Gi Physiology

Front 1

Where are pH chemoreceptors located?

Back 1

esophagus, stomach, duodenum, and rectum

(ESDR)

Front 2

Where are AA chemoreceptors located?

Back 2

in the duodenum and jejunoileum

Front 3

Where are lipid chemoreceptors located?

Back 3

in the duodenum and jejunoileum

Front 4

Where are sugar chemoreceptors located?

Back 4

in the duodenum and jejunoileum

Front 5

Where are glucose osmoreceptors located?

Back 5

in the stomach, duodenum, and jejunoileum

(SDJ)

Front 6

Which hormones occur in the stomach?

Back 6

gastrin, ghrelin, and somatostatin

Front 7

Which hormones occur in the PAncreaS?

Back 7

amylin, PP, and somatostatin (PAS)

Front 8

Which hormones are part of the CCK family?

Back 8

motilin, CCK, gastrin, and grehlin (MCGG)

Front 9

What occurs during the cephalic phase for responses to occur?

Back 9

The stimulus goes to higher brain centers, to the dorsal vagal complex, to increase PS outflow.

Front 10

Which PS nerves innervate the descending colon and everything below it?

Back 10

pelvic nerves (NOT vagal)

Front 11

Which sympathetic nerves innervate the descending colon and everything below it?

Back 11

prevertebral ganglia (NOT superior cervical)

Front 12

What is the pH and tonicity of saliva?

Back 12

pH between 6 and 7.8. Saliva is always hypotonic but increases in tonicity as flow rate increases.

Front 13

During the swallow reflex, which nerves are involved in the sensory part?

The motor part?

Back 13

Sensory--5,9,10
Motor--5,7,9,10,12

Front 14

What are the functions of the body/fundus of the stomach?

What are the functions of the antrum/pylorus?

Back 14

a reservoir, tonic force during emptying

mixing, grinding, sieving, regulation of emptying

Front 15

What do surface and neck cells secrete? And what are their functions?

Back 15

mucus, HCO3, and trefoil peptides. They function in lubrication and protection.

Front 16

What do endocrine cells secrete and what is their function?

Back 16

They secrete gastrin, histamine, and somatostatin. They regulate acid secretion.

Front 17

What stimulates pepsinogen secretion during the cephalic phase? "PAG"

Back 17

Ach and gastrin

Front 18

What occurs during the gastric phase?

Back 18

Both the vago-vagal reflex and endocrine release stimulate this phase. When the vagus senses distension, it causes an increase in H, pepsinogen, Ach, and gastrin. Also, gastrin increases H and pepsinogen levels.

Front 19

What are the 3 mechanisms by which the parietal cell is stimulated?

Back 19

1. neuron stimulates GRP to release gastrin, which then stimulates the ECL cell to release histamine.

2. Direct action of histamine on the parietal cell.

3. neuron stimulates Ach release which acts on the ECL cell and parietal cell.

4. Direct action of gastrin on the parietal cell.
5. Direct action of acetylcholine on the parietal cell.

Front 20

For each of these hormones, describe the pathway by which it works, and the receptor it binds to:

1. Gastrin
2. Histamine
3. Acetylcholine

Back 20

1. on the CCK receptor by the IP3 pathway
2. on the H2 receptor by the cAMP pathway
3. on the muscarinic M3 receptor by the IP3 pathway

Front 21

What stimulates somatostatin?

Back 21

acid in the antrum. The SST will then inhibit gastrin. This occurs when the pH is less than 3.5

Front 22

Which two hormones inhibit parietal cell acid secretion?

Back 22

CCK and secretin

Front 23

What is interesting about gastric juice and plasma?

Back 23

They stay isotonic at all secretory rates.

Front 24

How do the gastric glands get more acidic?

Back 24

carbonic acid dissociates and makes a hydrogen. And by a proton pump (with active transport), the hydrogen enters the gland.

Front 25

How does chloride get into the gastric gland?

Back 25

It first gets to the parietal cell from the blood via an exchange molecule with bicarbonate.Then it diffuses in, following the positive charge of hydrogen.

Front 26

How does potassium leave the parietal cell?

Back 26

It uses the proton pump as an exchanger with H+.

Front 27

What causes receptive relaxation and antral contraction in the stomach?

Back 27

Vagal afferents respond to changes in tension in smooth muscle in the gastric wall. This afferent activity is processed in the dorsal vagal complex in the medulla and results in changes in vagal efferent outflow. These changes in excitatory and inhibitory parasympathetic outflow result in changes in motor functions of the proximal gastrointestinal tract.

Front 28

How is gastric emptying regulated?

Back 28

Nutrients (and H+)(fat also via CCK) in the duodenum exert negative feedback over gastric motor function resulting in a decrease in the rate of gastric emptying. This is brought about by changes in motor function of different regions of the stomach that are coordinated in a way to regulate the emptying of contents from the stomach. This negative feedback is mediated through neural and humoral pathways activated by the nutrients.

Front 29

What occurs when gastric emptying is being INHIBITED?

Back 29

decreased tone in the body of the stomach

decreased amplitude of contractions at the antral region

increases amplitudes of contraction at the sphincter and pyloric regions to increase flow resistence

increased amplitude of contractions in the duodenum

Front 30

How does pH affect gastric emptying?

Back 30

The lower the pH, the slower the emptying. Secretin would appear to be the leading hormonal candidate to modulate this effect since acid in the duodenum is the prime stimulus for its release and secretin has been shown to delay gastric emptying. The mechanisms involved in the secretin inhibition of gastric emptying are: (1) decreased intragastric pressure due to decreased tone in the proximal stomach, and (2) decreased frequency and force of antral peristalsis. Secretin's effect on pyloric function, if any, is unclear. In addition, neural receptors which respond to acid are present in the duodenum. Because of the rapidity of the inhibition of gastric emptying produced by acid in the duodenum, it is likely that the neural feedback is predominant.

Front 31

How does caloric contents affect gastric emptying?

Back 31

Caloric fluids decrease the rate of gastric emptying. The duodenum controls the rate of gastric delivery of calories, as well as hydrogen ions and "osmoles", by a negative-feedback mechanism. The rate of delivery of calories to the duodenum is kept within a very narrow range, regardless of whether the calories are presented as carbohydrate, protein, fat, or as a mixed meal. The duodenum releases hormonal messages in response to intraluminal nutrients: CCK is released by fat, protein digestion products, and glucose and gastric inhibitory peptide (GIP) is released by glucose. PYY and GLP-1 from the distal small intestine and large intestine also inhibit gastric emptying.

Front 32

What is the Intrinsic Myenteric Defecation Reflex?

Back 32

The entry of feces into the rectum causes the distention of the rectal wall. This stretching triggers signals to the descending and sigmoid colon via the myenteric plexus to increase peristalsis.

Front 33

What is the gastrocolic reflex?

Back 33

distention of the stomach while eating or immediately after a meal triggers mass movements in the colon.

Front 34

What is the gastroiliel reflex?

Back 34

distention of the stomach while eating or immediately after eating triggers the relaxation of the ileocecal sphincter and speeds up peristalsis in the ileum (end portion of the small intestine). This causes the contents of the ileum to rapidly empty into the colon.

Front 35

What is the enterogastric reflex?

Back 35

distention and/or acidic chyme in the duodenum slows stomach emptying and reduces peristalsis.

Front 36

What is the duodenocolic reflex?

Back 36

distention of the duodenum a short while after eating triggers mass movements in the colon.

Front 37

What are the S cells responsible for, and where are they located?

Which other two factors potentiate the effect of S cells?

Back 37

They secrete secretin in the duodenal mucosa and sense the pH there. At a pH less than 4.5, they will promote sodium bicarbonate secretion into the pancreatic ducts, bile ducts, and duodenal mucosa.

Ach and CCK.

Front 38

How is H+ transported in the pancreas?

Back 38

H+ resulting from production of HCO3- is transported out of the duct cell by a Na+/H+ exchange pump. This pump is indirectly coupled to the Na+/K+ ATPase, found on the basolateral membrane of the duct cell, which supplies the energy for Na+/H+ exchange.

Front 39

How are most electrolytes transferred in the pancreas?

Back 39

Na+, K+, Cl-, and H2O in pancreatic juice enter the duct lumen mainly by passive diffusion (driven by electrochemical and osmotic forces) between duct cells.

Front 40

How are chloride and HC03 transferred in the pancreatic cell?

Back 40

http://student.biology.arizona.edu/honors97/group7/cftrpage.html

Opening of the chloride channel/pump (the cystic fibrosis gene product) in the apical membrane allows Cl- ions to move from cell to lumen. Cl- then re-enters the cell by exchange for HCO3- across the basolateral membrane. The process is mediated by cAMP which induces a series of phosphorylation steps resulting in activation of the Cl- channel/pump.

Front 41

How do the three digestion phases affect pancreatic enzyme secretion?

Back 41

Cephalic and gastric stimulate an increase in secretion through an increase in PS activity.

The intestinal phase has the greatest effect. It is mediated by CCK.

Front 42

How is CCK released in the pancreas?

Back 42

The presence of nutrients in the small intestine release CCK from CCK entero‑endocrine cells, called I cells.

Monitor peptide is released from acinar cells in the pancreas and acts on CCK cells. In addition, in the duodenal lumen the presence of a CCK releasing peptide (CCK‑RP) has been established that can release CCK. In the absence of protein or digestive products of protein, CCK‑RP and monitor peptide are broken down by enzymatic digestion and thus are not available to release CCK.

Front 43

How is CCK released in the pancreas?

Back 43

CCK may act through a vagal afferent pathway to reflexly stimulate pancreatic secretion via a vago‑vagal reflex. CCK receptors have been found on vagal afferents innervating subdiaphragmatic viscera and CCK increases vagal afferent fiber discharge. The importance of this reflex in the response to a meal in man is unclear but the ability of a hormone to act via a neural pathway is intriguing.

Front 44

What promotes the release of contents from the acinar cells?

Back 44

The vagal efferents synapse with neurons in the enteric nervous system in the pancreas. Efferent neurons from the enteric nervous system release at least three neurotransmitters that cause enzyme secretion from the pancreatic acinar cell. These neurotransmitters are acetylcholine (Ach), gastrin releasing peptide (GRP) and vasoactive intestinal peptide (VIP). Ach and GRP interactions with their specific receptors lead to intracellular phosphoinositide and calcium signals, whereas VIP interaction with its receptor leads to cellular cyclic AMP signals. Through intracellular signal interactions, the secretory response to a combination of VIP and either Ach or GRP leads to a synergistic response.

Front 45

What signals occur in the pancreatic acinus and duct?

Back 45

The neurotransmitters, Ach, GRP, VIP and the hormone, CCK, each interact with the acinar cell receptors to cause a digestive enzyme secretory response. In addition, there are synergistic responses when the acinar cell is exposed to VIP and one of the other three agonists. The synergistic response is due to an interaction between the intracellular messengers generated by the receptor‑agonist interaction. VIP increases cellular cyclic AMP, whereas the other agonists increase phosphoinositide and calcium changes. Thus, the interaction between the cyclic AMP and phosphoinositide/calcium signaling system leads to the synergistic responses.
The duct cells express receptors for secretin and CCK. Both act as humoral agents. Secretin is the primary stimulant of ductal cell secretion acting by increasing cellular cyclic AMP. CCK causes little or no secretion itself, but it augments secretin‑stimulated secretion presumably through its ability to increase phosphoinositide and calcium changes.

Front 46

What is the role of bile?

How is the bile concentrated?

Back 46

It is necessary for the digestion and absorption of lipids.

It is concentrated by 5-15 fold by active sodium reabsorption.

Front 47

Describe how the gallbladder treats bile acids.

Back 47

the gallbladder epithelium promotes significant absorption of water from the bile entering it by solute transport­mediated mechanisms. An interesting point is that the absorption of water in the gallbladder causes concentration of biliary constituents without changing the osmolality of the bile. Osmolality does not change because the major component, bile acids, forms micelles as the water is removed. In a micelle, the bile acids act as a single osmolar unit.

Front 48

What are the solute components of bile?

Back 48

Bile acids are the major component. Cholesterol and bilirubin are excretory products. Both bile acids and phospholipid secretion are important in maintaining cholesterol in a soluble state. Cholesterol precipitates and stones form in the gallbladder when bile acids and/or phospholipid concentrations are insufficient to maintain cholesterol in the soluble state.

Front 49

What are some functions of the biliary tract?

Back 49

Notice that the presence of microvilli are only on the canalicular membrane. The canaliculus secretes oxidized glutathione, and canalicular transport systems are also responsible for exocytosis of vesicles into the canaliculus. Canalicular membrane proteins mediate Cl-/ HCO3- exchange, and have been reported to salvage biliary constituents by transporting them back into the hepatocyte. Secretion of organic anions such as conjugated bilirubin induces only a very small fraction of bile flow. Biliary ductules secrete bicarbonate in response to secretin and absorb secondary solutes.

Front 50

What three mechanisms are used for transportation of substances in and out of the canaliculus?

Back 50

Active transport, Na/K ATPase, and osmotic filtration.

Front 51

How are water and sodium absorbed in the gallbladder?

Back 51

Sodium inside the epithelial cells is transported into the interstitium by an active process involving Na/K-ATPase pumps. This transport causes an increase in the luminal-to-interstitial fluid movement of sodium, which produces an increase in interstitial osmolarity relative to luminal osmolarity. As a result water flows by osmosis across the cells and through tight junctions from the lumen to the interstitium. The resulting increase in interstitial fluid hydrostatic pressure causes bulk flow of water and ions from the interstitium into the capillaries.

Front 52

How does bile enter the duodenum?

Back 52

CCK release on the biliary system is through vagal pathways. The CCK released activates sensory neurons containing CCK receptors. The sensory signals are carried by way of afferent vagal neurons to the dorsal vagal complex. There the signals lead to activation of vagal efferents that, in turn, interact with the enteric nervous system in the gallbladder and the sphincter of Oddi. Its involvement with the gallbladder leads to enteric nerve release of acetylcholine (Ach) which interacts with the smooth muscle to cause contraction. The interaction at the sphincter of Oddi leads to enteric nerve release of vasoactive intestinal peptide (VIP) and nitric oxide (NO) which interact with the smooth muscle cells that are tonically contracted (by Ach) to cause relaxation. Thus, both the contraction and relaxation effects of CCK are mediated by nervous pathways.

Front 53

How are bile salts created?

What does amphipathic mean?

What conformation are bile salts in, in the bile and the gut?

Back 53

They are made from cholesterol.

Bile acids have planar molecules with all polar groups on one surface.

Micellar

Front 54

What is special of primary bile salts?

What is special of secondary bile salts?

What is special of conjugated bile salts?

Back 54

The polar molecules that are located in the colon, and can be reabsorbed (cholate and chenodeoxycholate).

They are formed in the colon by bacterial dehydroxylation (deoxycholate and lithocholate).

Bile salts are usually ionized (to glycine and taurine in the liver), soluble, and exist mainly as sodium salts.

Front 55

How are conjugated BA absorbed into the ileal enterocyte?

Back 55

Uptake of ionized, conjugated bile acids involves a Na+-coupled cotransport. Energy for the transport is provided by the Na+ concentration gradient; low intracellular [Na+] is maintained by Na+ / K+ ATPase.

(The exit of bile acid anions across the basolateral membrane is considered to be mediated by an ion-exchange protein that moves an ion such as bicarbonate or sulfate into the cell, while simultaneously moving the bile acid anion out of the cell. )

Front 56

How is bile salt synthesis inhibited?

Back 56

Bile salts inhibit the rate-limiting step (cholesterol hydroxylase) in bile salt synthesis from cholesterol (negative feedback).