Physiology of the Pancreas Flashcards

1
Q

What cells in the pancreas secrete enzymes?

A

acinar cells

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2
Q

Do islet hormones have an influence on exocrine secretion?

A

yes –> venous blood from islets perfuse neighboring acini, insulin stimulates enzyme synthesis/secretion and somatostatin/glucagon inhibit enzyme secretion –> local effects only

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3
Q

Functions of exocrine secretions of pancreas

A

digestive enzymes, neutralizing bicarbonate, receptors for hormones and neurotransmitters

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4
Q

What hormone a major stimulus for water and bicarbonate?

A

secretin –> activates adenylate cyclase in duct cells –> opens CFTR that exchanges bicarbonate for intraluminal chloride

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5
Q

Functions of secretin

A

increase bicarbonate secretion, retard gastric emptying/secretion, promotes mesenteric blood flow

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6
Q

Which pancreatic enzymes are stored and secreted in an active form?

A

amylase and lipase

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7
Q

How are most pancreatic enzymes stored and secreted

A

proenzymes

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8
Q

How are proenzymes activated?

A

enterokinase of intestinal brush border activates trypsinogen to trypsin which activates other proenzymes

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9
Q

Why are proteolytic enzymes stored in zymogen granules and secreted as inactive precursors?

A

to prevent autodigestion

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10
Q

What is peptide inhibitor of trypsin?

A

PSTI/SPINK1 can inactivate 10% of trypsin in zymogen granules –> if inactive, linked to pancreatitis

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11
Q

At what pH does amylase function?

A

neutral

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12
Q

Products of amylase digestion

A

maltose, maltotriose, dextrins –> further digested by brush border enzymes

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13
Q

Major source of triglyceride and phospholipid lipases

A

pancreas

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14
Q

4 etiologies of steatorrhea

A

excess gastric acid/ZES, inadequate enzyme/bicarb excretion/pancreatic insufficiency, poor bile flow/cholestasis, intestinal dysmotility/scleroderma, mucosal malabsorption/crohns/infections

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15
Q

3 main proteolytic pancreatic enzymes

A

trypsin, chymotrypsin, elastase

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16
Q

Where are zymogen granules stored in pancreatic cells?

A

apical/apex side

17
Q

2 cellular controls of enzyme secretion in exocrine pancreas

A
  1. vip/secretin increase cyclic amp/pka

2. cck, ach, grp, substance p increase IP3 –> calcium

18
Q

Functions of CCK

A
  1. major stimulus of pancreatic secretion
  2. contracts gallbladder, relaxes sphincter of Oddi
  3. delays gastric emptying
19
Q

Where is CCK produced?

A

upper intestinal cells –> regulated by monitor peptide and CCK-RP

20
Q

Phases of pancreatic secretion

A

stimulatory: cephalic, gastric, intestinal
inhibitory: postprandial

21
Q

What nerve mediates the cephalic phase?

A

vagus nerve –> sham feeding produces about 50% of maximal enzyme secretion

22
Q

What inhibits the cephalic phase?

23
Q

What causes the intestinal phase?

A

acid and chyme in intestine –> ph below 4.5 releases secretin –> enzyme secretion

24
Q

What mediates postprandial inhibition?

A
  1. excess intraluminal trypsin inhibits CCK release by digesting monitor peptide and CCK releasing peptide
  2. oleic acid in ileum/colon via peptide YY
    glucose/iv AA
25
Tests for pancreatic function
1. fecal fat (>10 abnormal) 2. sudan stain for fat 3. duodenal secretions 4. secretin stimulation test 5. imaging --> need 90% loss of lipase to get a change in fecal fat
26
Bile functions
1. excrete polar metabolites of lipid waste/bilirubin 2. fat and fatsoluble vitamin absorption 3. excrete cholesterol 4. IgA
27
Where are different components of bile secreted?
1. organic components = hepatocytes into canaliculi 2. electrolyes and water= hepatocytes into ducts some salts increase/reduce canalicular flow
28
Rate limiting step in secretion of bile salts
secretion of components against concentration gradient in canaliculi
29
Nuclear control of intracellular bile salts
farnesoid X factor senses intracellular bile salt --> stimulation suppresses bile salt synthesis and increase in canalicular secretion --> feedback suppression of toxic cellular bile salt level
30
Rate limiting step in cholesterol synthesis
HMGCoA reductase
31
How are primary bile salts formed?
7alpha hydroxylation and carboxylation side chain of cholesterol in liver
32
How are secondary bile salts formed?
bacterial 7alpha dehydroxylation or isomerization in colon
33
What does water solubility of bile salts depend on?
ionization of side chain --> secondary bile acids are more water soluble
34
Bile salt conjugation
before secretion into bile, salts are conjugated with taurine/glycine --> stronger acids which ionize upper small intestine and prevent back diffusion of bile --> bind to specific ileal receptors and form clusters/micelles once above critical micellar concentration
35
Addition of what molecule increases ability to solubilize cholesterol in a mixed micelle?
lecithin
36
What limits proximal intestinal absorption of bile salts?
ionization (conjugation)
37
How do bile salts return to the liver?
portal vein
38
What is the effect of small bowel stasis on bile salts?
premature deconjugation due to bacterial overgrowth leading to precipitation of bile salts and fat/vitamin malabsorption
39
What products may protect mucosa against toxicity of bile salts?
cholesterol and phospholipids