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51 Cards in this Set
- Front
- Back
True or False
Acinar cells synthesize and secrete proteins and isotonic fluid. |
True
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True or False
Duct cells transport fluid and electrolytes. |
True
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? stimulate basolateral membrane receptors.
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Secretagogues
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Make sure to go over TABLE 2-1
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Make sure to go over TABLE 2-1
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The parietal cell has receptors for what 3 things?
--therefore 3 different pathways to stimulate HCl secretion!!! |
CCK-B ==> Gastrin
M3 ==> ACh H2 ==> Histamine |
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? inhibits acid secretion by a PARACRINE mechanism whereby histamine release by the ECL cells is blocked.
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Somatostatin (SST)
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Histamine is secreted by the ? cells.
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Enterochromaffine-Like Cells
(ECL) |
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? in the gastric antrum inhibits G Cell secretion of gastrin and stimulates secretion of ? by the ? cells.
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Excess H+ (pH < 3)
Somatostatin (SST) by D cells |
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Fine tuning of control of the ECL cell is mediated through receptors for ? , ? , and ?
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ACh
Gastrin SST |
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REMEMBER
inhibition of HCl secretion can also be done by secretin CCK GIP Prostaglandin E2 |
REMEMBER
inhibition of HCl secretion can also be done by secretin CCK GIP Prostaglandin E2 |
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What are the 4 phases of Gastric Acid Secretion?
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Basal (interdigestive) Phase
Cephalic Phase Gastric Phase Intestinal Phase |
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Describe what happens in the Basal Phase.
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Rate of acid secretion is LOW but the luminal [H+] is HIGH because of the absence of the buffering effect of food in the stomach.
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Describe the Cephalic Phase
**this phase accounts for 30% of TOTAL ACID SECRETION |
sight, smell, taste, and thought stimulate the DORSAL MOTOR NUCLEUS of the VAGUS NERVE.
ACh stimulates Parietal cells, ECL cells, release of GRP and INHIBIT D cells |
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Describe the Gastric Phase
**this phase accounts for about 60% of the TOTAL ACID |
Distention activates release of ACh locally via Vago-Vagal Reflex
Hydrolyzed proteins and amino acids stimulate G CELLS to secrete GASTRIN low pH stimulates D cells to release SST |
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Describe the Intestinal Phase
**this phase accounts for about 10% of TOTAL ACID |
hydrolyzed protein in the duodenum stimulate duodenal G Cells ---> Gastrin
unknown mechanism -- absorption of amino acids in duodenum stimulates GASTRIC secretion of acid Fat, acid, and hyperosmolar contents ==> inhibit acid secretion via SECRETIN and SST, GIP, CCK, Prostaglandins |
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List the stimulus and mediator for the given site in regards to mechanisms for controlling gastric acid secretion:
Duodenum (2) Duodenum and Jejenum Gastric Antrum |
protein products ==> Gastrin
Acid pH < 4.5 ==> Secretin // Enterogastric Reflex Fatty acids, glucose, amino acids ==> GIP and CCK Acid pH < 3 ==> Somatostatin |
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Pepsinogens are from ? cells and are active at pH ?
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Chief Cells
pH < 5 |
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? from parietal cells is critical to the absorption of Vitamin ?
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Intrinsic Factor
Vitamin B-12 |
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? are potent stimulators of mucus secretion.
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Prostaglandins
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What are the consequences of a damaged gastric mucosal barrier?
figure 3-3 |
What are the consequences of a damaged gastric mucosal barrier?
figure 3-3 |
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A patient has Zollinger-Ellison Syndrome and has symptoms of ulcers, diarrhea, malabsorption, possible vitamin deficiencies, and steatorrhea.
What is the cause ? |
Gastrinoma secretes GASTRIN
==> causes excess HCl gastric glands proliferate |
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A patient has increased NH3 production, increased Gastrin, decreased SST, and increased HCl.
What is a possible reason for this? |
H. Pylori infection
colonizes under the gastric mucus layer risk for gastritis, ulcers, and gastric adenocarcinoma |
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REMEMBER
use of NSAID results in decrease mucus decrease HCO3- decrease prostaglandin E2 increase Gastrin |
REMEMBER
use of NSAID results in decrease mucus decrease HCO3- decrease prostaglandin E2 increase Gastrin |
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Pancreas acinar cells have basolateral membranes that possess receptors for ? and ? that stimulate phosphorylation of structures proteins via cAMP.
via Ca2+ second messenger? |
VIP (cAMP)
Secretin (cAMP) ACh (Ca2+) CCK (Ca2+) |
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MAKE SURE TO COVER FIGURE 4-1 and 4-2 and TABLE 4-1 IN LECTURE
pH osmolarity and electrolyte concentration changes in pancreatic fluid |
MAKE SURE TO COVER FIGURE 4-1 and 4-2 and TABLE 4-1 IN LECTURE
pH osmolarity and electrolyte concentration changes in pancreatic fluid |
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Pancreatic Acinar cells secrete what type of products?
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Proteases
Amylolytic Enzyme Lipases Nucleases |
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Pancreatic Duct cell functions in the fed state are ---?
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secrete isotonic NaHCO3-
via Cl- / HCO3- exchange channel =>linked to apical Cl- channel (CFTR) and Cl- recycling source of HCO3- from Basolateral Na / HCO3 co-transport and CO2 + OH- catalyzed by Carbonic Anhydrase |
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Describe the regulation of pancreatic secretions during fasting
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Cephalic phase I = secretion lowest
Gastric phase II = increase Intestinal phase III = secretion highest |
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Describe the regulation of pancreatic secretion in the Fed Period.
Cephalic Phase? Gastric Phase? Intestinal Phase? |
Cephalic phase - initiated by sight, taste, smell and chewing via VAGAL EFFERENTS --20% total response
Gastric Phase - food in stomach and is via VAGO-VAGAL REFLEX --minor significance Intestinal Phase - CHYME entering duodenum --80% total secretion. |
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Chyme stimulates the release of ? , ? and ? during the Intestinal Phase of the pancreas.
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Secretin
CCK ACh (vagovagal response) |
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in regards to the pancreas...
? is a potent stimulator of water and bicarbonate secretions. The stimulus for ? is long-carbon chain fatty acids and amino acids. |
Secretin
CCK |
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What is the role of CCK in the pancreas--
what cell does it affect? Released by ? Regulated by ? |
binds to CCK-A receptors on Basolateral Membranes of ACINAR Cells
I cells of the duodenal mucosa CCK-RP => response to fatty acids and amino acids Monitor Peptide => acinar cells |
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Describe the role of SECRETIN in pancreas.
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binds to basolateral receptor
=> G protein to Adenyl Cyclase => cAMP targets PKA => PKA phosphorylates CFTR channel in APICAL MEMBRANE of DUCT CELLS |
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Hepatocytes synthesize primary bile acids from ? and conjugate them with ? or ?
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Cholesterol
conjugate with GLYCINE or TAURINE |
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How is Canalicular Bile formed?
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bile acids are actively secreted across the canalicular membrane.
pulls water and solutes and absorbs them passively |
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What is Ductule Bile?
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product of CHOLANGIOCYTES (columnar epithelial cells) that line the ductules.
Hepatic Bile emerges from the ductules prior to entering the Gallbladder |
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? from hepatocyte membranes combine with Bile Acids form mixed ?
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Phosphatidylcholine
Micelles |
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Active absorption of bile acids occurs in the ?
Absorbed bile acids return via portal circulation to the liver bound to ? where hepatocytes extract them. |
ILEUM
Albumin |
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The volume of bile secreted in response to recycling of bile acids is called the ?
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Bile Acid - Dependent Fraction
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Bile acid synthesis is regulated by negative feedback control by ? which is the RATE LIMITING STEP.
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7 α-hydroxylase
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How are bile acids extracted from portal blood?
What is this dependent upon ? |
via co-transport with Na+
(basolateral surface) dependent on Na+ / K+ pump |
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Secretion of bile is accomplished by WATER TRANSPORT coupled to TRANSPORT OF Na+.
What hormones help with this process? |
Bile Acid-Independent
Secretin --stimulates secretion of water and HCO3- CCK --potentiates this activity |
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Make sure to go over Hepatocyte Transporters
Table 5-1 |
Make sure to go over Hepatocyte Transporters
Table 5-1 |
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CONTRACTIONS of gallbladder begin within an hour of eating due to ? and ?
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CCK binding to CCK-A receptors in gallbladder Smooth Muscle.
CCK --> Activation of the Vago-Vagal Reflex releases ACh |
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What causes Gallstones?
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hypersecretion of Cholesterol
or diminished Bile Acid Pool |
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Summary of regulation of Bile Flow
for each stimulus given list the TARGET and EFFECT Bile Acids Secretin CCK Vagus Nerve |
bile acids --> HEPATOCYTES --> increase bile flow, inhibit bile acid SYNTHESIS
Secretin --> Bile Ducts (liver) --> stimulates secretion of water and HCO3- CCK --> Gallbladder --> stimulates CONTRACTION CCK --> Sphincter of Oddi --> stimulates RELAXATION Vagus N. --> Gallbladder --> stimulates Contractions (minor) |
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How does Cl- enter the enterocytes from the basolateral membrane?
How does Cl- leave the cell and enter the lumen? |
Na+ / K+ / 2 Cl- cotransporter
CFTR channel |
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What activates the CFTR channel?
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increase cAMP
increase cytosolic Ca2+ |
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Cl- moving through the CFTR channel will cause ? and ? to enter the lumen paracellularly.
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Water and Na+
enter into the lumen paracellularly |
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What primarily controls the CFTR and Na+/K+/2Cl- cotransporter
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Submucosal Plexus
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Where does the HCO3- secretion by the duodenum come from?
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Comes from the ALKALINE TIDE and from the actions of CARBONIC ANHYDRASE
Na+ / HCO3- Cotransporter from plasma into cell Cl- / HCO3- Exchanger for lumen |