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GI anatomy and secretions

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David Hartmann

on 14 February 2013

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Transcript of GI anatomy and secretions

N-K strat. squamous epithelium + lamina propria + muscularis mucosa (smooth muscle-longitudinal-outer; circular-inner)
Mucosal glands top 1/3 and bottom 1/3 ESOPHAGUS Mucosa Submucosa Houses blood and lymph vessels, submucosal nerve plexus (Meissner's)
Contains glands for middle 1/3 of esophagus Muscularis externa Longitudinal outer and circular inner layers (LOCI) w/ myenteric nerve plexus (Auerbach's
Skeletal for superior 1/3 of esophagus; mixed middle; smooth muscle for bottom 1/3 of esophagus Serosa Blends with connective tissue of trachea (upper 1/2) or thoracic cavity (lower 1/2) Esophagus Physiology No digestion, mostly motility function
Peristalsis along the length of the esophagus is coordinated by the brainstem according to when swallowing occurred and the distension of esophagus
Primary wave = peristalsis along entire esophagus (swallowing)
Secondary wave = peristalsis only within the smooth muscle portion of esophagus (reflux, clearing bolus)
Rate of swallowing determines rate of peristalsis
peristalsis turned off during guzzling
Tone of UES increased by reflux, distension, liquid
ACh and substance P constrict sphincter
Tone of LES increased by ACh and gastrin
NO and VIP relax sphincter and cardiac stomach ("receptive relaxation") Esophagus Pathophysiology Vomiting Vomiting controlled by "vomiting center" in medulla
5-HT, D2 receptors, area postrema ("chemoreceptor trigger zone)
Retching occurs before vomiting (movement from stomach to closed glottis)
Intrathoracic pressure elevates, respiration suppressed, vomiting occurs
Alkalotic (loss of stomach acid); hypokalemic (low H+/K+ exchanger activity in collecting tubule/duct) Achalasia Failure to relax LES. Food builds up. Sx: Heartburn and dysphagia. GERD LES relaxation leads to acid reflux, irritating esophogeal tissue
Can lead to tissue damage
Increased odds of GERD during pregnancy Gastro-esophogeal junction "Z-line"
Abrupt change from strat. squamous of esophagus to simple columnar of stomach
Muscularis mucosa of stomach wider than that of esophagus
"Physiological sphincter", meaning the muscularis externa is not specialized into a sphincter like we would see at the gastroduodenal junction esophagus stomach Cardiac Region arrowheads-glands w/ mucus-secreting cells
arrow-muscularis mucosa Short pits with coiled glands that have wide lumen
Coiled glands
"Cardiac glands" seen beneath pits
Wide lumen
Release mucous and lysozyme
Mostly built to resist acid (hence all the mucus) Body and Fundus Short pits with very long glands & darkly stained cell clusters in deep regions of mucosa
Contains 75% of stomach's "oxyntic glands" (HCl), details later
Site of receptive relaxation--a vagovagal reflex to distension of stomach (NO, VIP)
BER, promoted by
ACh and gastrin musc mucosa muscularis
(longitudinal, circular, oblique) arrowhead-neck of gland w/ neck mucous cells (regenerative stem cells) Mucous Cells Surface epithelium of stomach
Simple columnar, NOT goblet cells
Mucous forms protective coat
Contains HCO3- PGE2 helps form protective mucous layer
-NSAIDS block PGE2
H. pylori live within mucous layer Body/Fundus Oxyntic Gland Body/Fundus
Gland Surface mucous cell Parietal Chief Parietal and Chief Cells Parietal Cells Release HCl, intrinsic factor (B12 absorption)
Undergo tubulovesicular transformation during secretion
Secretions guide proliferation/differentiation of stomach cells
Contain receptors for histamine (H2), ACh (M3), gastrin (CCK-B) that promote HCl production/secretion
Luminal distension and digestion of peptides promote HCl also
HCl production inhibited by PGE2, somatostatin, enterogastrones Chief Cells Pepsinogen and lipase release
Stimulants for pepsinogen release = those for acid release
Most important is Vagus-ACh, gastrin
Pepsinogens cleaved to active pepsins at pH = 5 Parietal cells activate pepsinogens via HCl K+ H+ to stomach lumen, HCO3- to blood
-"alkaline tide"
-Lots of mitochondria Regulation of Parietal Cell +EtOH, caffeine ACh (M3R) (H2R) ECL cell (CCK-BR) somatostatin
(released at low pH)
some neural control PGE2 (decreases H2-cAMP signaling)
somatostatin (inhibits HCl, hista & gastrin) cephalic phase gastric phase intestinal phase ECL Cells Base of ECL cells always touch basement membrane, but apex of cell often not in the lumen
Release contents from the membrane opposite the lumen, towards the basal side
Various ECL cells in stomach release gastrin, histamine, somatostatin
Gastrin-CCKB and PNS signals promote histamine release
Histamine produced by histidine decarboxylase
Inhibited by somatostatin, PGE2 many histamine-containing vesicles Pyloric Region Pylorus lubricates and protects opening to duodenum
Deep pits, shallow glands
No chief or parietal cells
Glands have mucous-secreting and ECL cells
Specialized ECL: D cells (somatostatin) and G cells (gastrin)
Enteric nerves release gastrin-releasing peptide GRP Digestion and Absorption General Plan for GI cell layers Mucosa-
epithelium: absorption with enterocytes. Secretions by mucous, endocrine, exocrine cells
lamina propria: connective tissue w/ blood, lymph, immune cells, nerve fibers
muscularis mucosa-longitudinal outer and circular inner layers (LOCI)
submucosal n plexus, major blood vessels
glands in middle esophagus and ileum (Peyer's patches)
Muscularis Externa-
thicker muscle layer, same LOCI arrangement as musc mucosa
myenteric n plexus
connective tissue found throughout GI tract except in esophagus and rectum Control of GI blood flow: Sympathetic: Major locus of control for GI blood flow
Constrict GI vessels to reroute blood (as during hemorrhage) with ADH, AngII, (nor)epinephrine Parasympathetic: Acts only via indirect mechanisms to effect vasodilation
can increase glandular secretions, thereby increasing local digestion which leads to vasodilation
synapses onto interneuron of ENS which will release vasodilator Other: After a meal, a functional hyperemic response ensues
metabolic substrates inc. blood flow
ENS releases VIP and NO w/o CNS influence to promote vasodilation
Hypoxia -> adenosine -> vasodilation Neural Control of GI function Sympathetic: Via greater (T5-9), lesser (T10-11), lumbar (L1-2) splanchnic nerves
SNS activity decreases motility and secretions
Afferent fibers explain referred pain dermatomes Parasympathetic: Via vagus n. (CN X) foregut and midgut, and pelvic splanchnic nerves (S2-S4) for hindgut
Increases motility and secretions ("rest and digest")
Afferent fibers allow vagovagal reflexes Enteric NS Communication b/t submucosal and myenteric plexuses
Afferent: Receptors for mechanical, stretch, osmolarity, chemical (sugars, fats, peptides) in GI wall
Efferent: Excitatory (ACh, Sub P) and Inhibitory (VIP, NO) to smooth muscle
ENS can complete short (small GI segment), medium (longer GI segment), and long (involving the CNS) reflexes
Serotonin-promotes (5HT-3) or delay (5HT-1) gastric emptying depending on receptor gut lumen receptor Stuff enters the stomach Receptive relaxation Vagus n. and mechanosensors elicit NO and VIP release to relax the stomach
Distention > gastrocolic and ileocecal reflexes Gastric Emptying Fastest: large volumes of isotonic, noncaloric fluid
Hyper and hypotonicity slows emptying
Adding calories slows emptying of fluid
Slowest: small volume of fatty, high-calorie meal
Glucose digested more rapidly than complex carb/protein
Fats slow emptying Regulation of emptying: 1. acid decreases gastric contractions via ENS and perhaps secretin
2. fat causes CCK and GIP release, inhibiting emptying
3. hypertonicity inhibits emptying (mechanism unknown)
4. gastrin increases antral contractions and closes pyloric sphincter; net effect is inhibition of gastric emptying
5. neural-PNS and instrinsic > NO release > pyloric sphincter opens
CNS can override and slow gastric emptying (fear, depression, etc.) Small Intestine Motility Segmentation Segmentation duration is longer with higher calories
Intensity of contractions influenced by ENS w/ ACh Peristalsis
Oral to anal
Stretch, mechano, chemical activation
Intrinsic GI reflex (ACh=contract, VIP=relax) MMC Fasting
Coordinated by ENS
and motilin (stim'd by ACh)
3 phases of MMC
Phase III-appreciable [motilin]
Sweeping contraction across GI
Starts at pylorus of stomach,
takes 2 hrs to reach terminal ileum
Does not propagate into colon Gastroileal Reflex Increased secretory and motor activity of stomach signals the ileocecal valve to relax, allowing chyme into cecum
Usually after a meal Intrinsic Factor Released in parallel with acid
Binds B12 in proximal sm intestine Exocrine acinus of pancreas Acinar cells: Release digestive enzymes
Stimulated by
ACh & VIP from vagus
CCK, which also potentiates vagal stim.
Gastrin Centroacinar cells: Release fluid similar to plasma w/ elevated HCO3-
Stimulated by
Secretin (when pH in duodenum < 4.5)
CCK potentiates secretin effects All work best at ~neutral pH
Release stim'd by vagus n. (VIP, ACh); CCK; gastrin
Trypsin activates all zymogens shown here
activated by enterokinase in duodenum
inhibited by "trypsin inhibitor"
Carboxypeptidase A& B: ectopeptidases
Lipase works with a colipase HCO3- Secretion from Centroacinar Cell HCO3- release into lumen is driven by high luminal [Cl- ] created by CFTR
Stimulated by secretin, which increases CFTR expression via cAMP
CCK potentiates this effect
HCO3- neutralizes chyme in duodenum, allowing pancreatic enzymes to operate at their optimum pH (~neutral) Secretion in Small Intestine Enterokinase on brush border of duodenum converts trypsinogen to trypsin, which then activates other zymogens Cl- released through CFTR determines small intestine H20 secretion
VIP and PGE2 elevate cAMP, keep CFTR open longer, induce more water secretion
Bacteria can increase cAMP, causing water loss through diarrhea Carbohydrate Digestion 1. Carbohydrates acted upon by salivary and pancreatic amylase
can only cleave certain 1,4 glycosidic bonds
maltose, maltotriose, alpha-limit dextrans with 1,4 and 1,6 glycosidic linkages remain after amylase action
2. Isomaltase, sucrase, glucoamylase, lactase are brush border enzymes that digest everything to sugars that can be absorbed
treatments for diabetes block these enzymes to prevent spikes in blood sugar
3. Internalization of 3 sugars:
Glucose and galactose via Na+ coupled SGLT1
Fructose via Na+ independent GLT-5
4. Export all sugars to blood via GLT-2 Protein Digestion and Absorption Digestion begins in stomach and absorption is nearly completed by end of jejunum
Pepsinogens in stomach activated to pepsins by HCl
Pancreatic proteases require activation by trypsin, neutral pH
Most of digestion occurs via pancreatic enzymes
Brush border aminopeptidases and carboxypeptidases finish the job to make aa's or 2-4 aa oligopeptides
Many different lumenal aa transporters
PEPT-1 absorbs oligopeptides w/ H+ cotransport
Some do require Na+ cotransport, others do not
75% end up as single aa's entering blood, 25% 2-4 aa peptides 75% 25% P= pit; G=gland; M=muscularis mucosa pyloric stomach duodenum Gastroduodenal Junction Physiologic and anatomic sphincter
large muscularis externa (ME)
Simple columnar both stomach and duodenum
Finger-like extensions of mucosa into the lumen = intestinal villi, seen in duodenum (V)
Duodenum has submucosal glands-"Brunner's"
secrete alkaline mucous
house lymphocytes
Duodenum has goblet cells, stomach does not Duodenum Villus: Curved arrow in image
Only in duodenum, jejunum, ileum
Simple columnar epithelium with lamina propria core
muscularis mucosa does not extend into villi
blood and lymph lacteals in villus core
Lymphocytic aggregations (arrowheads)
Apex of villus
enterocytes-absorption, digestion w/ brush border enzymes
goblet cells-mucous secretion
Base of villus = Crypts of Liberkuhn
enterocytes, goblet cells also down here
enteroendocrine cells- stem cells
paneth cells-antimicrobial lysozyme release
Crypts also in large intestine
Tight junctions between epithelial cells of S.intestine Base of Crypt Arrowhead pointing to Paneth cell
purple vesicles containing lysozymes
Note muscularis mucosa is lumenal in relation to the glands, automatically indicating these are submucosal glands and we are therefore in the duodenum Diffuse Immune System Arrows pointing to lymphocytes
can be intraepithelial
Mast cell circled
always in lamina propria
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