chapter17 GIT Flashcards
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Congenital abnormalities GIT
AtresiaDuplicationsFistula
Most common congenital is ______. Developmentally incomplete
Atresia
It rsults to mechanical obstruction due to replacement of noncanalized cord.
Esophageal atresia
Atresia most commonly occurs in the _______. It is usually assoc with a _____ connecting the upper and lower esophageal pouches to a bronchus or trachea.
Near tracheal BifucationFistula
Is less common than esophageal atresia but it frequently involves the duodenum and is characterized by a segment of bowel lacking a lumen.
Intestinal Atresia
It is an incomplete form of atresia in which the lumen is reduced in caliber as a result of fibrous thickening of the wall resulting in partial or complete obstruction.Most commonly affected is in the esophagus and small intestine.
Stenosis
The most common congenital intestinal atresia due to failure of the cloacal diaphragm to involute.
Imperforate anus
Are saccular or congenital cystic masses that contain redundant smooth muscle layers. May be present in the esophagus,intestines or colon.
Congenital duplication cyst
What is the tx of ménétrier dse
- Supportive 2. IV albumin 3. Parenteral nutritionSevere cases: gastrectomy
A disease caused by gastrin-secreting tumors, gastrinomas, that are most commonly found in the small intestine and pancreas.Px often present with duodenal ulcer and chronic diarrhea.Within the stomach the most remarkable feature is DOUBLING OXYNTIC MUCOSAL THICKNESS DUE TO A FIVEFOLD INCREASE IN PARIETAL CELLS
Zollinger Ellison Syndrome
Gastric polyps and tumors
- Inflammatory and hyperplastic polyps2. Fundic gland polyps3. Gastric adenoma4.gastric adenocarcinoma5. Lymphoma6. Carcinoid tumor7. Gastrointestinal stromal tumor
Nodules or masses that project above the level id the surrounding mucosa and are i.d in up to 5% of upper GI endoscopiesIt may develop as a result of epithelial or stromal cell hyperplasia, inflammation, ectopia or neoplasia.
Polyps
Approx 75% of all gastric polypsAre most common in indiv bet 50-60 yo.Polyps that usually develop in assoc with chronic gastritis, which initiates the injury and reactive hyperplasia that leads to polyp growth.In indiv with H.pylori, regresses after removal of insult.
Inflammatory and hyperplastic polyps
Occur sporadically and in indiv with FAP.Increased gastric secretion, in response to reduced gastric acidity, and the resulting glandular hyperplasia.5x more commom in women and an average of 50y0.May be asymptomatic or assoc with nausea, vomiting, or epigastric pain.Morphology:Occur in gastric body and fundusWell circumscribed lesions with smooth surfaceSingle or multipleCystically dilated irregular glands lined by flattened parietal and chief cellsInflammation is typically absent or minimal.
Fundic gland polyps
10% of all gastric polyps.Incidence increases progressively with age. Bet 50-603x more in malesLike fundic gland polyp it is assoc with FAPRisk of gastric ca is related to the size of lesion and is elev in leasion greater than 2cm in diameter
Gastric adenoma
Morphology:Usually solitary lesions less than 2cm in diameterMost commonly loc in the antrumMajority are composed of intestinal-type columnar epithelium.
Gastric adenoma
Is the most common malignancy in the stomach.90% of all gastric ca.Early symptoms resemble those of chronic gastritis, including,Dysphagia, dyspepsia, and nausea.Often discovered at advanced stages when symptoms such as wt loss, anorexia, altered bowel ha its, anemia a s hemorrhage trigger further diagnostic evaluation.It is. Ore common in lower socioeconomic status and in indiv with multifocal mucosal atrophy and intestinal metaplasia. PUD doesnt impart as risk factor except to those who had partial gastrectomy for PUD.Majority is not inherited.
Gastric adenocarcinoma
What is the pathogenesis in gastric adenocarcinoma?
Germline mutations in CDH1 which encodes E-cadherin , a protein that contributes to epithelial intercellular adhesion are associated with familial gastric ca of which is a diffuse type.
What is the pathogenesis of intestinal-type gastric ca?
Mutation in beta-catenin, a protein that binds to both E-cadherinand adenomatous polyposis coli ( APC ), as well as microsatellite instability and hypermethylationof several genes including TGF B RII, BAX, IGFR II and p16 /INK4.
Morphology charac:Irreg enlargement of gastric rugae.Some areas appear polypoid.Enlarged rugae present in body and fundus except antrum( gen spared)Most characteristic feature: HYPERPLASIA OF FOVEOLAR MUCOUS CELLS.THe glands are elongated with CORK-SCREW appearance and cystic dilation is common.Inflammation is only modest although some cases show marked intraepithelial lymphocytosis.Diffuse or patchy glandular atrophy, evident as hypoplasia or parietal and chief cell is typical
Ménétrier dse
2 diseases associated in hypertrophic gastrophaties
- Ménétrier dis2. Zollinger ellison syndrome
Uncommon diseases charac by GIANT CEREBRIFORM ENLARGEMENT OF THE RUGAL FOLDS due to epithelial hyperplasia W/O inflammation.As expected they are linked to excessive GF release
HYPERTROPHIC GASTROPHATIES
Rare d/oCaused by x’ss secretion TGF-alphaCharac by: diffuse hyperplasia of foveolar epithelium of the. Body and fundus and hyperproteinemia due to protein losing enteropathySecondary symptom: wt loss, diRrhea, peripheral edema.Pathologic feature in children same in adult but pedia dse is self- lim and often follows respi infection.Risk of gastric adenocarcinoma is ⬆️ in adult.
Ménétrier dse
Intestinal obstruction occurs at any level but which is commonly affected and why?
Small intestine because of its narrow lumen
what are the collection of intestinal obstruction?
- hernias
- intussuception
- volvulus
- adhesions
this account for 80 % of intestinal obstructions
volvulus
how many percent does tumors account for intestinal obstruction?
10-15%
what are the clin manifestation of intestinal obstruction?
abdomina pain and distention
vomiting
constipation
What is the weakness or defect in the wall of the peritoneal cavity that may permit protrusion of a serosa-lined pouch of peritoneum
hernial sac
Acquired hernias most commonly occured in the?
It is via?
anterior
inguinal, femoral canals, umbilicus, or sites of surgical scars
The resultant stasis and edema increases the bulk of the herniated loop, leading to permanent entrapment called _______. In which overtime, arterial, and venous compromise ______ develpps that can result in infarction.`
incarceration
strangulation
Surgical procedures, infections, or other causes of peritoneal inflammation, such as endometriosis, may result in development of _______ between bowel segmens, the abdomina wall and operative sites.
adesions
Complete twisting of a loop bowel about its mesenteric base of attachment is called _____ and produces both luminal and vascular compromise. Thus presentation includes features of obstruction and infarction. It occurs most often in large redundant loops of sigmoid colon, followed in frequency by the :
cecum
small bowel
stomach
or rarely transverse colon.
Because this is rare, it is often missed clinically
volvulus
It occurs when a segment of the intestine, constricted by a wave of peristalsis, telescopes into te immediately distal segment. Once trapped, the invaginated segment is propelled by peristalsis and pulls the mesentery along. If left untreated may result in or progress into intestinal obstruction, compression of mesenteric vessels and infarction.
When encountered in infants no underlying cause but come cases are associated with_______.
In older children and adults an intraluminal mass or tumor generally serves as the point of traction that causes this.
Intussusception
Rota virus
Acute compromise of any major vessel can lead to infarction of several meters of intestine. Damage can range from______.
- mucosal infarction
- mural infarction
- transmural infarction
Infarction extending no deeper than te muscularis mucosa
mucosal infarction
Infarction extending of mucosa to submucosa
mural infarction
infarction involving all three wall layers
transmural infarciton
Mucosal or mural infarctions are often secondary to____
acute or chronic hypoperfusion
transmural infarciton is generally caused by _____
acute vascular obstruction
what are the two major variables in IBD?
- Time frame which it develops
- vessels affected
Intestinal segments at the end of their respective arterial supplies are particularly susceptible to iscemia. These are called_______ which includes:__________
Watershed zone
splenic flexure where the superior and inferior mesenteric arterial circulation ends
to a lesser extent the sigmoid colon andrecutm where inf mesenteric, pudendal and iliac arteries circulations end.
What is a morphologic signature of iscemic intestinal disease? why?
Surface epithelial atrophy or even necrosis and sloughing with normal or hyperproliferative crypts .
The reason is intestinal capillaries run alongside the glands, form the crypt to surface, before making a hairpin turn at the surface to empty into the post-capillary venules. This allows oxygenated blood to supply crypts but leaves the surce epithelium vulnerable to ischemic injury. This anatomy protects the crypts which contain the epithelial stem cells.
Microscopic examination showing ATROPHY OR SLOUGHING OF SURFACE EPITHELIUM. In contrast, crypts may be hyperproliferative. Inflammatory infiltrates are initially absent in acute ischemia nut neutrophils are recruited within hours of reperfusion. Chronic ischemia is accompanied by fibrous scarrring of the lamina propria and uncommonly stricture forms.
IBD
In acute phase of IBD bacterial superinfection and enterotoxin release may induce pseudomembrane formation that can resemble ______
C. difficile- associated pseudomembranous colitis
It tends to occur in older individual with coexisting cardiac or vulvular disease. Acute transmural infarction typically presents wit sudden abdominal pain and tenderness, sometimes accompanied by nausea, vomiting, bloody diarrhea, or grossly melanotic stool.
Patients may progress to shockand vascular collapse within hours as a result of blood loss. Peristaltic sound diminished or disappear and muscular spasm creates board- like rigidity of the abdomina wall.
These physical signs overlaps with other abdominal emergencies that results in delayed or missed diagnosis.
IBD
These themselves may not be fatal. However, may progress to more extensive infarction if the vascular supply is not restored by correction of the insult or in chronic dse by dev of adequate collateral supplies. Diagnosis is partially difficult since there may be a confusing array of nonspecific abdominal symptoms including intermittent bloody diarrhea and intestinal psuedo-obstruction.
Mucosal and mural infarction
May masquarade as IBD with episodes of bloody diarrhea interspesed with periods of healing
chronic ischemia
This causes iscemic GI dsew due to viral tropism for and infection of endothelial cells. This is a complication of an immunosuppressive therapy
CMV
This occurs when the GI tract is irradiated. In add to epitelial damage, radiation-induced vascular injury may be significant and produce changes that are similar to ischemic disease. The presence of BIZARRE “ RADIATION FIBROBLAST” within the stroma may provide important clue to the etiology. It manifest as anorexia, abdominal cramps, and a malabsorptive diarrhea while chronic radiation enteritis or colitis is often more indolent and may present as an inflammatory colitis.
Radiation enterocolitis
Is an acute do of the small and large intestines that can result in transmural necrosis. It is the most common acquired GI emergency of neonates, particularly those who are premature of LBW and occurs most oftenat the time of oral feeding.
NEC
Characterized by malformed submucosal and mucosal blood vessels. It occurs most often in the CECUM or RIGHT colon because cecum has the largest diameter that develops tha greatest wall tension. It is usally after the 6th decade of life. Prevalence is < 1 % in adult, it accounts for 20 % major episodes of lower intestinal bleeding; intestinal hemorrage may be chronic and intermittent, acute and massive. Pathogenesis is attributed to mechanical and congenital factors.
angiodysplasia
Presents most commonly as chronic diarrhea characterized by defective absorption of fats, fat- and water- soluble vit ,proteins, carbohydrates,electrolytes and mineral and water.
Malabsorption
It is accompanied by wt loss, anorexia, abdominal distention, borborygmi and muscle wasting.
chronic malabsorption