Reference no: EM133855149
Aside from the fact that there is a genetic component (ET tends to run in families), there also appears to be nongenetic influences (diet and toxins) that may have a role in developing ET. The authors wrote, "Consumption of many nutritional antioxidants did not differ between ET patients and controls according to a previous study, but the MeDi, being a composite dietary pattern, may be better at capturing the overall antioxidant effect of the diet." This speaks to the idea that a total and/or synergistic effect of the MeDi is perhaps more powerful than taking a handful of antioxidant supplements every day.
1. How effective is parathyroid hormone in the management of osteoporosis? Please explain the mechanism.
2. 1. What is the recommended treatment for severe osteogenesis imperfecta?
2. Where two siblings have already been born with severe osteogenesis imperfecta, what is the risk of subsequent children of the same parents being born with this condition?
3. Why does achondroplasia not affect the mandible (when all other bones are affected)?
4. If an elderly patient with rheumatoid arthritis who has been taking myocrisin (injectable gold) for several years presents with pancytopenia, should the gold treatment be stopped? If so, what treatment should replace it?
5. In a patient with dermatomyositis, what laboratory tests should be ordered to exclude systemic lupus erythematosus (SLE)?
6. What treatment is recommended for tarsal tunnel syndrome?
7. In a patient with documented antiphospholipid syndrome, should lupus anticoagulant be investigated for? If it is found to be present, will this necessitate the use of anticoagulants?
8. What are the findings to be looked for during routine fundus examination in patients on long-term chloroquine or any other antimalarial therapy for the treatment of systemic lupus erythematosus (SLE)?
9. What is the sensitivity of plain X-ray in detecting ankylosing spondylitisrelated spine lesions in both early and late disease, and is there a specific diagnostic test for this?
10. It is reported by the Oxford Handbook of Clinical Medicine that glucosamine and chondroitin sulphate have failed an NEJM trial for the treatment of osteoarthritis? Is there still a valid use for these compounds?
11. Can high serum titres of C-reactive protein (CRP) with normal erythrocyte sedimentation rate (ESR) indicate relapse of rheumatoid arthritis in established rheumatoid arthritis which is in remission?
12. What is the positive predictive value of hyperuricaemia in the diagnosis of gout?
13. What is Scheuermann's disease? And is this a specific clinical or radiological or haematological disease? What is the treatment for this disease?