Term
| What is the primary mechanism of secretion for glands in the GI tract? |
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Definition
| first they secrete either digestive enzymes or mucus, then they secrete water and electrolytes to push the substances toward the desired area |
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Term
| What are the types of secretory glands? Give examples of each and the function of each |
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Definition
a. simple cell - mucus cells or goblet cells
b. simple tissue - indentations in the epithelium (crypts of Lieberkühn);
c. tubular gland - acid-secreting oxyntic
d. complex - salivary or pancreas |
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Term
| What factors control the rates of secretion in the GI tract? |
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Definition
a. local stimulation, such as tactile, distension, or irritation
b. nervous input from PSNS or SNS
c. hormones |
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Term
| What effect does PSNS have on the rate of secretion? How about SNS? |
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Definition
1. increases rate of secretion
2. by itself, it increases secretion but decreases blood flow to the area; combined with PSNS, it will decrease secretion due to decreased blood flow |
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Term
What is the average daily quantity and approximate pH of the following secretions: saliva, gastric, pancreatic, bile, small intestinal, Brunner's gland, and large intestinal.
What is the average total volume of daily secretion? |
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Definition
1. 1 L, 6.0-7.0 pH
2. 1.5 L, 1.0-3.5 pH
3. 1 L, 8.0-8.3 pH
4. 1 L, 7.8 pH
5. 1.8 L, 7.8-8.0 pH
6. 0.2 L, 8.0-8.9 pH
7. 0.2 L, 7.5-8.0 pH
8. 6.7 L |
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Term
| What are the functions of mucus in the GI tract? |
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Definition
| it adheres to the GI walls, it coats the walls, it acts as a lubricant, it is cohesive, it resists digestion, it can act as a buffer, and it causes fecal material to stick to other fecal material |
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Term
| What is mucus composed of? |
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Definition
| primarily water, electrolytes, and glycoproteins (with some HCO3- mixed in to increase buffering capabilities) |
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Term
| What are the functions of saliva? |
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Definition
| lubication, solubizing food, initiate starch digestion, oral hygiene (destruction of bacteria via proteolytic activity and thiocyanate activity) |
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Term
| Describe the two types of salivary secretion. What is the maximum rate of secretion? What is the average salivary secretion rate? |
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Definition
1. a. serous - watery, containing α-amylase
b. mucous - contains mucin for mubrication
2. about 4 ml/min
3. 0.5 mL/min |
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Term
| What are the types of salivary glands, how much of the saliva do they secrete, and what kind of saliva do they secrete? |
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Definition
a. parotid - serous saliva
b. submandibular - mucous/serous saliva; this and the parotid secrete about 90%
c. soblingual - mucous/serous saliva (mostly mucous); about 10%
d. buccal - mucous saliva; less than 1% |
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Term
| What is the pH levels of saliva and why is that helpful? |
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Definition
| about 6.0-7.0; it is the optimal pH for the ptyalin (amylase) to function |
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Term
| What are the stages of salivary secretion? How does the tonicity of saliva compare to plasma? |
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Definition
1. acini secretion and salivary duct reabsorption/secretion
2. saliva is hypotonic |
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Term
| How do the following concentrations compare between plasma and salivary fluid: sodium, bicarbonate, chloride, potassium. How do these compare with increased salivary rates? |
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Definition
1. lower
2. higher
3. higher
4. lower
5. they are all closer to plasma levels with increased salivary rates (decreased K+ and HCO3- levels and increased Na+ and Cl- levels) |
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Term
| What are stimuli for salivary secretion? What are inhibitory for salivary secretion? What is the neural pathway for the PSNS? For the SNS? |
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Definition
1. conditioned reflexes, chewing, taste/smell of good food, smooth objects, nausea
2. sleep, fatigue, dehydration, rough objects, fear
3. stimuli send impluses to the nuclei salvatori in the medulla, which will send impulses through CN VII, IX, and CN X to release ACh from the salivary gland and influence secretion, the myoepitheal contractions, and vasodilation
4. stimuli cause impulses from T1-T3 to be sent to the superior cervical ganglia and then to the salivary gland to release norepinephrine at the gland, limiting blood supply but increasing secretion |
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Term
| What is xerostomia? What causes it? What is the treatment for drooling? |
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Definition
1. dry mouth
2. drug side effects, insufficient capillary perfusion, radiation treatment, autoimmune disease
3. anticholinergics, surgicaal removal of the sublingual glands and retroposition of the submandibular ducts |
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Term
| How can cystic fibrosis affect salivary secretion? How does Conn's syndrome affect salivary secretion? |
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Definition
1. Ca+2, Na+, and protein are elevated in the saliva (as well as pancreatic juice, bronchial secretions, and sweat) and have reduced or no Cl- secretion
2. Na+ and Cl- secretions are nearly zero and K+ secretions are high |
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Term
| Why do CF patients have such low Cl- levels in their saliva, sweat, etc? |
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Definition
| the luminal side of the secretory cells have CFTR (cystic fibrosis transmembrane conductance regulators), which allow secretion of Cl- that has built up in a cell from the Cl-/Na+ symporter; CF patients have dysfunctional or no CFTRs |
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Term
| Cellularly, how are H2O, Na+, and Cl- transported from ECF to the salivary secretory ducts? |
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Definition
a. H2O follows the osmotic gradient paracellularly
b. Na+ follow the electrical gradient paracellularly
c. CFTR channels, activated by cAMP, allow Cl- secretion |
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Term
| What are the most common secretory glands in the esophagus? What do they secrete and what is that used for? What other glands are present in the esophagus, where, and what are they used for? |
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Definition
1. simple mucous glands
2. mucous are lubricant
3. compound mucous glands near the pharynx prevent esophageal excoriation from newly entering food while compound mucous glands near the stomach prevent damage from acid reflux |
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Term
| What are the types of secretory cells in the stomach? Where are they located and what do they secrete? Which one is most common? |
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Definition
a. gastric (oxyntic) - located in the body of the stomach; secretes HCl, pepsinogen, intrinsic factor, mucus, and rennin (chymosin); most common gland
b. pyloric - located near the pyloric sphincter; secretes gastrin, mucus, and small amounts of pepsinogen |
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Term
| Describe the placement of cells in a typical oxyntic gland. What does each cell type secrete? |
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Definition
| mucous neck cells exist in layers near the surface of the gland (secretes alkaline mucus), oxyntic (parietal) cells are deep to that (secretes HCl and inrinsic factor), peptic (chief) cells are deep to that (secretes large amounts of pepsinogen), and enterochromaffin-like cells at the bottom of the gland (secretes histmine) |
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Term
| What stimulates the secretion of mucous cells, chief cells, and parietal cells? |
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Definition
1. mechanical stimulation by contents
2. ACh and gastrin
3. ACh, gastrin, and histamine |
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Term
| In the stomach, what is the function of the following: intrinsic factor, pepsinogen, alkaline mucus, HCl? |
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Definition
1. facilitates absorption of vitamin B12
2. when activated, begins protein digestion
3. protects mucosa against mechanical, pepsiin, and acidic injury
4. activates pepsinogen, breaks down tissue, kills microorganisms, and denatures proteins |
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Term
| In the stomach, what is the function of the following: histamine, gastrin, somatostatin? |
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Definition
1. stimulates parietal cells
2. stimulates parietal, chief, and ECL cells
3. inhibits parietal, G, and ECL cells |
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Term
| Describe the placement of cells in a typical pyloric gland. What does each cell type secrete? |
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Definition
| mucous cells exist at the top of the gland (secrete alkaline mucus), chief cells are deep to that (secrete pepsinogen), and G cells that (secrete gastrin) and D cells (secrete somatostatin) are both at the bottom of the pyloric gland |
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Term
| What is the mechanism for pepsin production? |
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Definition
| chief cells produce and secrete pepsinogen, which is enzymatically split and converted into pepsin |
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Term
| What are the stimuli for the cephalic phase of gastric secretion? The gastric phase? |
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Definition
1. seeing, smelling, tasting, chewing, swallowing food
2. protein, distension, caffeine, calcium, or alcohol in the stomach |
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Term
| What is the mechanism for secretion via the cephalic phase? |
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Definition
| 1. stimuli stimulate the vagus nerve, which stimulates intrinsic nerves and G cells; intrinsic nerves release additional ACh, which activated chief and parietal cells, which causes gastric secretion; G cells secrete gastrin, which activates chief and parietal cells and ECL cells, the latter of which releases histamine, which also activates chief and parietal cells |
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Term
| What is the mechanism for secretion via the gastric phase? |
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Definition
| stimuli stimulate the vagus nerve; it and the stimuli stimulate the intrinsic nerves and the G cells; intrinsic nerves release ACh, which activates chief and parietal cells, which cause gastric secretion; G cells secrete gastrin, which activates chief and parietal cells and ECL cells; ECL cells release histamine, which also activates chief and parietal cells |
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Term
| What stimuli inhibit gastric secretion? |
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Definition
| removal of protein and distension as the stomach empties; accumulation of acid in the antrum or duodenum; or fat, acid, hypertonicity, or distension in the small intestine |
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Term
| What is the mechanism of inhibited gastric secretion in the stomach due to decreased protein and/or distension? |
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Definition
| those cause inhibition to the intrinsic and vagus nerves and to the G cells, the latter of which causes less gastrin, meaning less histamine; inhibition of those nerves and less histamine means less secretion |
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Term
| What is the mechanism of inhibited gastric secretion in the stomach and duodenum due to build-up of acid? |
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Definition
| acid stimulate the D cells, causing increased somatostatin, which inhibits parietal, G, and ECL cells, the inhibition of all of which cause decreased gastric secretion |
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Term
| What is the mechanism of inhibited gastric secretion in the stomach due to increased fat/acid/hypertonicity/distension in the duodenum? |
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Definition
| those cause activation to the enterogastric reflex and increased release of enterogastrones (CCK and secretin); the reflex and the enterogastrones inhibit parietal, chief, and smooth muscle cells, which causes decreased secretion and motility in the stomach |
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Term
| Describe a parietal cell in the stomach. |
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Definition
| it has an invagination with canals called canaliculi and many villus-like formations from the membrane into the canaliculi, from which the HCl is secreted |
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Term
| What transporter the main cause of the high acid levels in secreted stomach acid? Which does it need to function? What is the pH of secretions in the canaliculi? |
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Definition
1. H+/K+-ATPase
2. ATP and Mg+2
3. 0.8 |
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Term
| What ions are secreted into the lumen of the canaliculus? Which are reabsorbed from the lumen? Which are transported from the ECF into the cell? Which are reabsorbed into the ECF from the cell? |
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Definition
1. H+, K+, Cl-, Na+
2. K+, Na+
3. CO2, K+, Cl-
4. HCO3-, Na+ |
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Term
| What transporters are present in the basolateral side of oxycentic cells? The luminal side? |
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Definition
1. HCO3-/Cl- antiports, Na+/K+ ATPases
2. Na+ transporters, H+/K+ ATPases, and Cl- channels |
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Term
| What is the mechanism for HCl secretion in the parietal cells? HCO3- formation? |
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Definition
1. H2O splits into OH- and H+; the H+ is transported out via H+/K+ ATPase; H+ and Cl- associate in the lumen
2. CO2 diffuses into the cell; OH- and CO2 combine to make HCO3-, which is transported into the ECF via the HCO3-/Cl- antiport |
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Term
| Define: achlorhydria, pernicious anemia. |
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Definition
1. lack of stomach acid secretion
2. lack of matured RBCs because of a deficiency of vitaming B12 (which stimulates bone marrow) |
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Term
| What are the phases of gastric secretion? |
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Definition
| cephalic, gastric, and intestinal |
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Term
| What is the tonicity of gastric juice between meals? After meals? What is the secretion rate between meals? After meals? How do the ion concentrations vary from between and after meals? |
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Definition
1. isotonic
2. isotonic
3. low
4. high
5. between meals gastric juice has high NaCl concentration and after meals it has high HCl concentration |
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Term
| At what pH is pepsinogen optimally active? At what pH is it inactive? |
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Definition
1. 1.8-3.5
2. it is reversibly inactivated at pH = 5 and irreversibly at pH = 7-8 |
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Term
| Describe how dietary vitamin B12 is taken in. |
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Definition
| in the stomach it is bound to binding proteins, which are later digested by pancreatic proteases; vitamin B12 then binds to intrinsic factor, which helps B12 get absorbed in the ileum |
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Term
| What does chymosin do? Why is it not common in adults? |
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Definition
1. it is a proteolytic enzyme that causes milk to curdle in the stomach
2. its maximal secretion is in the first few days after birth, after which pepsin replaces it as the main gastric protease |
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Term
| What effect do the following have on gastrin secretion: atropine, gastrin-releasing peptide, somatostatin, antrum pH of 2, antrum pH of 4, antrum pH of 6, amino acids |
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Definition
1. no effect
2. stimulates gastrin release
3. inhibits gastrin release
4. inhibits gastrin release
5. no effect
6. no effect
7. stimulates gastrin release |
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Term
| How is gastrin release regulating by the vagus nerve? |
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Definition
| the vagus nerve can release ACh to different postsynaptic nerves, which can either release GRP to the gastrin cell to stimulate gastrin release or release ACh to a somatostatin cell, which will release somatostatin to the gastrin cell, which will inhibit gastrin release |
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Term
| What stimulates the proliferation of ECL cells? In what situations can excess ECL cells show up? |
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Definition
1. excessive gastrin
2. gastrin-secreting tumors or long-term therapy with acid secretion-blocking drugs |
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Term
| What effect does atropine have on gastric secretion? What about cimetidine? |
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Definition
1. ACh stimulates gastrin and histamine secretion; atropine blocks this
2. histamine stimulate gastrin and ACh secretion; cimetidine (as an H2 blocker) blocks this |
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Term
| How much acid secretion occurs during the cephalic phase? Gastric phase? Intestinal phase? How much occurs in a basal state? |
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Definition
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|
Term
| What would block the cephalic phase of gastric secretion? |
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Definition
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Term
| What factors can weaken the mucosal barrier? What can a weakened barrier cause? What can strengthen it? |
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Definition
1. H. pylori, NSAIDs, ethanol, bile salts
2. gastritis or ulcers
3. mucus, HCO3-, secretion, gastrin, prostaglandins, epidermal growth factor |
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Term
| What is the mechanism for the beginning of a gastric ulcer? |
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Definition
| the mucosal barrier is damaged (somehow), and H+ leaks back into the cell in exchange for Na+; decreased pH kills cells; damaged ECL cells leak histamine, which causes vascular damage, which causes local ischemia, which causes more H+ leakage |
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Term
| What are possible treatments for peptic ulcer disease? What is the mechanism by which they help? |
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Definition
a. antacids - neutralize acid
b. anticholinergics - inhibit ACh-stimulated acid secretion
c. H2 blockers - inhibit histamine-dependent acid secretion
d. omeprazole - inhibits H+/K+-ATPase
e. coating agents (sucralfate, CBS) - provides a protective layer
f. prostaglandins - inhibit acid secretion and enhance cytoprotection |
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Term
| Describe the structure of the compound exocrine gland of the pancreas and what the cell types secrete. |
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Definition
| in the deep part of the gland are acinar cells, which secrete digestive enzymes; superficial to that (and superficial to the duct) are duct cells, which secrete NaHCO3- |
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Term
| What are the proteolytic enzymes secreted by the pancreas and how do they work? Carbohydrate enzymes and how do they work? Lipases and how do they work? |
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Definition
1. trypsin, chymotrypsin, carboxypeptidase; the first two cleave proteins into polypeptides and the third cleaves polypeptides into amino acids
2. pancreatic amylase; it cleaves starches and glycogen into disaccharides
3. pancreatic lipase, phospholipase, and cholesterol esterase; the first cleaves fat into FFAs and monoglycerides, the second coverts phospholipids into FFAs, and the third converts cholesterol esters into FFAs |
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Term
| Systemically, how is pancreatic secretion regulated? |
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Definition
| acid from the stomach stimulates the wall of the duodenum to release secretin and fats and amino acids cause the release of CCK; CCK and secretin are absorbed into the blood stream, where they travel to the pancreas; there secretin stimulates the secretion of pancreatic fluid and bicarbonate and CCK stimulates the secretion of enzymes; vagovagal stimulation also causes the release of enzymes into the acini |
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Term
| Cellularly, how is acinar cell secretion regulated? |
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Definition
| Secretin and VIP bind to their receptors and activate AC to produce cAMP, which activates protein kinases and causes the exocytosis of secretory vesicles; ACh, CCK, Bombesin, and substance P bind to their receptors and activate the PIP2/IP3 system, which causes the release of Ca+2, which causes the release of NO, which causes the production of cGMP, which activates the protein kinases mentioned before |
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Term
| Why doesn't the pancreas digest itself? |
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Definition
| proteolytic enzymes are stored and secreted in an inactivate form and a trypsin inhibitor (which prevents trypsinogen cleavage) is present in the cells, acini, and ducts; without this inhibitor, trypsinogen turns into trypsin, chymotrypsinogen turns into chymotrypsin, and procarboxypeptidase turns into carboxypeptidase, and the pancreas becomes acutely inflamed |
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Term
| What causes trypsinogen to be cleaved and become active? |
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Definition
| trypsinogen is secreted into the pancreatic duct with its inhibitor and aqueous secretion washed the inhibitor and the enzymes out of the duct; without the inhibitor diluted, trypsinogen is converted by enterokinase, which is released by mucosal cells in the intestine |
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Term
| What is the mechanism for pancreatic bicarbonate formation/secretion? |
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Definition
| CO2 + H2O combine and are converted into H2CO3 by carbonic anhydrase; H2CO3 makes H+ and HCO3- and H+ is exchanged by H+/Na+ antiport on the basolateral membrane (via a Na+ gradient established by Na+/K+ ATPase); HCO3- moves across the apical membrane with Na+ |
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Term
| What are the phases of pancreatic secretion and what percent of the secretion is due to each phase? |
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Definition
a. cephalic - 20%
b. gastric - 5-10%
c. intestinal - 70-80% |
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Term
| What stimulates the release of secretin? Where is it stimulated for release? |
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Definition
1. pH below 4.5; pH = 3 causes maximal secretion of secretin
2. in the duodenum or jejunum; in the ileum it is less effective, but still effective |
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Term
| What will happen if pancreatic enzymes are not release? What can cause this? |
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Definition
1. 60% of fat is not absorbed and 30-40% of protein/carbs are not absorbed
2. pancreatitis or removal of the pancreatic head |
|
|
Term
| What causes chronic pancreatitis? Acute pancreatitis? |
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Definition
1. usually alcohol (mostly in adults) or CF (most common in children)
2. gallstones, usually |
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Term
| How common is the CF allele? What does CF cause? |
|
Definition
1. 1/29 Caucasians carry 1 copy of the mutated CFTR and 1/2000 Caucasians have both alleles (i.e. have CF)
2. an abnormality in the CFTR, which transports Cl- at the apical membrane of various tissues; it can cause watery ductal secretion in the pancreas to decrease, concentrating secretions and threatening pancreatitis and pancreatic autodigestion |
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Term
| How does liver bile compare to gallbladder bile? How do these changes occur? |
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Definition
1. liver bile is more dilute of almost all active ingredients and contains more water, salt, and HCO3- than gallbladder bile
2. bile becomes concentrated when it is stored in the gallbladder |
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Term
| What are the stages of bile secretion? |
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Definition
| hepatocytes secrete bile acids and cholesterol into the bile canaliculi and it flows to the terminal bile ducts, the hepatic bile ducts, and the common bile duct; NaHCO3- and water are added to the bile by bile epithelia (stimulate by secretin) |
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Term
| How much bile can the gallbladder hold? How does it concentrate the bile? |
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Definition
1. 30-60 mL
2. it has active transport of Na+ across the epithelia and CL- and H2O follow the Na+ |
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Term
| How is bile secretion regulated? |
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Definition
| Secretin in the blood stimulates liver ductal secretion and CCK in the blood stimulates gallbladder contraction and the relaxation of the sphincter of Oddi, which is at the junction of the bile duct and the duodenum; vagal stimulation also causes weak contraction of the gall bladder and bile acids in the blood stimulate hepatic secretion |
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Term
| How do bile acids get into the blood? |
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Definition
| 95% of bile acids are reabsorbed by the terminal ileum and recycled by enterohepatic circulation |
|
|
Term
| What acids are included in bile acids? How much bile salt does the liver make per day? |
|
Definition
1. chenodeoxycholic acid (cholesterol derived), glyco- and tauro-conjugated bile acids (glycine and taurine derived)
2. about 6 g |
|
|
Term
| How do bile salts assist with digestion? |
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Definition
| bile salts emulsify fats, making them easier to be absorbed into lymphatic lacteals |
|
|
Term
| What are Brunner's glands? What are they stimulated by? What are they inhibited by? |
|
Definition
1. compound alkaline secreting mucus glands
2. local irritation (stimulation via the vagus nerve)
3. sympathetics |
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|
Term
| What are crypts of Liberkühn? How is its secretion regulated? |
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Definition
1. invaginations in the SI and LI; in the SI they exist adjacent to villi
2. secretion is stimulated by PSNS stimulation |
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|
Term
| What use is bile secretion besides the assistance with fat digestion and absorption? |
|
Definition
| bile secretion can aid with the excretion of various waste products, including excess cholesterol and bilirubin |
|
|
Term
|
Definition
| excress water or bile acids are reabsorbed from the bile, too much cholesterol is in the bile, or the epithelium becomes inflammed |
|
|
Term
| Describe the cells in the crypts of Lieberkühn. |
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Definition
| goblet cells secrete mucus to lubricate surfaces and neutralize acid and enterocytes secrete large quantities of water and electrolytes; these secretions are rapidly reabsorbed by the villi, providing a vehicle in which nutrients can be reabsorbed |
|
|
Term
| Where do the small intestine digestive enzymes come from? |
|
Definition
| they are contained in the enterocytes of the villi and other mucosa surfaces and digest food as it is being absorbed |
|
|
Term
| Name the disaccharidases present in enterocytes. |
|
Definition
| sucrase, maltase, isomaltase, and lactase |
|
|
Term
| How are enterocytes recycled? How long do enterocytes usually last? |
|
Definition
1. in the crypts of Lieberkühn, enterocytes undergo mitosis and migrate up the crypt walls; once they cross the border between the crypts and the villi, they can no longer differentiate and are part of the villi
2. about 5 days |
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