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Lordosis, kyphosis, and scoliosis
Osteomalacia and rickets
Paget disease of bone
Calcium pyrophosphate deposition disease (pseudogout)
Juvenile idiopathic arthritis
Inclusion body myopathy
Degenerative disc disease
Spinal disc herniation
Achilles tendon rupture
Anterior cruciate ligament injury
Iliotibial band syndrome
Patellar tendon rupture
Patellofemoral pain syndrome
Carpal tunnel syndrome
Thoracic outlet syndrome
Radial head subluxation (Nursemaid elbow)
Rotator cuff tear
Lambert-Eaton myasthenic syndrome
Limited systemic sclerosis (CREST syndrome)
Mixed connective tissue disease
Systemic lupus erythematosus
Developmental dysplasia of the hip
Osgood-Schlatter disease (traction apophysitis)
Slipped capital femoral epiphysis
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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On your rounds, you see Ashvir, a 50-year-old man who complains of severe pain and swelling in his first toe on the right foot.
This is the first time he has experienced this and the symptoms developed in the last 5 hours.
He described the pain as very severe and that it’s causing him to limp.
On examination, he is obese and the toe is swollen, red, warm, and painful to the touch.
Then you see Bianca, a 22-year old who also came in with a pain and swelling of the left big toe and left knee, which developed yesterday.
However, unlike Ashvir, she is not overweight and has a history of hemochromatosis.
Synovial fluid analysis was performed in both, detecting negatively bi-refringent crystals in Ashvir, and weakly positively birefringent crystals in Bianca.
Now, both seem to have some type of crystalline arthropathy.
But let’s talk about physiology first.
Purines, together with pyrimidines, are key components of nucleic acids like DNA and RNA.
Purines are first broken down into adenosine monophosphate or AMP and guanosine monophosphate or GMP.
AMP is converted to inosine via two different mechanisms; either by removing an amino group to form inosine monophosphate or IMP, which is quickly converted to inosine, or by removing a phosphate group to form adenosine, which is also converted to inosine.
Inosine is then converted to hypoxanthine, and hypoxanthine to xanthine, which is finally metabolized to uric acid.
These last two steps are catalyzed by the enzyme xanthine oxidase.
GMP is converted to guanosine, which is then converted to guanine.
Guanine is deaminated to form xanthine, which is oxidized by xanthine oxidase to form the final product, uric acid.
Now, under normal physiologic conditions, uric acid circulates in plasma and synovial fluid as urate an-ions.
However, human tissues have a limited ability to metabolize urate; thus, it is quickly eliminated by the kidney and the gut to maintain urate homeostasis.
Another way the body can avoid excess uric acid is by recycling purines via the purine salvage pathway.
This is when organs convert hypoxanthine back to IMP via hypoxanthine-guanine phospho-ribo-syl-transferase or HGPRT, which then gets converted to AMP to make new purines; conversely, we can take guanine and convert it to GMP by HGPRT to make new purines;
Now, gout is a monoarticular inflammatory disease where monosodium urate crystals cause joint damage.
When plasma becomes saturated with urate acid molecules, these bind sodium to form monosodium urate crystals, especially in areas with slow blood flow, like the joints and the kidney tubules.
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