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GIS > GIS18 Control Of Biliary And Pancreatic Exocrine Secretions > Flashcards

GIS18 Control Of Biliary And Pancreatic Exocrine Secretions Flashcards

1
Q

Pancreas secretion

A

Exocrine

  1. Enzymatic component
    - secreted by **Acinar cells / Exocrine cells
    - contains enzymes for digestion
    - stored as **    zymogen granules, released by exocytosis
    - proteases secreted as inactive forms
  2. Aqueous component (HCO3 / water):
    - secreted by **Duct cells / **Epithelial cells of pancreatic ductules and ducts
    - **largest supply of HCO3 in the duodenum (> biliary ductules and duodenal epithelial cells)
    - neutralises acid chyme from stomach, **    stops action of pepsin
    - provide optimal pH (7-8) for the action of pancreatic enzymes

Endocrine (Endocrine cells / Islets of Langerhans)

  1. Insulin
  2. Glucagon
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2
Q

***Pancreatic enzymes

A
  1. Endopeptidases: **Trypsin, **Chymotrypsin, elastase
    - protein —> peptide
  2. Exopeptidases: ***Carboxypeptidase A, B (+ Aminopeptidase)
    - splits off terminal amino acid from Carboxyl end of protein
  3. Lipase
    - TAG —> MG + 2 fatty acids
    (- + Lipid esterase + Phospholipase A2)
  4. Amylase
    - polysaccharide —> glucose, maltose
  5. Ribonuclease, Deoxyribonuclease
    - nucleic acid —> free mononucleotides
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3
Q

Proteolytic digestion by pancreatic enzymes in intestine

A

Proteolytic enzymes:

  • secreted as inactive precursors
  • converted to active enzymes only when they reach the lumen of the small intestine
  • Trypsinogen is converted to active Trypsin by membrane-bound ***Enterokinase
  • Active Trypsin cleaves the other precursors of proteolytic enzymes (e.g. Chymotrypsin, Proelastase) —> make them active

Non-proteolytic enzymes (Amylase and Lipase):
- secreted as active forms by pancreas

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4
Q

Proenzyme and active enzyme (ALL converted by Trypsin)

A

Endopeptidase:

  • Trypsinogen —> Trypsin
  • Chymotrypsinogen —> Chymotrypsin
  • Proelastase —> Elastase

Exopeptidase:

  • Procarboxypeptidase A —> Carboxypeptidase A
  • Procarboxypeptidase B —> Carboxypeptidase B
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5
Q

HCO3 secretion

A
  1. Primary secretion (intralobular ductal system)
    - slightly ***hypertonic to plasma
  2. Secondary secretion (extralobular ductal system)
    - HCO3 secretion —> ↑ concentration of HCO3 (exchange with Cl-)
    - H2O secretion —> dilution —> become ***isotonic to plasma

(vs Saliva: **Isotonic (NaCl + H2O secretion) —> **Hypotonic (NaCl reabsorption + KHCO3 secretion))

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6
Q

HCO3 secretion from pancreatic duct cell

A

Formation of HCO3:

  1. Inside cell: formation of HCO3 from CO2 and H2O by ***carbonic anhydrase
  2. From blood: transported into the cells by ***Na/HCO3 co-transporter (NBC-1)

—> **HCO3 transported into lumen via **Cl/HCO3 exchanger (apical membrane)
—> Cl recycled into lumen via Cl channel (CFTR cystic fibrosis transmembrane conductance regulator)
—> ***osmosis of H2O down osmotic gradient into lumen

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7
Q

Cystic fibrosis

A 
- defect in CFTR
—> cannot drive Cl- out into lumen
—> no osmosis of water into lumen
—> very viscous
—> pancreatic insufficiency / pancreatitis
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8
Q

***Control of pancreatic secretion by small intestine

A

Hormonal control:
—> ***Secretin, CCK (paracrine) mostly secreted by duodenum and jejunum during Intestinal phase

Neural control:
—> **Vagal during Cephalic phase
—> **Vagovagal during Gastric phase

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9
Q

***Control of pancreatic secretion of HCO3

A
  • Controlled by Intestinal phase (stimulus on small intestine)

↑ **Acid from stomach
—> ↑ stimulus to **S cells in duodenal lumen
—> ↑ **Secretin secretion
—> ↑ **HCO3 from pancreatic ***duct cells
—> ↑ HCO3 into small intestine
—> ↑ neutralisation of acidic chyme from stomach (-ve feedback to S cell)
—> enzymes in small intestine work best at neutral pH

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10
Q

Action of secretin on pancreatic duct cells

A

Secretin ↑ HCO3 secretion by:
—> ***↑ opening of CFTR (via ↑ cAMP)
—> ↑ outflow of Cl- (into lumen)
—> ↑ exchange of HCO3 into lumen (Cl- back into cells) via Cl/HCO3 exchanger on apical membrane

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11
Q

***Control of pancreatic enzyme secretion

A
  • Controlled by Intestinal phase (stimulus on small intestine)
  • Stimuli: fatty acids / amino acids

↑ intestinal **f.a. and a.a.
—> ↑ stimulus to **I cells in duodenal lumen
—> ↑ **CCK secretion by I cells in small intestine
—> ↑ plasma CCK
—> ↑ **enzyme secretion by pancreatic ***acinar cells
—> ↑ enzymes in small intestine
—> ↑ digestion of fats, proteins and carbohydrates

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12
Q

Action of CCK on pancreatic acinar cells

A
  1. Directly acting on ***CCK-1 receptor on acinar cells
  2. Indirectly activates **Vagovagal reflex from small intestine
    —> activate pancreatic enteric neurones to release **    neurotransmitter (VIP, GRP, ACh)
    —> stimulate receptors on basolateral side
    —> stimulate acinar cells to increase pancreatic enzymes secretion
    —> enzyme washed into duodenum by ductular secretion
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13
Q

Biliary secretion

A
  • secreted by liver cells
  • concentrated and stored in gall bladder
  • bile contains water, electrolytes, organic molecules including bile acids, cholesterol, phospholipids, bilirubin
  1. **Bile salts: synthesised from **cholesterol, for fat digestion
  2. **HCO3 in bile: secreted by bile duct **epithelial cells
  3. ***Cholesterol: extracted from blood, secreted by liver into bile, then excreted as faeces (cholesterol homeostasis in blood)
  4. ***Bilirubin / bile pigments: excretion, from RBC breakdown
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14
Q

Stages of biliary secretion

A
  • First stage: **Hepatocytes secrete fluid rich in **Bile salts, ***Cholesterol and other organic components into canaliculi, then flows into bile ducts
  • Second stage: **Ductal epithelial cells add watery, **HCO3 rich secretion to modify bile as it flows through the bile ducts
  • Bile stored and concentrated in gall bladder between meals through ***absorption of H2O, Na, Cl and other electrolyte, but retaining and concentrating all organic molecules
  • Gall bladder contracts and empties bile into duodenum in response to meal
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15
Q

Digestion of lipids

A
  • Most ingested fat in form of TG, some in phospholipids and cholesterol
  • mainly in small intestine by ***Pancreatic lipase
  • Emulsification:
    —> mechanical disruption into small droplets by contraction of stomach and small intestine
    —> non-polar portions of phospholipid and bile salt associate with the non-polar portion interior of the lipid droplets
    —> polar portions exposed at the water surface, repelling other lipid droplets
    —> prevent re-aggregating back into larger droplets
    —> allow digestion by water soluble pancreatic lipase at surface of lipid droplet (since fat are insoluble in water and lipase is in aqueous phase)

Formation of micelles:
**Bile salts + Fatty acids + Phospholipids + Monoglycerides
—> all cluster together with polar ends towards micelle’s surface and non-polar ends forming the core
—> cholesterol and fat-soluble vitamins inside core of micelles
—> **micelles ↑↑ solubility of lipid and fat-soluble vitamins in the intestine
—> facilitate their absorption

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16
Q

Fat absorption

A
  • free molecules of fatty acids and MG diffuse into intestinal epithelial cells
  • resynthesized into **TAG in **sER
  • droplets of TAG secreted as ***chylomicrons which also contain cholesterol + fat-soluble vitamins
  • chylomicron passed into ***lacteals
  • lymph empties into systemic veins via ***thoracic duct
17
Q

Enterohepatic circulation

A
  • ~95 % bile salts reabsorbed into blood at the ***Ileum
  • return via ***Hepatic portal vein to liver
  • absorbed by hepatocytes and re-secreted into bile
  • re-circulated several times in a single meal
  • 5% lost in faeces replenished by synthesis in liver from cholesterol
  • bile salts remain ionised —> unabsorbed to ensure full digestion before conjugation
18
Q

***Control of biliary secretion

A

Bile salts secretion increased after absorption of bile salts in the blood from ileum

  1. Acid in duodenum
    —> **Secretin secretion
    —> stimulates **    HCO3 secretion by bile duct (effect like in pancreatic duct)
  2. Fatty acids in duodenum
    —> **CCK secretion
    —> stimulates 1. **    Contraction of gall bladder and 2. ***Relaxation of sphincter of Oddi (this time not stimulate enzyme secretion)
    —> increase bile flow to duodenum
  3. ***Vagus nerve: stimulation of contraction of gall bladder
19
Q

Bilirubin metabolism

A

Liver conjugates water-insoluble bilirubin (Free bilirubin)
—> water-soluble bilirubin-glucuronide (Conjugated bilirubin)
—> excreted into bile
—> Conjugated bilirubin —> ***Urobilinogen by bacteria in intestine

  1. reabsorbed and go to liver
    —> Urobilinogen -(kidneys)-> Urobilinogen -(oxidation)-> ***Urobilin (excreted in urine)
  2. unabsorbed
    —> Urobilinogen —> Stercobilinogen -(oxidation)-> ***Stercobilin (excreted as faeces)
20
Q

Summary of functions of biliary secretions

A

Digestive functions:

  1. Bile acids
    - aid fat digestion and absorption
    - promote absorption of fat soluble vitamin
    - emulsification and formation of micelles
  2. HCO3
    - neutralises acidic chyme and provide optimal pH for enzyme action

Excretory functions:

  1. Bile pigments
  2. Excess cholesterol
  3. Drugs
21
Q

Clinical relevance

A
  1. Chronic pancreatitis
    —> pancreatic insufficiency leads to **fat indigestion —> **steatorrhoea
  2. Cystic fibrosis
    —> genetic disease, mutation in gene that encodes Cl channels
    —> **impairs water and electrolyte transport
    —> pancreatic ducts, acini and small airways clogged with **    viscid mucus
    —> imparted pancreatic exocrine function, ***fat digestion and absorption (carbohydrates and protein digestion can be compensated by other glands)
    —> also respiratory problems
  3. Gallstones
    —> ***obstruction of common bile duct impairs fat digestion and absorption
    —> also impairs absorption of fat soluble vitamins
  4. Jaundice
    —> increased bilirubin level in the blood, yellowish colouring of skin

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