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Gastro > Pancreas & liver physio > Flashcards

Pancreas & liver physio Flashcards

1
Q

functional division of pancreas (2)

A
  • exocrine pancreas
  • endocrine pancreas
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2
Q

what does the exocrine pancreas secrete (3)

A
  • Enzyme secretion (acinus)
  • Electrolyte secretion (duct)
  • Mucin (goblet)

acinar cells + ductal cells form a gland together

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3
Q

what does the endocrine pancreas secrete

A
  • Insulin
  • Glucagon
  • (Somatostatin)
  • Pancreatic polypeptide

**ALL FROM ISLETS OF LANGERHANS

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4
Q

what regulates enzyme secretion by acinar cells

A
  • hormone CCK (cholecystokinin) increases production of enzymes
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5
Q

what regulates ductal fluid secretion by ductal cells

A
  • hormone SECRETIN
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6
Q

why is ductal fluid produced by ductal cells alkaline

A
  • ductal cell contains carbonic anhydrase -> convert CO2 to H2CO3 -> produce HCO3- which is excreted out of cell
  • HCO3- is exchanged for Cl- at the lumen site
  • H+ produced from H2CO3 dissociation is pushed into blood with exchange for Na+
  • alkaline solution favours enzymatic activity of small intestines
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7
Q

how does pancreas protect itself from its enzymatic secretions (4)

A
  • packaging protease as PRECURSOR FORMS (zymogens) -> protease inactivated, cannot digest pancreas
  • presence of PROTEASE INHIBITORS (eg trypsin inhibitor) -> protect pancreas from unlikely case that protease is activated
  • protease are COMPARTMENTALISED away from main cells, cannot do damage
  • protein exist in LOW pH environment -> will denature if activated
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8
Q

how are pancreatic enzymes activated

A
  • enterokinase present in luminal walls of intestine -> cleaves trypsinogen in pancreatic juice to trypsin
  • active trypsin continues on to cleave remaining zymogens in pancreatic juice (chymotrypsinogen, proelastase, procarboxypeptidase A, procarboxypeptidase B)
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9
Q

pancreatic enzymes that are secreted in ACTIVE form & function

A

Pancreatic α-amylase
– Hydrolyzes glycogen, starch, complex carbohydrate
(except cellulose) into disaccharides

Pancreatic lipases
– Water-insoluble esters require bile salts to work
– Water-soluble esters do not require bile salts

Nucleases

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10
Q

what is pancreatic secretion stimulated by (2)

A

Neural
- vagus nerve

Hormonal
- secretin -> ductal cell secrete water, electrolytes & HCO3- rich secretion
- CCK -> acinar cell produce enzyme rich secretion

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11
Q

what stimulates secretin release

A
  • gastric acid stimulus (acid from stomach entering duodenum)
  • sensed by pH sensors in DUODENUM -> presence of H+ leads to secretin production in S cells of duodenum -> boost HCO3- secretion from ductal cells
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12
Q

what stimulates CCK secretion

A
  • LCFA (long chain fatty acid), amino acid, gastric acid stimulus -> stimulate I cells in duodenum to secrete CCK
  • CCK causes increase secretion of enzyme rich pancreatic fluid + increase hepatic secretion of bile salts -> pancreatic fluid & bile released into duodenum
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13
Q

how does vagus nerve stimulate secretin & CCK release (2)

A

CEPHALIC & GASTRIC PHASE (30%)
cephalic phase
- sight/smell/taste of food
gastric phase
- presence of food in stomach

cephalic + gastric phase -> CNS effect -> vagus nerve act on M3 receptors on acinus & ductal cells (ACh neurotransmitter) -> release secretin & CCK

INTESTINAL PHASE (70%)
- protein + lipid breakdown -> stimulate vagovagal reflex -> stimulates primarily ACINAR cells

**hormonal control of secretin & CCK secretion also falls under INTESTINAL PHASE (ie intestinal phase = vagus + hormones; cephalic & gastric = only vagus)

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14
Q

how is pancreatic secretion regulated according to amount of food in stomach

A
  • by CCK-RP (releasing peptide) and monitor peptide -> similar function, both binds to I cells in duodenum to increase CCK production
  • CCK-RP & monitor peptides are broken down by TRYPSIN

too much food in stomach
- all available trypsin are used to digest food -> CCK-RP & monitor peptide not broken down -> binds to receptor on I cells -> stimulate more CCK secretion & enzyme secretion

stomach empty
- many free trypsin -> digest CCK-RP & monitor peptide -> no longer binds to receptor -> I cells do not secrete CCK

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15
Q

functions of CCK (4)

A
  • contraction of gallbladder (push bile out)
  • acinar secretion in pancreas
  • reduce rate of stomach emptying
  • relax sphincter of Oddi (allow bile to flow out when gallbladder contracts)
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16
Q

how is pancreatic function lost

A
  • loss of exocrine pancreas cells -> loss of digestive enzymes & malabsorption -> steatorrhea (fat in faeces)
  • loss of endocrine pancreas cells -> loss of islet cells > diabetes
17
Q

how to assess pancreatic function

A

Indirect
- stool fat -> indicates absorption
- stool elastase, chymotrypsin -> reflects pancreatic secretion

Direct
- inject secretin and obtain the amount of secretion from secretin injected

18
Q

what are hepatocytes

A

Epithelial cells one cell thick separating two fluid compartments
– canalicular lumen (bile)
– sinusoids (blood)

Presence of hepatocyte polarity
– Apical membrane faces the canalicular lumen
– Basolateral membrane faces perisinusoidal space (space of Disse)

19
Q

do bile canniculi and sinusoids flow in the same direction?

A
  • NO. countercurrent flow
20
Q

what do liver lobules (hexagons) contain

A
  • a central vein that drains into
    a BRANCH of HEPATIC VEIN -> eventually drain into IVC
  • periphery contains portal triad (hepatic artery + bile duct + portal vein) -> formed from BRANCHES of PORTAL VEIN -> sends blood to sinusoids
21
Q

how does hepatocyte carry out its excretory function

A
  • sinusoid endothelial contains large gaps -> products from blood (even albumin) can diffuse into hepatocyte
  • products are metabolised and drained into bile canaliculus -> released via bile duct
22
Q

basal daily bile secretion & its contents

A

500-600mL

  • majority bile acids
  • bile pigments (bilirubin)
  • lecithin & phospholipids; cholesterol; proteins; electrolytes
23
Q

describe bilirubin transport within hepatocyte

A
  • ALB(albumin):UCB(unconj. bili) from sinusoid diffuse into space of disse -> UCB moves into hepatocyte easily (UCB is non polar)
  • UCB converted eventually to bilirubin diglucuronide (water soluble) -> discharged to bile canaculi by MRP2 (multidrug resistance associated protein 2)
24
Q

how is bile release regulated

A

CCK
- gallbladder contraction -> push bile into common bile duct
- sphincter of Oddi relaxation -> release bile from common bile duct into duodenum

25
Q

types of bile acids

A

pri bile acids
- cholic & chenodeoxycholic acids

sec bile acids
- deoxycholic & lithocholic acids
- formed from pri bile acid by bacteria in gut

bile salt
- sec bile acids conjugated to glycine or taurine

26
Q

characteristics of conjugated bile acids (bile salt)

A
  • bound to glycine, taurine
  • more amphiphatic -> easier to form micelles (aid fat absorption), reabsorb poorly thus stay longer in gut
  • resistant to hydrolysis by pancreatic enzymes -> stable in gut lumen
27
Q

how are bile salts excreted by hepatocytes

A
  • bile salt enter hepatocyte from sinusoids
  • excreted into bile canaliculus via BSEP (bile salt export pump); ACTIVE TRANSPORT (similar to bilirubin)
28
Q

function of bile acids

A
  • Promote bile flow
  • Solubilise cholesterol, phospholipids in GB
  • Enhance dietary lipid digestion and absorption by mixed micelle formation (detergent function)
29
Q

where and why are bile acids reabsorbed

A
  • 80-90% of bile salts absorbed in terminal ileum by active Na dependent process
  • bile acid synthesis is energy intensive
30
Q

effects of loss of bile salts

A
  • bile salts are limited (energy intensive production) -> need to recycle by reabsorption at terminal ileum
  • loss of bile salts -> diminished fat digestion -> fat malabsorption -> loss of calorie & vitamins ADEK (fat soluble) deficiency

Gastro (20 decks)

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