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Pathology-8
STOMACH
| Question | Answer |
|---|---|
| cardia is made up of what cells? | mucous cells (cardia glands) |
| the fundus is made up of what cells? | parietal, chief, oxyntic glands, scattered endocrine |
| body is made up of what cells? | oxyntic: parietal/chief, scattered endocrine cells |
| the pylorus is made up of what cells? | mucous secreting/endocrine |
| the antrum is made up of what cells? | mucous secreting/endocrine, G cells |
| mucous cells are located? secreting? | cardia/antral (secreting mucous and pepsinogens |
| where are parietal cells located in the oxyntic gland? | in the upper part, toward the surface |
| what do parietal cells secrete? | intrinsic factor, H+ |
| what is the function of intrinsic factor? | it binds vitamin B12 in teh duodenum and permits absorption in the ileum |
| where are chief cells located in the oxyntic gland? | the lower part, toward the base |
| explain how pepsin is activated? | parietal cells secrete H+ which lowers the pH, which activates pepsinogen 1 and 2 secreted by chief cells, which is converted to pepsin |
| where are the main endocrine cells located? | G cells, in the antrum |
| what are the endocrine cells in the body of the stomach for? | they release histamine, which activates parietal cells, decreasing pH, increasing acid production |
| B: explain how the cells interact during feeding? | see food (celiac phase) activ Ach rec, which act parietal cells by influx of Ca2+, decreases pH. G cells were also stimulated so gastrin incr Ca2+ influx, and activ Histamine incr acid |
| what problems are associated with pyloric stenosis? | trisomy 18, turner syndrome, esophageal atresia |
| who is most affected by pyloric stenosis? | male infants |
| what is the typical presentation of congenital pyloric stenosis? | projectile vomiting and regurgitation in the 2nd or 3rd week |
| severe congenital diaphragmatic hernias can be associated with what? | all of GI out into thorax--> hypoplasia of lung (severe respiratory distress) |
| acquired pyloric stenosis arise from? | tumors or fibrosis, often associated with gastric ulcers (scarring) |
| Helicobacter pylori, causing gastritis, most likely manifests where? | antrum (90%) |
| what is the most impt cause of chronic gastritis? | helicobacter pylori |
| What diseases is Hpyloir associated with? | chronic gastritis, peptic ulcer ds, gastric carcinoma, Gastric MALT lymphoma (definitive) |
| GASTRIC MALT LYMPHOMA is always associated with what? | Hpylori infx |
| what are the common etiologies for gastritis? | autoimmunity, alco/cig, post-surgical, radiation, granulomatous inflamm (Chron's), GVHD |
| acute gastritis is usually caused by what? | NSAIDS, alcohol |
| acute gastritis usually involves what part of the stomach? | body, fundus, antrum |
| acute gastritis is characterized by what type of lesions? | SUPERFICIAL |
| where does chronic gastritis usually locate? | body/fundus, hardly ever the antrum |
| what is the most common cause of chronic gastritis? second most common? | Hpylori (1) autoimmune (2) |
| autoimmune chronic gastritis is usually to ______ cells | parietal |
| autoimmune chronic gastritis is usually associated with what? | pernicous anemia, Hashimoto's thyroiditis, Addison's disease, DM type 1 |
| You suspect gastritis in a pt. What tests can be done non-invasively? | serology, fecal bacterial detection, urea breath test |
| You have exhausted all non-invasive tests on a patient for which you still suspect gastritis. Which invasive tests? | rapid urease tests, PCR, biopsy (often done), culture |
| You obtain a biopsy on a pt with suspected gastritis. What will be done with this biopsy. | Silver stain will look for superficial HP cells on the mucosal lining that look like seaguls |
| what typically defines a peptic ulcer? | solitary lesion <4cm, but can see >4cm |
| What size of peptic ulcer is the worst? | peptic ulcers are graded based on size; a small may be malignant where a large may be benign |
| where are peptic ulcers usually located? | lesser curvature (antrum) or first part of duodenum |
| what is the trx for peptic ulcers? | they normally heal spontanously, but can recur |
| what are complications for peptic ulcers? | can cause massive hematemasis in addition to varicies, if perforates past muscularis mucosa or sometimes wall |
| You tell a pt you think their peptic ulcer has healed, bc you know they heal spontanously. She thanks you say much. What do you say? | They can recur |
| what is the pathogenesis of a peptic ulcer? | either increased aggressive forces or decreased body protection |
| what are the increased aggressive factors that can lead to peptic ulcer? | HPylori infx, NSAID, aspirin, cigs/alc, impaired regulation of acid/pepsin secretion |
| what are the decreased body protections that can lead to peptic ulceration? | ischemia, shock, delayed gastric emptying, duodenal reflux |
| what are the complications for peptic ulceration? | bleeding (M/C), perforation, edema/scarring, pain |
| 25% of peptic ulcer deaths are due to? | bleeding |
| what is the most common complication in peptic ulcer? | bleeding |
| what is the common morphology of acute gastric ulceration? | multiple lesions (that may be superficial or deep) mainly in the stomach (less in duodenum) |
| what is the typical situation underlying acute gastric ulceration? | extensive burns, shock, trauma, head injury |
| Menetrier's Disease? | rare, hyperplasia of the superficial mucosal cells with glandular atrophy |
| hypertrophic hypersecretory gastropathy? | rare, hyperplasia of chief and parietal cells |
| hyperplasia of the chief and parietal cells? | hypertrophic hypersecretory gastropathy, rare |
| hyperplasia of the superficial mucosal cells with glandular atrophy? | Menetrier's disease, rare |
| Zollinger Ellison Syndrome? | rare, hypertrophic gastropathy, hyperplasia of gastric glands, secondary to gastrin production, multiple intractable ulcers, unbearably painful |
| what does a Zollinger Ellison syndrome slide look like (morphologically)? | cerebriform hyperplasia of rugal fold, brain |
| what is the clinical significant of Zollinger-Ellison syndrome? | it may mimick carcinoma of the stomach bc of changed rugal pattern |
| hyperplasia of gastric glands, causing excess gastrin production? | Zollinger-Ellison syndrome, multiple intractable ulcers, unbearably painful |
| Most Benign Gastric Polyps are ______? Less commonly they are ---? | hyperplastic (90%); adenomatous |
| You have a pt with a benign adematous polyp. Why are you clinically monitoring and being very thorough in your benign diagnosis? | 40% of aden. polyps have a carcinoma focus on dx, and the risk of carcinoma in the adjacent mucosa is as high as 30% |
| gastric carcinoma is associated with? | diet, smoking, Group A blood, chronic atrophic gastritis, HP infx, gastric adenoma, partial gastrectomy, Barret's esophagus |
| Barrett's esophagus may lead to what----? | adenoCAR of esophagus and gastric carcinoma |
| what is the most common location for gastric carcinoma? | pyloris and antrum, along the lesser curvature |
| How are gastric CAR's classified? | intestinal (polypoidal or ulcerated) vs diffuse (Linitus plastica) |
| Diffuse gastric carcinoma? | Linitus plastica |
| what defines gastric carcinoma as being advanced? | Linitus plastica (diffuse) or excavated (extending into the muscularis propria) |
| what do you notice histologically for Linitus plastica? | diffuse lesion, no distinct epi lesion, wall is thickened, signet ring cells |
| If you have a gastric carcinoma with no signet ring cells, how do you classify? | poorly differentiated |
| what are the clinical features of gastric carcinoma? | weight loss, abd pain, anorexia, vomiting, hemorrhage, anemia |
| what is the prx for gastric car? | good prx if detected early |
| what is the most common site for extranodal lymphomas? | stomach, weird..we're in the stomach section |
| GIST. what is the suspected cell of origin? | interstitial cell of Cajal |
| GIST is associated with what? | Carney's Triad: gastric GIST, paraganglioma, pulmonary chondroma |
| what is Carney's Triad? | GIST, pulmonary chondroma, gastric GIST |
| You're in the NICU with 4 projectile vomiting male infants. You know 1 of them has cong. pyloric stenosis. What's a good way to tell by evaluating the vomit? good way to tell on gross finding? good way to tell genetically? Treatment? | look for NON-BILOUS vomit bc it hasn't touched the stomach yet; grossly for esophageal atresia, visible peristalsis, or palpable mass; genetically trisomy 18, turner's syndr; tx is surgical splitting "knick" |
| You have a pt with antral gastritis and peptic ulcers. He's had this for 10years. Increases risk for? | acquired pyloric stenosis |
| why are NSAIDS the main cause for acute gastritis? | they inhibit prostaglandins which inhibit vasodilation of backflow vessels removing acid when it needs to be; prostaglanding also increases bicarb, which is now decreased |
| You see a gastric mucosa with hyperemic, punctate dark spots grossly. what do you suspect? what are common causes? | acute gastritis--common causes aspirin/Rheumatoid arthritis |
| B: what accompanies chronic gastritis histologically, concerning the mucosa? | mucosal inflammatory changes: mucosal atrophy and intestinal metaplasia, usually in the absence of erosions |
| How does Chron's disease involve the stomach? | it can cause chronic gastritis |
| Helicobacter infx increases with ____. | age |
| Most people (have/don't have) HPylori infx, which are mostly (symptomatic/asymptomatic)? | most have; most asymptomatic |
| All bacteria don't survive in the stomach. Does Hpylori have something special? | urease (produces ammonia to buffer acid) and flagella to move away from acid |
| Why is blood group A more prone to gastric carcinoma? | Increased risk for infex, and association with Helicobacter pylori |
| B: what is the target for the autoanitbody in autoimmune gastritis leading to pernicious anemia? | the H-K ATPase of parietal cells, gastrin receptor, and IF |
| autoimmune gastritis (a chronic gastritis) is at increased risk for _______? | gastric carcinoma and endocrine carcinoid tumors |
| Why is there usually no damage to the antrum in autoimmune chronic gastritis? | there are no parietal cells in the antrum |
| B: what do you typically see in terms of acid release in autoimmune chronic gastritis? | increased gastrin and achlorochondria |
| There are many subtypes of hypertrophic gastropathies. How are they all similar | They all produce cerebriform giant enlargement sof rugal folds of the gastric mucosa and they are all RARE |
| B: In hypertrophic gastrophy, specially Zollinger-Ellison syndrome, why does the gastric galnd undergo hyperplasia secondary to gastrin secrtion? | in the settin gof a gastrinoma |
| B: Why are hypertrophic gastropathies clinically significant? | On endoscopy they mimick gastric carcinoma or lymphoma, and (2) Zollinger Ellison or Hypertrophic-Hypersecretory gastropathy can predispose to peptic ulcers |
| B: Menetriers disease is a type of _________ that may be associated with ___secondary disease___? | protein-losing gastroenteropathy |
| B: Gastric varicies? | most often co-present with esophageal varicies, usually due to portal HTN, hard to see, most lie within 2 cm of GE jxn |
| B: Tumors of the stomach, just like in esophagus and intestines, predominantly arise from _____? | mucosa, not mesenchyme or stroma |
| B: In the alimentary canal, the term polp is reserved for mass lesions in teh mucosa, but you may ocassionally get a submucosal ______ or _________ that may protrude, generating a "polypoid" lesion. | lipoma or leiomyoma |
| gastric polyps common or uncommon? | uncommon |
| peptic ulcers...common or uncommon? | common |
| B: when you say that 90% of gastric polyps are hyperplastic, what do you mean? | the foveolar epithelium is hyperplastic; benign (no dysplasia); also get cystically dilated glandular tissue, with a lamina propria with increased infl cells and smooth muscle |
| Most hyperplastic polyps are ________(morphology) and are located in the _____? | sessile; antrum |
| Stomach adenomas comprise _____% of the polypoid lesions of the stomach? | 5-10% |
| B: how do hyperplastic and adenoma polypoid lesions differ? | adenomas are dysplastic, meaning they have malignant potential |
| Adenomatous polyps are much more common in ______ (location)? | colon |
| Gastric adenomas may be ___________ (morphology) and are most commonly located in _____? | sessile or pedunculated; antrum |
| B: How do adenomas of the stomach and colon differ? | In the stomach they can cover a large area of flat gastric mucosa without forming a mass lesion; colon they cover small areas. In the stomach they arise with a background of inflammation and intestinal metaplasia, where in colon arise from normal mucosa |
| B: inflammatory fibroid polyp (eosinophilic granuloma)? | typically at distal stomach, may cause acute gastric outlet obstruction |
| B: when are hyperplastic polyps most likely seen? | in the setting of chronic gastritis |
| What is the most comon tumor of the stomach? | gastric carcinoma |
| B: order of tumors from incr freq to decr regarding gastric tumors? | gastric CAR>lymphomas>carcinoids> mesenchymal tumors> GI stromal tumors> leiomyosarcomas> schwannoma |
| what is the second most common tumor in the world? | gastric carcinoma |
| Gastric CAR more likely to affect? | men, other countries, lower socioeconomic status |
| What is the leading cause of cancer deaths worlwide? | gastric carcinoma |
| B: what are the major differences between intestinal and diffuse gastric carcinomas? | INTESTINAL (bulky, glandular, M>F, high risk areas, precurser lesions, 55yo) DIFFUSE (poorly diff, discohesive malig cells, constant areas, no precurser, 48yo, M=F) |
| B: incr incidence of gastric carcinoma (risk factors ass with intestinal type; diffuse not really known) | ENVIROM (Hpyl, nitrites, smoked/salted foods, lack of fresh fruit, low socio, cigs); HOST (chronic gastritis, hypochl, gastric adenoma, barrets esophagus);GENETIC (blood groupA, hx, HNPCC, E-cadherin mut) |
| B: Why are partial gastrectomies a risk factor for gastric carcinoma? | it disrupts mucosa leaving it in a state of shock and thus hypochlorochondria, which favors bacterial growth, bile reflux, and chronic gastritis. |
| B: Why does Menetrier's disease have an incr risk for gastric carcinoma? | bc it causes hyperplasia of the mucosal cells and glandular atrophy which disrupts mucosa and turns acid production off (hypochlorochondria) favoring bacterial gastritis. |
| B: the favored location for gastric carcinoma is the _________ curvature in the _____ region? | lesser; antropyloric region |
| B: what morphologic feature has the best cooreclation with clinical outcome in gastric car? | depth of invasion |
| B: what separates an early vs advanced gastric carcinoma? | early (mucosa+submucosa confined); advanced extends below the submucosa into the muscular wall |
| For unknown reasons, all gastric carcinomas eventually invade and become advanced (bc of serosa) and frequently metastasize to ______nodes? | Virchow's nodes (supraclavicular sentinel), periumbilical region (foriming a subq nodule called a Sister Mary Joseph nodule) |
| Sister Mary Joseph Nodule? | gastric carcinoma |
| Krunkenberg Tumor | metastatic adenocarcinoma from gastric carcinoma spreading to ovary |
| interstitial cell of Cajal? | GIST, cells that control GI peristalsis |
| GIST tumors are thought to be involved in a tumor syndrome? | Carney's Syndrome (GIST, paraganglioma, pulomonary chondroma) |
| B: On a histologic slide you see a "lymphoepithelial lesion" from the stomach? | Gastric MALT lymphoma |
| B: majority of GIST tumors are positive for? | C-Kit |
| What is a gastric carcinoid tumor? | a gastric neuroendocrine cell |
| B: breast and lung cancer metastasis can mimick _____ in the stomach? | linitus plastica |
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