Secretions of the intestine, liver, gall bladder and pancreas Flashcards
Cell in villi
Goblet cells: secrete mucus
Enterocytes with microvilli: absorbs nutrients and electrolytes.
Enteroendocrine cells: secretes hormones
Succus enterius
Intestinal juice produced by the small intestines
Payer’s patches
Masses of lymphatic tissue found throughout the ileum.
Monitors bacterial population and provides immune defense.
Crypt-villus unit
Functional unit of the intestines composing of:
- Crypt of Lieberkuhn
- Villus
Villus tip:
- Contains enterocytes where absorption of nutrients, fluid and electrolytes occur.
Maturation zone:
- Stem cells from the crypt and differentiating towards the villus tip.
Crypt (of Lieberkuhn):
- The intestinal gland
- Contains stem cells that rapidly divide.
- Site of fluid secretion.
Crypt of Lieberkuhn
The intestinal gland where fluid secretion occurs.
Contains stem cells that rapidly divide and gradually replace old cells.
Contains:
- Paneth cells
- Enterocytes
- Enteroendocrine celles
Paneth cells
One of the cell types in the crypts of Lieberkuhn.
Secretes lysosomes which hydrolyses bacteria.
Enterocytes
One of the cell types in the crypts of Lieberkuhn and in villi.
Columnar epithelial cells which absorb nutrients, electrolytes and fluid.
Enteroendocrine cells
Cells of the GI tract and pancreas- secretes hormones.
Different cells have different functions in the intestines:
I cells—> secrete CCK.
D cells—-> secretes somatostatin
S cells—-> secretes secretin
Brunner glands
Gland in the submucosa that secretes alkaline fluid into the crypts of Lieberkuhn.
- This fluid protects the tissue from acidic (chyme) damage.
Histological differences between the duodenum, jejunum and ileum
- Duodenum contains Brunner glands which secrete alkaline fluid to protect the epithelium from acidic damage by chyme.
- Jejunum has the most extensive intestinal folds as it is the site for absorption.
- Ileum contains Peyer’s patches.
Celiac sprue [celiac disease]
Malabsorption disorder caused by hypersensitivity to gliadin, in wheat.
The immune system destroys intestinal villi.
Symptoms: Diarrohea Steatorrhea Abdominal bloating Flatulence
Overall function of pancreas in digestion
Secretion of alkaline fluid:
- Neutralises chyme.
Secretes pancreatic digestive enzymes
Exocrine glands in the pancreas
Acini and ductal cells:
Acini= secrete digestive enzymes Duct= secretes bicarbonate.
Pancreatic juice released contains both digestive enzymes and neutralising alkaline fluid.
The juice is secreted into the pain pancreatic duct then into the intestinal lumen (duodenum)
Prevention of pancreatic autodigestion
Enzymes secreted from the acini are secreted as zymogens.
Zymogens are sequestrated in vesicles then released via exocytosis.
Zymogens are only activated in the small intestines by trypsin.
Trypsin inhibitor is secreted by the pancreas to prevent trypsin activation.
Enterokinase
Enzyme that converts trypsinogen to trypsin.
Enterokinase is found on apical membrane of enterocytes that line the small intestines.
Trypsin can then activate zymogens.
Enzymes in pancreatic juice
Mainly proteolytic
Amylolytic
Nucleases (breaks down nucleic acids)
Lipolytic enzymes
Enzyme secretion agonist of the pancreas
Ach:
- Binds to receptors on acini cells.
Vasocative intestinal peptide:
- Increase blood flow, stimulates more fluid secretion
CCK:
Released from I cells in response to fats, amino aicds
CCK
Cholecystokinin
Pancreatic secretion agonist.
Stimulates secretion in response to:
- Monoglycerides and fatty acids.
- Amino acids
Alkaline secretion agonist
Secretin: from S cells in duodenum
- enters the blood via ducts
- stimulates by low pH
Action is potentiates to Ach and CCK.
Pancreatitis
Inflammation of the pancreas cause by inappropriate activation of enzymes in the pancreas.
Cause: alcohol, gallstones.
Symptoms:
Epigastric pain
Mechanism of enzyme secretion in the pancreas
Enzymes are secreted by acini cells.
- Enzymes are made in ribosome as inactive proenzymes.
- Proenzymes eventually transferred to acid condensing vacuoles to form zymogen granules.
- CCK, Ach and secretin secreted in the blood acts on acini cells. Stimulates release of Ca2+ and cAMP.
4 Subsequent signals causes fusion of zymogen granules and its exocytosis into ductal lumen.
Primary secretion of NaCl in pancreatic acini cells.
- Basolaterally, Na/K- ATPase remove Na from cell to set up Na+ electrochemical gradient.
- Na+ transported back into the cell via Na/ 2Cl/ K symporter.
- K+ channels basolaterally remove K+ from the cell.
- Cl- enters lumen via Cl- channels on apical membrane.
- Na+ enters the lumen with water paracellular.
Regulation of NaCl- in acini cells
CCK and M3 receptors allows CCK and M3 to bind on the basolateral membrane.
This stimulates intracellular rise in Ca2+—> activates protein kinase.
Protein kinase activates Cl- and K+ channels.
Mechanism of secretion from pancreatic ductal cells.
- Bicarbonate is secreted into the lumen via Bicarbonate-chloride exchanger on luminar membrane.
- HCO3- made from carbonic anhydrase - Cl- taken back out to lumen via CFTR channel.
- Carbonic anhydrase produces H+—-> H+ leaves cell basolaterally via Na/ H+ and K/H+ exchanger.
- Sodium potassium pump brings K+ back into cell.
- Na+ in interstitial space travels with water paracellularly into lumen.
Reason for neutralising chyme in duodenum
This provides the optimum pH for pancreatic digestive enzymes.
Protects mucosa from acidic erosion.
Rate of secretion and pancreatic juice compositon
The slower the rate of secretion:
- Lower HCO3- composition
- Higher Cl- composition
Due to less time for Cl- reabsorption
Cystic fibrosis
Genetic condition with defective CFTR channel.
- Cl- cannot be recycled so HCO3- cannot be released into lumen.
This blocks the duct with mucus and impairs secretion of enzymes.
Cephalic regulation of pancreatic secretion
Regulates 20% of secretion
Secretion is initially triggered by sight, smell, and thought of food.
Ach release via vagal fibres to acinar cells.
Ach increase HCO3- secretions from ductal cells.
Ach also stimulates water release in acini lumen.
Gastric phase of pancreatic juice secretions
Regulates 10% of pancreatic secretion
Peptides in antrum of stomach stimulate gastrin release from G cells.
Postganglionic vagal fibres release GRP which stimulates gastrin release.
Gastrin acts on CCK receptors on acini cells to stimulate secretion.
Intestinal phase of pancreatic juice secretion
Regulates most of pancreatic secretion (70%).
Trigger: Chyme entry into duodenum
S cells in duodenum: senses low pH and secretes secretin.
= bicarbonate secretion
I cells: senses MG, FA and a.a = CCK secreted
- CCK acts on acini cells
= Enzyme rich secretions + potentiates gastrin.
Vago-vagal reflex: triggered by lipids and proteins= increases secretion.
Composition of bile
Water, Ions
Bilirubin
Biliverdin
Bile salts
Bile salts
Secreted from the gallbladder to emulsifies lipids.
- Synthesised from cholesterol.
Allows for lipid absorption.
Functions of bile
Exocrine secretion of the liver stored in the gallbladder.
Has alkali properties to help neutralise acid.
Produces bile salts to facilitate absorption of fats.
Acts as a vehicle for excreting blood cell components.
Bilirubin
Yellow-green bile pigment formed from the breakdown of haem in the spleen.
It is conjugated by hepatocytes and excreted as bile.
Urobilinogen
Brown bile pigment formed from converted conjugated bilirubin.
It is excreted through the kidneys.
Enterohepatic circulation
The recycling of bile acids from the ileum back into the liver.
After bile salts have been used for digestion, conjugated bile salts are completely reabsorbed
- In terminal ileum
- Returns to liver via hepatic portal vein.
25% of bile salts are also deconjugated by bacteria after being used for absorption in the ileum.
- Some returned to hepatic portal vein
- Some converted back to primary bile acids (mainly lithocholic acid) and lost in faeces
Bile acid-dependent fraction
Mechanism of bile secretion where bile acids are actively transported from the blood into bile canaliculi.
- Hepatic bile is only made when enough bile acid is present.
- Hepatocytes make bile acids from cholesterol and are conjugate them to form bile salts.
- In the intestines, some of the primary bile salts are converted to secondary bile salts by bacteria.
Acid-dependant secretion rate
This is dependent on the rate of bile salts returned via enterohepatic circulation.
Hyoerbilirubinea
Hepatic jaundice- accumulation of bilirubin the the blood.
- Caused by hepatitis or cirrhosis
Consequences:
- Impairs uptake by hepatocytes
- Impairs conjugation of bilirubin
Control of bile release
CCK: released from duodenal cells in response to FA and chyme.
- Stimulates peristalsis in gallbladder and relaxation of the sphincter of Oddi.
Vagus nerve: causes weak muscle contraction of gallbladder
Cholelithiasis
Gallstones
Can cause biliary colic: intermittent pain in right upper quadrant.
Can block ducts and lead to cholecystitis or pancreatitis.
Cholecystitis
Inflammation of the gallbladder.
Symptoms:
- Right upper quadrant abdominal pain.
- Nausea
- Vomitting
Caused mainly by the blockage of cystic duct by gallstones- prevents release of bile.
Risk factors:
- COCP
- Pregnancy
- Obesity
- Diabetes
Choledocholithiasis
Blockage of the common bile duct by gallstones.
Can lead to cholecystitis
Ascending cholangitis
Blockage of the common bile duct leading to infection of the bile duct.
Caused by bacteria ascending from the duodenum into the common bile duct when it is blocked.
