Updated hyperuricemia
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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.
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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.
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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
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.
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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.
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For UnderGraduates and Orthopaedic Surgeons
Hyperuricemia and gout
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 and the kidneys
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.
Gout present by sarim .....
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.
Relationship between Adiposity, inulin resistance and gout.
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.
Gout - all you need for primary care
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
Gout
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 & its treatment by srota dawn
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 Hyperuricemiadbm
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.
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.
ICD Revision Beta 2013 - Internal Medicine
This is a presentation on ICD Revision current status in Internal Medicine TAG summarizing the latest developments in Beta Phase including the Review Process, Field Trials and next steps
Gout & Hyperuricemia
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.
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Relationship between Adiposity, inulin resistance and gout.
Relationship between Adiposity, inulin resistance and gout.
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Correlations of Serum Level of 25(OH)D and Bone Mineral Density (BMD) among c...International Multispeciality Journal of Health
—Chronic patients of spinal cord injury has been detected severe reduction of bone density. Patients with SCI show mostly osteopenia or osteoporosis of the hip and spine. Vitamin D deficiency may contribute to development of osteoporosis in SCI. So a study was conducted on 100 chronic SCI patients to find out status of correlation of Vitamine D and bone mineral density (BMD). Blood samples were collected and investigated routine biochemistry with serum 25(OH)D. DXA scan of hip and spine was also done. This study observed that 55% patients had suboptimal vitamin D. Positive correlation was found between vitamin D & bone mineral density. It is concluded from this study that monitoring of Serum 25(OH)D levels and annual surveillance of bone mineral density is crucial among persons with chronic SCI to reduce progression of osteoporosis and minimize the risk for further fractures. Keywords: 25(OH)D: 25 Hydroxy Vitamin D, DXA: Dual Energy X-Ray Absorptiometry, BMD: Bone Mineral Density.Distinguished Professor Lecture
The document summarizes the work of the Linus Pauling Institute at Oregon State University over the past 13 years. It discusses the Institute's focus on determining the roles of micronutrients, antioxidants, and other dietary factors in promoting optimal health and preventing disease. Key areas of research include cancer prevention, cardiovascular health, aging, and the protective effects of certain foods/compounds against oxidative stress and inflammation. The Institute has grown from half a researcher in 1996 to 12 full researchers and 4 research assistants currently. The work described emphasizes the important influence of diet and lifestyle on gene expression and chronic disease risk, beyond just genetic factors.
Effects of Different Proportions of Salvianolic Acid and Hydroxysafflor Yello...
In this experiment, SD rats were injected intravenously with different proportions of test samples to observe the protective effect of intravenous injection of pituitrin (PIT) that induced myocardial ischemia in rats, and to determine the lipid peroxidation product of Malondialdehyde (MDA) in rat brain and the content and activity of Superoxide Dismutase (SOD), Creatine Kinase (CK) and Lactate Dehydrogenase(LDH). The role of the anti–myocardial ischemia model in the test and its optimal ratio were studied. Each group of test samples was injected through the tail vein and the Ⅱ lead ECG was traced. After injection for 30 min, the rats were sublingually injected with 2U/kg pituitrin, and Ⅱ lead ECG was recorded for 5 min. After 3 hours’ observation, the rats were sacrificed from the cervical spine, and the hearts were removed and placed in a refrigerator at –20 °C to measure various biochemical indicators. Intravenous injection of each group of tested products has the effect of reducing the content of MDA, LDH, and CK in myocardial tissue, which can enhance the activity of SOD in myocardial tissue, and has statistical significance compared with the model group (P≤0.05 or P≤0.01). Through comprehensive comparison, the A:B=1:10 dose group was found to have the best results.
Optemising hd prescription 2018
This document discusses optimizing dialysis outcomes through various aspects of dialysis prescription and management. It covers:
1. Providing adequate dialysis dose as measured by Kt/V targets of 1.2-1.4 to reduce mortality risk and ensure solute clearance.
2. Controlling fluid status and electrolytes through achieving dry weight targets, avoiding excessive fluid gains and sodium intake between sessions.
3. Managing anemia through iron supplementation and erythropoiesis-stimulating agents to maintain hemoglobin in target ranges.
4. Addressing other factors like nutrition, blood pressure control, and bone mineral disease management to further optimize patient outcomes on dialysis.
Managing comorbidities in heart failure
heart failure , comorbidities , niddm , sglt2, coronary artery disease, chronic kidney disease, iron deficiency
Role of Antioxidant in Rheumatoid Arthritis
introduction:
Rheumatic diseases
RH and its histopathology
pathophysiology
complications
symptoms
diagnosis
treatment
medication
|
Nutrition & RA:
MNT
Oxidative stress
Antioxidant status
Dietary antioxidants
Antioxidant supplement
|
Studies
Raccomandazioni della iof (international osteoporosis foundation) sull’impieg...
This position paper from the International Osteoporosis Foundation makes recommendations for vitamin D intake in older adults. Based on randomized controlled trials, daily vitamin D intake of 20-25 μg (800-1000 IU) is estimated to achieve a target serum 25OHD level of 75 nmol/L (30 ng/ml), which is associated with reduced risk of falls and fractures. Higher daily intakes may be needed for those with risk factors like obesity, limited sun exposure, or malabsorption. Doses above 20 μg/day have not been thoroughly evaluated, so higher intakes cannot be generally recommended at this time.
Vitamin D deficiency and nutritional management of patients within FLS_Slidek...
This document summarizes a presentation on vitamin D and nutritional management of patients in fracture liaison services. It discusses:
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- Recommendations that vitamin D levels below 30 ng/ml are insufficient for fracture prevention and muscle function. Supplementation with calcium and vitamin D can reduce fracture risk.
- The importance of adequate protein intake of 0.8-1.3 g/kg daily for older adults to prevent sarcopenia and fractures. Malnutrition in hospitals can increase risks of poor outcomes.
- Fracture liaison services provide an opportunity to address secondary fracture prevention through vitamin D and nutritional
180e9b4f-ef1f-468e-adba-790bc4a151f3-160809053930.pdf
Iron deficiency anemia (IDA) is the most common type of anemia globally, affecting approximately 1.6 billion people. It results from prolonged negative iron balance in the body due to inadequate intake, decreased absorption, increased demand, or losses. Diagnosis involves a complete blood count and serum iron studies showing microcytic anemia and low iron stores. Treatment focuses on oral iron supplementation of 200 mg elemental iron daily for 3-6 months to replenish stores and resolve symptoms, with intravenous options for intolerances or malabsorption. Education aims to prevent recurrences through lifestyle modifications.
180e9b4f-ef1f-468e-adba-790bc4a151f3-160809053930.pdf
This document discusses iron deficiency anemia (IDA), including its definition, epidemiology, etiology, diagnosis, and treatment. Some key points include:
- IDA is the most common type of anemia worldwide, affecting approximately 1.6 billion people. It occurs when iron levels and stores in the body are depleted.
- Risk factors for IDA include blood loss, inadequate iron intake, increased iron demands, and impaired iron absorption. Young children, women of childbearing age, and those with chronic blood loss are most at risk.
- IDA is diagnosed based on low hemoglobin and iron indicator levels. Treatment involves oral or intravenous iron supplementation to replenish iron stores. Managing the underlying cause is also important for preventing
Update on the 18th International Conference on Co-morbidities and Adverse Dru...
Update on the 18th International Conference on Co-morbidities and Adverse Dru...UC San Diego AntiViral Research Center
The document summarizes key points from the 18th International Conference on Co-morbidities and Adverse Drug Reactions in HIV. It discusses findings related to bone health, cardiovascular health, and physical activity levels in people living with HIV. Regarding bone health, studies showed bone mineral density loss with tenofovir-containing antiretroviral therapy and PrEP. Loss was also seen with glucocorticoid use. For cardiovascular health, studies suggested lower risk of atherosclerotic events with NNRTI-based initial ART and possible lower risk with atazanavir. Physical activity levels were associated with comorbidity risk, with higher risk at lower activity levels.Iron Deficiency Anemia (IDA)
IDA is the most common form of anemia worldwide, affecting approximately 50% of anemia cases. It results from prolonged negative iron balance in the body due to factors like inadequate iron intake, decreased absorption, increased demand, or blood loss. Diagnosis involves a complete history, physical exam, and lab tests showing low indicators of iron stores like serum ferritin and iron, along with an elevated TIBC. Treatment aims to replenish iron stores and typically consists of oral iron supplementation of 200mg elemental iron per day for 3-6 months.
Dr. Maureen McMahon Presents "“Heart Disease and Preventive Measures” at Lupu...
Pro-inflammatory HDL (piHDL) may help predict risk of atherosclerosis (ATH) in patients with systemic lupus erythematosus (SLE). The study found 45% of SLE patients and none of the healthy controls had piHDL. PiHDL was significantly associated with carotid plaque and greatly increased the risk of plaque in SLE patients. Traditional risk factors did not fully explain the risk of ATH in SLE. PiHDL could be a useful marker for predicting ATH risk in SLE patients. Further research is needed to develop new treatments targeting piHDL and risk profiles including piHDL.
Hyperhomocysteinemia and its implications in atherosclerosis ppt copy (2) ...
This document discusses hyperhomocysteinemia and its implications for atherosclerosis in India. It begins by defining homocysteine and its metabolism. It then discusses the various causes of hyperhomocysteinemia, including genetic and nutritional factors. It notes the high prevalence of hyperhomocysteinemia in India compared to worldwide, due to common vegetarian diets, vitamin deficiencies, genetic factors like MTHFR deficiency, and environmental factors. It discusses the mechanisms by which hyperhomocysteinemia promotes atherosclerosis and cardiovascular disease. It concludes by summarizing various Indian studies finding associations between hyperhomocysteinemia and more severe, premature, and fatal coronary artery disease.
ANEMIA_IN_CKD.pptx
This document discusses anemia in chronic kidney disease (CKD). It notes that anemia is associated with increased risks of cardiac disease, stroke, mortality, and hospitalization in CKD patients. The main causes of anemia in CKD are decreased erythropoietin production and iron deficiency/restriction. Evaluation involves assessing red blood cell indices, iron status, and ruling out other causes. Management includes red blood cell transfusions, erythropoiesis-stimulating agents (ESAs) like epoetin alfa and darbepoetin alfa, and iron therapy. ESAs effectively treat anemia in CKD and reduce transfusion needs but must be used cautiously due to potential cardiovascular risks with high hem
What are we missing in CKD-MBD management? - prof. Magdy El Sharkawy
This document discusses gaps in the current definitions and management of chronic kidney disease-mineral and bone disorder (CKD-MBD). It notes that while CKD-MBD is now defined more broadly than just renal osteodystrophy, clinical definitions are still lacking. Guidelines for phosphorus management need clarification on organic vs. inorganic phosphorus and dialysate calcium guidelines could be more precise. Role of magnesium and biomarkers like alkaline phosphatase are underexplored. PTH assays and their relationship to bone remodeling is also in need of better definition. Overall, this highlights several areas where CKD-MBD understanding and treatment could be improved.
1. Gallieni CKD.MBD 2006.pdf
This document summarizes the concept of chronic kidney disease-mineral and bone disorder (CKD-MBD). It defines CKD-MBD as a systemic disorder due to abnormalities in calcium, phosphorus, PTH, or vitamin D metabolism, as well as abnormalities in bone health and soft tissue calcification. The document then discusses key aspects of CKD-MBD pathogenesis including the roles of phosphorus retention, PTH, FGF23, and vitamin D. It highlights the importance of controlling phosphorus levels even in early CKD to prevent downstream effects on bone and mineral metabolism.
orthopedics.pdf
This document discusses the importance of vitamin D and other micronutrients for orthopedic patients. It summarizes that vitamin D plays a key role in bone metabolism and calcium homeostasis. Vitamin D deficiency has been linked to impaired fracture healing and increased risk of falls. The document recommends maintaining vitamin D levels of 30-35 ng/mL or higher for optimal bone health in orthopedic patients. Other micronutrients discussed include calcium and the roles of various vitamins and minerals in bone health and orthopedic outcomes.
Cardiorenal syndrome DR Osama EL-Shahat
1. Cardio-renal syndrome (CRS) describes conditions where acute or chronic dysfunction in one organ induces acute or chronic dysfunction in the other organ.
2. Management of CRS is challenging and involves diuretics, ACE inhibitors, beta blockers, and dialysis. However, treatment outcomes remain poor, with high mortality and rates of rehospitalization.
3. While advances have been made, CRS continues to significantly impact morbidity and mortality. Early multidisciplinary management may help improve outcomes, but effective new therapies are still needed to better treat and prevent this challenging condition.
Conti Laura. Emicrania e Trombofilia. ASMaD 2011
1. The document discusses the relationship between migraine and thrombofilia, specifically looking at the MTHFR C677T polymorphism which is associated with higher homocysteine levels and cardiovascular disease risk.
2. One study found the TT genotype was less common in migraine patients but conferred higher risk of ischemic stroke in those with migraine with aura.
3. A meta-analysis found conflicting data on the association between migraine and the C677T polymorphism with high heterogeneity between studies related to ethnicity.
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Webinar interventions Dr Abdallah Allam
provides basic knowledge of ultrasound guided interventions and used injectants
Hosted by : smile makers
Sponsored by hyalomed
Ultrasound Guided Minimally Invasive Interventions for the Common Painful Con...
Ultrasound guided minimally invasive interventions can effectively treat common painful hand and wrist conditions like carpal tunnel syndrome, trigger finger, and de Quervain's disease. For carpal tunnel syndrome, a study of 129 patients found 100% had relief of symptoms after ultrasound-guided injections with no complications. For trigger finger, ultrasound-guided injections and partial releases provided relief in 81.7% of patients at 6-month follow up. For de Quervain's disease, ultrasound-guided injections and releases led to 91.4% relief within 1 month and no recurrences at 6-month follow up. The techniques allow for accurate needle placement and treatment of these painful conditions with minimal invasiveness and good patient outcomes.
Ultrasound Guided Botulinum Toxin Injection and Nerve Block for Management of...
Presented at the annual congress of the Tunisian society of Physical Medicine and Rehabilitation.
Disclosure: Sponsored by IPSEN Tunisia
Case presentation. Cairo MSK US grand-round 9-2018
A 26-year-old right-handed female presented with chronic bilateral hand tingling. Ultrasound revealed bilateral carpal tunnel syndrome caused by extension of the myotendinous junction of the flexor digitorum superficialis tendons of the index and middle fingers on both sides. Surgery was performed to address the condition.
Ultrasound guided intervention treatment for knee osteoarthritis: Tips and T...
Ultrasound guided treatment can help with knee osteoarthritis. It is important to visualize the needle and scan the knee before injecting medications. The proper injectate choice depends on the stage of osteoarthritis - corticosteroids, hyaluronic acid, platelet-rich plasma, or Botox may be used. Early stage patients may benefit from dry needling or PRP while moderate cases use PRP with hyaluronic acid and advanced or systemic cases use bone marrow concentrate or laser ablation synovectomy. Injections can also target the adductor canal, popliteal plexus or genicular nerves. Proper technique is important for successful treatment.
Case presentation ESRD 40th
This document describes a case study of a 38-year-old female farmer who was diagnosed with De Quervain's tenosynovitis (DQT) in her right wrist. She was initially treated with NSAIDs and corticosteroid injections, which provided only temporary relief. When her symptoms recurred and surgery was recommended, she was instead treated with ultrasound-guided injections of methotrexate into her wrist. This led to gradual improvement in her pain levels over subsequent weeks and months, with no pain reported after 10 months. The document discusses DQT and the rationale for using methotrexate injections as an alternative to surgery or repeated corticosteroid injections.
Ultrasound guided interventions; Knee - Ankle - Foot
This document discusses various musculoskeletal conditions including osteoarthritis of the knee, posterior tibial tendon dysfunction, and plantar fasciopathy. It then outlines pharmacological treatments for pain such as local anesthetics, corticosteroids, and hyaluronic acid. Regenerative medicine techniques are also mentioned including dry needling, platelet rich plasma, and stem cells. Potential complications of interventions like neurovascular injury, allergic reactions, vasovagal responses, and infection are briefly listed.
Ultrasound guided interventions for the Brachial Plexus
This document discusses various types of arm pain including those caused by neurovascular injury, allergy, and vasovagal responses as well as drug related issues. It then categorizes arm pains into those originating from the spine such as radicular pain or complex regional pain syndrome, and those involving the shoulder, elbow, forearm, hand and wrist. Finally, it recommends selective root blocks for treating radiculopathy that has resisted conservative measures.
Sonography of the Normal Brachial Plexus
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
Neuro-muscular Ultrasound; Focus on pathology of nerves
This document discusses nerve pathology and interventions for nerve entrapments. It covers indications for diagnostic interventions like nerve blocks and hydrodissection. Examples of different nerve pathologies are provided along with cases showing muscle changes distal to the level of injury. Non-invasive interventions like nerve blocks and hydrodissection are described to help diagnose and treat entrapments like carpal tunnel syndrome while avoiding injury to nearby nerves.
Updated Musculoskeletal US Examination of the Foot
This document provides an anatomical overview of the ligaments, tendons, fascia, and nerves in the dorsal and plantar aspects of the midfoot. Key structures mentioned include the dorsal talonavicular and calcaneocuboid ligaments, Lisfranc ligament, plantar fascia and its lateral cord, peroneal tendons, flexor tendons and plantar plate under the metatarsal heads, and the heel fat pad.
Updated Musculoskeletal US Examination of the Ankle
This diagram labels the major nerves and vessels of the leg. It shows the anterior tibial nerve and vessels on the front of the leg, the superficial peroneal nerve on the side, and branches of the posterior tibial nerve including the saphenous and sural nerves on the back.
Updated Musculoskeletal US Examination of the Hip
This document lists different types of hip pathologies including anterior, lateral, medial, and posterior structures as well as longitudinal and transverse structures of the hip. It also lists common hip conditions such as rheumatoid arthritis, osteoarthritis of the hip, calcium pyrophosphate deposition disease, and greater trochanteric pain syndrome.
Case presentation ( Cairo round)
A 35-year-old female patient with a history of SLE, corticosteroid use, and a prior THR presents with chronic right medial knee pain. An ultrasound revealed a fixed subluxation of the medial meniscus entrapping the infrapatellar branch of the saphenous nerve. The diagnosis is a trapped IPS nerve causing her pain. Treatment options discussed include weight loss, lateral wedge insoles, and regenerative medicine. A video link is also provided about dynamic subluxation or dislocation of the medial meniscus.
Musculoskeletal Ultrasound examination of the Foot
This document provides an anatomical diagram of the ligaments and structures on the dorsal and plantar surfaces of the midfoot. It depicts the dorsal talonavicular ligament, dorsal calcaneocuboid ligament, and Lisfranc ligament dorsally. Plantarly it shows the proper plantar fascia, lateral cord of the plantar fascia, heel fat pad, peroneus brevis and longus tendons, metatarsal heads, and flexor tendon and plantar plate.
Case presentation 9-3-2017
A 26-year-old male carpenter suffered cuts to the left ring and little fingers during a quarrel, requiring repair and a splint for 4 weeks. He was referred for rehabilitation due to stiffness, pain, and numbness. Treatment included NSAIDs, neurotonics, pregabalin, pulsed ultrasound, and range of motion exercises, with gradual improvement in range of motion and pain but not the numbness. The document discusses anatomy, causes including fractures and lacerations, diagnosis through history, examination, nerve tests, and ultrasound, and treatments including medical management, rehabilitation, ultrasound-guided interventions, and surgery.
Updated Elbow Musculoskeletal US Examination
This document provides an anatomical diagram of the posterior forearm and lists the muscles of the superficial and deep forearm extensors. Key muscles identified include the extensor carpi radialis longus and brevis, brachioradialis, supinator, anconeus, extensor pollicis longus and brevis, and extensor indicis proprius. The diagram orients the reader to the anterior, medial, lateral, and posterior aspects of the forearm as well as superficial and deep muscle layers.
Ultrasound examination of the Ankle
This diagram labels the major nerves and vessels of the lower leg, including the anterior tibial nerve and vessels on the front of the leg, the superficial peroneal nerve on the side of the leg, and branches of the posterior tibial nerve like the saphenous nerve and sural nerve in the back of the leg.
Basic sonoanatomy of ultrasound guided interventions of cervical and lumbar s...
This document discusses pain management techniques for the lower back, including facet joint medial branch blocks, sacral hiatus injections, and sacroiliac joint injections. These techniques involve injecting therapeutic medications into specific areas to diagnose and potentially treat sources of lower back pain.
Updated lecture about Ultrasonography of the knee
The document describes the three grades of medial collateral ligament injuries: Grade I involves microscopic tears or strains and edema near the ligament. Grade II is a partial tear extending into the ligament with edema and thickening. Grade III is a complete rupture where the ligament is fully disrupted and there is hematoma formation. MRI and ultrasound can be used to identify the grade based on edema, fluid patterns, and ligament continuity or disruption.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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Updated hyperuricemia
- 3. Treat or not to treat Foe Friend Review
- 4. Hyperuricemia, usually defined as PUA >7 mg/dL Hershfield MS et al 2010
- 5. Alexander So and Bernard Thorens (2010): Uric acid transport and disease, JCI. 120(6):1791–1799. Reno-vascular or Parenchymal disease
- 7. UA accounts for approximately half of the antioxidant properties of human plasma Masseoud D, Rott K, Liu-Bryan R, Agudelo C. Overview of hyperuricaemia and gout. Curr Pharm Des 2005;11:4117-24.
- 8. PUA protects humans from cancer and other life- shortening disorders. low PUA is a cause of neurodegenerative diseases and that raising PUA may be an effective therapy for these disorders Hershfield MS et al 2010
- 9. Uric acid protects cultured rat hippocampal neuronal cells from oxidative stress, and administration of uric acid 24 hours prior to middle artery occlusion also attenuated brain injury induced by acute ischemia in rats Yu ZF et al(1998): Uric acid protects neurons against excitotoxic and metabolic insults in cell culture, and against focal ischemic brain injury in vivo. JNR. 53:613–625
- 11. Alexander So and Bernard Thorens (2010): Uric acid transport and disease, JCI. 120(6):1791–1799.
- 12. Alexander So and Bernard Thorens (2010): Uric acid transport and disease, JCI. 120(6):1791–1799.
- 14. 365 Peri- and postmenopausal Women (60.5ys) Baseline BMD + BMI DEXA At least 1 repeat measure on average 9.7 ys later Annual rate of change in BMD was calculated UA was measured at each visit Calciotropic hormones and bone turnover markers were measured at final visit only
- 16. ↑ SERUM URIC ACIDANTI OXIDANT OXIDATIVE STRESS ↓ BMD URIC ACID ↓ OXIDATIVE STRESS ↑ BMD (NOT FOR HIP MAY BE MECHANICAL)
- 17. ↑ BMI ↑ BMD BMI IS DIRECTLY CORRELATED WITH SERUM URIC ACID MAY BE AN EXPLANATION FOR INCREASE SERUM URIC ACID↑ BMD
- 18. THE HIGHER THE SERUM URIC ACID THE HIGHER CHOLESTEROLE & TRIGLYCERIDES AND THE LOWER LDL ATHEROGENIC LIPID PROFILE LOW BMD
- 19. Joanna Makovey et al concluded Higher serum UA levels appear to be protective for bone loss in peri- and postmenopausal women and this relationship is not affected by changes in body composition measures
- 21. Ito S et al 2012
- 22. Meek I L et al 2014
- 23. Brian F. Mandell CLEVELAND CLINIC VIRTUAL GRAND ROUNDS 2013
- 25. Alexander So and Bernard Thorens (2010): Uric acid transport and disease, JCI. 120(6):1791–1799.
- 26. Sautin Y Y and Johnson R J (2008): URIC ACID: THE OXIDANT–ANTIOXIDANT PARADOX, Nucleosides Nucleotides Nucleic Acids; 27(6): 608–619.
- 27. Hyperuricemia Cell Purine Uric Acid SMC Proliferation Vasoconstriction Inflammation RAS COX-2 Hypertension Inflammation Renal disease progression Endothelial dysfunction and CVD Tissue hypoxia Cell death Insulin resistance
- 30. Intra cellular Plasma Hydrophobic Hydrophilic Adipose tissue And LDL Ascorbic acid And methionine
- 37. Carnovale C et al 2014