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GIT& Special Senses
Nwhsu GIT
| Question | Answer |
|---|---|
| Define digestion | breaking down complex molecules into simple molecules |
| Mechanical digestion | Chewing |
| Chemical digestion | Enzymes (catalysts) |
| Parasympathetic activity | Facilitate movement of food, promotes secretion, Ach/Peptides |
| Sympathetic | Norepinepherin |
| T or F GIT has its own nervous system | Ture, Enteric Nervous System |
| Gastrin: Source, Function, Receptor Cell | S: G cells in the antrum, F: Increase H+ secretion by parietal cells & stimulate GROWTH of Gastric Mucosa, RC: PARIETAL Cells -stimulated by A.As, stomach wall distention by food, pH, vagal stimulation, GRP/bombesin |
| Factors that can damage gastric mucosa | Stress, NSAIDS, Alcohol, Smoking |
| Imbalance of what can cause Gastric Ulcers | Acid production/secretion & mucosal protection |
| CCK: Source, Function, Receptor Cell | S: Duodenal & Jejunal "I" cells, F: promotes FAT digestion& Absorption, RC: (2) CCKa&CCKb -stimulated by monoglycerides and fatty acids & A.As |
| CCKa vs CCKb | CCKa found on pancreatic Acinar cells & Gallblader (selective to CCK), CCKb found on STOMACH & in the Brain (sensitive to gastrin and CCK) |
| Actions of CCK (5) | Contraction of gallbladder -Secretion Enzymes (Lipase, Amylase, Proteases) -Secretion of bicarbonate ions (HCO3-) -Trophic effects on gallbladder & Pancreas -INHIBITION of gastric emptying & Increase gastric emptying time |
| Can the Pancreatic enzymes function in acidic environment? | No, they need a basic environment, need Bicarbonate ions (HCO3-) |
| Lipase converts: | Fats-->Fatty Acid |
| Amylase converts: | Starch--> Glucose |
| Trypsin converts: | Protein-->A.As |
| Secretin: Source, Function, Receptor Cell | S: S cells Duodenal glands, F: secretion of pancreatic &biliary HC03- from ductal cells, reduces gastric motility & secretion (INHIBITS GASTRIN) RC:ductal cells -stimulated by LOW pH in Stomach |
| Define GIP | Glucose dependent Insulinotropic Peptide |
| GIP: Source, Function, Receptor Cell | S: K cells in Duodenal&Jejunal glands, F: stim Insulin secretion, Inhibit Gastric H+ secretion, Limits Gastric Emptying RC** - secreted in response to Glucose, A.A &FAs |
| Molitin Hormone: Source, Function | S: Enterochromaffin cells F: Increase stomach and intestinal MOTILITY, Intestinal "HOUSEKEEPER" & "MIGRRATING MOTOR COMPLEX" |
| Function of Pancreatic polypeptide Hormone | Inhibits pancreatic secretion of HCO3- |
| Function of Enteroglucagon Hormone | Increase glycogenolysis and gluconeogenesis in Liver |
| T or F Somatostatin is a Paracrine | TRUE |
| GIT Somatostatin: Source, Function, Receptor Cell | S: D cells F: inhibits secretion of other hormones and Gastric H+ secretion |
| Histamine (paracrine) function | Stimulates H+ secretion with Ach and gastrin |
| Zantac antagonist of ? | Histamine (blocker) |
| Causes relaxation of SM (2) | VIP & Neuropeptide Y |
| Causes contraction of SM (2) | Enkephalins & Substance P |
| Increases saliva | Substance P |
| GIT all smooth muscle except | Pharynx, Upper 1/3 esophagus and External Anal Sphincter (all SK muscle) |
| GI smooth muslce pacemaker (synchronizes contraction & generates ATP) | CAJAL CELLS |
| CHEWING function | Increases surface area, facilitates swallowing, mix food w/ saliva, stimulates taste buds, initiates secretion of enzymes & bile |
| Chewing starts by | stretch in mechanoreceptors that orchestrates REFLEX OSCILLARTOR pattern of muscles |
| Swallowing (deglutition) receive affterents via | Vagus & glossopharyngeal |
| What compacts food into a bolus | TONGUE |
| CN that stimulates opening of lower esophageal sphincter | CN 10 VAGUS |
| Relaxation of Lower Esophageal Sphincter leads to | RECEPTIVE RELAXATION of ORAD region of stomach |
| Stomach can accommodate | 1.5L of food |
| Steps of Motility (4) | Reception--> Mixing --> Gastric Emptying --> Retropulsion (if food isnt properly mixed) |
| What shuts during retropulsion | pyloris |
| caudad region includes | lower body and antrum |
| Orad region includes | Fundus & upper body |
| Innervation of stomach PE & E | PE: Myenteric plexus, E: Celiac ganglion |
| Neurotransmitter of Vasovagal reflex | VIP |
| Due to strong peristaltic contraction, Majority of Mixing occurs | in the ANTRUM |
| Inhibitor of Gastric Emptying (4) | FAT, ACID, Hypertonicity, Distention |
| Primary method of motility (thorough mixing occurs) | SEGMENTATION |
| Does PE or E activity INCREASE segmentation? | PE, E decreases segmentation |
| Segmentation occurs when chyme enters the | Duodenum |
| Peristalsis between meals that sweeps the inestine clean is known as | Migrating Motility Complex, 3 steps forward, 2 steps back |
| What 2 hormones are involved in the | Gastrocolic Reflex |
| What coordinates the vomiting reflex | Medulla |
| Saliva's Tonicity? | Hypotonic (less salt) |
| Antibody in saliva | IgA |
| Enzymes in saliva that start Fat Digestion | Salivary amylase &Lingual lipase |
| Antagonist of PE that blocks Muscarinic R on Acinar Cell | ATROPINE, dry mouth |
| B12 deficieny can lead to DDX | Pernicious anemia |
| The Mucus cells provide (3) | Lubrication, Protection against self digestion by pepsin & acid injury |
| Chief cellssecret | pepsinogen |
| What converts Pepsinogen into Pepsin | HCL |
| G cells secrete | Gastrin |
| Parietal cells secrete (2) | HCL & Intrinsic factor |
| What 2 things can be absorbed in the stomach | Asprin & Alcohol |
| Gastric Gand contains | chief cells and parietal cells |
| Ach and gastring stimulate the release of | Histamine |
| Histamine stimulates which cells | parietal |
| Phases of Gastric secretion | Cephalic, Gastric, Intestinal |
| What occurs in the Cephalic reflex phase | Sensory stimulation --> Gustatory centers -->Vagal nuclei and intricsic plexuses |
| What occurs in the Gastric phase | Added stimulation of food and POTENTIATION PE & ENS |
| Which phases are EXCITATORY to gastric secretion | Cephalic & Gastric |
| In the Intestinal phase, what happens to secretion in the stomach? | Contents empty into intestine and thus LESS PROTEIN and DISTENTION to stimulate secretion in stomach |
| Which cells are stimulated in intestinal phase | D-Cells (SOMATOSTATIN), inhibiting release from parietal, chief & ECL cells and PEPSIN & HCl |
| H+ ions for HCl (H+/K+ATPase)secretion in gastric Parietal Cell come from which PUMP/Exchanger? | CO2&H20 ….Chloride Bicarbonate exchanger slide 36 |
| What are the agents that stimulate H+ secretion | Vagus (Ach), G cells (Gastrin), ECL cells (Histamine) |
| What are the agents that inhibit H+ secretion | Somatostatin & Prostaglandins |
| OMEPRAZOLE (prilosec) inhibitor of | H+/K+ATPase action inhibiting H+ secretion! |
| What is in the protective barrier | HCO3- and Mucus |
| What are protective factors on the mucosa | HCO3- & mucus, Prostaglandins, Mucosal blood flow, Growth Factor |
| What are Damaging factors on the mucosa | H+, Pepsin, H.Pylori, NSAIDs, Stress, Smoking, Alcohol |
| In Peptic Ulcer Disease there is an imbalance between | Mucus secretion and Acid protection |
| Pancreatic secretions contain | Amylase, Lipase, Protease, CHOs, Fats, Proteins, HCO3- |
| 80% of pancreatic secretions goes into the ? | Intestine |
| Pancreatic secretions's TONICTY? | Hypotonic |
| Liver Functions | Regulation of metabolism, Synthesis of proteins, storage of vitamins and IRON, degrading Hormones, inactivating excreting drugs and toxins |
| Major source of Cholesterol production and Only source of Excretion | LIVER |
| Which organ converts Chylomicron to VLDL, then HDL and LDL | Liver |
| Bile is responsible for | Emusification of FATS |
| Enterohepatic Circulation | Circulation of Bile Salts |
| Bile is stored in _________ and Formed in the _________ | Gallbladder, liver |
| What happens in the Gallbladder | Bile is concentrated |
| Bile consists of | 50%salts, 40%phospholipids, 4%cholesterol, 2%bilirubin |
| Salt when conjugated with Na+ is | bile acid |
| The end product of heme catabolism | Bilirubin |
| Cholesterol -->Liver--> = | Primary bile acid |
| Cholesterol--->Liver---> Primary bile acids--> intestinal Bacteria ---> = | Secondary bile acid |
| Primary bile acids (2) | cholic acid, chenodeoxycholic acid |
| Secondary bile acids (2) | Deoxycholic acid, Lithocholic acid |
| Emptying of gallblader is caused by ______ binding to ____ | CCK to CCKb |
| Opening of the sphincter of oddi is caused by | CCK |
| Bile is ejected in steady spurts or stream? | Spurts |
| Only IRON and CALCIUM absorption is… | adjusted to the body's needs (not indiscriminately) |
| B12 and Bile salts are absorbed in | Ileum |
| Enzyme that breaksdown Starch | alpha amylase |
| Lactose is broken down into | Glucose and Calactose (via lactase) |
| Sucrose is broken down into | Glucose and fructose (via sucrase) |
| Maltotrios is broken down into glucose via | sucrase |
| Final digestion of maltose, sucrose and lactose occurs in | microvilli |
| fructose is absorbed into the blood by | Facilitated diffusion only |
| Protein digestion in the stomach occurs via which enzyme | Pepsin ...Protein-->pepsin--> AMINO ACID &oligopeptides |
| Protein digestion in the small intestine, which enzymes | trypsin, chymotrypsin, elastase, carboxy A&B |
| Makeup of a MICELLE | Chol, MG, LysoPL, FFA |
| Make up of Chylomicron | PL, ApoB (Chol E, TG) |
| Vitamins are absorbed by sm intestine, H20 soluble Vit? | B1,B2,B6 and B12, C |
| Fat soluble | A, D,E,K |
| B12 absorption requires__ and is absorbed in ____ | Intrinsic factor, Ileum |
| B12 is stored in | Liver |
| B12 has ____ years worth maintained in the liver | 3-6 years |
| B12 is required for (2) | Proper myelination in the CNS & Nucleic acid synthesis |
| Vitamin C increases IRON absorption by | Reducing Fe+++ to Fe++ |
| Transferrin (Iron bound to BetaGlobulin) transports it from ____ to _____ | Sm intestine to the liver |
| Heme iron is digested by | lysosomes & is transported with apoferritin into blood |
| Vit D stimulates absorption of Ca++ against [gradient] by | activating Ca++ transporter protein (calbindin-D-28K) |
| 2 transporters of Ca++ exist in ________membrane | basolateral |
| The 2 Ca++ transporters are | Ca++ATPase & Ca++/Na+ ANTIporter |
| where is the HCO3-/Cl- exchanger located | epithelial cell of Illeum |
| Passive absorption for Na+ occurs | Btw Adjacent epithelia cells & Interstitial fluid |
| Active absorption for Na+ occurs | through epithelial ceels requiring ATP& 2carriers |
| Deposition of Ca++ in the lense causes | cataracts |
| Photoreceptors in the retina are (2) | Rods & cones |
| Rods & Cones detect what | Rods=Dark (shades of grey), Cones=Light (color vision) |
| Where is the blind spot located | At the optic disk |
| Which portion of the retina are cones are most abundant | Center (macula) |
| Portion of retina where Rods are most abundant | Periphery |
| Rhodopsin | Rod photopigment |
| Human ear is sensitive to a range of _______ (Hz of sound frequency) | 20-20000 |
| Sound pressure is expressed as | dB |
| what sound pressure can cause damage to aud. Apparatus | >100 dB |
| what sound pressure can cause pain to aud. Apparatus | >120 dB |
| CN for hearing | 8, Vestibulocochlear |
| Inner hair cells of scala media are located on the _____ membrane | basilar |
| Is endolymph or perilymph in the scala media? | endolmph (high in K+) |
| Contain vestibular hair cells covered by cupula | Semi-circular canals |
| Detects angular acceleration | Semi-circular canals |
| Responds selectively to TILTING of HEAD away for a HORIZONTAL position (get up from bed) | SACCULE |
| Responds to vertically and directed linear acceleration | jumping up and down, elevator |
| Sound waves are not conducted through external and middle ear | Conductive deafness |
| Physical blockage of canal is what type of deafness | Conductive deafness |
| Bony adhesion btw stapes and oval window is what type of deafness | Conductive deafness |
| Sound waves are not TRANSLATED into nerve signals | sensorineural defnesss |
| What is Neural Presbycusis | degenerative age related process that occurs as hair cells wear out |
| Golf Proteins | olfactory transuction |
Created by:
kfrancis
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