Physiology Exam Iii - Gi - Secretions

Front 1

What happens when parietal cells become stimulated?

Back 1

Lots of mitochondria are present due to the high metabolic demand for acid production. Stimulation of cell (via vagus, gastrin, Hist) causes the tubular vesicular membrane to form cnals called canaliculi for acid production and this increases the surface area for acid secretion.

Front 2

Parietal cells secrete acid against a million fold concentration gradient... how?

Back 2

-Tight Junctions: prevent H+ ions from leaking back into the cell.
-Active Transport: using H+/K+ ATPase within the parietal cell membrane.

Front 3

Where is the site of parietal cell regulation?

Back 3

The H+/K+ ATPase
The stimulation of the cell to secrete acid will put more pumps onto the lumen
The inhibition of acid secretion can be accomplished by a proton pump inhibitor.

Front 4

How does HCL form?

Back 4

CO2 + H20 <>H2CO3<> HCO3 + H+

HCO3 leaves the cell via a basolateral HCO3/CL antiporter. When there is alot of acid production there is a lot of HCO3 going into the blood. It can be called an alkaline tide, where the blood leaving the stomach is alkaline, which can then go and buffer the blood.
The H+ ion will be pumped into the lumen via H+/K+ pump.
(Remember the high levels of K in the gut)
K+ enters the cell via Na/K ATPase and then enters the lumen via K/CL cotransporter.
The Cl enters the cell via the HCO3/CL antiport and via Na/CL symport. Many charges ions are present in the lumen, so the CL will follow it's electrochemical gradient into the lumen. It is important to bring CL into the lumen so you can make HCL and KCL.
Cl is the most prevalent molecule in Gastric Acid. Then comes H, then K, then Na.
In the saliva, Na is the highest concentration... then HCO3, CL, then K.

Front 5

What are the major stimulators of gastric acid secretions?

Back 5

Stimulate Parietal Cells:
-PNS (ACh):vagal stimulation ^ HCL secretion.
-Gastrin: stretch/chyme in the antrum and duodenum cause gastrin secretion into the blood that will stimulate parietal cells.
-Histamine: local factors present in gastric pits that stimulate parietal cells in a paracrine fashion.

Front 6

What are the major inhibitors of gastric acid secretions?

Back 6

Inhibitor of Parietal Cells
-Secretin: inhibits HCL secretion by acting on G-cells to decrease gastrin.
-Somatostatin (SS) - acts on parietal cells in a paracrine fashion. Local SS works in the same manner as circulating SS from the pancreas. The local effects include sensing and modulating the environment.
Gastric Inhibitory Peptide (GIP) or Glucose Insulin Peptide (GIP): in addition to working on parietal cells GIP stimulates insulin release.
CCK: (cholecystokinin): decreases HCL secretion at a parietal cell level.

Front 7

What happens at low secretory rates?
What happens when the secretory rate increases?

Back 7

At low secretory rates (unstimulated cells) some acid is produced, but mostly buffer is made in the form of NaCl.
As the cell is stimulated Na secretion decreases, H+ secretion increases, K increases, Cl stays high.

Front 8

How do people get stomach ulcers?

Back 8

Helicobacter is resistant to HCL. It produces a urease that is converted into ammonium. Ammonium destoys the bicarbonate mucosal barrier that protects the gastric epithelium. H. pylori then burrows into the gastric mucosa and allows the inflitration of acid, which creates ulcerations.
Aspirin and NSAIDs are lipophilic and can cause disruption of the bicarbonate mucosal layer, allowing acid to reach the tissue. In addition, Prostaglandins provide protection to the mucosal layer and they can be suppressed by aspirin. (Stress and caffiene can also cause ulcers)
The treatment of ulcers is long-term antibiotics and omeprazole (proton pump inhibitor.

Front 9

What is the gastric mucosa made up of?

Back 9

The mucosal lining has pits and secretions come out of the pits into the lumen. Progenitor cells move up and down the pit to replace the surface mucus cells and the cells in the lower part of the pit. There is a large blood supply around so hormones will have an effect on parietal cells.
Surface mucousal cells will secrete mucours to trap bicarb. The bicarb maintains a pH of 2 in the mucous layer even though the stomach has a pH of 2.

Front 10

How is acid secretion in the stomach controlled?

Back 10

Neural Control of Acid Secretion: Three Phases
1. Cephalic - The anticipation or presence of food in the mouth will stimulate the vagus n. The vagal stimulation will stimulate the parietal cells to secrete acid. It will also stimulate Gastrin.
2. Gastric: The presence of food in the stomach stimulates the gastric phase. This phase is mediated by vagal, enteric n.s, local factors, mechanoreceptors and gastrin.
3. Intestinal: Food in the intestine will cause the release of hormones in the duodenum. These hormones will feedback to reduce gastrin release and thus HCL secretions. They also work to decrease gastric emptying.

Front 11

Where do secretions from the small intestine come from?

Back 11

Secretions from the SI come from cells in the Crypts of Lieberkuhn:
-Brunner's glands: secrete mucous and proteases for protection.
-Paneth Cells: secrete bicarbonate and electrolytes to provide buffers.
-Endocrine cells: produce hormones
-Enterokinase: is produced to activate trypsin

Front 12

What are the hormones released into the SI?
(IMPORTANT! KNOW THIS!)

Back 12

1. Gastrin (G-cells): increases HCL secretions! ALSO, it aids in digestion by increasing pepsinogens. It increases intestinal motility responsible for mass movements in the colon. Released by the antral and duodenal G-cells in response to peptides and aa's. Also released in the stomach in response to stress.
2. Secretin: Released in response to acid (acidic chyme in stomach entering duodenum). It stimulates pancreatic, biliary, and intestinal secretions. Stimulates buffer and bicarbonate release. And it decreases HCL secretion by modulating gastrin release.
3. CCK: Released in response to peptides and fats. Stimulates pancreatic enzyme secretion. Increases motility in intestine and mass movements. Gall bladder contraction to get bile out into the intestine in the presence of fat.
4. GIP: Released in response to fatty acids, aa, and glucose. Decreases HCL secretion. Inhibitory: decreases gastric emptying, motility, and mixing.
Peptide YY: Released after chyme is out of higher part of intestine. Shuts down the acid secretion and motility in the stomach.
Fat is present on top of chyme and this stimulates the release of GIP, CCK, and Peptide YY.

Front 13

What is the function of the Pancreas?

Back 13

Endocrine and Exocrine functions.
Endocine Pancreas: Secretions come out into blood. (3 things secreted)
1. Insulin - GIP stimulates insulin in response to small carbs and fatty acids. When glucose is sensed in the duodenum, there is an immediate alarm sent out telling the pancreas to start insulin release. Insulin also increase HCL secretion and stomach mixing by depolarization of the slow waves in the stomach.
2. Glucagon: opposite effect of insulin. Decreases HCL and motility.
3. SS: inhibits both insulin and glucagon release. It also decreases HCL and motility.
EXOCRINE PANCREAS: secretions come out in ducts (two things secreted)
1. Acinar Cells: store and secrete enzymes as zymogens to protect the pancrease. Some of the enzymes are secreted are pancreatic lipases, proteases, and amylases that are responsible for 70-75% of digestion, which happens rapidly. These enzymes are primarily stimulated by CCK and also stimulated by Secretin.
2. Centroacinar cells: secretes buffers (esp HCO3) and electrolytes. (iso-osmotic w/ plasma) These secretions release are stimulated primarily by Secretin, but also by CCK. Vagus also helps stimulate secretion release b/c PNS is pro-digestion.
Enzymes in the Pancreas are stored as zymogens to keep them from destroying the Pancreas. Trypsin Inhibitor ("The Fire Extinguisher") is present In the pancreas, pancreatic duct, and bile duct. This keeps trypsin from auto-activating itself and the proteases around it!
In Chronic Pancreatitis there is an absence of trypsin inhibitor that allows auto-activation of trypsin and this chews the pancreas up.
Pancreatic juice and Bile juice are good buffers b/c they have lots of bicarb and Na+ (why is sodium a buffer?). They are both secreted into the duodenum to buffer stomach acid. They are both iso-osmotic w/ plasma. Also, salivary juice is hypotonic to plasma and is a slight buffer.

Front 14

What goes on in the ileum in terms of secretions?

Back 14

When chyme reaches the ileum, the pancreatic secretions need to stop. Hormones such as SS, glucagon, pancreatic polypeptide, and peptide YY help to turn off the pancreatic secretions.
In the iluem gas is constantly being exchanged so CO2 and water will form H and HCO3 in the presence of carbonic anhydrase. There will be excretions of H and HCO3 with a net excretion of HCO3.

Front 15

What goes on in the colon in terms of secretions?

Back 15

Secretion of K+ due to Aldosterone sensitivity. Cells rich in K are constantly being sloughed off in the lumen.
Colonic Salvage: Na+ coming into the cell will bring in water resulting in drying of the chyme to form feces.