pancreatic & biliary (3) Flashcards Preview

unit 6: physiology > pancreatic & biliary (3) > Flashcards

Flashcards in pancreatic & biliary (3) Deck (45)
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1
Q

what is the function of proteases? list 4

A
digest proteins
o	Trpsinogen
o	Chyomtrysinogen
o	Procarboxypeptidase A
o	Procarboxypeptidase B
2
Q

what is occurring during pancreatitis?

A

the pancreas becomes inflamed because the digestive enzymes are activated before they reach the intestine

3
Q

what are the two pancreatic exocrine secretions?

A
  • aqueous juice high in HCO3 from centro-acinar and duct cells
  • enzyme juice from acinar cells
4
Q

what is the function of the pancreatic endocrine secretions?

A

they come from the islets of langerhanns and regulate blood sugar & metabolism

5
Q

what cells secrete glucagon?

A

alpha cells

6
Q

what do the beta cells secrete?

A

insulin

7
Q

what cell secretes somatostatin?

A

delta cells

8
Q

what is the function of bicarbonate?

A

it neutralizes acid from stomach and allows pancreatic cells to function at their optimal neutral pH

9
Q

where are digestive enzymes stored in the acinar cells?

A

in mature zymogen granules

10
Q

what is the function of VIP

A

it a neurotransmitter in the gut that is not normally important in pancreatic secretion but becomes important in pancreatic tumors known as vipomas which result in watery diarrhea

11
Q

what type of relationship does secretin and CCK have?

A

there are synergists

12
Q

what is the effect of secretin and CCK on zymogens?

A

they cause zymogens to secrete their contents

13
Q

what two neurotransmitters trigger Cl- release?

A

CCK and ACh

14
Q

what is most likely the mechanism by which ACh and CCK stimulate NaCl secretion?

A

through phosphorylation of basloateral and apical ion channels

15
Q

what is the role of secretin in the bicarb secretion from pancreatic duct cells?

A

it uses cAMP (as its 2nd messenger) activates the CFTR Cl- channel which then replenishes luminal Cl- needed for the Cl-/HCO3- exchange

16
Q

what happens to the concentrations of HCO3- and Cl- when the pancreatic flow rates change

A

their concentrations change in a reciprocal manner

ex. if rate of secretion is high, the bicarb in the secretion will be high

17
Q

what happens to the Na and K concentrations when the flow rate of secretions change?

A

they remain constant

18
Q

in relation to the pancreas, what is happen in patients with CF

A

CFTR channel is defective, pancreatic secretions are thick & viscous with the secretions of enzymes and they clog the pancreatic ducts which leads to inference with digestion
-The aqueous secretion isn’t there to dilute the pancreatic enzymes and reduce the viscosity

19
Q

what are the 3 stages of pancreatic secretion?

A
  • cephalic
  • gastic
  • intestinal
20
Q

what two phases does vagal stimulation act on?

A

cephalic & gastric

21
Q

which phase is these events occurring during?
“antral distension releases gastrin which stimulates acinar cells to secrete enzymes (and antral distenion to release oxyntic parietal cells to secrete HCl)”

A

gastric phase

22
Q

what phase is this describing?
“CCK and secretin enter blood stream and induce secretion of enzyme rich pancreatic juice; secretin cause copious secretion of bicarb rich pancreactic juice”

A

intestinal phase

23
Q

what hormone is the following describing?

“27 AA peptide hormone released into blood by S cells”

A

secretin

24
Q

what cells secrete pepsinogen?

A

gastric chief cells stimulated by secretin

25
Q

describe the following characteristics of pancreatic aqueous secretion (in terms of high or low)

  • volume
  • HCO3- concentration
  • enzyme content
A
  • volume: high
  • HCO3- concentration: high
  • enzyme content: low
26
Q

what type of products entering the duodenum will trigger CCK release?

A

fatty acids or AA

27
Q

what type of duodenal mucosal cells secrete CCK?

A

I cells

28
Q

what peptide cause gallbladder contraction?

A

CCK

29
Q

what peptide causes relaxation of the sphincter of Oddi?

A

CCK

30
Q

what peptide slows gastric emptying?

A

CCK

31
Q

what are the functions of bile sats?

A

emulsify fat
facilitate fat & cholesterol absorption
help solubilize choelsterol

32
Q

what is the rate limiting step in bile acid formation?

A

hydroxyl group at the position 7 by cholesterol 7-alpha hydroxylase

33
Q

how is the expression of the 7- alpha hydroxylase enzyme affected by bile acid and cholesterol concentrations

A

it is reduced by bile acids and increased by cholesterol

34
Q

what is the definition of choleretic?

A

an agent that stimulates the liver to increase the output of bile

35
Q

what is the function of bile acid sequestrants?

A

they bind bile acids and prevent reabsorption from the gut and can be used to lower cholesterol

36
Q

what two materials are bile salts conjugated with?

A

glycine -75%

or taurine- 25%

37
Q

what is the effect of conjugating bile salts?

A

conjugation reduces the pK from 7 to 4.. therefore conjugated bile salts are anionic at neutral pH and are very water soluable. They are also very amphipathic

38
Q

what are the two specific transporters in the liver than take up bile?

A

sodium taurocholate cotransporting polypeptide (NTCP) and organic anion transporting polypeptide (OATP)

39
Q

what is bile bound to when it returns to the liver?

A

albumin

40
Q

how are most bile acids reabsorbed?

A

most bile acid are reabsorbed as conjugated bile salts in the terminal ileum through an Na+ coupled cotransporter (ASBT)

41
Q

what is the consequence of bile salt malabsorption caused by terminal ileum

A

chronic diarrhea

42
Q

what are the primary components of micelles?

A

bile salts
lecithin
cholesterol

43
Q

what type of gallstones are most common in the US

A

cholesterol gallstones

44
Q

list and describe the 3 stages of cholesterol gallstone formation

A
  1. Supersaturation of cholesterol-occurs in liver
  2. Nucleation & precepitation-seeding of cholesterol crystals or microstones-prob occurs in gallbladder
  3. Growth of microstones to form macrostones
45
Q

what is cholecystitis?

A

inflammation of the gallbladder caused most commonly by the blockage of the cystic duct by a gallstone
this causes backup of bile in the gallbladded potentially damaging organ