secretions of the intestine, liver, gall bladder & pancreas Flashcards

1
Q

what is the function of the small intestine?

A

governs the majority of chemical digestion and absorption of nutrients, electrolytes and water

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2
Q

what are the 3 primary secretions of the small intestine?

A
  • intestinal juice
  • pancreatic juice
  • bile
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3
Q

what key endocrine hormones regulate bile and pancreatic secretions?

A
  • secretin
  • cholecystokinin (CCK)
  • glucose dependent insulinotrophic peptide/gastric inhibitory peptide (GIP)
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4
Q

what are the 3 main secretory cells in the small intestine and their function?

A
  • villi: absorptive enterocytes and mucus secreting goblet cells
  • intestinal glands: enterocytes secreting isotonic fluid, enteroendocrine cells, paneth cells
  • Brunner’s glands (duodenum only): secrete mcus and HCO3-
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5
Q

what is contained in the secreted intestinal juice?

A

electrolytes, water, lysozyme, mucus, alkaline mucus containing fluid

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6
Q

what is contained in the secreted exocrine pancreatic juice?

A

bicarbonate/digestive enzymes

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7
Q

what are the key endocrine hormone secretions into the vasculature of the small intestine?

A
  • CCK stimulate pancreatic and gallbladder secretion
  • secretin stimulates pancreatic and biliary bicarbonate secretion
  • GIP may inhibit acid secretion/stimulate insulin release
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8
Q

what does the exocrine pancreas secrete?

A

pancreatic juice containing bicarbonate rich secretion (pH 8) and digestive enzymes essential for normal digestion and absorption

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9
Q

what is the pancreatic structure?

A
  • the pancreas consists of glandular epithelial clusters
  • 99% exocrine acinar clusters secreting pancreatic juice (water, electrolytes, sodium bicarbonate and pro-enzymes)
  • 1% endocrine pancreatic islet (islets of Langerhans) of 4 types of secreting glucagon (alpha), insulin (beta), somatostatin (delta) and pancreatic polypeptide (F cell)
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10
Q

how is exocrine pancreatic secretion regulated by acinar enzyme production?

A
  • acetylcholine released via P/S vagus stimulation
  • CCK trigger is chyme containing fat and protein products
  • produces lower volume enzyme rich pancreatic juice
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11
Q

how is exocrine pancreatic secretion regulated by ductal bicarbonate and water?

A
  • secretin trigger is H+ in highly acidic chyme

- produces copious, HCO3- rich, lower enzyme pancreatic juice

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12
Q

what are the different pancreatic enzymes and their functions?

A
  • proteolytic enzymes: secreted in inactive form, convert proteins to peptides
  • amylase: hydrolyses starch, glycogen and other carbohydrates other than cellulose to form di and trisaccharides
  • lipase: hydrolyses fat into fatty acids and monoglycerides
  • nucleases: digest RNA and DNA to nucleic acids
  • trypsin inhibitor: prevents activation of trypsin to prevent pancreatic digestion
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13
Q

how are proteolytic enzymes activated?

A
  • proteolytic enzymes are produced as inactive precursors called zymogens
  • small intestinal brush border enterokinase enzyme cleaves hexapeptide to form active trypsin form trypsinogen
  • trypsin cleaves and activates other proteolytic enzymes
  • process prevents pancreatic auto digestion
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14
Q

how do ducts secreted sodium bicarbonate?

A
  • secretin stimulates high volume HCO3- rich pancreatic juice
  • HCO3- secretion out of cell and into duct lumen is via Cl-/HCO3- exchange at the apical cell membrane
  • Cl- is recycled out of the cell via the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel under secretin stimulation via cAMP
  • Na+ is secreted transcellularly into the duct lumen following HCO3- secretion down electrochemical gradient, water follows by osmosis
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15
Q

what happens with unstimulated channels?

A

low secretory rate: electrolyte content is similar to that of plasma

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16
Q

what happens with stimulated channels?

A

higher secretion rate and rise in HCO3- from ductal cells inversely related to reduced concentration of Cl- in pancreatic juice

17
Q

what happens to patients with a dysfunction in ductal CFTR Cl- channel?

A
  • cystic fibrosis
  • lack a functional Cl- CFTR channel in the luminal membrane, which results in defective ductal fluid secretion
  • the ducts become blocked with precipitated enzymes and mucus and the pancreas undergoes fibrosis
  • blocked ducts impair secretion of needed pancreatic enzymes for digestion of nutrients, resulting in malabsorption
  • treatment of this type of malabsorption includes oral pancreatic enzyme supplements taken with each meal
18
Q

what happens to patients with a dysfunction in the enzyme activation process?

A
  • pancreatitis
  • an inflammatory disease where pancreatic enzymes are activated within the pancreas resulting in auto digestion of the tissues
  • the most common causes are gallstones and alcohol abuse where obstruction of the pancreatic duct occurs
19
Q

what are the 2 main roles of bile in digestion?

A
  • required for digestion and absorption of fats from the small intestine
  • elimination of waste products
20
Q

how does bile diets and absorb fats from the small intestine?

A

bile salts emulsified fats for digestion by pancreatic lipase, solubilise fat digestion products into micelles for absorption across the mucosa

21
Q

what waste products does bile eliminate?

A
  • bile pigment bilirubin form harm in red blood cell degradation
  • cholesterol
  • drugs
22
Q

how is bile synthesised and secreted in the liver?

A
  • bile is constantly synthesised by hepatocytes linen sinusoidal blood vessels in the liver anicus
  • hepatocytes are the key functional cell of the liver forming 80% of the liver mass
  • bile drains into the blind ended canaliculi and into the bile duct for storage in the gall bladder or direct drainage into the duodenum
23
Q

how is bilirubin excreted in bile?

A
  • haem from old/faulty RBC is converted to bilirubin and oxidised from biliverdin transported to liver bound to albumin in unconjugated form
  • conjugated with glucuronic acid to bilirubin diglucuronide by hepatocytes excreted in bile
  • gut bacteria hydrolysis deconugated bilirubin to form urobilinogen
  • urobilinogen reduced to stercobilin, secreted in faeces
  • enterohepatic reabsorption or urobilinogen most re-secreted in bile
24
Q

what is jaundice?

A

the build up of bilirubin

25
Q

what are the 3 main causes of jaundice?

A

1) pre-hepatic: excessive RBC breakdown, build up of unconjugated bilirubin due to overload of progressing mechanisms
2) hepatocellular/congenital: altered hepatocyte function
3) post-hepatic: obstruction to normal bile drainage, build up of conjugated bilirubin

26
Q

what is an example of pre-hepatic jaundice?

A

haemolytic anaemia

27
Q

what is an example of hepatocellular/congenital jaundice?

A

Crigler-Najjar syndrome

28
Q

what is an example of post-hepatic jaundice?

A

gallstone obstruction of bile flow

29
Q

how is bile secreted and regulated?

A
  • CCK released in response to fat content of duodenum: gall bladder contracts and sphincter of hepatopancreatic ampulla relaxation
  • secretin released in response to acidic chyme: liver ductal secretion of HCO3- and H20
  • minor role for vagal and enteric ACh stimulation: bile flow, gall bladder contraction
30
Q

how does enterohepatic circulation work with bile salts?

A
  • enterohepatic circulation: bile salts secreted by hepatocytes into bile and continuously recycled through active reabsorption from the ileum and then re-secreted into bile
  • 94% bile salts return via portal vein to drive bile synthesis in liver
  • many hydrophobic drugs are deactivated by the liver and excreted into bile; enterohepatic recycling frequently occurs; slowing rate of drug elimination
31
Q

what are the common causes of gallstones?

A
  • excessive water and bile salt reabsorption from bile
  • excessive cholesterol in bile causing precipitation
  • inflammation of epithelium
32
Q

what is gall bladder disease?

A

occurs in several forms, ranging from asymptotic cholelithiasis (gallstones) to biliary colic affecting different areas of the biliary tract