bhom14's version from 2017-12-09 23:40

Section 1

Question Answer
GastrinG cells (antrum of stomach, duodenum)
SomatostatinD cells
CholecystokininI cells (duodenum, jejunum)
SecretinS cells (duodenum)
Glucose dependent insulintropic peptideK cells (duodenum, jejunum)
motilinsmall intestine
VIPParasympathetic ganglia in sphincter, small intestine, gallbladder
Intrinsic factorparietal cells (stomach)
gastric acidparietal cells (stomach)
pepsinchief cells (stomach)
bicarbonatemucosal cells; Brunner glands (duodenum)

Section 2

Question Answer
gastrinH+ secretion
somatostatinsomatoSTOPtin: decrease GI secretions; decrease insulin/glucagon release
CKKincrease digestive secretions from pancreas and gallbladder; relaxes the sphincter of Oddi; slows gastric emptying
which GI regulatory substance decrease secretion of insulin and glucagon?somatostatin
secretinincrease bicarb (pancreas) and bile secretion; decrease gastrin release
What does GDIP/GIP do?increase insulin; decrease gastric H+ secretion
Relaxes sphinchters and small intestine?VIP
Increase intestinal water and electrolyte secretionVIP
where is a VIPoma located?in pancreas; causing watery diarrhea, low K, no HCl
Increased LES tone in achalasia could be due to loss of what GI regulatory substance?nitric oxide
ghrelin increases in what genetic disorder?Prader Willi syndrome
what stimulates gastric acid release? where does it come fromfrom parietal cells. stimulated by histamine, gastrin, ACh
what inhibits gastric acid?somatostatin, secretin, Prostaglandins, GIP
Pepsindigest proteins; from chief cells of stomach
How is pepsinogen activated?by H+; becomes active form (pepsin to break down proteins)
what is secreted from the pancreas?alpha amylase, lipase, Proteases (zymogen form)
what converts enteropeptidase
Motilinproduce MMC (migrating motor complexes for peristalsis)
what are the activated forms of proteases?break down protein: trypsin, chymotrypsin, elastase, carboxypeptidase
what enzyme activates protease zymogens?trypsin
what activates trypsinogen to trypsin? where is this located?enteropeptidase / enterokinase (located at the brush border of the duodenum and jejunum)
what substances help relax GI sphinctersVIP, NO
what type of infection may cause secondary achalasiaT cruzi infection (Chagas disease)
etiology of achalasialoss of myenteric (Auerbach) plexus, which leads to loss of post-symp. INHIBITORY neurons with NO and VIP
what microbes can cause esophagitis in immunocompromised patients?candida, CMV, HSV-1
white pseudomembrane in esophaguscandida infx
ulcers in esophagus in immunocompromised - what are possible causes?HSV-1 (punched out), CMV (linear)
how does GERD affect LES tone?TRANSIENT decreases in LES tone
esophageal manifestations in achalasiaincreased LES tone; uncoordinated or absent peristalsis down the esophagus
hematemesis in alcoholics or bulimicspossibly Mallory Weiss syndrome (mucosal lacerations at gastroesophageal junction due to severe vomiting)
Plummer Vinson syndromedysphagia, iron deficiency anemia, esophageal web. Increased risk of esophageal squamous carcinoma (plumber's DIE)
Sclerodermal esophageal dysmotility - what happens to the LES tone?decreases.
etiology of scleroderma esophageal dysmotilityatrophy of esophageal smooth muscle --> fibrosis at the LES, therefore done decreases -> acid reflux --> barrett esophagus, stricture and aspiration.
scleroderma esophageal dysmotility is party of ____ syndrome.CREST. (E = esophageal dysmotility)
CREST syndromeCalcinosis, Raynaud's phenomenon, Esopphageal dysmotility, Sclerodactyl, Telangiectasis
Barrett esophagusreplacing esophageal epithelium with intestinal epithelium in distal esophagus, due to GERD. increased risk of adenocarcinoma.
eosphageal epitheliumnonkeratinized stratified squamous epithelium.
intestinal epitheliumconciliated columnar with goblet cells
adenocarcinomalower 1/3. Adenoma = America, common. GERD, Barrett's, obesity (smoking, achalasia)
squamous cell carcinomaupper 2/3. common worldwide. alcohol, hot liquids (smoking, achalasia)

Section 3

Question Answer
SGLT1glucose, galactose (Na+ dependent)
GLUT 5fructose (facilitated diffusion)
GLUT 2transport all monosaccharides from the enterocyte into the bloodstream
what is the d-xylose absorption test?distinguish GI mucosal damage from other forms of malabsorption.
Iron is absorbed in the ___duodenum
Folate is absorbed in the ___small bowel
Vit B12 is absorbed in the ___terminal ileum along with bile (needs IF)
what is in bile?bile salts (water soluble form of bile acids), phospholipids, cholesterol, water, ions, and bilirubin
what enzyme is needed in the RLS of bile acid synthesis?cholesterol 7alpha hydroxylase
why is bile important?Break down lipids, absorb fat soluble vitamins; antimicrobial; eliminates cholesterol.
what enzyme converts heme into bilirubin?heme oxygenase
Direct bilirubinconjugated with glucoronic acid; water soulable
indirect bilirubinunconjugated; water Insoluble
where is heme broken down into bilirubin?macrophages
how does unconjugated bilirubin travel in the bloodstreamsince it is water insoluble, it binds to albumin to travel in the bloodstream
what enzyme is needed to conjugate bilirubin?UDP-glucuronyosyl-transferase
what happens to bilirubin?excreted as bile --> urobilinogen (via gut bacteria). becomes brown poop, yellow urine, or gets recycled back to liver.
salivary gland tumor with chondromyxoid storm and epitheliumpleomorphic adenoma (benign mixed tumor, most common)
salivary gland tumor with mutinous and squamous componentsmucoepidermoid carcinoma (malignant)
salivary gland with cystic tumor and germinal centerpapillary cystademona lymphphomatosum (Warthin)
why does NSAIDS cause gastritisNSAIDS inhibit PGE2, which normally provides gastric mucosa cell protection
Cushing ulcer caused by burns; hypovolemia --> gastric mucosal ischemia --> acute gastritis
curling ulcercaused by brain injury; increased vagal stimulation --> ACh --> H+ secretion
chronic gastritismucosal inflammation leads to atrophy and intestinal G cell metaplasia (increased gastrin)
H pylori associated with...peptic ulcer disease, MALT lymphoma
types of chronic gastritis? where do they infectType A"autoimmune": autoimmune (fundus); Type B"bacteria": H. pylori (antrum first);
autoimmune gastritisautoantibodies to parietal cell and intrinsic factor (leads to pernicious anemia).
Menetrier diseasehyperplasia of gastric mucosa = looks like brain gyri (loss of protein and parietal cells)
signet ring cell (musician filled cell with peripheral nuclei)diffuse gastric cancer (NOT associated with H pylori). gross = thickened, leathery.
gastric cancer associated with H pyloriintestinal type. on lesser curvature commonly. gross = ulcer with raised margins
Peptic ulcer disease: which type is associated with post-prandial pain?Gastric peptic ulcer (greater with meals). vs Duodenal (Decreases with meals)
which type of peptic ulcer disease is associated with risk of carcinoma?gastric (greater risk with cancer)
Hypertrophy of Brunner gland is associated withduodenal ulcers (PUD)
common cause of ulcersH pylori
unique cause of gastric ulcerNSAID use
unique cause of duodenal ulcerZollinger-Ellison syndrome
ulcers at lesser curvature of stomach can lead to bleeding from what artery?left gastric artery
ulcers at posterior wall of stomach can lead to bleeding from what artery?gastroduodenal artery
Perforation due to duodenal ulcers can cause what type of pain? location?referred pain to shoulder (due to phrenic nerve).
ulcer perforation: how does this appear on CTfree air in diaphragm

Section 4

Question Answer
celiac disease - due to allergy to ___. what does it cause?gliadin. causes villous atrophy
IgA-antitissue transglutaminase (IgA tTG)celiac disease
anti endomysialceliac disease
anti deaminated gliadin peptide antibodiesceliac disease
D-xylose test. what decreased levels indicate?passively absorbs in small intestine. blood and urine levels decrease with mucosal defect of bacterial overgrowth
normal Dxylosepancreatic insufficiency
celiac disease affect which part of small intestine?distal duodenum or proximal jejunum
lactulose hydrogen breath test testGive lactulose, then measure H+ levels. value above 20 confirms lactulose malabsorption
celiac manifestationmalabsorption and steotorrhea
lactulose deficiencyosmotic diarrhea with low stool pH
why does lactulose deficiency increase H+ in stool and breath?colonic bacteria ferments lactulose.
what causes pancreatic deficiencyobstructing cancer, CF, chronic pancreatitis.
manifestation of pancreatic insufficiencymalabsopriton of fats and fat soluble vitamins (ADEK) also Vit B12; decrease in duodenal pH (loss of bicarb from pancreas); decreased fetal elastase
Tropical Sprue resemebles ____. How do you tell the difference?celiac disease. Tropical Sprue responds to abx (can also involve ileum over time)
Tropical Sprue associated with defiance in ____folate and vit B12 (leads to megaloblastic anemia).
Whipple Disease - caused by what organism?Tropheryma whipplei (intracellular gram +)
foamy macrophages in lamina propria. What are the sx?Whipple disease. CAN = cardiac, arthralgia, neuro "Foamy whip in a CAN". diarrhea/steatorrhea in later stages

Section 5