General Principles of Alimentary Tract Secretion
Anatomical Types of Glands (1) Single-cell mucous glands (2) Pits/crypts of Lieberkühn (3) Tubular gland
(4) Complex glands-
salivary glands, pancreas, and liver
Basic Mechanism of Secretion by Glandular Cells Stimulation of secretion by-
(1) Effect of Contact of Food with the Epithelium—Function of Enteric Nervous Stimuli.
(2) Autonomic Stimulation of Secretion
(3) Regulation of Glandular Secretion by Hormones
Secretion of Saliva
Saliva contains two major types of protein secretion:
(1) a serous secretion that contains ptyalin (an alfa-amylase), which is an enzyme for digesting starches,
(2) mucus secretion that contains mucin for lubricating and for surface protective purposes
.
ACINI
SALIVARY DUCT
Function of Saliva
(1) Flow of saliva itself helps wash away pathogenic bacteria as well as food particles
(2) Saliva contains several factors that destroy bacteria.
One of these is thiocyanate ions
another is several proteolytic enzymes—
most important, lysozyme—that
(a) attack the bacteria(IgA), (b) aid the thiocyanate
(c) digest food particles(Lingual lipase, alpha
amylase/Ptyln)
(3) Saliva often contains significant amounts of protein antibodies that can destroy oral
bacteria, including some that cause dental caries.
Patients with deficient salivation (xerostomia) have a higher than normal incidence of dental caries.
(4) Facilitates speech, increases taste of food,
helps in mastication & swallowing, in some
animals regulate temperature.
Regulation of salivary secretion by the parasympathetic nervous system
(B) Sympathetic stimulation (C)Reflex Secretion
APPLIED
(1) Xerostomia
(2) Sialorrhea
(3) Sialolithiasis
(4) Infections
Gastric Secretion
Structure of a gastric( oxyntic) gland from the fundus and body of the stomach
Oxyntic cells
Peptic
Enterochromaffin-like cells
Basic Mechanism of Hydrochloric Acid Secretion
Postulated mechanism for secretion of hydrochloric acid
Stimulation of Gastric Acid Secretion
Some of the proteins from meats or other protein-containing foods,
reach the antral end of the stomach, it have a special stimulatory effect on the gastrin cells in the pyloric glands to cause release of gastrin
gastrin goes rapidly to the ECL(enterochromaffin-like cells) cells in the body of the stomach, causing release of histamine directly into the deep oxyntic glands.
ECL cells can also be stimulated by-
(a) acetylcholine released from stomach vagal nerve endings and
(b) probably also by hormonal substances secreted by the enteric nervous system
Histamine then acts quickly to stimulate gastric hydrochloric acid secretion.
The rate of formation and secretion of hydrochloric acid by the parietal cells is directly related to the amount of histamine secreted by the ECL cells.
Regulation of Gastric acid & Pepsin secretion
SYNERGISM
Pareital cell receptor & Cell Modification
Phases of Gastric Secretion
(A) Cephalic Phase- normally accounts for about 20 percent of the gastric secretion. It results from the sight, smell, thought, or taste of food. Neurogenic signals originate in the cerebral cortex and in the appetite centers. They are transmitted the vagus nerves to the
stomach.
(B) Gastric Phase- Once food enters the stomach, it excites
(1) long vagovagal reflexes from the stomach to the brain and back to the stomach,
(2) local enteric reflexes, (3) the gastrin mechanism,
It accounts for about 70 per cent of the total gastric secretion associated with eating a meal.
(C)Intestinal Phase.- The presence of food particularly in the duodenum,will continue to cause stomach secretion of small
amounts of gastric juice, probably partly because of small amounts of gastrin released by the duodenal mucosa.
Phases of Gastric Secretion
Pancreatic Secretion
Pancreatic Digestive Enzymes
Pancreatic Digestive Enzymes
The most important of the pancreatic enzymes for digesting proteins are trypsin, chymotrypsin, and carboxypolypeptidase.
The pancreatic enzyme for digesting carbohydrates is pancreatic amylase.
The main enzymes for fat digestion are
(1) pancreatic lipase, which is capable of hydrolyzing neutral fat into fatty acids and monoglycerides
(2) cholesterol esterase, which causes hydrolysis of cholesterol esters
(3) phospholipase, which splits fatty acids from phospholipids.
**Secretion of Trypsin Inhibitor Prevents Digestion of the
Pancreas Itself.(APPLIED- ACUTE PANCREATITIS)
ACUTE PANCREATITIS
Trypsin activates phospholipase A2 enzyme which converts the Phosphatidylcholine in pancreatic ducts (PC, normal constituent of bile) into Lyso-PC which damages the cell membrane of pancreatic tissue.
Small amount of pancreatic enzymes leaks into circulation which further enhances in acute pancreatitis condition so plasma
Amylase or Lipase measurement is of
diagnostic values.
Secretion of Bicarbonate Ions by pancreatitis ductules
Cystic Fibrosis- Defect in CFTR-gene Chr 7 mutation- Decrease Cl channel, Decrease Cl entry into cell along Na & H2O, thick secretion- Pancreatic insufficiency(with Progressive Pulmonaty ds)
BASIC STIMULI CAUSES PANCREATIC SECRETION
(1) Vagal nerve- Ach
(2) Cholecystokinin- Fats & protein products (3) Secretin- Acid
PHASES OF SECRETION- (a) Cephalic- Vagal 5-10%
(b) Gastric- Vagal 5-10%
(c) Intestinal- Secretin, Cholecystokinin 80%
Regulation of Pancreatic Secretion
MULTIPLICATIVE EFFECTS OF DIFFERENT STIMULI
(PHOSPHOLIPASE C)
(C-AMP)
(PHOSPHOLIPASE C)
Conditioned reflex(Vagal)
LIVER SECRETION & GALLBLADDER EMPTYING
Composition of Bile
HUMAN BILE ACIDS
PRIMARY BILE ACIDS- Cholic acid, Chenodeoxycholic acid SECONDARY BILE ACIDS- Deoxycholic acid, Lithocholic acid, Ursodeoxycholic acid
PHYSICAL FORM OF BILE ACIDS
LIPIDS DIGESTION & PASSAGE TO INTESTINAL MUCOSA
CIRCULATION OF BILE ACIDS(ENTEROHEPATIC CIRCULATION)
Synthesis of bile acid from cholesterol- 1/ Bile acid conc. in hepatic portal blood Bile acid dependent secretion- Bile acid conc. in hepatic portal blood
BILE FLOW
HCO3- (active)
Cl- (c-AMP dependent Cl- channel
HCO3- (Na+/K+ ATPase, Na+/H+
exchanger,HCO3- transport system)
Bile salt,Cholesterol,Phospolipids,bilirubin (Bile salt-Na symport, Na+/K+ ATPase, bile acid carrier)
BILE SALT SECRETION
BILIRUBIN METABOLISM & EXCRETION
OATP,Organic anion transporter polypeptides
UDP-Glucuronyl transferase
MRP-2
Formation of gallstones
1) Bile stasis
2) Supersaturation of bile with cholesterol(B:L:C=10:3:1) 3) Mix of nucleation factor
Cholesterol stone Ca+ bilirubinate stone
Secretions of the Small Intestine
(A)Secretion of Mucus by Brunner’s Glands in the Duodenum- located in the wall of the first few
centimeters of the duodenum, mainly between the pylorus of the stomach and the papilla of Vater, in response to
(1) tactile or irritating stimuli on the duodenal mucosa;
(2) vagal stimulation,
(3) gastrointestinal hormones, especially secretin.
APPLIED- Brunner’s glands are inhibited by
sympathetic stimulation; therefore, such stimulation in very excitable persons is likely to leave the
duodenal bulb unprotected and is perhaps one of
the factors that cause of peptic ulcers.
(B) Secretion of Intestinal Digestive Juices by the Crypts of Lieberkühn
Digestive Enzymes in the Small Intestinal Secretion. The enterocytes of the mucosa, especially those that cover the villi, do
contain digestive enzymes that digest specific food substances. These enzymes are the following:
(1) several peptidases for splitting small peptides into amino acids,
(2) four enzymes— sucrase, maltase, isomaltase,and lactase—for splitting
disaccharides into monosaccharides, and (3) small amounts of intestinal lipase for splitting neutral fats into glycerol and fatty acids.