Colon Information and Courses from MediaLab, Inc.
These are the MediaLab courses that cover Colon and links to relevant pages within the course.
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|Calculating and Reporting the Myeloid:Erythroid (M:E) Ratio|
Once the bone marrow cell count is completed and recorded, the M: E ratio should be assessed. This is performed by calculating the total myeloid precursors in proportion to the total erythroid precursors. Remember that this does not use the total white blood cell tally; the myeloid cells alone are counted, excluding lymphocytes, monocytes, macrophages, plasma cells, megakaryocytes, osteoclasts, osteoblasts, and other non-myeloid cells. In most circumstances, it is quite simple to divide the myeloid total by the erythroid total to find the ratio. This is always reported as a whole number ratio, and is normally around 3:1 (reference range= 2:1 to 4:1). In some situations where the erythroid portion is increased, or the myeloid series is decreased, the M:E ratio is reversed. This would still be expressed as a whole number ratio (example: 1:2). A simple way to perform the calculation is to always divide the larger value by the smaller. Which side of the colon, the 1 is placed on, is dependent on which cell type was larger. The 1 always belongs on the side of the cell type found in lower numbers.For example:Myeloid total 120 : Erythroid total 40 M:E ratio = 120 ÷ 40 = 3 or 3:1 So, the M:E ratio is 3:1Another example:Myeloid total 30 : Erythroid total 150Divide the larger number by the smaller (notice that the placement is reversed).150 ÷ 30 = 5 So, the M:E ratio is 1:5
|It is important to establish a species identification of C. septicum in blood culture isolates because of its close association with carcinoma of the colon.||View Page|
Lorimer JW. Eidus LB.: Invasive Clostridium septicum infection in association with colorectal carcinoma. Canadian Journal of Surgery. 37:245-9, 1994 The association between invasive Clostridium septicum infection and colorectal carcinoma is examined by the presentation of three cases and a review of the literature. In the first two cases the patients presented with nontraumatic metastatic clostridial gas gangrene. In the third case a patient with chemotherapy-induced myelosuppression from concomitant multiple myeloma had a necrotizing transmural infection of the right colon. The apparent portal of entry of Clostridium septicum was an occult carcinoma of the ascending colon. The increasing evidence for a strong link between this organism and some cases of neutropenic enterocolitis is reviewed.
Kornbluth AA. Danzig JB. Bernstein LH.: Clostridium septicum infection and associated malignancy. Report of 2 cases and review of the literature. Medicine. 68(1):30-7, 1989 We report 2 patients with myonecrosis due to Clostridium septicum and associated colon carcinoma and have reviewed the English language literature for all reported cases of atraumatic C. septicum infection. A total of 162 cases of C. septicum infection have been reported. Eighty-one percent of these patients had an associated malignancy. Thirty-four percent of all patients had associated colon carcinoma, while 40% had a hematologic malignancy. Thirty-seven percent of reported patients had an occult malignancy at the time of their infection with C. septicum. In many patients, the portal of entry was found in the large intestine. In a particularly lethal form (79% mortality) of C. septicum infection, known as "distant myonecrosis," infection metastatic from the initial site of infection causes severe myonecrosis, gangrene, and often death within hours of clinical detection. Overall, survival of patients with C. septicum infection is only 35%. Review of all cases of C. septicum infection suggests several conclusions. 1) Patients with malignancy, particularly colonic or hematologic, and patients with cyclic neutropenia who develop signs and symptoms of sepsis, especially with associated findings of abdominal pain or pain in an extremity, should be treated for possible clostridial infection. 2) C. septicum infection does not appear to be a result of a single specific defect in either humoral or cell-mediated immunity. Rather, it may occur in patients who are granulocytopenic and therefore prone to an enterocolitis. 3) Patients in whom an infection with C. septicum is found must undergo a vigorous search for malignancy.
|Match the species of anaerobes and frequently associated conditions.||View Page|
|Each of the following statements is true concerning Clostridium septicum infections EXCEPT:||View Page|
|A clinical condition often associated with Streptococcus anginosus ("milleri") is:||View Page|
|Match tumor markers with corresponding sites of tumor origin:||View Page|
|An increase in CEA levels is most closely associated with which of the following organs:||View Page|
Mucins are generally categorized as Neutral Mucins or Acid Mucins for the purpose of histotechnique. Increased mucin production is indicative of many adenocarcinomas, including cancers of the pancreas, lung, breast, ovary, colon and other tissues. Mucins can also be overexpressed in lung diseases such as asthma, bronchitis, chronic obstructive pulmonary disease (COPD) or cystic fibrosis.
|Medical Complications of Metabolic Syndrome|
In addition to cardiovascular disease, stroke, and diabetes, that are closely associated with metabolic syndrome, there are several medical complications and conditions that could also potentially occur. An individual with metabolic syndrome is susceptible to: Fatty liver disease Other liver diseases Cholesterol gallstones Asthma Sleep apnea Osteoarthritis Pulmonary disease Renal disease Ocular complications Polycystic ovary syndrome Colon, endometrial, and breast cancers
|Which of the following are possible medical complications for an individual diagnosed with metabolic syndrome?||View Page|
|Which of the following specimens would not be considered suitable for anaerobic culture:||View Page|
Clostridium difficile is the cause of antibiotic associated diarrhea (AAD) and pseudomembranous colitis (PMC). PMC is an inflammatory disease of the colon caused by toxins of C. difficile.C. difficile produces two potent toxins: Toxin A (TcdA), an enterotoxinToxin B (TcdB), a cytotoxin It is the production of these toxins in the gastrointestinal tract that ultimately leads to disease. There is a relationship between toxin levels, the development of pseudomembranous colitis (PMC), and the duration of diarrhea. For many years, toxin A was regarded as more important than toxin B in the disease process. Later on, disease producing strains producing only toxin B were identified. These strains produced serious disease, and toxin B was found to be responsible for more serious damage to intestinal cells.
Another organism that has more recently become problematic is Clostridium difficile. Usually, normal gut flora resist overgrowth and colonization by this organism. However, antibiotic use that suppresses the normal gut flora, allows proliferation of C. difficile. The organism releases toxins that cause inflammation and damage to the mucosal lining of the colon, leading to severe diarrhea. An antibiotic-resistant strain has developed that can result in colitis, sepsis, and death. Elderly patients, patients with severe underlying illness, and patients undergoing immunosuppressive therapy are at higher risk of becoming infected since their immune response to the bacteria and its toxins is diminished.
Most Clostridium infections arise from endogenous sources. That is, many of the Clostridium species that are associated with disease in humans are part of the normal intestinal microflora, which is true of Clostridium difficile.The organism was originally isolated in 1935 as a component of the normal intestinal flora of healthy newborns. It was dubbed difficile because the organism grows slowly and is difficult to culture. Early investigators also noted that the organism produced a potent toxin, but the relationship between C. difficile antibiotic-associated diarrhea (AAD) and pseudomembranous colitis (PMC) was not elucidated until the 1970's. PMC is an inflammatory disease of the colon caused by toxins of Clostridium difficile. Normal intestinal flora is an important factor in host response to an infectious microorganism. Resistance to intestinal infection is significantly reduced when there is a reduction in the normal flora as a result of antibiotic treatment. The most common manifestation of this decreased host resistance is the development of PMC.
|Pathogenisis of C. Difficile-Associated Diarrhea|
Clostridium difficile is the leading cause of hospital-acquired diarrhea in the United States, with the number of cases rising annually over the last three decades. This is largely due to the increased frequency of antibiotic usage, the development of better detection methods, and the fact that hospital environments are increasingly contaminated with spores of C. difficile. The definition of C. difficile diarrhea includes > 6 episodes of non-formed diarrheic stool per 24 hours, along with prior antibiotic treatment. At least three events must occur in the pathogenesis of C. difficile-associated diarrhea (CDAD): Alteration of the normal fecal flora Colonic colonization with toxigenic C. difficile Growth of the organism with elaboration of its toxins"Colonization resistance" is the term used to describe the mechanism by which indigenous flora control overgrowth of C. difficile. This resistance may be compromised by the use of antimicrobial compounds, underlying illness, or therapeutic procedures. Infection begins with the ingestion of either the organism itself or spores, usually via the fecal-oral route. Spores in particular are able to survive the acidity of the stomach and germinate in the colon to produce vegetative organisms. Toxinogenic strains subsequently produce Toxin A, Toxin B, and/or the Binary Toxin leading to colitis, pseudomembrane formation, and watery diarrhea. Significant complications of the clinical disease associated with infection are hypoalbuminemia, toxic megacolon (acute toxic colitis with dilatation of colon), and pseudomembranous colitis (PMC).