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Step 1 12.18.12
GI II
| Question | Answer |
|---|---|
| What is a hernia? | protrusion of peritoneum through an opening usually a site of weakness |
| What is a diaphragmatic hernia? What type is most common? | abd structures enter the thorax. most commonly a hiatal hernia in which the stomach herneates upward through the esophageal hiastus of the diaphragm |
| Who most commonly gets a diaphragmatic hernia? | infants as a result of defective defeloment |
| What is a sliding hiatal hernia? | GE junction is displaced, most common type. See "hourglass" stomach |
| What is a paraesophageal diaphragmatic hernia? | GE junction is normal. cardia moves into the thorax |
| What is the pathophys of an indirect inguinal hernia? | goes through the INternal (deep) inguinal ring, external (superficial) inguinal ring, and INto the scrotum. |
| Where does an indirect inguinal hernia enter the internal inguinal ring? | lateral to inferior epigastric artery |
| What layers cover an indirect inguinal hernia? | follows path of descent of testes so is covered by all 3 layers of spermatic fascia |
| Who gets an indirect inguinal hernia? Why? | occurs most commonly in male infants due to failure of the process vaginalis to close (can get hydrocele). |
| What is the pathophys of a direct inguinal hernia? | protrudes through the inguinal triangle ( Hesselbach's). bulges directly through abdominal wall medial to inferior epigastric artery. |
| What ring does a direct inguinal hernia go through? | only through superficial (external) inguinal ring |
| What layers does a direct inguinal hernia have? | only external spermatic fascia |
| Who gets a direct inguinal hernia? | mostly older men |
| What is a mnemonic for the anatomic relationships of direct and indirect inguinal hernia? | MD's don't LIe: medial to inferior epigastric=direct hernia. Lateral to inferior epigastric= indirect hernia |
| What is the pathophys of a femoral hernia? | protrudes below inguinal ligamanet through femoral canal lateral to pubic tubercle. more common in women |
| What type of hernia is a leading cause of bowel incarceration? | femoral hernia |
| Who gets femoral hernias? | more common in women |
| What composes Hasselbach's triangle? | inferior epigastric artery, lateral border of rectus abdominis, inguinal ligament |
| What is the source and action of gastrin? | Source: G cell in antrum of stomach. Action: incr gastric H+ secretion, incr growth of gastric mucose, incr gastric motility |
| How is gastrin regulated? | incr in stomach distention/alkalinization, amino acids, peptides, vagal stim, decr by stomach pH <1.5 |
| `What AA are potent stimulators of gastrin? What diesease is gastrin highly elevated? | Phenylalanine, Tryptophan. gastrin is highly incr in Zolliger-Ellison syndrome |
| What is the source and action of cholecytokinin? | I cells in duodenum and jejunom. ActionL incr pancreatic secretion, incr gallbladder contraction, decr gastric emptying, sphrincter of Oddi relaxation |
| How is cholecytokinin regulated? | incr by presence of FA and AA |
| How does colecytokinin cause pancreatic secretion? | via a muscarinin pathway |
| What is the source and action of secretin? | S cell of duodenum. Action: incr pancreatic HCO3 secretion, decr gastric acid secretion, incr bile secretion |
| How is secretin regulated? | incr by acid, fatty acids in lumen of duodenum |
| Why do you need secretin to cause HCO3 release? | Hco3 neutralizes the pH of the SI allowing for pancratic enzymes to work |
| What is the source and action of somatostatin? | D cells of pancreatic islets, GI mucosa. Action: decr gastric acid and pepsiongen secretion, decr pancreatic and small intestine fluid secretion, decr gallbladder contraction, decr insulin and glucagon release |
| How is somatostatin regulated? | incr by acid, decr by vagal stim |
| What is the overall role of somatostatin and what effect might it have on growth? | inhibitory hormone, antigrowth hormone effects (you need digestion to grow) |
| What is the source and action of glucose dependent insulinotropic peptide (GIP)? | K cells of duodenum jejunum. Action: exocrine: decr gastric H+ secretion. endocrine: incr insulin release |
| How is GIP regulated? | incr by FA, AA, oral glucose |
| Which is used more rapidly? An oral or IV glucose load? | oral |
| What is the source and action of vasoactive intestinal peptide (VIP)? | parasympathetic ganglia in sphincter, gallbladder, and small intestine. Action: incr intestinal water and electrolyte secretion, relaxation of intestinal SMM and sphincters |
| How is VIP regulated? | incr in distention and vagal stim, decr by adrenergic input |
| What is a VIPoma? What are the sx? | none alpha, non beta islet cell pancreatic tumor which secretes VIP. see copious diarrhea |
| What is the action of nitric oxide in the GI? | incr SMM relaxation, including the lower esopageal sphincter |
| In what condition is loss of NO secretion implicated? | incr lower esophageal tone seen in achalasia |
| What is the source and action of motilin? | small intestine, produces migrating motor complexes (MMCs) |
| How is motilin regulated? | incr in fasting state |
| How are motili receptor agonisits used pharmacologically? | used to stimulate intestinal peristalsis |
| What is the source and action of intrinsic factor? | parietal cells of stomach. action: vit B12 binding protein required for B12 uptake in the terminal ileum |
| What happens if parietal cells are destroyed by an autoimmune process? | chronic gastritis and pernicious anemia |
| What is the source and action of gastric acid? | from parietal cells (stomach), action is to decr stomach pH |
| How is gastric acid regulated? | incr by histamine, ACH, gastrin. decr by somatostatin, GIP, prostaglandin, secretin |
| What is a gastrinoma? What can it cause? | gastrin secreting tumor that causes contiuous high levels of acid and ulcers |
| What is the source and action of pepsin? | chief cells of stomach. does protein digestion |
| How is pepsin regulated? | incr by vagal stimulation, local acid |
| How does pepsinogen get activated? | via the gastric acid |
| What is the source and action of HCO3- in the GI? | mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner's glands (duodenum. neutralizes gastric acid |
| How is GI HCO3 regulated? | incr pancreatic and biliary secretion with secretin |
| How is HCO3 "trapped" in the stomach? | trapped in the mucus covering the gastric epithelium |
| What is the source and action of saliva? | ecretion from parotid, submandibular, sublingual glands stimulated by SNS and PSNS activity |
| What enzyme in the mouth digests starch? | amylase |
| What does HCO3- in the mouth do? | neutralizes bacterial acids |
| What is the major effects of atropine on the stomach? | blocks vagal stim of parietal cells. vagal stim of G cells is unaffected as GRP not ACH is used on these cells |
| What is the mechanism of gastrin incr acid secretion? | via its effects on ECL cells (hitamine release) rather than directly acting on parietal cells |
| What is the mech of prostaglandins/misoprostol, somatostatin decr acid secretion? | inhibits the cAMP pathway that activates the H+ ATPase |
| What is the function of Brunner's glands? Where are the located? | secrete alkaline mucus to neutralize acid contents entering the duodenum. located in duodenal submucosa (only GI submucosal glands) |
| What happens to Brunner's glads in peptic ulcer disease? | they hypertrophy |
| What is the difference between high flow and low flow pancreatic secretions? | low=high Cl-, high flow= high HCO3- |
| What the 3 major classes of pacreatic secretions? | 1. alpha amylase 2. lipases 3. proteases |
| What is the role of alpha amylase, how is it secreted? | starch digestion, secreted in its activated form |
| What are the 3 lipases made by the pancreas? What is their role? | lipase, phospholipase A, colipase. digest fats |
| What are 4 major proteases made by the pancreas? | trypsin, chymotrypsin, elastase, carboxypeptidases |
| What is the role of trypsin, chymotrypsin, elastase, carboxypeptidases? how are they secreted? | protein digestion, secreted as zymogens |
| How is trypsinogen activated? | converted to trypsin by enterokinase/enteropeptidase which is secreted by the duodenal mucosa. Trypsin activates itself along with other proenzymes |
| What is the mech of salivary amylase and what does it produce? | starts digestion, hydrolyzes alpha 1,4 linkages to yield disaccharides (maltose and alpha limit dextrins) |
| Where is pancreatic amylase found? What are the products of its digestion? | highest conc in duodenal lumen, hydrolyzes starch to oligosaccarides and dissacarides |
| Where is oligosaccaride hydrolases found? Whatd othey produce? | at brush border of intestine, rate limiting step in carbohydrate digestion, produce monsaccarides from oligo and disaccarides |
| What types of carbohydrates can enterocytes absorb? | only monosaccarides (glucose, glactose, fructose). |
| How is glucose taken up by enterocytes? | via SGLT (Na+ dependent) |
| How is fructose taken up by enterocytes? | via facillitated diffusion by GLUT-5 |
| How are all monosacarides tranported to the blood by enterocytes? | GLUT-2 |
| What is the use of the D-xylose absorbtion test? | distinguishes GI mucosal damage from other causes of malabsrobtion |
| How and where is iron absorbed? | as Fe2+ in the duodenum |
| Where is folate absorbed? | jejunum |
| Where is B12 absorbed? What goes with it? | absrobed in ileum along with bile acids, requires intrinsic factor |
| What are Peyer's patches? Where are they located and what do they contain? | unencapsulated lymphoid tissue found in lamina propria and submucosa of small intestine. contain specialized M cells which take up Ag |
| What happens to the B cells located in Peyer's patches? What ab do they use? | differentiate into IgA secreting plasma cells which ultimately reside in the lamina prpria |
| How is IgA used to deal with intraluminal Ag in the gut? | receives a protective secretory component, then tranpsorted across the epithelium to gut to deal with intraluminal Ag |
| What is the composition of bile? | composed of bile salts (bile acids conj to glycine or taurine making them water soluable), phospholipids, cholestrol, bilirubin, water, ions |
| What are the 3 major functions of bile? | 1. digestion and absorbtion of fats and lipid soluable vitamins 2. cholesterol secretion (only means to eliminate it) 3. antimicrobial activity (via membrane disruption) |
| What is bilirubin? What is a general idea of how it is excreted? | product of heme metabolism. removed from bloos by liver, conjugated by glucuronate, excreted in bile |
| What is direct bilurubin? | conjugated with glucoronic acid; water soluable |
| What is indirect bilirubin? | unconjugated; water insoluable |
| How do you get from RBCs to unconjugated bilirubin? | RBC's-->heme-->unconjugated bilirubin. this takes place in macrophages |
| How do you get from unconjugated bilirubin to indirect bilirubin? | albumin is added in bloodstream to make an unconjugated albumin bilirubin complex which is indirect bilirubin |
| How and where does indirect bilirubin become direct bilirubin? | in the liver via uridine glucoronyl transferase which conjugates bilirubin and makes it water solubel direct bilirubin |
| Where does direct bilirubin become uribillinogen how? | gut bacteria in the gut convert direct bilirubin to urobillinogen |
| What are the 2 fates of uribillonegen? What % goes to each? | can either be excreted in feces as stercobilin (color of stool) (80%), or can be recylced to the liver or kidneys (20%) |
| What happens to the urobillinogen that is recycled to the kidneys and liver? | Liver: it's reconjugated into direct bilirubin Kidney (10%): excreted in urine as urobilin which gives the color of urine |
| What is the aggression and location of salivary gland tumors? | generally beingng and occur in the parotid gland |
| What are some of the major types of salivary gland tumors? | 1. pleomorhpic adenoma (painless, movable mass) 2. Warthin's tumor: (benign; heterotopic salivary gland trapped in lymph node) 3. mucoepidermoid carcinoma ( most common maligngnat tumor) |
| What is the globus sensation? | a.k.a. globus hystericus, globus pharyngis. lump in the throat without clinical signifance triggered by strong emotional activity |
| What is achalasia? | failiure of relaxation of lower esophageal sphincter due to loss of myenteric (Aurbach's) plexus |
| What are the sx of achlasia? | high LES opening pressure and uncoordinated peristalsis which leads to progressive dysphagia to solids and liquids (vs obstrction which would be solids only) |
| What does a barium swallow show in achalasia? | dilated esophagus with an area of distal stenosis. "Bird's beak" |
| What condition can cause a secondary achalasia? | Chaga's disease |
| What is seen with the lower esophageal sphincter in sclerodcerma? | associated with esophageal dysmotility invovling low pressure proximal to LES |
| What does achalasia carry as a long term risk? | incr risk of esophageal carcinoma |
| How does gastroesophageal reflux disease present? | commonly presents as heartburn and regurgitation upon lying down. may also present as nocturnal cough and dyspnea |
| How does esophageal varicses present? | PAINLESS. bleeding in submucosal veins of lower 1/3 of esophagus |
| What are some major causes of esophagitis? | reflux, infection (HSV-1, punched out ulcers, CMV:linear ulcers, Candida : white pseudomembrane), chemicals |
| What is Mallory-Weiss syndrome? who gets it? | mucosal lacerations at the gastroesophageal junction due to severe vomiting. leads to hematesis. usually found in alcoholics and bulimics |
| What is Boerhaave syndrome? | transmural esophageal rupture due to violent retching (Been-heaving syndrome) |
| What are esophageal strictures associated with? | lye ingestion and acid reflux |
| What is Plummer-Vinson syndrome? | Triad: 1. dysphagia doe to esophageal webs 2. glossitis 3. iron deficiency anemia |
| What is the pathophys of Barrett's esophagus? | glandular metaplasia: replacement of non keratinized (stratefied) squamous epithelium with intestinal columanr epithelium in distal esophagus. |
| What causes Barrett's esophagus and what sx might it be associated with? | chronic GERD is the cause. associated with esophagiits, esophageal ulcers, incr risk of esophageal cancer |
| How does esophageal cancer present? | progressive dysphagia first solids then liquids, and wieght loss |
| What are some major RF for squamous cell carcinoma of the esophagus? | alcohol/achlasia, cigarettes |
| What are some major Rf for adenocarcinoma of the esophagus? | Barrtet's esophagus, esoophageal web/ esophagitis, diverticula (ex. Zenker's) |
| What is a mnemonic for the RF for the 2 types of esophageal cancer? | SAC on ABED (see above) |
| What is the prevalence of squamos cell vs adenocarcinoma of the esophagus? | wordwide squaomous cell> adenocarcinoma. in US squamous cell=adeno |
| What part of the esophagus does adenocarcnioma vs quamous cell affect? | squamous cell: upper 2/3 adenocarcinoma: lower 1/3 |
| What can malabsorbtion syndromes cause? | diarrhea, steatorrhea, weight loss, weakness |
| What is a mnemonic for the malabsorbtion syndromes? | These Will Cause Devastating Absorbtion Problems: Tropical sprue, Whipple's disease, Celiac sprue, disaccaridase deficiency, Abeta-lipoportienemia, pancreatic insufficency |
| What causes tropical sprue? What does it affect? | possibly infectious as it responds to abtx. similar to celiac sprue but can affect entire small bowel |
| What causes Whipple's disease and what is seen on histology? | infection with Tropheryma whipelii (G+). see PAS positive foamy macrophages in intestinal lamina propria aand mesenteric nodes |
| Who gets Whipple's diease? What are the major Sx? | older men, get arthralgias, cardiac and neurologic symptoms |
| What is celiac sprue? What causes it? | autoAb to gluten (gliadin) in wheat and other grains. proximal small bowel primarily |
| What is the pathophys of disaccaride deficiency? | most common is lactase= milk intolerance |
| What sx are seen in disaccaride deficiency? | normal appearing villi with osmotic diarrhea |
| When might a dissacaride deficiency happen in a healthy person? Why? | can have a self limited one after injury by virus as lactase is located on tip of the villi |
| How do you test for lactose intolerance? | If: 1. administration of lactose causes sx 2. glucose rises <20 mg/dL |
| What is the pathophys of abeta-lipoproteinemia? | decr synth of apo B--> inability to generate chylomicrons---> decr decretion of cholesterol , VLDL into bloodstream-->fat accumulation in enterocytes |
| How and when does abeta-lipoprotenemia present ? | early childhood with malabsrobtion and neurological sx |
| What causes pancreatic insufficiency? | cystic fibrosis, obstructing cancer, chronic pancreatitis |
| What does pancreatic insufficency cause? | malabsrobtion of fat and fat soluable vitamin (ADEK), see incr in neutral fat in food |
| Who gets celiac sprue? | people of northern european descent |
| What are the key findings in celiac sprue? | auto Ab to gliadin and tissue transglutaminase, blunting of villi, lymphocytes in lamina propria, decr mucsal absorbtion of jejunum |
| What is a useful screen for celiac sprue? | serum levels of tissue transglutaminase Ab |
| What are 2 associations of celiac sprue? | associatred with dermatitis herpetiformis, moderately incr risk of malignancy (T cell lymphoma) |
| What is the pathophys of acute erosive gastritis? | disruption of mucosal barrier leading to inflammation |
| What are some major causes of acute erosive gastritis? | stress, NSAIDs (decr PGE2 leading to decr protection), EtOH, uremia, burns(curling's ulcer), brain injury (Cushing's ulcer) |
| What is Curling's ulcer and how does it happen? | decr plasma volume due to burns causing sloguhing of gastric mucosa |
| What is Cushing's ulcer and how does it happen? | incr vagal stim causes incr ACH and incr H+ production) |
| What populations especially get acute erosive gastritis? | alcoholics, those takings NSAIDs daily (RA) |
| What causes and what are the key findings in Type A (fundus/body) Chronic gastritis? | autoimmune disorder with autoAb to parietal cells, pernicious anemia, and achlorohydria |
| What causes Type B (antrum) chronic gastritis? What does it incr risk of? | most common type, caused by H. pylori. causes incr of MALT lymphoma |
| What type are most stomach cancers? What are their aggression characterisitcs? | almost always adenocarcinoma with early aggressive local spread and node/liver mets. |
| What are some major RF for stomach adenocarcinoma? | smoked foods (dietary nitrosamines), achlorohydria, chronic gastritis, type A blood. |
| How does stomach adenocarcinoma present? | acanthosis nigricans |
| What are the 2 types of stomach adenocarcinoma and what defines each? | 1. intestinal= resembles colonic adenocarcinoma 2. diffues= signet ring cells, grossly thickend and leathery (limits plastica) |
| What is Virchow's node? | invovlement of left supraclavicular node by stomach adenocarcinoma |
| What is a Krukenberg's tumor? | bilateral mets to ovaries with abundant mucus and signet ring cells of stomach adenocarcinoma |
| What is Sister Mary Joseph's nodule? | subcutaneous periumbilical metastasis |
| Who gets a gastric ulcer and how do they present? | often older pt. pain is greater with meals, associated with weight loss |
| What causes gastric ulcers? how do you test? | H. pylori (70%), will have positive urease breath test, chronic NSAID use also implicated |
| What is the mech of a gastric ulcer and what is it associated with? | decr mucosal protection against gastric acid. incr risk of carcinoma |
| What causes duodenal ulcers and how do they present? | almost 100% H pylori. pain decreases with meals, have weight gain |
| What is the pathophy of a duodenal ulcer? | due to incr gastric acid secretion (Zollinger-Eillison syndrome), or decr mucosal protection. |
| What do duodenal ulcers look like? What are they associated with? | have "punched out" margins unlike the raised or irregular margins of carcinoma. no incr in carcnioma risk |
| How do you treat peptic ulcers? | triple therapy with PPI, clarithromycin, amoxicillin ( metronidazole if allergic to penicillin) |
| What are 2 major complications of ulcers? | hemorrhage: gastric, duodenal (posterior> anterior). perforation: duodenal (anterior >posterior) |
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