front 1 lead into the liver | back 1 hepatic artery and hepatic portal vein |
front 2 lead out of the liver | back 2 hepatic veins and common hepatic duct |
front 3 be able to label the following on lobules | back 3 central vein, branch of hepatic artery, branch of portal vein |
front 4 big canal between hepatocyte cords | back 4 sinusoid |
front 5 small canal between hepatocyte cords | back 5 bile canaliculus |
front 6 modify the blood in the liver by adding or removing certain materials | back 6 hepatocytes |
front 7 special about liver, gives it direct access to blood | back 7 no endothelial layer |
front 8 can activate or inactivate drugs/chemicals in the liver | back 8 CYP enzymes |
front 9 additions/subtractions that CYP can do | back 9 hydroxylation, dealkylation, deamination, hydrolysis |
front 10 drugs that cannot be taken with grapefruit due to effect on CYP enzymes | back 10 Xanax, Lipitor, Allegra |
front 11 causes of variation in CYP affectiveness | back 11 genetics, liver failure due to age, alcoholism, or hepatitis |
front 12 phagocytes in the liver that remove foreign objects from the blood | back 12 Kupffer cells |
front 13 things placed in bile | back 13 cholesterol, bilirubin, HCO3-, water, bile salts |
front 14 where bile is stored | back 14 gallbladder |
front 15 be able to label the following organs and ducts involving bile | back 15 liver, common hepatic duct, common bile duct, pancreas, cystic duct, sphincter of oddi, pancreatic duct, duodenum |
front 16 how bile is let into the duodenum | back 16 the sphincter of oddi relaxes during eating periods to let it through |
front 17 what amount bile must be concentrated down to | back 17 50mL/12hr |
front 18 actively transported out of bile, followed by water | back 18 Na+ |
front 19 become more concentrated in bile after sodium and water leave | back 19 bile salts, HCO3-, bilirubin, and cholesterol |
front 20 can form gallstones | back 20 bilirubin and cholesterol |
front 21 symptoms gallstones can cause | back 21 poor digestion, jaundice, pain, toxicity, inflammation |
front 22 contractions of these cause bile to be released into the duodenum | back 22 CCK stimulates gallbladder contraction, sphincter relaxes |
front 23 neutralizes acid in duodenum | back 23 HCO3- |
front 24 how bile salts emulsify fats | back 24 attaches to them to form a micelle, which can be absorbed into the blood stream |
front 25 steatorrhea | back 25 fats in feces from lack of absorption |
front 26 stimulates islets for insulin secretion | back 26 incretin |
front 27 bicarbonate cycle | back 27 liver-->gallbladder-->duodenum-->blood-->liver again |
front 28 breakdown of proteins | back 28 into amino acids by pepsin and trypsin |
front 29 breakdown of carbohydrates | back 29 into sugars by amylase |
front 30 breakdown of nucleic acids | back 30 into nucleotides by nucleases |
front 31 breakdown of fats | back 31 into fatty acids by lipases |
front 32 3 step process of absorption | back 32 get into cytoplasm, get it to cross other side of cell, get it into blood or lymph |
front 33 modifications that maximize intestinal absorption | back 33 circular folds, villi, and microvilli |
front 34 absorption of sugar | back 34 cotransport with sodium, sodium is actively transported out |
front 35 absorption of fatty acids | back 35 micelles detach their phospholipids, which use flippases to flip across the bilayer and form into triglycerol |
front 36 protein coated micelles | back 36 chylomicron |
front 37 absorption of amino acids | back 37 can be absorbed in singles, pairs, or triplets, energy is from Na+ or H+ concentration gradient |
front 38 absorption of electrolytes | back 38 Positive ions use facilitated diffusion, negative ions use positive ions, water uses osmosis, potassium uses concentration gradient |
front 39 stimulates Na+ absorption | back 39 aldosterone |
front 40 stimulates Ca+2 absorption | back 40 PTH |
front 41 amount of fluid reabsorbed and added to digestive system | back 41 7 liters |
front 42 amount of fluid that must be consumed to avoid dehydration | back 42 2 liters |
front 43 types of ulcers | back 43 gastric and duodenal |
front 44 what ulcers are | back 44 erosions in the mucus membrane, exposed directly to stomach acid |
front 45 bacteria that causes ulcers | back 45 H. pylori |
front 46 hormones that stimulate proton potassium ATPase pump | back 46 gastrin, ACh, histamine |
front 47 bleeding ulcer | back 47 basement membrane broke and allowed blood in |
front 48 treatments for ulcers | back 48 antibiotics and proton pump inhibitors, histamine receptor antagonists, prostaglandin E1 analog, antacids |
front 49 why NSAIDs are counterproductive in ulcers | back 49 they inhibit prostaglandin production |
front 50 celiac disease | back 50 undigested gluten gets through villi into ISF, humoral immune system responds, neutrophils lyse and cause damage |