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Musculoskeletal system
Radial head subluxation (Nursemaid elbow)
Developmental dysplasia of the hip
Legg-Calve-Perthes disease
Slipped capital femoral epiphysis
Transient synovitis
Osgood-Schlatter disease (traction apophysitis)
Rotator cuff tear
Dislocated shoulder
Radial head subluxation (Nursemaid elbow)
Winged scapula
Thoracic outlet syndrome
Carpal tunnel syndrome
Ulnar claw
Erb-Duchenne palsy
Klumpke paralysis
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Unhappy triad
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Patellar tendon rupture
Meniscus tear
Patellofemoral pain syndrome
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Spondylolysis
Spondylolisthesis
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Back pain: Pathology review
Rheumatoid arthritis and osteoarthritis: Pathology review
Seronegative and septic arthritis: Pathology review
Gout and pseudogout: Pathology review
Systemic lupus erythematosus (SLE): Pathology review
Scleroderma: Pathology review
Sjogren syndrome: Pathology review
Bone disorders: Pathology review
Bone tumors: Pathology review
Myalgias and myositis: Pathology review
Neuromuscular junction disorders: Pathology review
Muscular dystrophies and mitochondrial myopathies: Pathology review
Gout
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gout and p. 477
for gout p. 477, 500
gout p. 726
treatment p. 726
acute gout attack p. 726
gout p. 477, 500
gout p. 251
gout exacerbation p. 477
in gout p. 500
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gout with p. 251
acute gout attack p. 726
gout p. 477, 500
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
gout p. 477
gout p. 477
acute gout drugs p. 501
gout p. 251
acute gout attack p. 726
gout p. 477, 501
gout p. 477
presentation p. 718
for gout p. 500, 726
gout p. 251
gout p. 251
gout p. 500
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.
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