TY  - CHAP
M1  - Book, Section
TI  - Joints and Bursae
A1  - Burton, John H.
A1  - Fortuna, Timothy J.
A2  - Tintinalli, Judith E.
A2  - Stapczynski, J. Stephan
A2  - Ma, O. John
A2  - Yealy, Donald M.
A2  - Meckler, Garth D.
A2  - Cline, David M.
PY  - 2016
T2  - Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e
AB  - Many  mechanisms  provoke  acute  joint  symptoms:  degradation  and  degeneration  of  articular  cartilage  (osteoarthritis),  deposition  of  immune  complexes  or  immune  system–related  phenomena  (rheumatoid  arthritis,  rheumatic  fever  and  possibly,  a  component  of  gonococcal  arthritis),  crystal-induced  inflammation  (gout  and  pseudogout),  seronegative  spondyloarthropathies  (ankylosing  spondylitis  [see  chapter  282,  "Systemic  Rheumatic  Diseases"]  and  reactive  arthritis  [postinfectious  with  HLA-B27  susceptibility]),  and  bacterial  invasion  (gonococcal  and  nongonococcal  septic  arthritis,  including  Lyme  arthritis)  or  viral  invasion  (viral  arthritis).  These  processes  impact  joint  capsules  and  surfaces,  resulting  in  a  cascade  of  reactive  and  inflammatory  events.  Septic  arthritis  is  invasion  of  a  joint  by  an  infectious  agent  with  organism  proliferation  and  associated  inflammation;  bacterial  arthritis  is  a  subset  of  septic  arthritis.  Under  ideal  conditions,  the  infectious  agent  is  recoverable  from  the  joint  fluid  in  septic  arthritis,  but  in  clinical  practice,  this  is  often  not  the  case.  This  chapter  reviews  the  common  causes  and  treatments  of  acute  nontraumatic  joint  pain.  Joint  injuries  are  discussed  in  section  22,  "Injuries  to  Bones  and  Joints,"  and  disorders  due  to  repetitive  use  syndromes  are  discussed  in  section  23,  "Musculoskeletal  Disorders,"  by  anatomic  site.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/16
UR  - accessmedicine.mhmedical.com/content.aspx?aid=1121518660
ER  -