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{| style="font-size: 85%;"
{| style="border: 2px solid #DCDCDC; font-size: 90%; width: 80%;"
! style="width: 80px; background: #4479BA; text-align: center;"|{{fontcolor|#FFF|Organ/Tissue}}
|+ '''Laboratory findings'''
! style="width: 720px; background: #4479BA; text-align: center;"| {{fontcolor|#FFF|Effect}}
|-
|-
| style="background: #F5F5F5; padding: 5px; text-align: center;"| '''[[Endothelial cells]]'''
! style="width: 80px; background: #4479BA; text-align: center;"|{{fontcolor|#FFF|Test}}
| style="background: #DCDCDC; padding: 5px;"| There is no clear evidence of endovascular damage
! style="width: 720px; background: #4479BA; text-align: center;"| {{fontcolor|#FFF|Findings}}
|-
|-
| style="background: #F5F5F5; padding: 5px; text-align: center;"| '''[[Liver]]'''
| style="background: #F5F5F5; padding: 5px; text-align: center;"| '''[[White blood cells]] count'''
| style="background: #DCDCDC; padding: 5px;"| Causes hepatocellular [[necrosis]] which could impair the synthesis of [[proteins]] of the [[coagulation system]]
| style="background: #DCDCDC; padding: 5px;"| Leucopenia (1000 cells/μL), with lymphopenia and neutrophilia
|-
|-
| style="background: #F5F5F5; padding: 5px; text-align: center;"| '''[[Adrenal cortex]]'''
| style="background: #F5F5F5; padding: 5px; text-align: center;"| '''[[Blood smear]]'''
| style="background: #DCDCDC; padding: 5px;"| Affects the synthesis of enzymes responsible for the synthesis of [[steroids]], leading to [[hypotension]], and [[fluid]] and [[electrolytes]] disturbances.
| style="background: #DCDCDC; padding: 5px;"| Left shift with atypical lymphocytes
|-
|-
| style="background: #F5F5F5; padding: 5px; text-align: center;"| '''[[Lymphatic system]]'''
| style="background: #F5F5F5; padding: 5px; text-align: center;"| '''[[Liver function tests]]'''
| style="background: #DCDCDC; padding: 5px;"| [[Necrosis of the [[spleen]], [[lymph nodes]] and [[thymus]]; [[Apoptosis]] of [[lymphocytes]] leading to [[lymphopenia]].  
| style="background: #DCDCDC; padding: 5px;"| Raised [[aspartate aminotransferase]] and [[alanine aminotransferase]], extended [[prothrombin time]] and [[partial thromboplastin time]].
|-
| style="background: #F5F5F5; padding: 5px; text-align: center;"| '''[[Proteins]]'''
| style="background: #DCDCDC; padding: 5px;"| [[Hyperproteinemia]].
|-
| style="background: #F5F5F5; padding: 5px; text-align: center;"| '''[[Urinalysis]]'''
| style="background: #DCDCDC; padding: 5px;"| [[Proteinuria]].  
|}
|}



Revision as of 18:58, 20 June 2014

The following table contains the main risk factors for CDI:[1][2][3][2][2]

Alterations in the coagulation system
Consumption of clotting factors
Increased concentrations of fibrin degradation products
Disseminated intravascular coagulation


Laboratory findings
Test Findings
White blood cells count Leucopenia (1000 cells/μL), with lymphopenia and neutrophilia
Blood smear Left shift with atypical lymphocytes
Liver function tests Raised aspartate aminotransferase and alanine aminotransferase, extended prothrombin time and partial thromboplastin time.
Proteins Hyperproteinemia.
Urinalysis Proteinuria.



table

Countries with a reported prevalence <15% of H. pylori resistance to clarithromycin
Diagnostic test North America South America Middle East Far East
ELISA (serology) detects:
  • Viral Antigen
  • IgM and IgG antibody | hol

There is a reported prevalence of 15% in the Northeast of the US.

  1. Hensgens MP, Goorhuis A, Dekkers OM, Kuijper EJ (2012). "Time interval of increased risk for Clostridium difficile infection after exposure to antibiotics". J Antimicrob Chemother. 67 (3): 742–8. doi:10.1093/jac/dkr508. PMID 22146873.
  2. 2.0 2.1 2.2 Knight, Christopher L.; Surawicz, Christina M. (2013). "Clostridium difficile Infection". Medical Clinics of North America. 97 (4): 523–536. doi:10.1016/j.mcna.2013.02.003. ISSN 0025-7125.
  3. Planche, Tim (2013). "Clostridium difficile". Medicine. 41 (11): 654–657. doi:10.1016/j.mpmed.2013.08.003. ISSN 1357-3039.