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Step 1 12.18.12


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)
Created by: tjs2123



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