Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Final Exam
Physiology
| Question | Answer |
|---|---|
| monosaccharides | glucose, fructose, galactose |
| disaccharides | sucrose and lactose |
| polysaccharides | starch and glycogen |
| t/f: fibers cannot be broken down into monosaccharides | true |
| insoluble fiber | cellulose |
| soluble fiber | pectin |
| what are triglycerides made of | glycerol and 3 fatty acids |
| what are triglycerides broken down into | free fatty acids and monoglycerides |
| what is protein broken down into | amino acids and small polypeptides |
| site of nutrient absoprtion | small intestine |
| accessory digestive organs | salivary glands, exocrine pancreas, liver, and gallbladder |
| serosa | secrete serous fluid to prevent friction |
| muscularis externa consists of | smooth muscle, inner circular and outer longitudinal layers & myentetic plexus |
| submucosa consists of | connective tissue and submucosal plexus |
| mucosa consists of | mucous membrane, lamina propria, muscularis mucosa |
| autonomous smooth muscle cells | pacemaker cells |
| what are the pacemaker cells of digestion | interstitial cells of cajal (muscularis externa); form a syncytium and produce slow wave potentials |
| intrinsic nerve plexus | submucosasl and myenteric plexus, neurotransmitters: Ach (+) and NO/VIP (-); intrinsic primary afferent (local stimuli) and efferent neurons (smooth muscle and endocrine/exocrine cells) |
| extrinsic nerves | Sympathetic nervous system-slows digestion Parasympathetic nervous system- vagus nerve, inc. smooth muscle contractions, (+) secretion of enzymes/hormones |
| GI hormones | endocrine cells of GI tract |
| 4 steps of digestion | 1. Motility- mixing and propulsive movement 2. Secretion- exocrine and endocrine 3. Digestion- hydrolysis of nutrients 4. Absorption- transfer of nutrients from intestinal lumen into blood/lymph |
| Gut microbiome | aids in fiber fermentation and produce vitamins and amino acids as byproducts |
| salivary amylase | breaks down starch → maltose and dextrins; inactivated by acid |
| lysozyme | antibacterial → breaks down bacterial cell walls |
| Stomach function | o Storage of food- intersititial cells of cajal produce slow wave potentials o Secretion of HCl and other enzymes for protein digestion o Production of chyme- strong antral peristaltic contractions mix food with stomach secretions |
| filling of stomach | vagus nerve mediated relaxation |
| gastric emptying | strong antral contraction pushes chyme through sphincter into duodenum |
| peristalsis | ring-like contractions of smooth m. that progressively move forward |
| 3 parts of the stomach | o Fundus- above esophageal opening o Body- middle/main part o Antrum- lower with heavy musculature |
| pyloric sphincter | barrier between stomach and small intestine |
| retropulsion | chyme propelled back to body then forward again |
| fluidity of chyme | the more fluid the faster the emptying |
| duodenal inhibits antral peristalsis when | o fat + release of CCK → - antral contractions and + pyloric sphincter o acidic chyme + secretin release → - gastric emptying o hypertonicity of intestinal content - gastric emptying o distention of duodenum due to inc. chyme - gastric emptying |
| how do emotions effect motility | o fear/stress: dec. motility due to SNS o anger: inc. motility o pain: dec. motility due to SNS |
| vomiting | forceful expulsion of gastric contents through the mouth |
| vomiting center in medulla leads to | inc. salivation, sweating, HR, and nausea |
| muscles involved in vomiting | diaphragm and abdominal muscle stimulates expulsion |
| things that can trigger vomiting | irritation/distention of stomach/duodenum, inc. intracranial pressure, motion sickness, chemical agents, psychological, touch back of throat |
| effects of vomiting | dehydration, metabolic alkalosis |
| what are gastric juices formed by | oxyntic mucosa (body and fundus) and pyloric gland area (antrum) |
| gastric pits | invaginations of luminal surface with gastric glands at the base |
| exocrine cells of stomach | o mucous cells: line gastric pits; secrete thin, watery mucus o chief cells: deep gastric glands; secrete zymogen pepsinogen o parietal cells: deep gastric glands; secrete HCl and intrinsic factor |
| t/f: no acid produced in pyloric gland area (PGA) and cells are joined by tight junctions which makes them impermeable to HCl | true |
| surface epithelial cells | between gastric pits; secrete sticky, alkaline mucus that forms over mucosa |
| stem cells | in gastric pits; become epithelial or glandular cells; entire mucosa replaced every 3 days |
| canaliculi | parietal cells form deep invaginations along luminal membrane to inc. surface area and secrete HCl into lumen; separate H+ and Cl- |
| H+ derived from water is secreted via what | H-K ATPase pump |
| why is blood leaving the stomach alkaline | basic byproducts of HCl production |
| HCl function | o Activates pepsinogen into pepsin o Breakdown of connective tissue and muscle that reduces food, denatures protein, and kills microorganisms o Inactivates salivary amylase |
| zymogen granules | pepsinogen stored in chief cells in secretory vesicles |
| autocatalytic process | active pepsin will activate pepsinogen into pepsin |
| 3 gastric secretion phases | cephalic, gastric, and intestinal |
| cephalic phase | ▪ inc. HCl and pepsinogen secretion ▪ Feedforward mechanism- vagal nerve (+) intrinsic plexus to inc. Ach, HCl, and pepsinogen and (+) G cells → inc. gastrin, HCl, and pepsinogen |
| gastric phase | ▪ Food reaches stomach ▪ Protein (+) vagal nerve → (+) secretory cells and gastrin → inc. HCl and pepsinogen ▪ Caffeine and alcohol (+) acidic juices without food which leads to discomfort |
| intestinal phase | ▪ Factors from small intestine affect gastric secretions ▪ Inhibitory phase ▪ inc. chyme in intestine gastric secretions via dec. protein in stomach, dec. pH (+) somatostatin, and (-) of gastric motility (fat, acid, hypertonicity, and distention) |
| digestion in body of stomach | little protein digestion, carb digestion by salivary amylase in center of mass not exposed to acid |
| digestion of antrum of stomach | chemical digestion; food is thoroughly mixed with pepsin and HCl |
| main functions of hepatocytes | o Secretes bile salts for fat digestion and absorption o Detoxification of wastes o Synthesis of plasma proteins o Nutrient storage o Activates vitamin D3 o Excrete cholesterol and bilirubin |
| Kupffer cells | remove bacteria and damaged RBCs |
| hepatic portal vein system | delivers blood from GI tract right after absorption in intestine before it circulates to the heart |
| liver lobule | consists of hepatic artery, hepatic portal vein, and bile duct |
| sphincter of oddi | connects bile duct to duodenum; when closed, bile is stored in gallbladder; when open, stored bile enter duodenum |
| bile is made of | o Bile salts o Cholesterol o Lecithin o Bilirubin o Alkaline fluid |
| bile salts | derived from cholesterol; important for fat absorption (emulsification) and digestion; reabsorbed in ileum ▪ Consists of cholesterol part (which binds to and dissolves in fat) and negatively charged part (projects from micelle and repels from others) |
| choleretic | compound that inc. bile secretion |
| examples of choleretics | bile salts, vagal nerve during cephalic phase, and CCK |
| emulsification | converted fat globules into small lipid droplets called micelles by adding negatively charged bile salts o Micelle core is hydrophobic and outer shell is water soluble o ↑surface area for pancreatic lipase |
| bilirubin | NO ROLE IN DIGESTION; WASTE BYPRODUCT OF DEGRADATION OF HEME o Hepatocytes take in bilirubin and modify to ↑solubility o Also modified in GI tract o cause of bile, urine, and feces color |
| Small intestine segmentation | motility during meal; mixes and slowly propels chyme with digestive juices and ↑surface area |
| segmentation is caused by | basal rhythm contractions are brought to threshold |
| strength of segmentation | determined by distention, gastrin, and extrinsic nerve activity ▪ SNS: (-) ▪ PSNS: (+) |
| gastrointestinal reflex | ileum segments in response to gastrin |
| migrating motility complex (MMC): | during fasting, “intestinal housekeeping” |
| phase 1 of MMC | long, quiet period with few contractions |
| phase 2 of MMC | shorter, little contractions |
| phase 3 of MMC | shortest, intense contractions from stomach → small intestine; pyloric sphincter is open; stomach "growling” |
| MMC is regulated by | motilin |
| Ileocecal sphincter | under neural and hormonal control; opens with gastrin |
| succus entericus | aqueous salt and mucus solution secreted by intestinal glands; ↑after meal |
| where is fat digestion completed | in lumen of small intestine |
| where is protein digestion completed | in microvilli |
| 3 membrane bound enzymes in brush border | enteropeptidase maltase, sucrase-isomaltase, and lactase aminopeptidase |
| Enteropeptidase | activates pancreatic trypsinogen |
| Maltase, sucrase-isomaltase, and lactase | targets maltose, α-limit dextrins, and dietary disaccharides |
| aminopeptidase | hydrolzye protein fragments into amino acids |
| increasing surface area | o Circular folds o Villi o Microvilli (brush border) |
| villi | epithelial cells joined by tight junctions; consists of capillary network and central lacteal |
| passive sodium absorption | favors Na moves from lumen to plasma through leaky tight junctions |
| active sodium absorption | Na passes through cell via Na-Cl symporter, Na-H antiporter, and Na-glucose/AA symporter |
| what carbs are absorbed | Monosaccharides: glucose, galactose, and fructose |
| t/f: Glucose and galactose are dependent on Na concentration for secondary active transport via SGLT symporter | true |
| what is the concentration gradient established by | Na-K pump on basolateral membrane |
| how is fructose absorbed | passively through GLUT5 |
| how do glucose, galactose, and fructose exit enterocytes and go into blood | GLUT2 |
| protein absorption | o AA-Na symporter o H-peptide symporter (tertiary active transport) |
| first step in fat absorption | Micelles reach epithelial cells |
| what happens after micelles reach epithelial cells in fat absorption | Free FA and monoglycerides passively diffuse into cell and reform triglycerides inside |
| what happens when triglycerides are reformed inside the epithelial cells (enterocytes) | Triglycerides form droplets and are coated with lipoprotein to make them water soluble and are now named chylomicrons |
| where are chylomicrons exocytosed | into ISF then central lacteal |
| t/f: fat absorption is technically active transport | true |
| Crypts of lieberkuhn | invaginations between villi; secrete water and salt for succus entericus; contain stem cells |
| paneth cells | in crypts; produce lysozyme and defensins |
| what do the acini cells do in exocrine pancreas | connect to ducts that empty into duodenum |
| what do pancreatic enzymes do | secreted in alkaline solution to neutralize acidic chyme |
| enzymes stored in zymogen granules | o Proteolytic enzymes o Pancreatic amylase o Pancreatic lipase |
| proteolytic enzymes | protein; trypsinogen, chymotrypsinogen, and procarboxypeptidase |
| pancreatic amylase | carbs; starch → disaccharides and α-limit dextrins; active |
| pancreatic lipase | fats; triglycerides → monoglycerides and free FA |
| what conditions do enzymes in zymogen granules work best in | basic conditions |
| t/f: enzymes in zymogen granules are stimulates by the intestinal phase | true |
| stimulation of secretin by zymogen granule enzymes | (+) by acid in duodenum → (+) duct cells → bicarb secreted |
| stimulation of CCK by zymogen granule enzymes | (+) by fat* and protein in duodenum → (+) acinar cells → enzymes secreted |
| pancreatic colipase | secreted with lipase; similar to bile salts in structure → helps lipase hydrolyze fats better |
| pepsin is found in the | stomach |
| pepsin | ▪ Inactive: pepsinogen ▪ Activated by: HCl ▪ Cleaves C side of phenylalanine, tryptophan, and tyrosine (aromatic AA) |
| trypsin is found in the | pancreas |
| trypsin | ▪ Inactive: trypsinogen ▪ Activated by: enteropeptidase ▪ Cleaves on C side of lysine or arginine |
| chymotrypsin is found in the | pancreas |
| chymotrypsin | ▪ Inactive: chymotrypsinogen ▪ Activated by: trypsin ▪ Cleaves hydrophobic AA (aromatic AA) |
| carboxypeptidase is found in the | pancreas |
| carboxypeptidase | ▪ inactive: procarboxypeptidase ▪ Activated by: trypsin ▪ cleaves C side |
| aminopeptidase is found in the | small intestine brush border (microvilli) |
| aminopeptidase | cleave peptide bonds |
| contents of the colon | consist of indigestible foods, biliary components, and remaining fluid |
| t/f: the colon extracts water and salt to dry and compact feces | true |
| colon main function | storage of feces |
| what provides bulk to the colon to maintain regular bowel movements | cellulose |
| GERD risk factors | obesity, delayed stomach emptying, pregnancy, fatty food, and smoking |
| GERD (gastroesophageal reflux) | reflux of food and gastric acid into esophagus due to open sphincter |
| GERD causes | Barrett’s esophagus cancer |
| Achalasia | nerve damage to esophagus that prevents food from propelling into stomach |
| Achalasia is caused by | neuromuscular disease, inflammation, and myasthenia gravis |
| Achalasia side effects | enlarged esophagus and respiration pneumonia |
| pernicious anemia | due to insufficient vitamin B12 absorption in ileum |
| pernicious anemia is caused by | dietary insufficiency, inflammation in ileum, lack of intrinsic factor (autoantibodies attack parietal cells) |
| peptic ulcers | damage to mucosal lining |
| peptic ulcers are caused by | helicobacter pylori, inflammation or physical damage, and medications like NSAIDS ■ NSAIDS block prostaglandins which function to decrease gastric acids production and increase mucus and HCO3 production (block prostaglandins inc. HCl and dec. bicarb |
| peptic ulcer treatment | H2 blockers (blocks one pathway of acid production) and proton pump inhibitors (reduces total acid production) |
| delayed gastric emptying (gastroparesis) | decreased motility and emptying |
| gastroparesis is caused by | inflammation, obstruction, or neurological (diabetes) |
| regurgitation | backwards flow of food |
| liver disease types | hepatitis, fibrosis, and cirrhosis |
| liver disease | reached regeneration limit and fibroblasts start displacing hepatocytes (fibrosis) |
| liver disease can be due to | hepatitis B and C, alcoholic liver disease, nonalcoholic fatty liver disease (obesity) genetic diseases (hemochromatosis and Wilson’s disease), diseases of bile ducts (primary biliary cirrhosis, primary sclerosing cholangitis, and biliary atresia) |
| liver disease symptoms | loss of appetite, edema, jaundice, etc |
| jaundice is caused by | bilirubin being formed faster than excreted |
| pre-hepatic jaundice | hemolytic anemia |
| hepatic jaundice | liver disease |
| post-hepatic jaundice | obstructive disease of bile ducts (gallstones) and lack of bilirubin excretion |
| liver function markers | ■ albumin: dec. with hepatic insufficiency ■ cholesterol: dec. with liver failure ■ bilirubin: used for hepatitis & cirrhosis ■ ammonia: used for hepatic insufficiency/portosystemic shunt ■ bile acids: used for portosystemic shunt/hepatic dysfunction |
| markers for hepatic injury | alanine transaminase (ALT): released upon injury from hepatocytes |
| markers for biliary disease | ■ alkaline phosphate (ALP): high with cholestasis ■ gamma glutamyltransferase (GGT): high with cholestasis |
| osmotic diarrhea | pulls water into intestinal lumen due to poorly absorbed solutes |
| osmotic diarrhea is caused by | lactose intolerance, citrate of magnesia, and maldigestion of food |
| altered motility diarrhea | increased motility |
| if altered motility diarrhea is decreased | constipation |
| secretory diarrhea | glands secrete more fluid |
| secretory diarrhea is caused by | decreased absorption, increased secretion, toxins produced by bacteria (Staph, E. coli, cholera) |
| maldigestion/alabsorption diarrhea | result of fat malabsorption (pancreatic insufficiency), Crohn’s disease, celiac disease, and decreased bile salt absorption (ASBT bile acid transporter in ileum) |
Created by:
k.murski
Popular Physiology sets