Gout
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Gout
Pathology
Bone disorders
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Cleidocranial dysplasia
Club foot
Craniosynostosis
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Genu valgum
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Osteogenesis imperfecta
Pectus excavatum
Pigeon toe
Lordosis, kyphosis, and scoliosis
Osteomalacia and rickets
Osteopetrosis
Osteoporosis
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Paget disease of bone
Musculoskeletal injuries and trauma
Degenerative disc disease
Sciatica
Spinal disc herniation
Spondylolisthesis
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Achilles tendon rupture
Anterior cruciate ligament injury
Iliotibial band syndrome
Meniscus tear
Patellar tendon rupture
Patellofemoral pain syndrome
Sprained ankle
Unhappy triad
Compartment syndrome
Rhabdomyolysis
Carpal tunnel syndrome
Erb-Duchenne palsy
Klumpke paralysis
Sciatica
Thoracic outlet syndrome
Ulnar claw
Winged scapula
Carpal tunnel syndrome
Dislocated shoulder
Erb-Duchenne palsy
Klumpke paralysis
Radial head subluxation (Nursemaid elbow)
Rotator cuff tear
Thoracic outlet syndrome
Ulnar claw
Winged scapula
Musculoskeletal system pathology review
Back pain: Pathology review
Bone disorders: Pathology review
Bone tumors: Pathology review
Gout and pseudogout: Pathology review
Muscular dystrophies and mitochondrial myopathies: Pathology review
Myalgias and myositis: Pathology review
Neuromuscular junction disorders: Pathology review
Pediatric musculoskeletal disorders: Pathology review
Rheumatoid arthritis and osteoarthritis: Pathology review
Scleroderma: Pathology review
Seronegative and septic arthritis: Pathology review
Sjogren syndrome: Pathology review
Systemic lupus erythematosus (SLE): Pathology review
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Gout
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Similar nodules are present on the left elbow and right external pinna of the ear. Further evaluation of this patient will most likely reveal which of the following?
External References
First Aid
2022
2021
2020
2019
2018
2017
2016
Alcohol use
gout and p. 477
Allopurinol
for gout p. 477, 500
gout p. 726
Chronic gout
treatment p. 726
Colchicine
acute gout attack p. 726
gout p. 477, 500
Cyclosporine
gout p. 251
Dehydration
gout exacerbation p. 477
Diuretics
in gout p. 500
Febuxostat
gout p. 477, 500, 726
Furosemide p. 253, 632
gout with p. 251
Glucocorticoids
acute gout attack p. 726
gout p. 477, 500
Gout p. 477
as drug reaction p. 251
drug therapy for p. 499
kidney stones and p. 628
lab findings p. 722
Lesch-Nyhan syndrome p. 35
loop diuretics and p. 632
presentation p. 718
treatment p. 726
Von Gierke disease p. 85
Indomethacin p. 499
gout p. 477
Metatarsophalangeal (MTP) joints
gout p. 477
Naproxen p. 499
acute gout drugs p. 501
Niacin
gout p. 251
Nonsteroidal anti-inflammatory drugs (NSAIDs) p. 499
acute gout attack p. 726
gout p. 477, 501
Podagra
gout p. 477
presentation p. 718
Probenecid p. 253
for gout p. 500, 726
Pyrazinamide p. 194
gout p. 251
Thiazides p. 633
gout p. 251
Tophi in gout p. 718
Uric acid
gout p. 500
Transcript
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Gout is an inflammatory disease in which monosodium urate crystals deposit into a joint, making it red, hot, tender and swollen within hours.
When this happens, it’s called a gouty attack.
The underlying cause is hyperuricemia—too much uric acid in the blood, which results in the formation of sharp, needle-like crystals, in areas with slow blood flow like the joints and the kidney tubules.
Over time, repeated gouty attacks can cause destruction of the joint tissue which results in arthritis.
To understand where the uric acid comes from, let’s start with purines, which, together with pyrimidines, are nature’s most common nitrogen-containing heterocycles.
A heterocycle being any molecular ring or cycle with different types of atoms.
Purines, as well as pyrimidines, are key components of nucleic acids like DNA and RNA, and when cells, along with the nucleic acids in those cells, are broken down throughout the body, those purines are converted into uric acid—a molecule that can be filtered out of the blood and excreted in the urine.
Uric acid has limited solubility in body fluids, though. Hyperuricemia occurs when levels of uric acid exceed the rate of its solubility, which is about 6.8mg/dL.
At a physiologic pH of about 7.4, uric acid loses a proton and becomes a urate ion, which then binds sodium and forms monosodium urate crystals.
These crystals can form as a result of increased consumption of purines, like from consuming purine-rich foods like shellfish, anchovies, red meat or organ meat.
Also, though, they can result from increased production of purines, for example high-fructose corn syrup containing beverages could contribute to the formation of uric acid by increasing purine synthesis.
Another way crystals could form is from decreased clearance of uric acid, which can result from dehydration from not drinking enough water or from consumption of alcoholic beverages, both of allowing uric acid to precipitate out.
Regularly eating these kinds of foods can also lead to obesity and diabetes, both of which are risk-factors for gout.
Hyperuricemia can also develop as a result of chemotherapy or radiation treatment, since cells die at a faster-than-normal rate.
Sources
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
- "Gout" The Lancet (2016)
- "Update on gout: new therapeutic strategies and options" Nature Reviews Rheumatology (2010)
- "Diagnosis of Acute Gout: A Clinical Practice Guideline From the American College of Physicians" Annals of Internal Medicine (2016)
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