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Gastritis,PUD,esoph
CMI - Fall 2011
| Question | Answer |
|---|---|
| What predisposes a person to Acid-peptic dz? | -^d acid production -Decrsd mucosal defense |
| What is the GI role of prostaglandin? | -Decrease acid produx (^mucus and bicarb secretion) -NSAIDS inhibit prostaglandins = more acid = ulcers! |
| What defends from acid? | -Mucus -Bicarb -Prostaglandin produx -Tight jxns |
| What defends from infex? | -Lymph tissue -Epithelial cell turnover -Stomach acid |
| Gastritis in inflamm of the stomach, what are some poss causes? | NSAIDS, H. pylori infex, Stress- related mucosal changes (intense physical stress-ICU), Atrophic gastritis (elderly,chronic H.pylori infex, autoimmune gastritis), alcoholic, infex |
| Is rebound of guarding seen in gastritis? | NO |
| Who would an H.pylori infex be most commonly seen in? | -Immigrants (SE Asia) ->60 y.o -Non-caucasion -Poor countries |
| H.pylori produces urease, which does what to the mucosal pH? | Raises it (H.pylori colonizes gastric mucosa adjacent to gastric epi cells) |
| Most likely route of transmission of H.pylori? | Oral - to - Oral Fecal - to - Oral |
| Most ppl w/ H.pylori are asymptomatic, but 85% end up w/pangastritis, while the other 15% end up w/ antral-type gastritis, what's the difference? | -Pangastritis: (acid hyposecretion)-can result in gastric CA -Antral-type: (acid hypersecretion)- can result in duodenal ulcer |
| Which commonly used drugs in the US damage the surface epi and NL protective barrier of the stomach? | NSAIDS |
| What is a major way that NSAIDs cause damage to stomach? | Inhibit prostaglandin produx =decrs blood flow,mucus and bicarb protection :( |
| NSAIDs inhibit prostaglandin thru inhibition of COX-1 and -2, what are these enzymes responsible for? | -COX-1:Regulates GI mucosal integrity -COX-2:Regulates inflammation |
| Ibuprofen is what kind of NSAID? | Non-selective=inhibits COX1 and COX2 (so does ASA) |
| Action of selective NSAIDS (celebrex)? | -Inhibit COX2 and relatively spares COX1=less GI AEs, but ^ CV risk |
| When and why does gastritis develop in critically ill/stressed pts? | ~w/in 72 hrs -Most likely d/t mucosal ischemia d/t decrsd gastric blood flow |
| Autoimmune gastritis is aka? | Pernicious anemia (results in absent or decrsd gastric acid and intrinsic fx = VitB12 malabsorp) |
| NL hgb in M and F? | Male: 14-18 Female: 11-16 |
| NL hct in M and F? | Male: 39-54% F: 34-47% |
| How many of those w/h.pylori infex progress to chronic infex w/diffuse mucosal inflamm? | Up to ~90% (about 15% develop a clinically significant ulcer) |
| What is the end result of an h.pylori gastritis infection? | -Atrophic gastritis (may predispose to gastric CA) |
| What is the role of COX-1 and COX-2 enzymes? | -COX-1: Regulates GI mucosal integrity -COX-2: Regulates inflammation |
| MC presentation of stress gastritis? | -GI bleeding |
| Autoimmune gastritis increases risk of what 3X? | Gastric adenocarcinoma |
| What are some general gastritis tx? | -Antacids (tums, rolaids) -H2 recep antagonists -PPIs -Sucralfate (coats stomach) -Avoid NSAIDs and other triggers -Treat UL cause -Lifestyle changes |
| Stress gastritis prophylaxis is routinely given to critically ill pts w/ RFs for sig bleeding, what is given? | -IV H2 recp blockers -IV PPI -Sucralfate suspension |
| What is the tx for stress gastritis once bleeding occurs? | IV PPI continuous infusion, sucralfate, endoscopy if poss |
| What is the order of the mucosal layers of the stomach from inside to outside? | 1.Mucosa 2.Submucosa 3.Muscularis 4.Serosa 5.Visceral peritoneum |
| What is PUD? | Break in gastric or duodenal mucosa that extends to the submucosa and is usually >5mm in diameter |
| What is the lifetime prevalence of PUD and who is it MC in? | -10% -Men |
| Duodenal ulcers most common in which ages? | 30-55 |
| Gastric ulcers most common in which ages? | 55-70 |
| What are the majority of ulcers related to? | NSAIDs or H.pylori |
| Where do gastric ulcers mostly occur? | Lesser curvature and antral rgn of stomach |
| How many of gastric ulcers are H.pylori +? and what must you do? | 70-90% -Acid produx may be NL or low -MUST bx-might be malignant (and then must rescope to make sure is gone) |
| 95% of duodenal ulcers are located where? | In the bulb or pyloric channel |
| Duodenal ulcer association w/ CA and how many test H.pylori +? | -Assoc w/decrsd risk for development of gastric adenocarcinoma -80-95% test + for H.pylori |
| What are the 2 MAJOR causes of PUD? | 1. NSAIDs/ASA use 2. H.pylori infex |
| NSAID/ASA use and relation to GUs and DUs? | -10-20% prevalence of GU & 2-5% prev of DU in long-tern users -Often develop in 1st 3mo of therapy -Age>60 -NSAID use w/ASA,steroids,anticoags |
| What is the syndrome of acid hypersecretion? | Zollinger-Ellison syndrome |
| What is more assoc w/GU and what is more assoc w/DU? | -NSAID use more assoc w/GU -H.pylori infex more assoc w/DU |
| Where do you most see H.pylori infected GU and DUs? | -GU in gastric body -DU in antrum |
| If pain from a peptic ulcer starts radiating or becomes constant, what might this indicate? | Ulcer may have penetrated all the way through |
| Which ulcer feels better with eating? | DU (better w/food, antacids,anti- secretory products) |
| Significant vomiting and wt loss are unusual w/uncomplicated ulcers and mat suggest? | -Gastric outlet obstrux (narrowing of pylorus) -Gastric CA |
| What is assoc w/epigastric pain, early satiety and post-prandial fullness? | Dyspepsia |
| TRUE or FALSE: you will see guarding or rebounding in a pt w/uncomplicated PUD? | FALSE - entire physical exam can be NL if PUD is uncomplicated |
| What labs should you FOR SURE do w/suspicion of PUD? | -CBC -H.pylori testing |
| What is the most accurate dx test for PUD? | Endoscopy (& should be doing bx's of gastric ulcers) |
| Tx for PUD w/+H.pylori? | -Tx w/anti-H.pylori regimen for 10-14days -Then after:Tx w/PPI or H2Blkr for 4-6wks |
| To confirm successful eradication of H.pylori, how long must you wait? | -4-6wks post tx for urea breath test -8wks for stool test |
| If a pt cannot stop NSAIDs, what should you do? | Prophylaxis w/PPI |
| How do you r/o Zollinger-Ellison syndrome? | -Do a fasting gastrin |
| What is the primary concern with a non- healing gastric ulcer? | Malignancy |
| What are some non-invasive methods for confirming H.pylori infection? | 1.Fecal antigen immunoassay-test for active dz 2.Urea breath test-test for active dz 3.Serologic tests-cheaper and widely avail, but not as accurate and cannot disting bw active vs past dz (bc IgG can stay elevated for a while) |
| Prior to non-invasive methods to test for H. pylori infection, what needs to be stopped? | -PPIs held for 14 days prior -Abx held for at least 28 days prior (bc could suppress infection) |
| When a scope is ordered for another issue, can get a gastric bx to test for active H. pylori infex, via? | Measure urease production |
| If pt has an UGI bleed or recently on PPIs or Abx, how do you test for H. pylori infex? | Histologic assessment (more$$) |
| What are 4 major complications with PUD? | 1.Bleeding 2.Perforation 3.Penetration 4.Obstruction |
| A gastric outlet obstruction may occur d/t? | Swelling, inflamm, scarring near pyloric channel |
| Hypergastrinemia and acid hypersecretion d/t gastrin-secreting neuroendocrine tumors is known as? | Zollinger-ellison syndrome (2/3 are malignant, 1/3 have metas. to liver @time of initial presentation) |
| What is the gradual, multi-step progression to gastic CA? | Gastritis>Atrophy>Metaplasia>Dysplasia>CA |
| RFs for gastric CA? | H.pylori (60-90%),diet high in salt and nitrates, smoking, pernicious anemia, atrophy |
| If a GU has failed to heal w/in 12 wks, what may the next tx step? | Surgery (malignancy suspicion) |
| A partial gastrectomy (+vagotomy) may be indicated for tx of ulcer, there are 2 methods: Billroth I and II, what are they and which is more common? | *Billroth I: Gastro-duodenal anastomosis *Billroth II: MOST COMMON--Gastrojejunal anastomosis |
| Postgastrectomy involving removal of part of antrum can ^risk of gastric CA ~15-20 yrs post-surgery, why? | -Removed antrum=decrsd stomach acid>atrophy> metaplasia>dysplasia>CA |
| Dyspepsia w/no obvious cause is aka? | Functional dyspepsia |
| Tx of fxnal dyspepsia? | -Lifestyle changes: reduce alcohol, caffeine, fatty foods -Meds limited success |
| When a bolus of food passes through the upper esoph sphincter, what initiates primary peristalsis? | Vagal stretch receptors in the wall of the esophagus detect distension & induce vagovagal reflex (=primary peristalsis) |
| After primary peristalsis, secondary peristalsis occurs, which is: | Another wave of peristalsis that clears the esophagus of food |
| Heartburn is aka? | Pyrosis |
| What can cause esophagitis? | -GER -Infections -Eosinophilic/Autoimmune -Drug-induced -Injury -excessive vomiting -Surgery or radiation to chest |
| What are the MC common causes of infectious esophagitis (rare and MC in immunocompromised)? | -Candida -HSV (may also have oral ulcers) -Cytomegalovirus (may have infected other sites, too) |
| Eosinophilic esophagitis is related to? | Allergies - MC in kids,esp MALES -Milk,egg,wheat,soy,pnuts,bean allergies |
| How is Eosinophilic esophagitis dx'd? | Labs:may see^eosinophils, IgE -Endoscope w/biopsy |
| Drug-induced esophagitis is from direct,prolonged mucosal contact, how can this be avoided? | Take pills w/4oz glass of H2O and sit up for 30 minutes, after |
| What is the MC cause of esophagitis? | GER |
| What is the MC type of hiatal hernia? | Sliding-type (95%) -Other =paraesophageal hiatal hernia(usually req surgery) |
| What is water brash? | Assoc with GER -Hypersalivation in response to reflux (unusual symptom) |
| Which symptom ALWAYS warrants reason for upper endoscopy?? | -dysphagia (AND bx) |
| What are some uses for barium esophagram? | -to ID area of stricture b4 endoscope -Hiatal hernia -Ulcers/erosions -Motility d/o |
| What are some foods that should be avoided in tx of GERD? | Chocolate,alcohol,citrus,tomato based produx, spicy foods that cause symptoms, fatty foods that delay gastric emptying |
| With GERD, should not eat within how many hours of going to bed? | 3 hrs |
| If medical management fails for GERD management, what is another option? | Surgical fundiplocation |
| What is the motility d/o involving loss of peristalsis in the distal 2/3 of the esophagus and impaired (reduced) relaxation of the LES? | Achalasia |
| What is the syndrome that involves nonpenetrating mucosal tears in the esophagus that are thought to be from events that increase trans-abd pressure, such as vomiting,retching,lifting? | Mallory-weiss syndrome |
| Which syndrome involves rupture/perforation of the esophagus, usually d/t a previous medical procedure? | Borhaave's syndrome |
| Where are esophageal webs and rings found? | Webs=upper or mid-esophagus Rings=distal esophagus |
| Esophageal rings are most likely assoc w/? | Hiatal hernia |
| What are esophageal varices? | Dilated submucosal veins in pts with underlying portal HTN |
| To prevent 1st episodes of variceal bleeding, what should be done? | Pts w/cirrhosis should have a dxtic endoscopy |
| Esophageal squamous cell carcinoma is almost always assoc w/? | Alc and Tobacco |
| Esoph adenocarcinomas are usually assoc w/? | GERD or Barret's Esophagus |
Created by:
ferrier.kath
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