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GIT Small bowel

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الكلية كلية طب الاسنان     القسم  العلوم الاساسية     المرحلة 3
أستاذ المادة علي زكي ناجي الاسدي       25/06/2019 10:05:55
GENERAL PATHOLOGY
Pathology of the bowel:
The small intestine in the human adult is approximately 6 meters in length, the first 25 cm of the small intestine, the duodenum, is retroperitoneal; the jejunum marks the entry of the small intestine into the peritoneal cavity, terminating where the ileum enters the colon at the ileocecal valve.
the colon (large intestine) approximately 1.5 meters. colon is subdivided into the cecum and the ascending, transverse, descending, and sigmoid colon .
Small intestinal mucosal lining show villi . These extend into the lumen as finger-like projections covered by epithelial lining cells. The central core of lamina propria contains blood vessels; lymphatics; a minimal population of lymphocytes and eosinophils. Between the bases of the villi are the crypts.
The muscularis mucosae forms a smooth, continuous sheet, serving to anchor the configuration of villi and crypts .
In normal individuals, the villus-to-crypt height ratio is about 4 to 5:1.
villi of the small intestinal mucosa are the site for terminal digestion and absorption of foodstuffs through the action of the columnar absorptive cells .
crypts secrete ions and water, deliver immunoglobulin A and antimicrobial peptides to the lumen, and serve as the site for cell division and renewal.
colonic mucosa has no villi and it surface is flat.
The mucosa is punctuated by numerous straight tubular crypts that extend down to the muscularis mucosa.
The surface epithelium is composed of columnar absorptive cells, which have shorter, less abundant microvilli than found in the small intestine, but numerous goblet cells.
Congenital Anomalies
1-Duplication of the small intestine or colon, usually in the form of saccular to long, cystic structures
2-Malrotation of the entire bowel, resulting from improper embryologic rotation of the gut
3-Omphalocele, in which the abdominal musculature fails to form, leading to birth of an infant with herniation of abdominal contents into a ventral membranous sac
ATRESIA AND STENOSIS
Duodenal atresia is most common; the jejunum and ileum are equally involved and the colon virtually never.
The obstruction may be complete (atresia) or incomplete ( stenosis).
Single or multiple lesions appear to arise from developmental failure, intrauterine vascular accidents, or intussusceptions (telescoping of one intestinal segment within another) occurring after the intestine has developed.
MECKEL DIVERTICULUM
Failure of involution of the vitelline duct, which connects the lumen of the developing gut to the yolk sac, produces a Meckel diverticulum.
This solitary diverticulum lies (85 cm) of the ileocecal valve.
This is a true diverticulum, in that it contains all three layers of the normal bowel wall: mucosa, submucosa, and muscularis propria. Meckel diverticula may take the form of only a small pouch or a blind segment having a lumen greater in diameter than that of the ileum and a length of up to 6 cm.
Meckel diverticula are present in an estimated 2% of the normal population, but most remain asymptomatic or are discovered incidentally
HIRSCHSPRUNG DISEASE "CONGENITAL AGANGLIONIC"
This disorder is characterized by the absence of ganglion cells in the large bowel, leading to functional obstruction and colonic dilatation proximal to the affected segment.
MORPHOLOGY.
Most cases involve the rectum and sigmoid only. Proximal to the aganglionic segment, the colon undergoes progressive dilation and hypertrophy. With time, the proximal innervated colon may become massively distended, sometimes achieving a diameter of 15 to 20 cm (megacolon). When distention outruns the hypertrophy, the colonic wall becomes markedly thinned and may rupture, usually near the cecum.
Clinical Features.
Hirschsprung disease occurs in approximately 1 in 5000 to 8000 live births. Males predominate 4:1.
Hirschsprung disease usually manifests itself in the immediate neonatal period by failure to pass meconium, followed by obstructive constipation. The major threats to life in this disorder are superimposed enterocolitis with fluid and electrolyte disturbances and perforation of the colon or appendix with peritonitis.
Celiac disease:
is a chronic disease, in which there is a characteristic mucosal lesion lead to impair nutrient absorption, which improves on withdrawal of wheat gliadins.
Pathogenesis.
The fundamental disorder in celiac sprue is a sensitivity to gluten protein component (gliadin) of wheat and closely related grains (oat, barley..).
Cell-mediated immunity appears to be important in the pathogenesis of this disease.
Morphology:.
The mucosa appears flat or scalloped.
Biopsy specimens demonstrate a diffuse marked atrophy or total loss of villi. The surface epithelium shows an increased number of intraepithelial lymphocytes. The crypts exhibit increased mitotic activity and are elongated, and tortuous.
Clinical Features
Symptomatic diarrhea and failure to thrive may be evident during infancy, yet adults may seek attention only in their forties. The classic presentation includes diarrhea, flatulence, weight loss, and fatigue. Extraintestinal manifestations of malabsorption may overshadow the intestinal symptoms.
Detection of circulating antigliadin favors the diagnosis.
Definitive diagnosis rests on:
(1) clinical documentation of malabsorption.
(2) demonstration of the intestinal lesion by small bowel biopsy.
(3) unequivocal improvement in both symptoms and mucosal histology on gluten withdrawal from the diet.
There is an increase risk of malignant disease. More than half of these malignancies are intestinal lymphomas, other malignancies include gastrointestinal and breast carcinomas.
Idiopathic Inflammatory Bowel Disease:
They are chronic, relapsing inflammatory disorders of obscure origin.
1- Crohn disease:
is a granulomatous disease that may affect any portion of the gastrointestinal tract from esophagus to anus but most often involves the small intestine and colon.
2- ulcerative colitis: is a non-granulomatous disease limited to the colon
Pathogenesis:
• Genetic predisposition:
• Infectious agents:
• Hyper-regulation of immune response.
Gross appearance:
gross involvement of the small intestine alone in about 40% of cases, of small intestine and colon in 30%, and of the colon alone in about 30%.
The intestinal wall is rubbery and thick, the result of edema, inflammation and fibrosis.
lumen is almost always narrowed
A classic feature of Crohn disease is the sharp demarcation of diseased bowel segments from adjacent uninvolved bowel.
When multiple bowel segments are involved, the intervening bowel is essentially normal (skip lesions)
Mucosal ulcerations.
Cobblestone appearance of mucosal surface.
Fissure formation with sinus tracts.
Microscopical appearance:
heavy transmural chronic inflammatory cells infiltrate with non-caceating granuloma formation.
The disease usually begins with intermittent attacks of relatively mild diarrhea, fever, and abdominal pain, spaced by asymptomatic periods lasting for weeks to many months.
Often the attacks are precipitated by periods of physical or emotional stress.
In those with colonic involvement, occult or overt fecal blood loss may lead to anemia over the span of time.
chronic disease complications:
• fibrosing strictures, particularly of the terminal ileum.
• fistulas to other loops of bowel, the urinary bladder, vagina, or perianal skin.
• Extensive involvement of the small bowel, including the terminal ileum, may cause marked loss of albumin (protein-losing enteropathy), generalized malabsorption, specific malabsorption of vitamin B12 (with consequential pernicious anemia), or malabsorption of bile salts, leading to steatorrhea.
• 5-6 folds increase possibility of GIT cancers


المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .
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