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NBPME GastroIntest
| Question | Answer |
|---|---|
| how can you eliminate central control of the GI tract and digestion | -vagotomy (cut CN 10), this eliminates the touch, hearing, seeing, smell of food on your GI system |
| what is the pineal gland in the brain responsible for | -your circadium rythyms, it tells you when it is night and when it is day, around 8pm it raises your melatonin levels to shut off your metabolism and anabolic pathways are most active |
| how can you trick the pineal gland | -bright lights |
| where are your hunger and satiety centers located | in the hypothalamus, they both respond to glucose and stomach distension |
| how does the hypothalamus respond to stomach stapling surgeries | -since the hunger and satiety centers are affected by distension, the stomach will be distended faster and the centers will think they are satisfied |
| the hypothalamus hunger and satiety centers respond to glucose and distension, but also to 5HT and norep; what drugs can affect this | -amphetamines, THC and other drugs that dec/inc 5HT will increase or decrease hunger |
| if the satiety centers are located in the hypothalamus, what might lesions of this area cause | -anorexia if lesion is in the satiety center-bulemia if the lesion is in the hunger center |
| amphetamines like dexatrim and ridalin release what that affect atiety and hunger | catecholamines (norep, HT) |
| what is the stress response | -when the brain perceives stress the parasympas dischrage followed by the sympathetic discharge, so when you are stressed you end up with a diarrhea/constipation cycle known as IBS |
| knowing that the body goes through a para/sympa cycle when stressed, what drug is given to all ICU due to the stressful situation | -H2 blocker due to the increase risk of peptic ulcers due to stress response |
| since our hunger and satiety is in the hypothalamus and can be controlled by norep/5HT what drug could treat eating disorders like anorexia and bulemia | -SSRI (serotonin uptake inhibitors) |
| what is Prader Willi syndrome | -genetic disorder that causes a lesion of the satiety center, so the child is constantly hungry |
| digestion begins with the central phase with the vagus, then the oral phase, where saliva is secreted from 8 diff saliva glands; what are they | -parotid, lingual, sublingual, submandibular, all of them are found in pairs with the parotid being the largest |
| all of the salivary glands with the exception of the parotid are innervated by what CN | -all are innervated by CN7, but the parotid is innervated by CN9; so saliva production will never quit b/c of the dual nerve innervation |
| what disease can cause acute parotitis (inflammation of the parotid) | mumps (mumps also causes orchitis and pancreatitis) |
| what bacteria can cause parotitis | staph during the intubation process |
| what are the muscles of mastication | -massester, temoporalis, lateral pterygoid, medial pterygoid-unlike other facial muscles that are innervated by facial nerve 7, the chewers are innervated by CN5 trigeminal |
| what is the enzyme found in the mouth that prevents the bacteria from sticking to the teeth | lysozome |
| what substance in the saliva starts to break down fat in the mouth | -salivary lipase |
| what does salivary amylase do | -breaks down sugar and carbs down in the mouth into disaccharides |
| sucrose, lactose, maltose and alpha dextrose are disaccharides that need sucrase, lactase, maltase and dextrase in the SI to break them down furthur...what makes up these sugars | -sucrose (glucose+fructose)-lactose (glucose+galactose)-maltose (1,4 glucose, glucose)-dextrose(form of glucose) |
| what are some causes of GERD | -obesity, restrictive lung disease, eating late at night, high fat meal, relaxing LES pressure(can be from estrogen, Ca etc.) |
| esophogitis or any other type of inflammation that has been present for awhile will have what cells present | -Tcells, macrophages and fibroblasts |
| Mallory Weiss disease | -bleeding from tears in mucosa of the esophagus-tears can be caused by severe vomiting, wretching or coughing |
| Boerhaave syndrom | -rupture of the esophageal wall into the pleural cavity (Been heaving) |
| there are two sphincter in the esophagus, upper and lower; the UES is voluntary due to skeletal muscle, what nerve innervates the swallowing muscles | -all of the swallowing muscles are innervated by CN10, except the stylopharyngus |
| The esophagus has two forms of peristalsis, primary and secondary...when is each used | -primary peristalsis moves food from the UES to the LES-secondary peristalsis kicks in when something gets stuck, doesnt depend on innervation but depends on Smooth muscle contracting when distended |
| what controls the contraction and the reaction of primary esophagus peristalsis | -the vagus causes contraction then the Auerbach complex causes the relaxation |
| in the esophagus food moves via peristalsis, in the small intestine food moves via segmentation and MMC(migrating myenteric complex), how does food move in the colon | -haustration(1) and mass movement(2) |
| what type of cells are very numerous in the GI to make mucous | Goblet cells |
| Achalsia is difficulty swallowing due to a missing... | Auerbachs plexus |
| what type of anemia is caused by LT GI bleeding | -hyperchromic mcrocytic anemia (Fe) |
| where does peristalsis in the stomach begin | -in the middle of the stomach because that is where food first falls |
| parietal cells are located in the stomach, what do they secrete and when | -when pH is alkaline, gastrin release is triggered from G cells which stimulates parietal cells to release HCl |
| parietal cells release HCl when the stomach is alkaline, what else do they secrete | -intrinsic factor which is needed for B12 absorbtion |
| what 3 things does the GI lining have to protect it | -mucous and mucosa, PG promote mucous secretion, bicarb from parietal cells |
| if PG's promote mucous secretion, what drugs can cause ulcers in the GI tract | -aspirin, NSAIDS, prednisone block PG production |
| once the stomach pH reaches 1-2; chief cells release pepsinogen, what does this start | -protein degradation |
| what is the only food constituent broken down in the stomach | -proteins |
| sliding hiatal hernia | -the fundus of the stomach slides up into the esophageal hiatus of the diaphragm |
| what are the clues for stomach cancer | -leather water bottle (thick wall),a.k.a. linnitus plastica, signet ring cells, virchows nodes, Krukenberg tumor (tumor that seeds onto the ovary) |
| what are the risk factors for stomach cancer | -smoking, alcohol, temp hot substances, nitrites from smoked foods |
| digestion of these are mainly in the mouth and stalled in the stomach | -carbs and fats |
| no digestion of this food component occurs in the mouth, it does begin in the stomach | proteins |
| stimulated by an acid environment, which causes the release of bicarb from the pancreas and gall bladder | -secretin, also causes a decrease in gastric motility adn causes pyloric sphincter constriction |
| this enzyme is stimulated by fat in the duodenum | CCK |
| what is the role of CCK | -tells the gall bladder to release bile and tightens the pyloric sphincter to slow release |
| what does motilin do | stimulates segmentation in the small intestin (produces MMC's) |
| what does somatastatin do | inhibits all gastric enzymes |
| alpha amylase is released from the pancreas, what does it do | breaks down the alpha 1,4 bonds in carbs |
| how are all sugars except fructose transported | -Na cotransport-fructose can pass by simple diffusion |
| name some enzymes needed to break down proteins until they are 3 amino acids in length | -trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase, proaminopeptidase |
| fats are continued to be broken down in the duodenum, they first need to be emulsified..how | -they need to be emulsified with bile salts and lecithin (this forms a micelle) |
| name the 3 components of a micelle | -fat, bile salts, and lecithin |
| how are bile salts made | -cholesterol is converted to bile salts, then conjugated with glycine or taurine to form bile salts |
| where are bile salts made | conjugated of bile acids with glycine or taurine occurs in the liver |
| once bile salts are made in the liver, where are they sent to | to the gall bladder |
| what is the major route of cholesterol secretion | excretion of bile salts (20% of bile salts are excreted in feces each day) |
| since bile salts are the main route of getting rid of cholesterol, what drug can be used to bing bile salts and excrete more cholesterol so the liver pools more cholesterol out of the plasma to replace them | -colestipol and Cholestyrimine |
| what are some S/E of cholesterol drugs | -if you loose too much chol., your steroid hormones will be affected-dry membranes like hair and skin-steatorrhea-vit deficiency of KADE |
| deficiency of K | bleeding (K dependent factors are 2,7,9,10,C,S) |
| deficiency of A | eyes |
| deficiency of D | bones |
| deficiency of E | RBC health |
| 20% of bile salts are excreted, 80% are returned to liver...what do the 80% enter | -the enterohepatic circulation where they are reconjugated and put back into the GI |
| when are new bile salts made | -between meals, because during a meal recycled bile salts from enterohepatic circulation are returning..so none are needed then |
| Most kidney stones are made of Ca, but most gall stones are made of cholesterol...low amounts of what chol product can cause high cholesterol and lead to gallstones | bile salts, if you dec bile salts, you wont be using up any cholesterol or excreting them as bile salts |
| what are the clinical signs of gallstones | -fat, 40, female-stone pain comes in waves due to its flow and muscle contraction around it, positive Murphys sign, RUQ pain |
| name the three types of FA and how each gets absorbed | -SCFA, MCFA, LCFA-short and long chain get absorbed into lacteals, a lymphatic capillary in the intesintal wall; MCFA cross the intestinal wall and bind to albumin and head to the liver |
| name the five major groups of lipoproteins that enable fats and cholesterol to move into the water based solution of the blood stream | -chylomicrons,VLDL,IDL,LDL,VLDL,HDL |
| SCFA and LCFA enter lacteals to meet up with ApoB48 to form what | -chylomicron |
| chylomicrons head to the liver to get broken down to drop off TG, what is needed to break them down | -lipoprotein lipase and C2 (from HDL) |
| where does VLDL come from | -when chylomicrons get broken down in the liver, the liver repackages it into VLDL with ApoB100 and E |
| VLDL travels with apoB100, where does it deliver TG to | -adipose tissue where it is broken down |
| where does IDL come from | -after VLDL is broken down in adipose tissue, it still has B100 and E with it (IDL with B100 and E) |
| where does IDL deliver TG | -everywhere else (it is metabolized by the ApoE it has with it) |
| after IDL is metabolized by ApoE, all that is left is cholesterol and B100..this is LDL...what attached to LDL receptors in the body | -the B100 that is with the LDL |
| Abetalipoproteinemia | inability to make lipoproteins due to deficiency in apo B100 and apoB48 |
| why is HDL good cholesterol | -it has the most protein, thus least cholesterol-it activates Lcat which emulsifies cholesterol left in the blood vessels to take it back to the liver |
| how are artery plaques formed from cholesterol | -fatty streaks are formed in artery by cholesterol, macrophages eat the cholesterol and form a foam cell, bunch of foam cells forms an atheroma, blood swirls around atheroma in the artery and damages endothelium, forming clots and scars, atherosclerosis |
| Hyperlipidemia caused by too many chylomicrons | -Type I, due to a lipoprotein deficiency (thats what breaks chylomicrons down) |
| which type of Hyperlipidemia is familial | -Type 2a, due to too much LDL, caused by absent or dec in LDL receptors |
| what is Type 4 hyperlipidemia | -too much VLDL |
| what group of drugs are used to lower cholesterol | -statins |
| how do statins lower cholesterol | -inhibits HMG CoA reductase, which is rate limiting enzyme in cholesterol synthesis-this dec chol synthesis in the liver and inc the number of LDL receptors, so more LDL is cleared from the plasma |
| what is high total cholesterol | -greater then 200 |
| why do xanthomas appear in pts with cholesterol problems | -they are fat pads on the extensor tendons (eldows, achilles) |
| LDL cholesterol is bad, what should it be | -below 130 |
| HDL cholsterol is good, what should it be | -above 35 |
| how can you raise HDL good cholesterol | -exercise, weight loss, moderate alcohol, estrogen (thats why women have lower chol) |
| where are the majority of things absorbed in the GI | -in the jejunum (except KADE B12, iron)-KADE, B12 are absorbed in the ileum-Iron is absorbed in the duodenum |
| where is iron absorbed | duodenum |
| where are vitamins KADE and B12 absorbed | ileum |
| 10% of fats, sugars, amino acids are absorbed in the duodenum, where is the other 90% absorbed | -the jejunum |
| what are the only 2 things absorbed in the ileum | -all KADE and B12, a little fat |
| what part of the intestine has the highest absorption capacity | jejunum (where most food components are absorbed) |
| which part of the intestine has the highest reabsorption capacity | -ascending colon (sucks stuff back in that it orignally got rid of) |
| what is the main cause of constipation in the US | dehydration |
| After you pass the ascending colon, everything gets... | excreted |
| where is the watershed of the colon and thus the area most prone to ischemia | -splenic flexure |
| there are two types of polyps in the colon...what are they and which are prone to cancer | -hyperplastic and adenomas-adenomas are pre malignant |
| disease where you have too many adenomas (pre malignant polyps) | -familial polyposis, autosomal dominant b/c it is structural thing and 100% risk of colon cancer |
| when the pt has familial polyposis and osteoma and sebaceous adenomas, what is it called | gardners syndrome |
| when the pt has familial polyposis and brain tumors, what is it called | Turcot syndrome |
| what is the number one risk for colon cancer | -low fiber diet causes hard feces that scrape the colon |
| where does celiac sprue affect | -jejunum (this can cause nutrition problems because most things are absorbed here) |
| what Gi disorder is caused by gluten sensitivity | celiac sprue |
| where does tropical sprue effect | -ileum (also a malabsorption disease) |
| whipples disease | -malabsorption in males caused by whippeli bacteria-PAS positive macrophages (macros with fat stuck in them) |
| list the signs of crohns | -malabsorption in middle aged female-starts in ileum then moves distally-skip lesions-transmural (through all cell layers)-fistula formation(holes that erode) |
| list the signs of ulcerative colitis | -more common in men-HLA-B27-mucosal involvement only (unlike transmural crohns)-continuous (no skip lesions)-toxic mega colon-lead pipe appearance (haustra are lost from scarring) |
| HLA-B27 is associated with ulcerative colitis and what other diseases | -psoriasis, Reiters, ankylosing spondylosis |
| ischemic colitis causes severe abdominal pain and bloody diarrhea..where does the ischemia occur | -in the watershed area of the colon, at the splenic flexure |
| there are 4 causes of SEVERE abdominal pain; pancreatitis, ischemic colitis..name two more | -kidney stones and abdominal aortic aneurysm |
| there are 2 enteric nerve plexuses in the Gi tract; Myenteric (Auerbachs) and Submucosal (Meissners)..what do each control | -Auerbachs; motility-Meissners: secretions, blood flow, absorption |
| branches of the celiac trunk are the main blood supply of the stomach, what are the branches | -common hepatic, splenic, left gastric |
| which salivary glands secret mostly mucous | -sublingual and submandibular |
| Zollinger Ellison syndrome | increased gastrin production |
| trypsinogen is secreted from the pancreas and is activated to trypsin...it then | -activates other proenzymes and more trypsinogen |
| Achalsia is difficulty swallowing bc you cant relax the LES | -caused by loss of Auerbachs plexus |
| Barrets Esophagus | -glandular metaplasia in the distal esophagus due to chronic acid reflux |
| what antibodies are present with Celiac sprue | -antigliadin antibodies |
| peptic ulcer caused by dec in mucosal protection(from NSAIDS) | gastric ulcer |
| peptic ulcer caused by H pylori or inc acid production | duodenal ulcer |
| Zenkers diverticulum | -false diverticula due to herniation of mucosal tissue at junction of pharynx and esophagus (causes smelly breath due to trapped food) |
| Hirschsprungs disease | -congential megacolon caused by lack of ganglion cells/enteric nervous plexues (auerbach and meissners); cant pass meconium-Chagas a S. American trypanosome eats the ganglion as well |
| what type of anemia would long term GI bleeding cause | hyperchromatic microcytic anemia (Fe) |
| smell stimulates the cortex, which then stimulates which nerve to cause Gi contraction | -the vagus is stimulated, without the vagus you would never enjoy food |
| anytime the body senses a stress, there is a para/sympa response, which fires first | -think of Point and shoot, parasympathetic causes erection and sympa causes ejaculation |
| chronic acid expoaure to the lower esophagus can cause the cells to change from squamous to tall columnar, what disease is this and what secondary condition is it associated with | -Barrets esophagus can lead to adenocarcinoma of the esophagus |
| parasympathetic stimulation will increase saliva production, what drugs can also do this | -cholinergics such as Ach, pilocarpine for galucoma, bethanecol for urinary retention, carbachol for post-op urinary retention |
| what is the difference between the two cholinergics ACh and bethanecol | -bethanecol is an anticholinesterase, so it istn degraded and stays around longer |
| which receptors does NE have a greater affinity for | alpha > beta |
| which receptors does Epi have a greater affinity for | beta > alpha (thats why it is used for anaphalactic shock) |
| what is cystic fibrosis | -genetic defect in Cl/HCO3 protein, this causes thick secretion because Cl remains in the saliva |
| is the buccinator muscle a masticator | -no, it slides the jaws sideways |
| what is achalsia and what can cause it | -esophageal motility disorder can be caused by a loss of auerbachs plexus or Chagas disease |
| Plummer vinson syndrome is associated with Fe deficiency anemia, what other esophageal defect is assocaited with it | esophageal webs (strips across the esophagus( |
| high pH in the stomach triggers G cells to.. | release gastrn, which stimulates parietal cells |
| what stimulates parietal cells | gastrin - which is released by G cells when sotmach pH is high |
| what does the parietal cell produce | -H+ and intrinsic factor, into the stomach and also secretes bicarb around the stomach lining to protect it |
| what vitamin needs instrinsic factor to be absorbed | B12 |
| for how long do the parietal cells pump HCl into the stomach | -until the pH reaches 1 or 2 |
| what are 3 things that protect the GI lining | -mucous and mucosa, PG promote mucous secretion, bicarb from the parietal cells |
| name 3 drugs that block PG production, thus causing stomach ulcers | -aspirin, NSAIDs, prednisone |
| once the stomach pH reaches 1 or 2, the parietal cells stop releasing HCl and the chief cells release | -pepsinogen which will activate pepsin which is the enzymes that start protein digestion |
| in what part of the GI does digestion end | -the small intestine, then absorption begins in SI and LI |
| what is the only thing digested in the stomach | proteins (fats are digested in the small intestine) |
| what are most gastric ulcers caused by | -breakdown in protection barrier |
| what are most duodenal ulcers caused by | H pylori or acid output |
| name the 3 parts of the small intestine in order | -duodenum,jejunum, ileum |
| does digestion occur in the large intestine | no, it ends in the small intestine |
| what is an esophageal hiatal hernia | -a sliding hernia where the first part of the stomach (the fundus) slides up through the esophageal hiatus in the diaphragm |
| gastric cancer is adenocarcinoma, what are 5 clues | -leather water bottle appearance due to thickened walls, signet ring cells, virchows nodes(METS to superclavicular nodes), krukenberg tumor (cancer seeds into the ovary) |
| what are the risk factors for stomach cancer | -smoke, alcohol, hot temp substances, nitrites |
| which food component is NOT digested at all in the mouth | protein, it begins in the stomach |
| very acid stomach slurry is ejected into the duodenum (first part of the small intestine)...what is secreted then | -secretin is secreted |
| secretin release is stimulated by acidity, it goes to the pancreas and gall bladder to cause...3 things | -release of bicarb, decrease gastric motility and gastrin release, pyloric spinchter constriction (so stuff is release slower from stomach) |
| what is CCK | -it is stimulated by fat in the duodenum and causes bile to be released from the gall bladder |
| what is motilin | -stimulates segmentation |
| what is somatastatin | inhibits everything in the GI |
| what are zymogens | -inactive enzymes in the pancreas, they are inactive so the pancreas doesnt self digest |
| what pancreatic enzymes are responsible for breaking down protein into amino acids | -trypsinogen, chymotrypsinogen, proelastasae, procarboxypeptidase, proaminopeptidase |
| how are proteins absorbed | -by Na co transport, as are most digested items except fructose has its own transporter |
| fats need to be emulsifed to be broken down in the duodenum, how does this occur | -fats combine with bile salts and lecithin to form a micelle |
| how are bile salts made | -cholesterol is turned into bile acids, then bile acids are conjugated with glycine or taurine to form bile salts |
| where are bile salts made | -in the liver, then transported to the gall bladder |
| what is the major route of getting rid of cholesterol | -20% of bile salts are excreted everyday |
| since excreting bile salts gets rid of cholesterol, how can you get rid of more cholesterol | -bind the bile salts with cholestipol or cholestyrimine, then the liver has to pull chol out of the plasma to make more bile salts |
| 80% of bile salts are reabsorbed and returned to the liver, what is this called | -enterohepatic circulation |
| are new bile salts made during a meal | -no because the enterophepatic circulation is bringing bile salts back to the liver for reconjugation rather then making new ones, new ones are made between meals |
| what are the S/E of cholesterol binding drugs (think of the role of chol in the body) | -cholesterol is used to make steroid hormones, so menstrual cycle, VitD etc will be affected, dry skin, dry hair, steatorrhea, vit deficiency of KADE, K bleeding, A eyes, D bones, E RBC health |
| what are the vit K dependent factors | 2,7,9,10,c,s |
| most kidney stones are calcium, what are most gallstones | cholesterol |
| what are the 3 type of fatty acid | SCFA, MCFA, LCFA |
| what is bilirubin | -breakdown product of heme in RBC and is excreted with bile, gives bile its color |
| how are SCFA absorbed | -via the lacteals(lymphatic capillary in villi of SI) |
| how are MCFA absorbed | -go through the intestinal wall, bind to albumin and albumin takes it to the liver |
| how are LCFA absorbed | -via the lacteals |
| what are the 5 main groups of lipoproteins that enable fats and cholesterol to move with the the water based solution of the blood stream | -chylomicrons, VLDL,IDL,LDL,HDL |
| short and long chain fatty acids enter the lacteal and meet up with Apo B48 to form... | chylomicrons |
| what fats make up chylomicrons | short and long chain fatty acids |
| what is abetalipoproteinemia | disorder that interferes with normal fat absorption because they cant make chylomicrons because they lack Apo B48 |
| chylomicrons head to the liver to drop off TG, lipoprotein lipase breaks it down into... | -the liver repackages it into VLDL with Apo B100 |
| which lipoprotein delivers fat to the adipose tissue | VLDL |
| which lipoprotein delivers fat to the liver | chylomicron |
| LDL travels with B100, the B100 attaches to what receptors | LDL receptors |
| why is HDL considered good cholesterol | because it has the most protein content and it activates Lchat to emulsify cholesterol lest in BV and take it to the liver |
| what is the process for atherosclerosis formation | -fatty streaks are formed by cholesterol, macrophages eat the fatty streak adn become a foam cell, a bund of foam cells form an atheroma and blood swirls around it and damages endothelium, this forms a clot and scarring known as atherosclerosis |
| which type of Hyperlipidemia can respond to diet alone | Type 1- due to too many chylomicrons |
| Type 2a Hypercholesterol | -familial cholesterol due to LDL receptor deficiency |
| Type 4 Hyperlipidemia | -familial hyperlipidemia caused by too much VLDL |
| how do statins treat high cholesterol of Type 2a | -they are HMG CoA reductase inhibitors which is the RL enzyme needed for chold synthesis |
| what are xanthomas and who gets them | -they are fat pads formed on extensor tendons (elbows and achilles) in pts with cholesterol problems |
| what is normal total cholesterol | -less then 200 |
| what is normal LDl | less then 130 |
| what is normal HDL | -greater then 35 |
| how can you raise your HDL | -exercise, weight loss, moderate alcohol consumptions, estrogen |
| where are the majority of food components absorbed (except Fe and KADE, B12) | jejunum |
| where is fe absorbed | duodenum |
| where are KADE, B12 absorbed | ileium |
| where are Peyers Patches located | -the ileum (responsible for immune response) |
| which part of the GI has the highest absorptive capacity | the jejunum |
| which part of the GI has the highest resorption capacity | -ascending colon (sucks stuff back in by Na/K pumps controlled by aldosterone) |
| what is the main cause of constipation | dehydration |
| after you pass the ascending colon, everything is meant for excretion, you cant get anything back | . |
| name the parts of the colon in order | ascending colon, right splenic flexure,transverse colon, left splenic flexure,descending colon, sigmoid colon, rectum |
| where is the watershed area of the colon | splenic flexure has the least blood supply |
| all sphincter are alpha 1, but is there sympa input to pooping | NO, there is not sympa input to pooping |
| chylomicron travels to the liver and lipoprotein lipase breaks it down and it becomes... | VLDL |
| what autosomal dominant polyp condition has a 100% risk of colon cancer | -familial adenomatous polyposis ( too many adenomas are present in the LI that become cancerous) |
| if someone has familial polyposis with osteomas and sebaceous adenomas what is it called | Gardeners syndrome |
| if pt has familial polyposis with brain tumors | Turcot syndrome |
| what is the main risk factor for LI(colon) cancer | low fiber diet (hard stools scrape colon) |
| what is Meckels Diverticulum | -congential problem that is a small bulge in the SI that can cause massive GI bleeding; it is a remnant of the umilical cord connected to the SI |
| what are the rule of 2's of Meckels Diverticulum | -2 feet from iliocecal valve (jxn of SI and LI), present in 2% of population,peaks at age 2,twice as common in males, 2 types of tissue; pancreatic and gastric |
| what is Peutz Jeugher | -hereditary intestinal hyperplastic polyps (not adenomatous) |
| celiac sprue | -effects the jejunum, so you mess with absoprtion of almost everything - wheat protein sensitivity that presents with blunting of vills border and pruitic rash known as dermatitis herpeformis, diarrhea after eating wheat |
| tropical sprue | -the same as celiac sprue, but it is in the ileum |
| Whipples Disease | -an infectious malabsorption disease that has PAS pos macrophages (macrophages with fat stuck in them) |
| Crohns disease | -malabsorption in middle aged female, skip lesions, granulomatous (so T cells and macros),cobblestoning due to granulomas, transmural,fistula formation(holes that erode) |
| ulcerative colitis | -more common in men, bright red bleeding,HLA-B27,mucosal involvement only,continous,toxic mega colon, lead pipe appearance bc haustra are lost from scarring |
| ischemic colitis | -sudden severe abdominal pain, splenic flexure is ischemic area b/c it is the watershed area |
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