Karteikarten
GI tract
Karten in diesem Stapel (118)
- 1What is the function of: 1. exocrine glands (salivary glands, liver, pancreas) 2. stomach 3. small intestine 4. large intestine1. secretion
2. storage & breakdown of food
3. digestion & absorption
4. storage & absorption - 2What are different layers of GI tract?Mucosa: epithelium, lamina propria, muscularis mucosae
Submucosa (w/SM plexus separating ME)
Muscularis externa: circular SM, longitudinal SM (w/myenteric plexus betwen circular & longitudinal SM)
Serosa: connective tissue, epithelium - 3What r different cell types in intestinal epithelium and their functions?Enterocyte/intestinal absorptive cell: simple columnar epithelia small intestine microvilli apical surface ↑surface A 4 digestion (breakdown of sugars, proteins, lipids) & absorption (uptake of ions, H2O, sugars, peptides & aa, lipids, vit B12, un-conjugated bile salts), secretory role (immunoglobulins)
Goblet cells: glandular modified simple columnar epithelia, secrete mucus, highly polarised (nucleus+organelles cell base, rest cytoplasm secretory granules w/ mucins), microvilli ↑surface A 4 secretion
Paneth cell: located below intestinal stem cells in intestinal glands (crypts of Lieberkuhn), large eosinophilic granules w/antimicrobial compounds & compounds important 4 immunity & host-defense occupy most cytoplasm
Enteroendocrine cells: endocrine function=>produce GI H/peptides in response various stimuli & release them in2 blood 4 systemic effect, diffuse them as local messengers or transmit 2 ENS (e.g. I cell: CCK=>bile secretion, exocrine pancreatic secretion, satiety; S cell: secretin=>exocrine pancreatic secretion) - 4What r the functions of GI tract?Digestion+absorption of nutrients
Absorption+retention of H2O+electrolytes
Elimination of toxins
Maintenance of barrier function
Immunological barrier - 5What diary V of fluid do we ingest? And produce (saliva, gastric secretions, bile, pancreatic secretions,intestinal secretions)? And absorb (small & large intestine)? And excrete?Ingest: 2L
Saliva: 1.5L
Gastric secretions: 2L
Bile: 0.5L
Pancreatic secretions: 1.5L
Intestinal secretions: 1.5L
Absorption small intestine: 8.5L
Absorption large intestine: 0.4-1L
Excrete: 0.1L - 6What is absorbed/secreted & function in: 1. oral cavity? 2. stomach? 3. duodenum? 4. ileum? 5. large intestine?1. Amylase (starch digestion), fluid (salivary glands), mucus (lubrication/ protection)
2. HCL (lumen pH~2-3), pepsin action (protein digestion), intrinsic factor (vit B12 absorption), alkaline mucus (protection) (2-4hr)
3. nutrient digestion & absorption, aborption of: vit, ions (Fe2+, Ca2+, PO4-, Na+, K+, Cl-, HCO3-), H2O (2-3hr)
4. absorption of vit B12, bile salt, Na+, Cl-, H2O (1-2hr)
5. Na+, Cl-, H2O absorption, K+&HCO3- secretion (12-24hr) - 7What %CO & %V blood does splanchnic circulation represent? What %BF 2 liver does splanchnic circulation (portal vein)& hepatic artery represent?20-25%CO, 30%V blood
Portal vein: 70%BF 2 liver
Hepatic artery: 30%BF 2 liver - 8Which organs does splanchnic circulation involve?Stomach (gastric artery), spleen (splenic artery), pancreas (splenic artery+superior mesenteric artery), small intestine (superior mesenteric artery), large intestine (inferior mesenteric artery)
- 9Which cells secrete gastric acid? How is gastric acid secretion controlled?Parietal cells=>HCL secretion=>stimulated by gastrin, histamine & ACh (enteric neurons) // inhibited by somatostatin
Gastrin (G cell) stimulate histamine release (ECL cell), somatostatin (somatostatin-releasing cell) inhibits gastrin+histamine - 10What is the function of the following endocrine H secreted by GI tract: 1. CCK (duodenum - I cells) 2. Secretin (duodenum - S cells) 3. Gastrin (stomach - G cells) 4. GLP-1 (ileum - L cells)1. Gall bladder contraction, GI motiliy, pancreatic exocrine secretion
2. pancreatic exocrine secretion
3. acid secretion
4. incretin activity (insulin secretion & glucagon inhibition), inhibits acid secretion & gastric emptying (stomach), satiation - 11Describe nervous control of GI function1. CNS: conditioned/unconditioned reflexes (association neutral stimulus w/food=>acquired by learning, cortex involved/reflex response 2 food in GI tract, no learning required)
2. ANS: PASY/SY (increases motility, GI BF, exocrine secretion/decreases motility,GI BF, no major control exocrine secretion)
3. ENS (local nerve reflexes): control mov GI tract, fluid & electrolyte transport, mucosal protection (mucus secretion) - 12What is ENS & how is it related 2 ANS?Myenteric plexus=motor function
SM plexus=sensory function
ENS called "gut brain" as contains 10^7-10^8 neurons, + than SC
ENS influenced by ANS but can perform many functions independently (peristaltic reflex, ion secretion...)
ENS secrete ACh, NA & many non-classical NT involved control GI motility, control fluid & electrolyte transport & mucosal protection - 13Compare long & short reflexes in GI tractCNS pathways (long reflex): R (gut wall)=> afferent fibres=>CNS=>ANS=>efferent fibres=>enteric neurons=>target cells (gut)
Local(enteric)nerve pathways(short reflex): R (gut wall)=>enteric neurons=>target cells - 14What r different GI exocrine secretions and where do they originate?Exocrine secretions originate glands w/ ducts. Exocrine glands secrete digestive juices: salivary glands (1.5L), liver (0.5L), pancreas (1.5L). Stomach gastric glands secrete HCL, mucus & pepsinogen. Duodenum Brunner's glands produce mucus rich alkaline secretion
- 15What r principles of exocrine secretion & its control? (model exocrine gland)Acinar cells produce primary secretion (isotonic) & duct cells modify it by ion exchange 2 produce final secretion. Both acina & duct tranport processes r regulated by endocrine, neurocrine, paracrine agents
- 16Describe salivary secretions in terms of glands, pH, V, functions, tonicity1-1.5L saliva/day; parotid gland: serous (H2O secretion), other salivary glands (sub-mandibular, sublingual): mucous secretion; secretion hypotonic; pH 6.5-7.5; facilitates speaking, chewing, swallowing, tasting; contains α-amylase: initiates carbohydrate digestion; antibacterial properties
- 17Which transport processes are involved in formation of saliva?Acinus/acinar cells: NKCC1=>cotransport Na+, 2Cl-, K+ in (BLM); Na+/K+ pump=>K+ in, Na+ out (BLM); K+ channels=>K+ out (BLM); CFTR=>Cl- out (AM); trans-cellular (aquaporins) & paracellular (tight junctions) H2O transport; paracellular Na+ transport (primary isotonic secretion rich in Na+, Cl-, H2O, HCO3- protein)
Duct/duct cells: Na+/K+ pump=>Na+ out, K+ in; CBE=>Cl- out, HCO3- in (final hypotonic secretion rich K+, HCO3-, H2O) - 18What determines osmolarity & ionic composition of saliva? How do they vary?Flow rate: high flow rate=less t modification
As flow rate increases, osmolarity increases
As flow rate increases, Na+, Cl- & HCO3- increase & K+ decreases - 19How is salivary secretion controlled?PASY nerves: increase flow rate, increase BF, contraction of myoepithelial cells
SY nerves: no major effect
H do not exert any control - 20What is Sjogren's syndrome?Inflammation salivary glands
Lack saliva impacts oral health - 21What r 4 layers wall tubular part GI tract? And what is their function?M (epithelium, lamina propria, MM): region-specific specialisations (mucus+ secretory glands-stomach, villi-SI, crypts-LI), epithelium interface luminal contents /gut wall=>digestion & absorption, secretion locally acting & circulatory H
SM: connective tissue w/blood+lymph vessels & SM plexus (ENS)
ME: circular & longitudinal SM, myenteric plexus (ENS), propulsion contents along digestive tract, mixing&storage functions
Serosa: single layer cells separate GI tract from peritoneum - 22Give examples GI endocrine & paracrine H?GI endocrine H: gastrin, secretin, CCK, GIP, GLP-1, GLP-2, PYY (acts on non-GI tissue)
GI paracrine H: somatostatin, histamine - 23What is the function of PYY? Why is special?PYY: GI endocrine H affects non-GI tissues =>released SI by luminal nutrients=> suppresses appetite & regulates food intake (acts specific CNS satiety neurons)
- 24How is ANS involved in control GI function?Vagal & splanchnic nerves convey SENSORY (afferent) & efferent info. Approx 90% vagal fibres r afferents as r 70% fibres splanchnic nerves & r thus part somatic NS. Efferent postG nerves synapse w/ENS w/in ME & SM layers&innervate SM,glands&mucosal cells
- 25What r 3 salivary glands, their secretions & general structure? What is function saliva?Parotid:serous(watery)secretion w/amylase
Submandibular: mucous & serous acini
Sublingual: largely mucous acini
Structure glands: acini (protein+fluid secretion)+ducts (ion exchange)
Functions saliva: digestion (α-amylase), lubrification (mucus), antibacterial, taste - 26How is saliva formed?Primary secretion: isotonic fluid (acini) w/ plasma-like Na+& Cl- c. Acinus only part net fluid secretion. H2O flow 2ndary electrolyte transport. 2ndary changes ion c - striated duct:Na reabsorption exchange K secretion (3:2). Ducts low H2O permeability (explains variation osmolarity & Na/K c w/ flow rate)
- 27How is salivary secretion controlled?Mostly through PASY efferent fibres from salivatory nuclei in medulla. Those neurons receive input from R in mouth, pharynx, olfactory A. Response modulated by facilitatory & inhibitory impulses from appetite A in HPT & taste-smell A in cerebral cortex. Conditioned (weak in humans, controlled higher cortical A) & unconditioned (initiated by stimulation R tongue/mouth, lower oesophagus & stomach/upper intestine) nervous reflexes operate.
- 28What r effects of PASY & SY stimulation of salivary glands? And H stimulation?PASY: abundant flow watery (serous) saliva from parotid glands, vasodilation
SY: no overall effect rate salivary secretion
No H control rate salivary secretion; ALDO reduces Na+ c (similar mechanism kidney) - 29What r functions of stomach?1. Stores food for 2-4hr
2. Secretes gastric juices
3. Allows controlled emptying stomach contents into small intestine - 30What major anatomic regions of stomach?Cardia (where contents oesophagus empty into stomach), fundus, body (major A exocrine secretion), pyloric antrum (major A endocrine secretion: production & release gastrin), pyloric canal (opening 2 duodenum, controls emptying of stomach)
- 31What's name & function internal folds stomach?Rugae: allow distension of stomach wall & increase A of secretion
- 32Compare structure gastric & pyloric glandsGastric glands: surface mucous cell, mucous neck cell, parietal cell (HCl, intrinsic factor), chief cell (pepsinogen), entero-chromaffin-like (ECL) cell (histamine)
Pyloric glands: surface mucous cell,
mucous neck cell, G cell (gastrin), D cell (somatostatin) - 33What is composition & function of gastric secretions?~2L gastric secretion/day, isotonic, pH 2-3, HCL (kills bacteria, denatures dietary proteins, activates pepsinogen, cofactor pepsin action), pepsin (initiates protein digestion), intrinsic factor (essential vit B12 uptake lower ileum)
- 34How does acid secretion & gastric pH change after eating?After eating, lumen pH increases & so does acid secretion until lumen pH back normal (pH~2) & acid secretion drops
- 35How is HCl produced in parietal cells?1. Plasma CO2 in=>CO2+H2O=carbonic anhydrase=>H2CO3=>HCO3-+H+
2. Cl- in <=CBE=>HCO3- (1) out plasma
3. K+ in<=Na+/K+ ATPase=>Na+ out plasma
4. K+ (3) & Cl- (2) out lumen channels
5. H+ (1) out lumen<=H,K-ATPase=>K+ in (4) - 36What is alkaline tide? What is [H+] difference between plasma & lumen?After meal, 2 produce HCl parietal cells (stomach) secrete HCO3- across BLM in2 blood=>temporary increase in pH
plasma [H+]=10^-8M; lumen [H+]=0.15M - 37What r subcellular changes observed in parietal cells during acid secretion?Resting parietal cell: tubulovesicles
Active: canaliculus (50-100 fold increase canalicular surface A) - 38How is pepsinogen activated?1. Pepsinogen (chief cells) & HCl (parietal cells) secreted into lumen
2. HCl converts pepsinogen 2 pepsin (active enzyme) - 39What is function of pepsin?Endopeptidase that initiates protein digestion (~15% protein digestion)
- 40Why is HCl so important 4 pepsin?Not only HCl converts pepsinogen in2 pepsin, but is also cofactor required 4 optimum protein activity (pH<2)
- 41What is the intrinsic factor and its function?Intrinsic factor: glycoprotein secreted from parietal cells, forms complex w/dietary B12 in upper SI which protects it from enzymatic digestion,
- 42How is vit B12 absorbed?In terminal ileum, R mediated endocytosis, only B12 transferred to blood, in circulation bound to B12 BP, excess B12 stored liver
- 43How is gastric secretion controlled?1. ANS: PASY nerves ↑secretion (direct & indirect mechanisms: HCL production, pepsinogen release, gastrin release, mucous release, gastric SM contraction), SY no major control over secretion, ENS SM & myenteric plexus ↑secretion (ACh)
2. Endocrine H: gastrin main endocrine H, promotes gastric secretion=>↑HCl production, pepsinogen&mucous release (also maintenance gastric mucosal structure & ↑motility GI SM); secretin=> endocrine inhibitor of H+ secretion (from upper SI epithelial cells)
3. Paracrine H: somatostatin (direct & indirect mechanisms: inhibits G cell/ gastrin, ECL cell/histamine, parietal cell/ HCl; stimulated by HCl), histamine (ECL cell stimulated by gastrin, histamine stimulates HCl secretion by binding H2-R on parietal cells).
Interaction between systems at parietal cell level - 44What r 3 phases gastric secretion?Cephalic phase (30-35% total secretion): b4 food enters stomach, short duration
Gastric phase (~60% total secretion): while food in stomach, long duration (2-4hr)
Intestinal phase (5-10% secretion): chyme enters duodenum, largely hormonal, long duration (hrs) - 45Describe function, stimuli & components of cephalic phase of gastric secretionFunction: prepares stomach receiving food
Stimuli: anticipation, sight, smell, chewing
Components: direct=>vagal stimulation & activation of SM plexus; indirect=>release gastrin from G cells - 46Describe function, stimuli & components of gastric phase of gastric secretionFunction: homogenise & acidify chyme, initiate digestion of proteins by pepsin
Stimuli: distension, elevated pH & peptides & aa in stomach
Components: distension initiates vago-vagal & enteric reflexes causing direct & indirect effects on parietal cells, peptides cause secretion of gastrin, NB: low luminal pH inhibits secretion (via D cell release of somatostatin) - 47Describe function, stimuli & components of intestinal phase of gastric secretionFunction: controls rate chyme entry into duodenum
Stimuli: duodenal stretch, presence lipids & CHO & decreased pH
Components: initial, short lived stimulation of gastric secretion by gastrin release in response to peptides in chyme
Release CCK & secretin have inhibitory effect on acid secretion&gastric emptying
Vago-vagal & ENS reflexes (from duodenal stretch) inhibit HCl secretion - 48With all the acid present during digestion, why doesn’t the stomach digest itself?Gastric mucosal barrier: surface cells secrete alkaline mucus (HCO3-) that neutralizes backdiffusion of pepsin & H+ (HCO3-+H+=>H2O+CO2) (pH~7 cell surface but 2 gastric juice); functional (HCO3-)+ structural(mucous,cell junctions) protection of gastric mucosa against acid & pepsin
- 49What factors increase & reduce effectiveness of gastric mucosal barrier? What r consequences?Effectiveness
-increased by: local factors that promote prostaglandin release
-reduced by: aspirin, Helicobacter pylori, alcohol, bile salts (barrier breakers)
=>leads 2 gastric ulcer formation - 50What is the origin of HCO3- 4 secretion by surface mucous cells?H+ secretion by parietal cells accompanied by delivery HCO3- into perfusing blood (alkaline tide). This HCO3- carried to surface epithelium where is secreted into surface mucosal layer
- 51What is importance of inhibition of gastric acid secretion? How is secretion inhibited? Which 1 is probably crucial feedback mechanism 4 controlling gastric pH?Ensures pH gastric/duodenal contents maintained optimal level processing chyme
Nervous (local & vago-vagal), endocrine (secretin) & local gastric (H+, somatostatin) mechanisms. Inhibition H+ secretion by low gastric pH crucial feedback mechanism - 52What is structure of pancreas?Endocrine portion of pancreas (Islets of Langerhans): insulin, glucagon=>blood
Exocrine portion pancreas:acinar+duct cells - 53What r acinar&duct cells secretions rich in?Acinar cells secretions: enzymes & Cl- rich
Duct cell secretions: aqueous NaHCO3- rich - 54What is function of pancreatic exocrine secretions?Digestion: lipase, amylase, proteolytic enzymes important 4 nutrient digestion
pH buffering: high levels HCO3- neutralise HCl emptying from stomach - 55What is V/day, tonicity & pH of pancreatic exocrine secretions?1-1.5L/day, isotonic, alkaline (pH~8.0)
- 56What is enzymatic component of pancreatic secretion? And function?Trypsin, chymotrypsin, elastase=>break peptide bonds forming peptide fragments
Carboxypeptidase=>splits off terminal aa from carboxyl end of protein
Lipase=>splits 2 FA from triacylglycerols forming free FA & monoglycerides
Amylase=>splits polysaccarides in2 glucose & maltose
Ribonuclease, deoxyribonuclease=>splits nucleic acids in2 free mononucleotides - 57Which enzymes r stored & released in zymogen granules?Trypsin, chymotrypsin, elastase, carboxypeptidase, lipase
- 58Why don't proteolytic enzymes digest acinar cells once released?Proteolytic enzymes require activation! Enzymes released from acinar cells by exocytosis, enzymes in zymogen granules activated in upper SI, enteropeptidase/ enterokinase (in duodenal epithelium) converts trypsinogen=>trypsin=>activates many other pancreatic enzymes+trypsin
- 59How does ion c (HCO3-, Cl-, K+, Na+) changes w/ secretion rate? Why?High Q rate=>↑[HCO3-],↓[Cl-],=[Na+],=[K+]
When food enters duodenum, ↑levels of secretin not only ↑rate fluid flow out of pancreas but accelerate CBE 2 neutralise acid stomach allowing digestive enzymes function optimal pH=>watery fluid (low enzyme content) rich HCO3- (4-5x plasma) - 60What r cellular mechanisms involved in pancreatic secretion (duct cells)?1. CFTR: Cl- out lumen
2. CO2 blood in+H20=>H2CO3=>HCO3-+H+
3. NBC-1: Na+ blood in, 2HCO3- blood in
4. CBE: Cl- (1) in, HCO3- (2,3) out lumen
5. NHE-1: Na+ in, H+ (2) out (+HCO3=>CO2)
6. Paracellular transport Na+ & H2O - 61What r causes & consequences of CF?Pancreatic acini secrete many enzymes. Cl- secreted ductal lumen via CFTR=> driving F fluid mov=>maintain solubility ductal enzymes. CF:impaired Cl-transport =>low V +acidic fluid (low activity CBE)=> enzyme precipitation=>obstruction ducts =>progressive pancreatic damage+ reduced efficiency nutrient digestion
- 62How is pancreatic secretion controlled?Nerves: PASY
H: CCK (SI), secretin (SI), gastrin (stomach) - 63What r 3 phases pancreatic secretion?Cephalic phase (~20% total secretion)
Gastric phase (~10% total secretion)
Intestinal phase (~70% total secretion) - 64How is cephalic phase pancreatic secretion controlled?Cephalic phase: sight, smell, taste, chewing =>vagal stimulation=>secretion ACh=> acinar&duct cell secretion(enzymes, HCO3) +gastric (local) nerves=>gastrin release (G-cells)=>acinar cell secretion (enzymes)
- 65How is gastric phase pancreatic secretion controlled?gastric distension=>vago-vagal reflex=> secretion ACh=>acinar & duct cell secretion (enzymes, HCO3)+gastric (local) nerves=> gastrin release (G-cells)=>acinar cell secretion (enzymes)
peptides antral lumen=>gastrin release (G-cells)=>acinar cell secretion (enzymes) - 66How is intestinal phase pancreatic secretion controlled?H mostly responsible: ↑[H+] (pH<3.5)=> secretin release=>secretion watery fluid (low enzyme content) rich in HCO3- (4-5x higher than plasma); fat&protein digestion products=>CCK release=>secretion pancreatic juice rich in digestive enzymes
- 67How does secretin control duodenal pH?↑[H+] (pH<3.5)=>↑secretin=>↑watery (low enzymes) pancreatic juice rich in HCO3- (neutralises acidic chyme)+↓gastric emptying+↓gastric acid secretion
- 68What r functions of liver?CHO metabolism, protein metabolism, lipid metabolism, iron storage, detoxification, synthesis & secretion bile
- 69What r main ducts in liver?Left+right hepatic ducts=>common hepatic duct+cystic duct (from gallbladder)=> common bile duct+pancreatic duct (from pancreas)=>ampulla of Vater (empties into duodenum)
- 70Describe structure of liver lobulePortal triad: bile duct (collects bile from bile canaliculi made by liver cells), hepatic artery & portal vein (empty blood 2 liver that is collected by central vein)
- 71What r characteristics of bile (V/day, tonicity, pH, colour, components)?0.6-1L/day, isotonic, pH 7.6-8.6; yellow-green in colour, components: cholesterol, bile salts & bile acids, H2O & electrolytes, bile pigments (bilirubin)
- 72How is bile produced?BA: derivatives cholesterol, synthesised by hepatocytes or extracted blood by active process, conjugated w/Gly, Tau in hepatocytes 2 form bile salts actively secreted 2 bile canaliculi, Cl-, HCO3-, Na+, H2O then added to hepatic bile as moves along bile duct, production: 0.3-0.5g/day
- 73Describe enterohepatic circulation of bilePrimary BA (derivatives cholesterol or actively extracted blood)=>conjugated Gly, tau=>bile salts=>bile stored gallbladder or secreted by bile duct into duodenum=>bile salts unconjugated from Gly, Tau by intestinal bacteria=> primary BA+2ndary BA (converted by microbiome)=>reabsorption in terminal ileum=>enterohepatic circulation 2 liver
- 74How much bile is produced, secreted & excreted per day?Production: 0.3-0.5g/day
Secretion: 15-30g/day
Excretion: 0.3-0.5g/day - 75What r cellular mechanisms involved in bile secretion?BA-dependent secretion: active Na+ dependent retrieval BA from portal blood & BA secretion into canalicular fluid
BA-independent secretion: active secretion Na+, C- & HCO3- in2 ducts w/H2O following passively - 76How is hepatic bile modified in bile duct?BLM: NKCC1=>Na+, K+,2Cl- contransport in, NBC=>Na+,HCO3- contransport in, NHE1=> Na+ in exchange H+ out, K+ out channel
Lumen: CBE=>Cl- in exchange HCO3- out, Cl- out (CFTR+cAMP - promoted by secretin; Ca2+ gated channel), H2O out (AQP)
Paracellular transport H2O+Na+ - 77What is the role of gallbladder?Stores up 2 50% hepatic bile during interdigestive phase; concentrates hepatic bile by absorbing Cl-, HCO3-, Na+ & H2O; BS concentrated up 2 20-fold; presence chyme in duodenum stimulates release CCK=> contraction gallbladder
- 78What r cellular mechanisms of bile modification in gallbladder?Lumen: NBC=>Na+ & HCO3- in; NCC=>Na+ & Cl- in; H2O transcellular transport blood
BLM: NBC=>Na+ & HCO3- out; Cl- out (channels), CBE=>Cl- in, HCO3- out; Na+/K+-ATPase=>Na+ out, K+ in; K+ out (channels) - 79How is bile secretion regulated?1. PASY (vagus/X)=>bile production by liver
2. FA+aa in chyme entering duodenum=> CCK=>blood=>contraction gallbladder
3. Acidic chyme=>duodenum=>secretin=> blood=>↑flow bile rich in HCO3- from liver - 80What is function of bile?1. Digestion: emulsification of fat=>↑ efficiency lipase action
2. Absorption: micelle formation (micellar solution differs emulsion=>fat-soluble compounds in solution, not suspension, much smaller particles=>greater stability) >essential uptake fat-soluble compounds
3. Excretion large hydrophobic products (e.g. bile pigments, mainly bilirubin) - 81Explain emulsification of fatIn stomach ingested fat=>large fat globules Fat globules (nonpolar) enter duodenum=> coated w/BS (amphipatic)=>fat droplets (FD)=> stable emulsion
- 82How do micelles form? What is their composition? What is their importance?Micelles formed 20-40 BS (liver) & lecithin (both amphipatic), absorb fat-soluble vit, cholesterol,FA&1glycerides (hydrophobic core),hydrophilic shell allow micelle cross unstirred H2O layer 2 epithelial surface, lipase (pancreas) breaks 3glycerides FD=> micelles=>1glycerides+FA=>enterocytes
- 83How does intestine absorb fat digestion products (1glycerides, FA)?1glycerides+FA cross PM enterocyte=>SER =>triglycerides+other lipids & proteins=> Golgi apparatus=>chylomicron=>crosses BLM=>absorbed by lacteal 2 lymph (too big to enter capillaries)=>general circulation
- 84Where does bile reabsorption occur? How?In terminal ileum by ASBT (apical Na+ BA- transporter)=>cotransport Na+ & BA- in2 enterocyte=>OSTα-OSTβ (heterodimeric organic solute transporter)=>transport BA- cross BLM=>portal vein=>liver
- 85What is the excretory role of bile?Senescent RBC(spleen)=>breakdown Haem =>biliverdin=>bilirubin=>plasma=>bilirubin conjugated glucuronic acid liver=>excreted bile=>hydrolysis by bacterial flora colon=> urobilinogen+stercobilin&urobilin=>excre-ted faeces/urobilinogen absorbed blood=> excreted urine/portal vein=>liver
- 86What is name of disease that happens when gallstone blocks bile secretion & that makes people yellow/greenish skin?Obstructive jaundice
- 87What is difference between BA & BS?Primary BA neutral pK=>undissociated at pH in biliary tract & upper SI (& plasma). Most BA not exist free acids but conjugated w/Gly or Tau. Conjugated forms lower pK=> present lumen +soluble dissociated BS-
- 88What is enterohepatic circulation?BS- recycled between liver&GI tract(90-95% BS- secreted in bile, mainly cholate & chenodeoxycholate, but also 2ndary BS- formed by gut bacteria). Active Na+-dependent process lower ileum. Gut bacteria can deconjugate BS-& free BA absorbed slowly by diffusion at SI/LI
- 89Why doesn't increasing BA c in gallbladder make bile lithogenic?No alter ratio BA:cholesterol:phospholipids (determines potential gallstone formation)
(just absorption H2O+electrolytes) - 90Why is higher c BA in gallbladder bile compared 2 liver bile so important?Allows "critical micellar c" 2 b exceeded=> micelle formation allows fat soluble molecules 2 cross "unstirred H2O layer" 2 epithelial surface 4 absorption
- 91How is bile secretion from bile duct (after bile fromation) 2 duodenum controlled?Contraction gallbladder SM + relaxation sphincter Oddi allows entry bile in2 duodenum. Process controlled by vagal & H (CCK) mechanisms (cephalic & intestinal phases). Sphincter Oddi relaxation also occurs in response increased contractile waves along bile duct.
- 92What r dimensions of villi? How much do they increase surface A?Villi~0.5-1.5mm high & increase surface A by 10 fold
- 93What r dimensions microvilli? How much do they increase surface A? What is estimated surface A 4 absorption?Microvilli (enterocytes)~1um long & ~0.1um diameter & increase surface A 20 fold. Estimated surface A 4 absorption ~200m^2
- 94Which solutes r transported in which parts of intestine (SI & LI)?Duodenum: Abs Fe2+ (10%) & Ca2+ (30%)
Jejunum & upper ileum: Abs nutrient digestion products (CHO>98%, most vit, Ca2+, PO4-3~70%, Na+ & K+, Cl- & HCO3-
Lower ileum: Abs vit B12, BA
Colon: Abs Na+ & Cl-, Sec K+ & HCO3-
H2O absorbed in all intestinal regions - 95Define: 1. Abs 2. Sec 3. transcellular transport 4. paracellular transport1. transcellular transport lumen 2 capillary
2. transcellular transport capillary 2 lumen
3. transport across cell (apical & BLM)
4. transport across tight junctions - 96What r pathways 4 intestinal fluid absorption?Transcellular: AQP or SGLT1 (Na+ glucose transporter: cotransport Na+ & solute, namely glucose, also playing role H2O Abs)
Paracellular (across tight junctions) - 97How r electrolytes transported across upper small intestine epithelium?AM: NHE3 (Na+ in exchange H+ out), Na+ dependent cotransport sugars, Pi, aa
CO2 diffuses in2 cell (HCO3-+H+)=>CO2+ H2O=>H++HCO3-=>CBE (Cl- in, HCO3- out)
BLM: CBE (HCO3- out, Cl- in),Na+/K+ ATPase (3Na+ out, 2K+ in), K+ channel (K+ out)
Paracellular: Cl-, H2O, K+ in2 interstitium - 98What r intestinal processes involved in digestion dietary CHO?Luminal digestion: polysaccharides (starch, glycogen)=amylase=>disaccharides
Brush border digestion: disaccharides (maltose, sucrose, lactose)=maltase, sucrase, lactase=>monosaccharides (glucose, gluc+fructose, gluc+galactose) - 99What r cellular mechanisms of intestinal sugar absorption?AM: GLUT2 (carrier glucose, galactose), GLUT5 (carrier fructose), SGLT1 (symporter Na+ & glucose, galactose)
BLM: GLUT2 (fructose, glucose, galactose), Na+/K+ ATPase - 100What is current model intestinal sugar transport?(between meals, digestive phase)Abs mainly jejunum. Between meals: SLGT1 dominant transporter at BBM (high affinity allow Abs low levels glucose lumen)
Digestive phase (luminal c>100mM): GLUT2 dominant transporter at BBM (high capacity route 4 glucose Abs) - 101How is intestinal GLUT2 affected in diabetes & obesity?GLUT2 up-regulated at BBM in rodent models diabetes & obese human patients
- 102Is GLUT2 at BBM in diabetes good or bad?Lean (low GLUT2): fasting=>low/no glucose Sec; sugar rich meal=>medium glucose Abs
Diabetic (high GLUT2): fasting=>medium gluc Sec; sugar rich meal=>high gluc Abs - 103What r processes involved in dietary protein digestion?Protein=HCl,pepsin(stomach)>denaturated & partially hydrolysed protein=trypsin, chy-motrypsin, carboxypeptidase, aminopepti-dase(luminal digestion SI)>small peptides, aa=endopeptidase,aminopeptidase(BB di-gestion intestinal lining)=dipeptidase, tripe-ptidase (INC digestion)=>aa bloodstream
- 104What r cellular mechanisms intestinal peptide & aa transport?AM: NHE3 (Na+in exchange H+ out), PepT1 (H+ & small peptides - hydrolysed by INC peptidases - cotransport in), aa carrier
BLM: Na+/K+ ATPase, K+ channel, aa carrier - 105How much Ca2+ do you take a day? Where is most absorbed? Why is vit D important? Which organs also regulate Ca2+ ECF level?Dietary Ca2+ intake: ~1g/day
~30% absorbed in duodenum
Abs increased by calcitriol(vit D metabolite)
Ca2+ level ECF also regulated kidney & Skel - 106How does body keep Ca2+ homoeostasis?Dietary intake: 1g=>Abs: 0.35g+Sec: 0.15g+ Faeces: 0.8g=>ECF: 1g+Exchangeable pool: 4g=>Skel: 1kg+reAbs: 0.5g+formation: 0.5g =>Kidneys: 99% reAbs (ECF)+urine: 0.2g
#Kidneys excrete same quantity Ca2+ as net amount entering body via GI tract# - 107What r cellular mechanisms of intestinal Ca2+ uptake?Low Ca2+ diet=>active (transcellular): TRPV6 (Ca2+channel AM)>calbindin-D9K (Ca2+BP: mediates Ca2+ transport across enterocytes apical 2 BL side)>PMCA1b (Ca2+ ATP pump BLM); Calcitriol binds VDR up-regulating TRPV6,Calbindin-D9K & PMCA1b expression+activity=>↑uptake
High Ca2+ diet=>passive (paracellular): across channels tight junctions - 108How is Ca2+ homoeostasis regulated?Low-normal dietary Ca2+ intake: calcitriol stimulates intestinal Ca2+ Abs (TRPV6, calbindin-D9K, PMCA1b) & kidney reAbs (TRPV5). If intestinal Ca2+ Abs not sufficient PTH (parathyroid H) preserves serum Ca2+ by acting kidney(TRPV5)+bone (Ca2+ reAbs)
- 109What r functions of colon?1) Electrolyte & H20 Abs (0.4-1L fluid reAbs/day, Na+ Abs stimulated by ALDO & SCFA produced by colonic microflora, HCO3- Sec/Cl- Abs coupled 2 Na+ Abs/K+ Sec=>net effect: increased NaCl uptake
2) Storage & expulsion faeces (chyme stored 12-24hr, mass mov contents in2 rectum initiates defecation)
3) Nutrition: role luminal bacteria (bacteria make up 50% faecal dry weight, synthesise small amounts vit (e.g. vit K), degrade toxic products, synthesise SCFA from undigested food matter) - 110What r cellular mechanisms electrolyte & H20 transport across colonic epithelium?AM: CBE (Cl- Abs/HCO3- Sec), SLC5A8 (Na+, SCFA cotransport in), BK channel (K+ out), ENaC (Na+ in, stimulated by ALDO)
BLM: Na+/K+ ATPase (3Na+ out, 2K+ in), NBC1 (Na+, HCO3- cotransport in), K+ channel (K+ out), CLC-2 (Cl- out)
Paracellular: H2O Abs, K+ Sec - 111Why is gut microbiome central to colonic function?Microbial fermentation undigested dietary polysaccharides=>SCFA colonic lumen=> colonocyte E source+Na+ Abs+fluid Abs+ mucus release+colonocyte proliferation & differentiation (butyrate)+retards growth pathogens (acetate)+anti-inflammatory+↑ motility+↑mucosal BF (acetate)
- 112What is difference prebiotic vs probiotic?Prebiotic: ingested digestion-resistant oligosaccharide that maintains healthy gut bacterial population
Probiotic: live microbial food supplement beneficially affects host=>improves gut microbial balance(↑ratio good:bad bacteria) - 113How does extent of Abs varies between nutrients?Wide variation: digestible CHO & proteins >98%, Fe2+ & Ca2+ transport regulated according body needs so much lower Abs
- 114Describe dietary protein digestion & AbsProteins hydrolysed 2 aa &small peptides (<3aa). Starts pepsin gastric juice, luminal phase completed SI (pancreatic enzymes) BB peptidases hydrolyse larger peptides 2 aa+small peptides. aa Abs across BBM via Na+ dependent transport. Transport di & tripeptides H+ dependent. Peptides hydrolysed in cell 2 aa that move blood by facilitated diffusion
- 115Describe dietary CHO digestion & AbsDigestible polysaccharides (starch, glyco-gen) luminal digestion salivary & pancre-atic amylase. Products (maltose, isomal-tose) & sucrose & lactose hydrolysed spe-cific BB enzymes (membrane digestion). Glucose (from lactose, sucrose, polysa-ccharides) Abs jejunum via BB transpor-ters SGLT1 (Na+-dependent) & GLUT2 (fa-cilitated diffusion). Galactose uptake also SLGT1. GLUT2 BLM transports glucose & galactose blood. Fructose (sucrose) trans-ported GLUT5 & GLUT2 at BBM & BLM.
- 116How is H20 uptake in GI tract?Most H20 entering GI tract Sec (salivary, gastric & pancreatic). Approx 9L/day H20 Abs via both paracellular (tight junctions) & transcellular (mainly AQP) routes. Some nutrient transporters e.g. SGLT1 also function as H20 transporters
- 117How is electrolytes uptake in SI?Upper SI (electrolytes+H20): Na+/H+ ex-change BB=>HCO3- uptake, K+ & Cl- follow gradient (paracellular), H20 down osmotic gradient generated solute transport (trans-cellular & paracellular). Lower SI: coupled transport Na+/H+ & Cl-/HCO3- at BB=> uptake NaCl w/ H20 following osmotically
- 118What is the importance of colonic bacteria?Close symbiotic relationship colonic microbes/colonic epithelial function. Colonic bacteria bulk of luminal contents. Indigestible CHO(<20% CHO)&lipids enter colon & fermented=>SCFA&various gases (NH3, CH4, H2). SCFA major anion colonic contents & key colonocyte metabolism. Colonic bacteria degrade BA, cholesterol, drugs, food additives.
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- Beschreibung
- Physiology Karteikarten am GI tract, erstellt von Francisco Sacadura am 09/04/2017.
- Erstellt von
- Francisco Sacadura
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