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Physiology Unit 6 > Pancreatic and Biliary Function > Flashcards

Pancreatic and Biliary Function Flashcards

1
Q

proteases

A
  • digest proteins
  • trypsinogen
  • chymotrypsinogen (trypsin activates)
  • procarboxypeptidase A and B
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2
Q

zymogens

A
  • inactive form of protein have no enzymatic activity
  • activated in gut
  • if activated too early-pancreatitis
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3
Q

pancreas

A
  • most important digestive gland
  • 1 liter secreted per day
  • exocrine secretions into ducts and lumen
  • aqueous juice high in HCO3 from centro acinar and duct cells
  • enzyme juice from acinal cells
  • endocrine secretions from islets regulate blood sugar and met
  • glucagon by alpha
  • insulin by beta
  • somatostatin by delta
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4
Q

pancreatic aqueous secretion

A
  • bicarbonate neutralizes acid from stomach and allows pancreatic enzyme to function at their optimal pH
  • pepsin is inactivated at neutral pH, and can’t attack duodenal mucosa
  • neutralization of pH prevents damage to duodenal and intestinal mucosa
  • dilutes enzyme juice
  • from centro acinar and epithelial cells of intercalary ducts
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5
Q

organization of exocrine pancreas

A
  • fundamental secretory unti is acinus and intercalated duct
  • acinar specialized for secretion
  • large condensing vacuoles are gradually reduced in size and form mature zymogen granules that store enzymes in the apical region
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6
Q

synthesis and secretion of enzymes

A
  • originates in pancreatic acinar cells

- RER to golgi to condensing vacuoles to zymogens

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7
Q

secretin

A
  • activates Gs protein and leads to PKA activation and increase cAMP
  • regulated by hormones
  • VIP also can activate this system
  • cAMP activates CFTR for exchanger
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8
Q

Ach and CCK

A
  • activate Gq protein and activate PIP, IP3, and PKC
  • increases intracellular calcium
  • secretin and CCK are synergistic
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9
Q

VIP

A

-important in vipomas- watery diarrhea

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10
Q

secretion of chloride by acinar cells

A
  1. Na-K pump creates inward directed NA gradient across basolateral membrane
  2. Na/K/Cl cotransporter produces the net Cl uptake, driven by Na gradien
  3. rise in intracellular K that results is shunted by basolateral K channels
  4. intracellular accumulation of Cl establishes gradient that drives Cl into acinar lumen through apical membrane Cl channels
  5. movement of Cl makes trans epithelial voltage more lumen negative, drives Na into lumen (with water)
    * CCK and ACh stimulate this
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11
Q

isotonic Na and HCO3 secretion by pancreatic duct cells

A
  1. bicarbonate secretion into the lumen occurs via a Cl-HCO3 exchange mechanism
  2. some of the HCO3 that enters the lumen directly enters the cell across the basolateral membrane via a Na/HCO3 transporter
  3. additional HCO3 is generated by carbonic anhydrase
  4. OH needed by CA comes from splitting water, which is driven by removing excess H by Na-H exchanger and H pump
  5. lumen negative voltage pulls Na into the lumen
    * *HCO3 secretion stimulated by secretin (through cAMP and PKA and phosphorylated CFTR)
    - CFTR puts Cl out and makes gradient for exchanger in first step
    - Ach also stimulates HCO3-Gq-increase Ca, primes na/k ATPase for secretin
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12
Q

features of aqueous solution

A
  • venous blood is acidified during secretion by and electrogenic proton pump and Na/H exchanger and negates alkaline tide
  • in intestinal phase- secretin and CCK stimulate aqueous secretion by pancreatic duct cells
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13
Q

composition of pancreatic juice and flow rate

A

-HCO3 increases the faster the flow rate

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14
Q

CF

A
  • CFTR channel defective
  • pancreatic secretions thick and viscous-clogging ducts and interfering with digestion
  • pulmonary mucous is also thick and viscous, causing dysnpea and premature death
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15
Q

regulation of pancreatic secretion

A
  1. during cephalic and gastric phase, stimulation from vagus fibers causes release of pancreatic juice
  2. in gastric phase, distension of the stomach results in the release of gastrin from the G cells
  3. acidic chyme entering the duodenum causes the enteroendocrine cells of the duodenal wall to release secretin, whereas fatty, protein rich chyme induces release of CCK
  4. CCK and secretin enter blood stream
  5. upon reaching the pancreas, CCK induces enzyme juice, secretin causes HCO3 juice
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16
Q

cephalic phase

A

-vagal stimulation has a greater effect on enzyme secretion from acini than on ductal aqueous secretion

17
Q

gastric phase

A
  • distension of body of stomach induces pancreatic enzyme secretion by vago-vagal replex
  • antral distension release gastrin
18
Q

intestinal phase

A

-secretin and CCK released into blood from intestinal cells in response to products of digestion

19
Q

intestinal phase regulation-secretin

A
  • secretin is a 27 aa peptide hormone released into blood by S cells in duodenal mucosa in repsonse to acid
  • natures antacid
  • inhibits gastric acid secretion and release of gastrin
  • stimulates chief cells to secrete pepsinogen
  • aq secretion by pancreatic duct cells
  • secretion is then high in vol, high in HCO3, low in enzyme content
20
Q

intestinal phase regulation-CCK

A
  • 33 aa peptide from I cells in duodenal mucosa in response to FA and aa
  • elicits enzyme secretion by acinar cells and potentials aq secretoin during intestinal phase
  • causes gallbladder contraction and relaxes sphincter of Oddi to release bile
  • slows gastric emptying
21
Q

composition of bile

A
  • yellow-green
  • alkaline solution
  • bile salts, bile pigments, cholesterol, neutral fats, phospholipids, electrolytes
  • cholesterol derivatives that emulsify fat, facilitate fat and cholesterol absorption, help solubilize cholesterol
  • enterhepatic circulation recycles bile salts
  • chief pigment is bilirubin, a waste product of heme
22
Q

biosynthesis of bile salts

A
  • rate limiting step is addition of hydroxyl group at position 7 by cholesterol 7 alpha-hydroxylase
  • that enzyme is reduced when excess bile acid and increased in excess cholesterol
  • made by liver and activate nuclear hormone receptor to regulate expression
  • choleretic agent stimulates the liver to increase bile
  • liver conjugates primary and secondary bile acids with glycine or taurine to their respective bile salts
  • the bile salt is named for the acid and the conjugating amino acid
  • see picture
23
Q

bile acids

A
  • salts
  • 2 primary (70%) synthesized in the liver and 2 secondary
  • conjugated with glycine or taurine in the liver
  • conjugation reduces pK from 7 to below 4
  • anionic at neutral pH and water soluble
  • amphipathic- helps them emulsify and solubilize ingested fats and steroids
24
Q

path of bile

A
  • secreted into canaliculi
  • canaliculi are guarded by tight junctions
  • produced by hepatocytes into canaliculi and then to ducts
  • then to sphincter, if closed back into gallbladder for storage
25
Q

path of bile 2

A

bile ducts-hepatic ducts-common bile duct-duodenum-cystic duct-gall bladder

  • stored and concentrated in gallbladder
  • CCK contracts gallbladder
  • 50% bile acids, 25% phospholipids, 4% cholesterol, 2% bile pigments, inorganic ions and IgA
26
Q

daily bile salt turnover

A

total pool 3-4g

  • secretion by liver 12-25 grams
  • reabsorbed and secreted twice during a meal and several times daily via the enterohepatic circulation
  • daily loss in feces and replaced by synthesis in liver is 0.5g
  • absorbed as conjugated bile salts
27
Q

biliary secretion

A
  • bile from intestine flows through the liver via the portal vein
  • absorbed by hepatocytes
  • secreted into canaliculus
  • returns to liver bound to albumin
  • taken up by sodium taurocholate cotransporting polypeptide and organic anion transporting polypeptide (NTCP, OATP)
28
Q

bile acid-independent secretion

A

-watery HCO3 rich fluid by cholangiocytes of the ducts and ductules similar to pancreatic aq secretion, stimulated by secretin

29
Q

bile acid dependent secretion

A
  • by hepatic parenchymal cells
  • stimulated to secrete by bile acids returning to liver in portal blood
  • synthesis of bile acids is inhibited by bile acids returning to the liver via portal blood
30
Q

terminal ileum

A
  • reabsorbed as bile salts through Na+ coupled cotransporter (ASBT)
  • bacteria de conjugate some
  • passively absorbed by nonionic diffusion
  • bacteria also take some to secondary acids from primary, some are captured and some are excreted
31
Q

BA concentration in gallbladder

A
  • active transport of Na, Cl, HCO3 out of lateral membrane and continued micellar formation
  • na-h exchange and Cl-HCO3 exchange in apical
  • basolateral Nacl absorption by Na/K pump and Cl channels
  • K channels for recycling
32
Q

release of bile from gallbladder

A
  • responds to cephalic stimuli
  • neural or hormonal
  • sphincter of Oddi relaxes and contracts gallbladder
33
Q

composition of salts

A
  • bile salts concentrated and form micelles
  • salts are less concentrated due to secretion
  • removal of normal salts concentrates the bile salts
34
Q

bile micells

A
  • lecithin and cholesterol
  • solvents for hydrophobic waste products to be removed from body and hydrophobic components of diet to be captured from the intestine
35
Q

formation of gallstones

A
  • cholesterol most common
  • pigment in far east and africa
  • supersaturation of cholesterol in liver
  • nucleation and precipitation- seeding of cholesterol crystals or microstones
  • growth of microstones to macrostones
  • below a certain point cholesterol is soluble but not above it

Physiology Unit 6 (12 decks)

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