Pancreatic exocrine secretions and control Flashcards
(16 cards)
explain the pancreas and its functional units
-secretions coming from pancreas join with gallbladder secretion via the common bile duct.
-these two secretions empty into duodenum via the ampullar of water
cross section of pancreas;
-ductal cells line lumen of pancreatic duct—> these secrete bicarbonate, water secretion .
-the ductal cell will make there way close to the islet cells associated with them.
-within pancreas, the islet cells that secrete insulin empty into the lumen of pancreas.
explain the contributions of the acinus and dcts to pancreatic exocrine secretions
-acinar cells secrete digestive enzymes
-acini form sacs —> connect to the ductal tree —> empty into duodenum.
-intercalated ducts –> squamous/cuboidal epothelial cells
-intralobular ducts- cuboidal or low columnar epithelial cells.
-extralobular ducts —> columnar epithelial cells
-interlobular ducts —> columnar epithelial/goblet cells
-pancreatic ducts, which enters the duodenum at the common bile duct
explain pancreatic exocrine functions
-secretes 1.5L of fluid (containg Na, albumin. globulin and digestive enzymes)
-acinar cells secrete digestive enzymes which break down carbohydrates, fats, proteins + nucleic acids.
-enzymes secreted in inactive form to prevent auto digestion.
-activation of enzymes occurs in the duodenum
explain alkaline secretions of pancreas
-HCO3- rich juice from the pancreas and gallbladder to help neutralise gastric acid.
-secretion from pancreas is similar to that in salivary gland but it is a HCO3- rich juice.
explain how composition of the juice is modified as it travels through the duct
-epithelial cells actively exchange Cl-/HCO3-
-H+ is actively eliminated by Na+/H+ exchanger
-H+ is exhanged for K+ driven by Na+/H+ exchanger
-H+ neutralises HCO3-
-CO2 and HCO3- produced in the blood
-CO2 diffuses in and from HCO3- and H20
explain what the concentration of HCO3- is proportional to
concentration of HCO3- in pancreatic juice is directly proportional to concentration of HCO3- produced in the blood
explain the effects of secretin on the composition and volume of pancreatic juice in humans
-there is a reciprocal change in concentrations of Cl- and HCO3- upon secretin infusion
-the reduced amylase and Cl- concentration upon secretin infusion may be a dilution effect due to increase in volume of the secreted pancreatic juice.
stimulated pancreas causes increased HCO3- rich secretions
explain enzyme secretion of the pancreas
major: proteolytic enzymes (trypsin, chymotrypsin, carboxypeptidase), amylase, lipase
-ribonuclease
-deoxyribonuclease
list the different enzymes and substrates the activator trypsin has
1) Elastase (enzyme) —> substrate is elastin
2) Phospholipase A2 (enzyme) —-> phospholipids (lecithin) substrate
3) Carboxypeptidase A and B (enzyme —-> proteins and polypeptides (substrate)
4) Colipase (enzyme) —-> fat droplets, work in concert with pancreatic lipase (substrate)
5) Chymotrypsin (secreted as chymotrypsin; activated by trypsin)—-> proteins and polypeptides (substrate)
explain proteolytic enzymes and give examples
-digestion of proteins ; so pancreas at risk of autodigestion
-enzymes secreted as proenzymes (like amylase)
e.g:
1) enterokinase; in the brush border of the duodenum and secreted as a response to CCK:
-converts trypsinogen to trypsin via auto catalytic chain reaction
-inhibitors of auto digestion
-acute pancreatis- trypsin activates phospholipase A in the pancreatic duct
-Isolecithin —> disruption of pancreatic tissue, membrane damage and necrosis.
-acute pancreatis —> increased pancreatic a-amylase
2) amylase:
-active; CHO digestion, polysaccharides —-> dissacharides
Lipase:
-fat digestion; triglycerides —> fatty acids and glycerol
-pancreatic insufficiency —-> poor digestion of lipids and their malabsorption which causes steatorrhoea
explain the function of chymotrypsin C and the fate of pancreatic enzymes in the duodenum
Chymotrypsin C= known to have a dual role; at high [Ca2+] of duodenum, it allows activation of trypsinogen but at low [Ca2+]of duodenum it is known to facilitate trypsin degradation.
Fate of pancreatic enzymes in the duodenum:
-digestive enzymes survive different lengths of time in the small intestine
-% of secreted enzymes that reach small intestine: amylase (75%), trypsin (20%), lipase (5%)
explain the control of pancreatic secretions
-neuroendocrine signals
-vagal (parasympathetic stimulation); enahcnes rate of secretion of enzymes and aquaeous components of pancreatic juice
-sympathetic stimulation; inhibits secretion
-secretin and CCK; stimulates secretion of pancreatic fluid (bicarbonate and enzyme rich secretions)
explain the phases of pancreatic secretions
1) Cephalic phase: vagal (Ach and VIP) stimulation of gastrin release from antrum—> some enzyme rich pancreatic juice
2) Gastric phase: distention (vago-vagal reflex on fundus or atrum), amino acid and peptide (in antrum)- stimulated gastrin secretion —> release of enzyme rich pancreatic juice
-vagotomy —> 50% decrease in response to acidic chyme
3) intestinal (duodenal) phase: secretin and CCK; enteropancreatic reflexes- acidic chyme in duodenum and jejunum induces secretion of pancreatic juice (HCO3- and enzymes) that gastrin is a weak agonist at stimulation the CCK receptors which are responsible for the secretion of pancreatic enzymes
give a summary of the 3 phases that stimulate pancreatic secretions
1) Cephalic:
-stimulant; sight, smell, taste, mastication
regulatory pathwayy; vagal pathways
percentage of max enzyme secretion; 25%
2) Gastric:
-stimulant; distention, gastrin
regulatory pathway; vagal-cholinergic
percentage of max enzyme secretion; 10-20%
3) intestinal:
stimulant; amino acids, fatty acids, H+
regulatory pathway; cholecytokinin, secretin, enteropancreatic reflexes
percentage of max enzyme secretion; 50-80%
give a summary of control of pancreatic secretions
-secretion from mucosa of duodenal and jejunum:
-induces pancreatic duct cells to secrete HCO3- rich pancreatic juice, but decrease enzyme content
-secretin also stimulates production of bile by the liver
CCK from duodenal and jejunum in response to fatty acids
-CCK stimulates pancreatic acinar cells to synthesise and release enzyme rich pancreatic juice + stimulates the secretion of concentrated bile from gallbladder for fat absorption,
-CCK contracts the gallbladder and relaxes the sphincter of Oddi —> release of bile into duodenum
-CCK potentiates the effects of secretin which is a weak agonist of acinar cells.
give pancreatic and intestine symptoms in patients with cystic fibrosis
pancreas:
-due to dysfunction of exocrine glands, sweat glands secrete excessive Na+ and Cl- which leads to blocked pancreatic ducts
Intestines:
-cannot fully absorb nutrients.
