OTHER QUESTIONS
Suggestions are welcome.
Q6). False about Non Obstructive Mesenteric Ischeamia. (NOMI)
a)Occurs due to treatment with vasopressors
b) Occurs in cardiac shock
c) Burns
d) Hypercoagulable state
Q7) Intestinal infarction all are signs on CT except?
a) Bowel walll thickening
b) Thumbprinting
c) Free Peritoneal air
d) Intramural gas
Q8) In short bowel syndrome false is
a) Jejunum has greater adaptability than ileum
b) Glutamine has a role to play in intestinal adaptation
c) Short Bowel syndrome is gut lenght less than 150cm normally
d) Megaloblastic anemia can occur
Q9) Caecal Volvulus true is
a) Maximum resolve with Colonoscopic method
b) It is the most common form of large gut volvulus
c) It can occur postoperatively
Q10) Which of the following statement(s)
is/are true concerning the immunologic functions of the small intestine?
a. The B lymphocytes of the small intestine do not produce
immunoglobulin A (IgA)
b. Peyer's patches, an example of an aggregated cellular portion of the
gut-associated lymphoid system tissue, are large collections of lymphoid
follicles found on the antimesenteric border of the ileum
c. The major immunoglobulin of the intestinal immune system is IgM
d. IgA produced by the intestinal immune system produces the classic Fc-mediated
inflammatory reactions to antigen stimulus
Answers
6) d
Nonocclusive mesenteric ischemia is one of the causes of mesenteric ischaemia. it contributes 20-30% cases of Mesenteric Ischaemia.
ITcan occur without any arterial or venous
abnormalities. Typically, patients have some degree of atherosclerosis of
the mesenteric vessels and report symptoms when external forces such as
intra-abdominal tumors compress the vessel or when they have poor perfusion
secondary to congestive heart failure, MI, or hypovolemia. It is generally a
syndrome of vasospasm and constriction that typically occurs in critically
ill patients who are in low-flow states (eg, from septic shock, cardiac
shock, burns, or hypovolemic shock).
Low-flow states cause peripheral vasodilation and shunting of the blood from
the gut to the periphery. Even treatment of mesenteric insufficiency by
revascularization can result in vasospasm and an ischemic episode.
Hypercoagulable state causes mesenteric venous thrombosis
Ref. Emedicine
emedicine.com/med/topic2726.htm
7) b
The most common CT finding in bowel ischemia is bowel wall thickening, although it is nonspecific. The thickened bowel wall is sometimes associated with the target sign, alternating layers of high and low attenuation within the thickened bowel wall, which results from submucosal edema or hemorrhage. However, the bowel wall is thinned or occasionally invisible when the involved bowel segment becomes gangrenous.
Other CT findings of bowel ischemia reported in the literature include arterial occlusion, mesenteric or portal vein thrombosis, bowel dilatation, engorgement of mesenteric veins and mesenteric edema, intramural gas (intestinal pneumatosis), mesenteric or portal venous gas, lack of bowel wall enhancement, increased enhancement of the thickened bowel wall, and infarction of other abdominal organs
The intramural gas is caused by dissection of luminal gas into the bowel wall across the compromised mucosa.
Mesenteric or portal venous gas is an even less common CT manifestation of ischemic bowel disease and represents the propagation of intramural gas into the mesenteric venous system. Free intraperitoneal gas is an ominous CT sign in ischemic bowel disease because it indicates perforation of an infarcted bowel segment . Absent or poor enhancement of the bowel wall appears to be the most specific finding for bowel ischemia.
Ref: radiographics.rsnajnls.org/cgi/content/full/20/1/29
Thumbprinting is seen in plain Xray Abdomen and Barium studies only.
8) a
The length of the small bowel in adults ranges from 365-600 cm. When extent of intestinal resection is considered, less than 50% can be tolerated quite well without any significant interventions; 50% to 75% often requires dietary manipulation, oral supplementation and medications to enhance intestinal absorption; and greater than 75% often requires prolonged parenteral nutrition (PN) . In terms of small bowel length, patients with at least 150 cm ending in a stoma or 60 cm to 90 cm anastomosed to a moderate length of colon can often be weaned off of PN
The bulk of nutrient absorption takes place in the first 150 cm of the small bowel in the region of the duodenum and proximal jejunum . The major consequence of intestinal resection is the loss of intestinal surface area and the diminished ability to absorb nutrients, electrolytes and water.
Intestinal adaptation is a process that takes place following extensive small bowel resection where the remnant bowel improves its ability to absorb nutrients.
This process begins immediately after intestinal resection and continues for up to two years. This process leads to morphologic changes, which increase surface area of the remaining bowel and improve the functional absorptive capacity of individual enterocytes and colonocytes. Factors which have been shown to enhance adaptation include: growth hormone, epidermal growth factor, insulin-like growth factors I and II, keratinocyte growth factor, peptide YY, glucagon-like peptide 2, soluble fiber, short-chain fatty acids, glutamine, polyamines, interleukines 3, 11 and 15, and pancreaticobiliary secretions.
Further reading: clevelandclinicmeded.com/selected_topics/shortbowel/summary/article.htm
9)c
10) b
Gut-associated lymphoid tissue (GALT) represent a major division of the immune system and is made up of aggregated (Peyer's patches, lymphoid follicles, mesenteric lymph nodes) and nonaggregated cellular components.
The lamina propria of the small intestine contains a wide array of nonaggregated lymphoid tissue including B cells, T cells, macrophages, eosinophils, and mast cells.
Some 80% to 99% of B cells are active producers of immunoglobulin A (IgA). In comparison, only 2% to 5% of B cells found in other lymphoid tissues of the body secrete IgA.
IgA is the major immunoglobulin of the intestinal immune system. The functional characteristics of IgA are unlike those of other antibodies. Unlike IgG or IgM, secretory IgA does not induce Fc-mediated inflammatory reactionsMost of the protective effect of IgA derives from its ability to bind the threatening antigen efficiently, while resisting enzymatic degradation by gut enzymes.
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