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===Diagnostic criteria ===
3 fractors determine the pathogeneis of the SBP:
A set of diagnostic criteria were proposed by Del Brutto et al based on the laboratory and imaging tests. The criteria were modified in 2001 to be: (22)
{| class="wikitable"
!Categories
!Details
|-
|Absolute
|
* Cystic lesions with the scolex in it on CT scan or MRI


* Histologic confirmation of the parasite on a biopsy from a lesion in the brain or spinal cord
Bacterial overgrowth in cirrhotic patients: Secondary to decreased intestinal motility and frequent use of PPIs in this population of patients.
* Visualization of subretinal parasites directly using funduscopic examination
Defensive intestinal barrier in the Both secretory and physical barriers are defective in cirrhotic patients: (1)
|-
Decreased immunity: both local and systemic immunity are decreased.
|Major
|
* Positivity of serum anticysticercal antibodies using enzyme-linked immunoelectrotransfer blot assay (EITB)


* Highly suggestive lesions of neurocysticercosis on neuroimaging
{{#ev:youtube|M502Byuiskw}}
* Resolution of small single enhancing lesions spontaneously
* Resolution of intracranial cystic lesions after trreatment with albendazole or praziquantel
|-
|Minor
|
** Lesions that are compatible with neurocysticercosis on neuroimaging (CT or MRI)
** Clinical presentation that is suggestive of neurocysticercosis.
** Positive findings from cerebrospinal fluid enzyme-linked immunosorbent assay (ELISA) for detection of anticysticercal antibodies or cysticercal antigens
** Diagnosing cysticercosis remotely (outside the central nervous system)
*
|-
|Epidemiologic
|
* Evidence of T.''solium'' infection in a household contact
* Individuals who are staying in or coming from an area of cysticercosis endemicity
* Household contact with an individual infected with ''T solium''
* History of travelling frequently to a disease endemic areas
|-
| colspan="2" |'''Certainity of diagnosis after applying the criteria'''
|-
|'''Certainity of diagnosis'''
|'''Details'''
|-
|Definitive
|
* Fulfilling 1 absolute criterion
* Fulfilling 2 major criteria in addition to 1 minor criterion and 1 epidemiologic criterion
|-
|Probable
|
* Fulfilling 1 major criterion in addition to 2 minor criteria
* Fulfilling 1 major criterion in addition to 1 minor criterion and 1 epidemiologic criterion
* Fulfilling 3 minor criteria in addition to 1 epidemiologic criterion
|}


==Specific for Neuro==


===EITB===
A. Bacterial overgrowth:
MaIN waknesses is that it has only 50% sensitivity in patients with single brain lesions and it can't differentiate between patients with only intestinal tapeworm and patients with cysticercosis (both will be positive)(23)


===Using monoclonal antibodies to detect parasitic antigen===
Intestinal mobility decreses with cirrhosis. Increased symapathetic drive and oxidant stress are believed to be the reasons for the decreased mobility.
CAn be used for following the response to treatment but less sensitive than EITB in detecting the disease. (23)
Also, cirrhotic patients administer PPIs more frequently than other populations.
The diminished intestinal mobility makes the intestinal contents more stagnant and allows the bacterial contents to flourish and overgrow and thus predisposes to cirrhosis. (2)
 
B. Increased bowel permeability:
Normally .. the intestinal mucosa is impermeable using 2 lines of defence.(1)
Secretory componenet which physical component. Both are affected with the development of cirrhosis.
 
Secretory defense mechanism is composed of mucins, immunoglobulins and bile salts.
Bile salts is protective through preventing adherence and internalization of bacteria.
Bile acids are decreased in cirrhosis partly due to decreased secretion from diseased liver and partly from increased conjugation by the flourishing intestinal flora. This gives bacteria easier access through the mucosa.
 
Physical componenet is the intestinal epithelium itself. Intestinal musosa is more permeable as a result of
Increased oxidant stress. NO proinflammatory cytokines
Increased intercellular spaces as a result of vasodilation, edema from portal hypertension.
 
Decreased local and systemic immune responses:
Kupffer cells (local macrophages of the liver) normally contribute in eradicating infection with neutrophils. But as a rsult of the extrahepatic porto-systemic shunts, bacteria in the circulation do not come in contact with these cells.
And as a result of defective liver secretory functions, complement levels decrease (in serum and ascitic fluid) and the neutrophils seems to have qualitative deficiencies.
 
Bacteria that translocates are carried through lymphatics. It can reach to the ascitic fluid either through the circulation then through the liver it can have access to the peritoneal cavity. Another way is through rupture of the lymphatic vessel carrying the contaminated lymph under pressure from the portal hypertension and the increased lymph content.

Revision as of 20:58, 19 April 2017

3 fractors determine the pathogeneis of the SBP:

Bacterial overgrowth in cirrhotic patients: Secondary to decreased intestinal motility and frequent use of PPIs in this population of patients. Defensive intestinal barrier in the Both secretory and physical barriers are defective in cirrhotic patients: (1) Decreased immunity: both local and systemic immunity are decreased.

{{#ev:youtube|M502Byuiskw}}


A. Bacterial overgrowth:

Intestinal mobility decreses with cirrhosis. Increased symapathetic drive and oxidant stress are believed to be the reasons for the decreased mobility. Also, cirrhotic patients administer PPIs more frequently than other populations. The diminished intestinal mobility makes the intestinal contents more stagnant and allows the bacterial contents to flourish and overgrow and thus predisposes to cirrhosis. (2)

B. Increased bowel permeability: Normally .. the intestinal mucosa is impermeable using 2 lines of defence.(1) Secretory componenet which physical component. Both are affected with the development of cirrhosis.

Secretory defense mechanism is composed of mucins, immunoglobulins and bile salts. Bile salts is protective through preventing adherence and internalization of bacteria. Bile acids are decreased in cirrhosis partly due to decreased secretion from diseased liver and partly from increased conjugation by the flourishing intestinal flora. This gives bacteria easier access through the mucosa.

Physical componenet is the intestinal epithelium itself. Intestinal musosa is more permeable as a result of Increased oxidant stress. NO proinflammatory cytokines Increased intercellular spaces as a result of vasodilation, edema from portal hypertension.

Decreased local and systemic immune responses: Kupffer cells (local macrophages of the liver) normally contribute in eradicating infection with neutrophils. But as a rsult of the extrahepatic porto-systemic shunts, bacteria in the circulation do not come in contact with these cells. And as a result of defective liver secretory functions, complement levels decrease (in serum and ascitic fluid) and the neutrophils seems to have qualitative deficiencies.

Bacteria that translocates are carried through lymphatics. It can reach to the ascitic fluid either through the circulation then through the liver it can have access to the peritoneal cavity. Another way is through rupture of the lymphatic vessel carrying the contaminated lymph under pressure from the portal hypertension and the increased lymph content.

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