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physio J2


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Impaired paristalis in the smooth muscle portion of the esophagus and failure of the LES to open due to selective loss of inhibitory enteric neurons that regulate peristalsis and LES opeing.
Antrum secretions
mucus, pepsinogen, gastricn and somatostatin.
Bile salts
Secreted by hepatocytes independent of neural and hormonal inputs. Stablilize fat droplets in the intestinal fluids, increase the surface area for lipase activity. Reesterified in the terminal illeum.
Embedded in the brus borders of enterocytes breaks oligo- and disacharides down to monosaccharides.
cathartic effect
Fas cause intestinal epithelial cells to secrete more ions and water into the lumen.
CCK(B) receptors
gastrin binds to these receptrs with a higher affinity than CCK, it induces acid secretion.
Cephalic phase of digestion
No food is in the tract, but the thought is there, sight, smell, taste are involved.
Crypt cells secrete CL through cAMP-regulated channels like this one. This happens in response to noxious stimuli after the NKCC transporter on the basolaterl side put ions into the cell.
Chief cells
Cells in gastric glands of oxyntic mucosa that secrete gastric lipase, and pepsin.
CCK is released by I cells in the duodenum and jejunum into the blood. Release is stimulated by peptides and Aas, Fas, and neural inputs. CCK potentiates pancreatic (acinar cells) and liver HCO3, inhibits acid secretion and gastric motility, and stimula
Good PGs (I2 and EIC), Leads to mucus production, increased blood flow to the stomach, and decreased acid secretion.
Valleys near the base of the intestinal villi that secret ions and water, in addition the crytps are the location of intestinal stem cells.
A defect in the luminal transporter of basic amino acids and cysteine.
digestive phase
When food is in the GI tract. This food causes distension and signalling from chemoreceptors that triggers responses in the enteric plexus as well as the CNS.
Forceful expulsion of intestinal and gastric contents through the mouth.
Na channels in the colon regulated by aldosterone which allow for maximal absorption of Na at the expense of losing K+.
Enterogastric reflex
Regulates how much food is released from the stomach. Volume, food components and low pH inhibit gastric emptying through local nerves, sympathetic extrinsic nerves, and hormones (e.g. CCK).
Enzyme in the SI that hydrolyzes trypsinogen to trypsin, which then activates other pro-proteases that have entered the SI. These hydrolyze proteins into large peptides, small peptides and Aas.
Excitation of Smooth muscle
Ca entry through Ca channels or from ER/SR -> activates MLCK -> Phosphorylates myosin light chain -> activates myosin ATPase, actin filaments slide. Response is graded by Ca++ concentration.
Crosses the luminal surface via GLUT-5, and the basolateral surface via GLUT2.
Functions of HCl
Acid environment for pepsin action, bacteriostatic, iron absorption (so iron doesn't form complexes).
G Cells
Release gastrin, they are found mainly in the antrum of the stomach, but are also scattered in the duodenum and jejunum of small intestine and in the pancreas.
Gastric Inhibitory Peptide
GIP is secreted by the duodenum in the presense of Peptides and Aas, FAs (>= 8 carbons), and oral glucose. It inhibits acid secretion, stimulates insulin release and inhibits gastric motility.
Endocrine secreted by the G cells in the antrum of the stomach, release is stimulated by petides and aminno acids, distension of the stomach, and neural inputs. Gastrin stimulates acid secretion by directly acting on the parietal cells, and stimulating h
Gastrin releasing peptide
During the cephalic phase (taste, smell, sight) of digestion chemoreceptor reflexes in the enteric plexus lead to release of AcH on EP neurons, which then release GRP on the basolateral surface of G-cells which then release gastrin.
Gastro-ileal reflex
Governs ileal motility. Increased ileal motility coupled to gastric secretion ad emptying after a meal. Extrinsic nerves mediate this, hormones too maybe.
LES can't maintain its town, reflux results. Caused by impaired esophageal clearence, transient LES relaxation, decreased resting tone of LES, impaired tissue resistance, and delayed gastric emptying.
Fructose, Glucose, and galactose crose the basolateral membrane via this Na-independent transporter.
H+/K+ ATPase Inhibitors
Omeprazole (prilosec), lansoprozole (prevacid), Rabeprazole (aciphex), Esomeprazole (nexium), pantroprazole (protonix), these compounds must be taken forever and regularly since pumps are replaced every 30-48 hours (all pumps cycled within 72 hours.
H2 histamine receptor antagonists
Used to treat GERD, cimetidine(tagamet), ranitidine(zantac), nizatidine(axid), famotidine(pepcid)
Hartnup disease
A defect in the luminal transporter for neutral Aas.
Slow segmental contractions of circular smooth muscle in the colon. 1-3 times a day there are also peristaltic contractions that lead to mass movement independent of external innervation.
Hyperosmotic solutions
In the duodenum, hyperosmotic solutions inhibit acid secretion.
I cells
Release CCK in response to peptides, Fas greater than or equal to 8 carbon chains, and monoglycerides of Fas, as well as neural inputs. Located in the duodenum, jejunum, and first part of ileum.
ICC (Interstitial Cells of Cajal)
Form a network close to smooth muscle that potentiates the contraction of smooth muscle. They have an endogenous rhythmic property.
Inhibition of the LES
Vagal inputs release AcH on interneurons of the enteric plexus, this interneurons release vasoactive intestinal peptide (VIP) which act on the smooth muscle of the LES causing it to relax.
Intestinal phase
refers to digestion in the small intestines.
Intestino-intestinal reflex
Excessive distension in one part of bowel inhibits contractile activity elsewhere.
Lactose intolerance
Lack of lactase leads to the metabolism of lactose by colonic bacteria to volatile Fas, short chain fas, lactic acid, methane, hydrogen gas, and CO2, this leads to distension, bloating and diarhea.
Large intestine
Very tight junctoins to absorb ions and water and to store feces. The Na-Cl gradient is maintained because of the tight junctions. No glucose absorption.
leaky tight junctions
As you move down the GI tract towards the colon, the junctions get tighter and tighter. There is a slight preference for Cations over anions.
Location of Tonic smooth muscle
Lower esophageal sphincter, orad stomach (fundus), pyorus, ileocecal sphincter, internal anal sphincter.
Lower SI
Somewhat leaky which allows for absorption of B12 and bile salts and some lipids.
Luminal Na+ absorption
Na/H exchanger, Na co-transporters with amino acids, glucose, etc. Na/Cl co-transporter, Na channels regulated by aldosterone.
Migrating Motor Complex
Cleans up after digestion. Seen when the stomach is empty, during periods of fasting. It is characterized by strong peristaltic contractions that essentially push everything through from stomach to caudad ileum. It has three phases, contractile quiescenc
Modulation of MMC
Feeding leads to replacement of MMC by basically continuous contractions, hormonal modulation: vagal, motilin stimulation, inhibition by gastrin.
Is secreted by the duodenum in response to neural inputs. It stimulates gastric and small intestine motility.
Mucosal protective agents
Sulfacrate (aluminum salt of sucrose sulfate), colloidal bismuth compounds (pepto), and prostoglandins.
Myenteric plexus (Auerbach's)
Mainly concerned with motility, it lives between the longitudinal and circular smooth muscle layers.
Na-dependent SGLT1
transports 2 Na along with one glucose or galactose.
Sympathetic neurotransmitter that leads to hyperpolarization of phasic smooth muscle, prevents action potentials, but may not suppress the slow waves.
Osmotic diarhea
Pathogens causing mucosal destructoin/loss, unabsorbed osmolytes present in the lumen. These osmolytes came in through food or pathogens, not produced by the body.
Oxyntic (Gastric) mucosa
Secretes mucus, pesinogen, HCL, intrinsic factor, lipase, bicarb, histamine, and somatostatin.
pancreatic amylase
30% of carbohydrate digestion is done by salivary amylase. Not necessary though since there is an excess of pancreatic. Breaks carbohydrates down to oligo and disaccarides.
Parasympathetic GI fibers
Mainly pre-ganglionic. The postganglionic are neurons of the enteric plexuses. Mainly excitatory through Ach. 70-80% are sensory afferents. Vagus carries fibers all the way down to the transverse colon.
Parietal cells
Secrete HCL and intrinsic factor.
H+/oligopeptide cotransporter in luminal membrane that is used by all small peptides.
Embedded in the brush border of the SI, break down peptide > 4aa for absorption.
Peristaltic reflex
Leads to contraction upstream and relaxation downstream, caudad directed movement. Depends on intrinsic nervous system. Aborad movement.
Peristaltic rush
Intesnse irritation (such as during infectious diarrhea) can cause powerful and rapid peristalsis over long distance in small intestine, sweep contents into colon.
Phases of Fat Digestion
Bulk phase: emulsification droplets are broken down, Acidic phase: Micelles are destabilized by the acidic envoronment near the luminal membrane causing the contents to dump and diffuse, Resterificatoin, Fas are reesterified inside the enteroyte.
receptive relaxation
The stomach relaxes when to receive the food that is about to enter it.
Reflex modulation of GI motility
If a segment receives enough material the downstream segment is stimulated and the upstream segment is inhibited. There are local enteric components, extrinsic sympathetic gangliar components, extrinsic CNS components, and hormonal components.
Reverse peristalsis
Wave of contraction starts in small intestine, moves in orad direction can start as deep as ileum, moves content to duodenum and stomach.
S cells
release, secretin, these cells are located in the duodenum.
secondary peristaltic wave
When food fails to clear mechanoreceptors in the smooth muscle layers of the esophagus send info to the EP which then transmits to the inhibitory interneurons that release VIP and begin peristalisis again.
Secreted by S cells in duodenum in the presence of Fas, acid, and neural inputs. Secretin potentiates pancreatic enzymes, inhibits acid secretion and gastric motility and stimulates pancreatic and liver HCO3.
Secretory diarrhea
Toxins cause Na and Cl secretion in excess of what the villi and colon can absorb. Secretory diarrhea can be caused by cholera toxins, E. coli toxins, or a VIP-secreting tumor. This is intended to help the body get rid of bugs.
Soluble fiber
Water soluble fiber that can be metabolized by bacteria in the small intestine. Important in gastric emptying and fermentation.
Paracrine secretion of the antrum of the stomach, inhibits gastrin secretion by g cells, inhibits histamine release by ECL cells, and inhibits acid secretion by parietal cells. Somatostatin is secreted by D cells in response to pH below 3-3.5. AcH inhibi
Submucosal plexus (Meissner's)
The submucosal plexus is mainly concerned with sensing the goings-on of the lumen, coordinatign secretion and absorption, regulating local microcirculation of small blood vessels, and the contraction of the muscularis mucosae. It lives between the circul
surface epithelia of the stomach
Secrete visible mucus and HCO3 rich fluid, replaced every 3 to 7 days.
Sympathetic GI neurons
Mainly post ganglionic, they regulated circulation through the large vessels of the GI tract. Mainly inhibitory, via NE.
Teniae coli
Arrangment of longitudinal smooth muscle in the large intestine.
Transports Fe through the basolateral membrane and throughout the blood stream.
Treatment of achalasia
Destroy LES, patient can't bend at the waste, and should take H/K-ATPase inhibitors.
Unidentified enterogastrone
Secreted in the small intestine this signalling molecule inhibits acid secretion.
Upper SI
Leaky tight junctions which allow for absorption of nutrients, vitamins and minerals. Na-Cl gradient cannot be maintained.
Vagovagal reflex
Chemoreceptors (peptides, Aas, Fas, H+, glucose) and mechanoreceptors send information up vagus to CNS, leads to vagal intra-pancreatic neuron release of Ach onto duct cells (bicarb), and acinar cells (digestive enzymes).
Vitamin D
Upregulates the Ca-ATPase in the basolateral membrane of the intestines. It also upregulates the Ca-binding proteins. It in turn is regulated by PTH.

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