Goodpasture syndrome: Difference between revisions
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==Management== | ==Management== | ||
*See [[Hemoptysis]] | *See [[Hemoptysis]] | ||
*See [[Glomerulonephritis]] | |||
*Plasmapharesis shown to be beneficial <ref> Levy JB, Turner AN, Rees AJ, Pusey CD. Long-term outcome of anti-glomerular basement membrane antibody disease treated with plasma exchange and immunosuppression. Ann Intern Med. 2001 Jun 5. 134(11):1033-42 </ref> | |||
*In severe cases may need: | |||
**Rheumatology eval: Immunosuppressants | |||
==Disposition== | ==Disposition== | ||
Revision as of 03:58, 24 January 2016
Background
- Goodpasture syndrome (60%): diffuse pulmonary hemorrhage + acute glomerulonephritis.
- Goodpasture disease: glomerulonephritis alone (30%,) pulmonary sx alone (10%,)
- Anti-GBM disease is most precise term for both entities.
- Type II hypersensitivty causing linear IG deposition in glomerular and alveolar BM.
- Triggered by:Sepsis, URI, inhalation injury, smoking, pulmonary edema.
Clinical Features
- Constitutional sx prior to pulmonary/renal complications
- Pulmonary
- Cough, dyspnea, chest pain, hemoptysis, respiratory failure or pulmonary hemorrhage
- Renal
Differential Diagnosis
Diagnosis
- Pulmonary
- Depends whether pt stable or not
- See hemoptysis
- Renal:
UA CBC Chemistry Albumin (often reduced in acute glomerulonephritis) C3, C4, ASO, ANCA
Management
- See Hemoptysis
- See Glomerulonephritis
- Plasmapharesis shown to be beneficial [1]
- In severe cases may need:
- Rheumatology eval: Immunosuppressants
Disposition
See Also
External Links
References
- ↑ Levy JB, Turner AN, Rees AJ, Pusey CD. Long-term outcome of anti-glomerular basement membrane antibody disease treated with plasma exchange and immunosuppression. Ann Intern Med. 2001 Jun 5. 134(11):1033-42