products and their combination with L-methionine prevent liver f...
The IOSR Journal of Pharmacy (IOSRPHR) is an open access online & offline peer reviewed international journal, which publishes innovative research papers, reviews, mini-reviews, short communications and notes dealing with Pharmaceutical Sciences( Pharmaceutical Technology, Pharmaceutics, Biopharmaceutics, Pharmacokinetics, Pharmaceutical/Medicinal Chemistry, Computational Chemistry and Molecular Drug Design, Pharmacognosy & Phytochemistry, Pharmacology, Pharmaceutical Analysis, Pharmacy Practice, Clinical and Hospital Pharmacy, Cell Biology, Genomics and Proteomics, Pharmacogenomics, Bioinformatics and Biotechnology of Pharmaceutical Interest........more details on Aim & Scope).
04_IJPBA_1841_20.pdf
This study investigated the effects of administering aqueous extracts of white grub and white grub waste to diabetic rats over two weeks. Biochemical analysis found that after one week, the extract-treated groups showed improvements in liver and kidney function indices compared to the untreated diabetic group. After two weeks, the white grub extract provided even greater benefits, lowering levels of liver enzymes and improving other liver and kidney parameters. The results suggest that the white grub extract did not harm liver or kidney function in diabetic rats and appeared to have protective effects.
CATABOLISM OF PURINE NUCLEOTIDES
Pawde Laxman presents on the catabolism of purine nucleotides. Purines are broken down through multiple steps into uric acid by enzymes like xanthine oxidase. Uric acid is then excreted. Disorders can occur if uric acid levels become too high, such as gout which causes painful joint inflammation and hyperuricemia. Gout treatment focuses on reducing uric acid through drugs inhibiting xanthine oxidase and dietary changes while anti-inflammatory drugs help gout symptoms.
Dietary Supplementation with Calcium in Healthy Rats Administered with Artemi...
Reports on the role of calcium on predisposition to cardiovascular disease have been rather inconsistent while studies on its interaction with other medications are ongoing. We therefore investigated the effect of separate and combine administration of calcium supplement with artemisinin-based combination drug on hepatic and serum lipid profile. Thirty two male wistar rats were randomly assigned into four groups of eight rats each. The control (group A) received normal saline. Group B and D were placed on 10mg/Kg calcium twice daily for four weeks. On the thirtieth day, therapeutic dose of artemisinin-based combination was simultaneously administered to group C and group D twice daily for three days. All the rats were then sacrificed after 12 hours fasting, blood was withdrawn and the liver removed and homogenized in an appropriate buffer. Biochemical analysis showed no significant (p>0.05) variation in hepatic triaacylglycerol in all the treated groups whereas calcium supplementation was observed to induce a significant (p<0.05) reduction in hepatic cholesterol. Significant elevations due to calcium supplementation were also observed in serum total cholesterol, LDL cholesterol level and atherogenic risk index with a concomitant reduction in serum HDL cholesterol. No significant change was observed in serum total cholesterol, triacylglycerol and serum lipoproteins in all other treatment groups. Our study suggests that calcium supplementation may predispose to cardiovascular disease and that its co administration with ACT may not aggravate nor reduced the predisposition risk.
SHER-E-KASHMIR UNIVERSITY OF AGRICULTURAL SCIENCES AND TECHNOLOGY, KASHMIR.pptx
This case study evaluated the hepatoprotective effects of formulations containing extracts of Berberis aristata, Solanum nigrum, and Aloe vera (Formulation A), and a decoction of Phyllanthus fraternus (Formulation B), on patients receiving antitubercular treatment. Patients taking the formulations showed no significant increases in liver enzymes, while the control group showed significant increases. The formulations helped prevent antitubercular treatment-induced hepatotoxicity and allowed patients to complete their treatment courses.
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Lactic acidosis (LA) is a type of metabolic acidosis caused by lactic acid buildup in the body. There are two main types - type A due to tissue hypoxia, and type B which is not caused by hypoxia. Type B includes subtypes B1 associated with underlying diseases, B2 caused by certain drugs and toxins, and B3 involving inborn errors of metabolism. LA can be diagnosed through patient history, symptoms, and laboratory tests showing acidosis and elevated lactate levels. Treatment focuses on addressing the underlying cause, improving oxygen delivery for type A, and correcting metabolic or drug issues for type B. Prognosis depends on the severity and underlying condition, with mortality rates over 60
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pathology & treatment of Gout
- 1. RAEBARELI Prepared by :- Gulam Navi Azad MS Pharma 1st year August 31,2018 Pharmacology & Toxicology National Institution Pharmaceutical Education & Research 1 1/27/2019
- 2. CONTENTS Introduction Fate of Uric acid Pathophysiology of Gout Diagnosis Treatment References 2 1/27/2019
- 3. INTRODUCTION Metabolic disease High blood uric acid Monosodium urate stones in joints, kidney& some soft tissues Its inflammatory disease Normal value of uric acid (2-6 mg/dl) Symptoms 1. Joints Pain 2. Swelling in the joints 3. Stiffness 4. Physical deformities 3 1/27/2019
- 4. RNA DNA purine hypoxanthine xanthine uric acid (low water soluble) PRODUCTION OF URIC ACID PRPP Xanthine oxidase Xanthine oxidase 4 1/27/2019 URATE EXCRETION HOAT 3 ( human renal organic anion transporter) 1. HUAT1 2. HUAT2 3. URAT1
- 5. 5 Fig :- Uric acid crystals ( source of Gout DR. G.Callie & DR. Michael B) 1/27/2019 GOUT PRIMARY GOUT SECONDARY GOUT TYPES OF GOUT
- 6. 6 PATHOPHYSIOLOGY OF GOUT Fig:- 94 etiology of &pathogenesis of hyperuricemia of gout Robert T. Keenan& Michael h.Pillinger 1/27/2019
- 7. 7 DIAGNOSIS JOINT FLUIDS ASPIRATION BLOOD TEST (SERUM URIC ACID LEVELS) X -RAYS 1/27/2019
- 8. TREATMENT OF GOUT Acute gout 1. NSAIDS 2. Colchicine 3. Corticosteroids Chronic gout 1. Inhibition of uric acid synthesis Allopurinol Febuxostate 8 1/27/2019
- 9. 2. Increase the uric acid excretion Probencid Sulphinpyrazole o IL 1bita inhibitors o Anakinra o Rilonacept o Canakinumab New treatment for gout 1. Pegloticase 2. Losartan ( URAT1 & GLUT9) 3. Fenofibrate ( URAT1) 4. Lesinurad 5. Ulodesine (under trial 3 phase) 6. Levotofisopam (under trial 2 phase) 9 1/27/2019
- 10. MODE OF ACTION Allopurinol Xanthine oxidase inhibitor Metabolism: liver (80% oxipurinol, 10% allopurinol) Elimination half-life: 2 h (oxipurinol 18-30 h) Febuxostat Potent than allopurinol Elimination half-life: ~5-8 hour Pregnancy category: US: C) Metabolism: via CYP1A2, 2C8, 2C9, UGT1A1 Lesinurad (200mg) USFDA approval on 22 Dec 2015 URAT 1 transporter inhibitors Combination with allopurinol 10 1/27/2019 Purine catabolism Hypoxanthine Xanthine Xanthine Oxidase uric acid Allopurinol
- 11. REFERENCES11 1. Saag KG, Mikuls TR, Abbott J. The Epidemiology of Gout and Calcium Pyrophosphate Dihydrate Deposition Disease in: Wortmann RL ed. Crystalinduced arthropathies: gout, pseudogoutand apatite- associated syndromes. Taylor and Francis 2006; 7-36. 2. Aromdee E, Michet C, Crowson C, O’FallonM, Gabriel S. Epidemiology of gout: isthe incidence rising? J Rheumatol 2002;29:2403–2406. 3. Wallace KL, Riedel AA, Joseph-Ridge N,Wortmann R. Increasing prevalence of goutand hyperuricemia over 10 years amongolder adults in a managed care population.J Rheumatol 2004; 31:1582–7. 4. Choi HK, Mount DB, Reginato AM.Pathogenesis of gout. Ann Intern Med 2005; 143:499. 5. Becker MA, Jolly M. Clinical gout andthe pathogenesis of hyperuricemia. In.Koopman W.J., Moreland L.W., ed. Arthritisand Allied Conditions: A Textbook of Rheumatology, (ed. 15) Lippincott Williamsand Wilkins Philadelphia, PA2005: 2303-39. 1/27/2019
- 12. 12 1/27/2019