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Module 104: Nutrition, Metabolism and Excretion > Theme 1: Lecture 6 - Secretions of the intestine, liver, gall bladder and pancreas > Flashcards

Theme 1: Lecture 6 - Secretions of the intestine, liver, gall bladder and pancreas Flashcards

1
Q

What are the 3 primary secretions into the small intestine

A
  • intestinal juice (mucus/HCO3-)
  • pancreatic juice (digestive enzymes/HCO3-, pH 8)
  • bile (bile salts)
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2
Q

Brunner’s glands

A
  • located in the submucosa of the duodenum.

- Secrete mucus and HCO3-

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3
Q

What are the key endocrine hormones involved with the small intestine

A

secretin, cholecystokinin (CCK), glucose dependent insulinotrophic peptide, GIP (AKA gastric inhibitory peptide) regulate bile and pancreatic secretions

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4
Q

What cells are located in villi of the small intestine

A
  • Absorptive enterocytes

- Goblet cells

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5
Q

What cells are located in the intestinal glands AKA crypts of Lieberkuhn

A
  • Enteroendocrine cells

- Paneth cells

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6
Q

What do absorptive cells in the small intestine do

A

Digest and absorb nutrients

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7
Q

What do Goblet cells in the small intestine do

A

Secrete mucus

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8
Q

What do enteroendocrine cells in the small intestine do

A

Secrete secretin, cholecystokinin (CCK) and glucose dependent insulinotrophic peptide AKA gastric inhibitory peptide (GIP)

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9
Q

What do paneth cells in the small intestine do

A

Secretes lysozyme and is capable of phagocytosis

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10
Q

Describe stem cell renewal of epithelial cells in the small intestine

A
  • rapid turnover of epithelial cells every 3-6 days

- vulnerable to radiation, chemotherapy

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11
Q

Describe intestinal juice

A

fluid containing electrolytes and water (secretory enterocytes), lysozyme (Paneth cells), mucus (goblet cells), alkaline mucus containing fluid (submucosal duodenal Brunner’s glands)

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12
Q

Where is cholecystokinin (CCK) secreted from

A

I cells

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13
Q

What does cholecystokinin do

A

stimulate pancreatic and gallbladder secretion

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14
Q

Where is secretin secreted from

A

S cells

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15
Q

What does secretin do

A

stimulate pancreatic and biliary bicarbonate secretion

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16
Q

Where is glucose dependent insulinotrophic peptide AKA gastric inhibitory peptide (GIP) secreted from

A

K cells

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17
Q

What does glucose dependent insulinotrophic peptide AKA gastric inhibitory peptide (GIP) do

A

may inhibit acid secretion/stimulate insulin release

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18
Q

Describe the structure of the pancreas

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 islets (Islets of Langerhans) of 4 types
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19
Q

What are the 4 types of islets of Langerhans cells in the pancrea

A
  • Alpha
  • Beta
  • Delta
  • F cell
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20
Q

What do the alpha cells of islets of Langerhans cells in the pancreas secrete

A

Glucagon

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21
Q

What do the beta cells of islets of Langerhans cells in the pancreas secrete

A

Insulin

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22
Q

What do the delta cells of islets of Langerhans cells in the pancreas secrete

A

somatostatin

23
Q

What do the F cells of islets of Langerhans cells in the pancreas secrete

A

Pancreatic polypeptide

24
Q

Describe secretion from acinar cells in the pancreas

A
  • Stimulated by Acetyl choline released via the parasympathetic vagus stimulation
  • Stimulated by CCK - trigger is chyme containing fat and protein products
  • Produces lower volume enzyme rich pancreatic juice
25
Q

Describe secretion from ductal cells in the pancreas

A
  • Stimulated by secretin - trigger is H+ in highly acidic chyme
  • Produces copious HCO3- rich, low enzyme pancreatic juice
26
Q

What enzymes are secreted by the pancreas

A
  • Proteolytic enzymes enzymes secreted in inactive form, convert proteins to peptides
  • Amylase hydrolyses starch, glycogen and other carbohydrates other than cellulose to form di and trisaccharides
  • Lipases hydrolyse fat into fatty acids and monogylcerides
  • Nucleases digest RNA and DNA to nucleic acids
27
Q

What other protein excluding enzymes is secreted by the pancreas

A

Trypsin inhibitor - prevents activation of trypsin to prevent pancreatic digestion

28
Q

Describe the activation of proteolytic enzymes

A
  • Proteolytic enzymes are produced as inactive precursors called zymogens
  • Small intestinal brush border enterokinase enzyme cleaves hexapeptide to form active trypsin from trypsinogen
  • Trypsin cleaves and activates other proteolytic enzymes
  • Process prevents pancreatic autodigestion (+trypsin inhibitor)
29
Q

Describe duct secretion of HCO3- in the pancreas

A
  • Secretin stimulates high volume HCO3− rich pancreatic juice
  • HCO3− secretion out of cell into the 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
30
Q

What does the ionic composition of pancreatic juice depend on

A

Secretory rate

31
Q

Describe ionic composition of pancreatic juice when it is unstimulated

A

Low secretion rate - electrolyte content is similar to that of plasma

32
Q

Describe ionic composition of pancreatic juice when it is stimulated

A

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

33
Q

Describe dysfunction of the ductal CFTR Cl- channel

A
  • Patients with 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 (hence the name of the disease)
  • 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
34
Q

Pancreatitis

A

an inflammatory disease where pancreatic enzymes are activated within the pancreas (and surrounding tissues), resulting in autodigestion of the tissues

35
Q

What causes pancreatitis

A

The most common causes of pancreatitis include gallstones and alcohol abuse where obstruction of the pancreatic duct occurs

36
Q

What is the role of bile in digestion

A
  • Required for digestion and absorption of fats from the small intestine
  • Bile salts (amphipathic with hydrophobic/hydrophilic regions) emulsify fats for digestion by pancreatic lipase, solubilise fat digestion products into micelles for absorption across the mucosa
  • elimination of waste products (bile pigment bilirubin from heme in red blood cell degradation, Cholesterol, drugs)
37
Q

Where is bile synthesised

A

Bile is constantly synthesised by hepatocytes lining sinusoidal blood vessels in the liver acinus

38
Q

What are hepatocytes

A

The key functional cell of the liver forming 80% of the liver mass

39
Q

Where does bile drain into once it has been synthesised by hepatocytes

A

Bile drains into the blind ended canaliculi and into the bile duct for storage in the gall bladder or direct drainage into duodenum

40
Q

What do liver duct epithelial cells do in response to secretin

A

add water, Na+, HCO3− to increase bile volume

41
Q

What does the gall bladder do to bile

A
  • Concentrates it
  • Water and electrolytes (Na+, Cl-, HCO3-) are reabsorbed across the gall bladder mucosa to concentrate bile salts, bilirubin and cholesterol
42
Q

Describe how bile pigment is excreted

A
  • Haem from old/faulty RBC is converted to bilirubin (orange) and oxidised form biliverdin (green) in the spleen/ liver kupffer cells.
  • Bilirubin is hydrophobic so is transported to liver bound to albumin in unconjugated form
  • Bilirubin is conjugated (made hydrophilic) with glucuronic acid to form bilirubin diglucuronide by hepatocytes, excreted in bile
  • Gut bacterial hydrolysis (b glucuronidase) deconjugates bilirubin to form urobilinogen
  • Urobilinogen is reduced to stercobilin, excreted in faeces (brown colour)
  • Enterohepatic reabsorption of urobilinogen can occur, most re-secreted in bile (small amount excreted in urine)
43
Q

What is jaundice

A

The build up of bilirubin (serum bilirubin >30-60 mmol.L-1) (yellow discoloration of skin in severe jaundice)

44
Q

What are the 3 groups that jaundice tends to be divided into

A
  • Pre hepatic
  • Hepatocellular/congenital
  • Post hepatic
45
Q

Pre hepatic jaundice

A

excessive RBC breakdown, build up of unconjugated bilirubin due to overload of processing mechanisms eg haemolytic anaemia

46
Q

Hepatocellular/congenital jaundice

A

altered hepatocyte function eg Crigler-Najjar syndrome (inborn error of metabolism - absence of hepatocyte bilirubin conjugating enzyme glucuronyl transferase results in increased unconjugated bilirubin)

47
Q

Post hepatic bilirubin

A

obstruction to normal bile drainage, build up of conjugated bilirubin eg gallstone obstruction of bile flow

48
Q

The role of CCK in relation to bile secretion

A
  • Released in response to fat content of duodenum
  • Causes gall bladder contraction
  • Also causes sphincter of hepatopancreatic ampulla (Sphincter of Oddi) relaxation
49
Q

The role of secretin in relation to bile secretion

A
  • Released in response to acidic chyme

- Liver ductal secretion of HCO3− , H20

50
Q

The role of vagal and enteric ACh stimulation in relation to bile secretion

A
  • Minor role

- Causes bile flow and gall bladder contraction

51
Q

Describe enterohepatic circulation of bile salts

A

bile salts secreted by hepatocytes into bile and continuously recycled through active reabsorption from the ileum and then re-secretion into bile

52
Q

Describe gall bladder disease

A

Occurs in several forms, ranging from asymptomatic cholelithiasis (gallstones) to biliary colic (blockage of the cystic duct) affecting different areas of the biliary tract

53
Q

What is gallstones commonly caused by

A
  • Excessive water and bile salt reabsorption from bile
  • Excessive cholesterol in bile causing precipitation (high fat diet)
  • Inflammation of epithelium (low grade chronic infection)

Module 104: Nutrition, Metabolism and Excretion (23 decks)

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