NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

GI SECRETIONS

Glands produce what they secrete. Production of secretions occur in the cells; they are stored in
secretory vesicles; stimulus leads to release of secretory substances.

Secretions include

1. Saliva

It is secreted by salivary glands found in the mouth. The salivary ducts open into the oral cavity.

Salivary secretions are characterised based on content; secretions with more proteins are serous
while those with less proteins are mucous. There are also sero-mucous secretions.

Salivary glands include;

a. Parotid glands: it is the largest of all the salivary glands. It produces 20-25% of salivary
secretions. It is innervated by glossopharyngeal nerve. Secretions are mainly serous. They
contains lots of enzyme ptyalin. Saliva secreted by parotid gland is emptied into oral cavity
via stensen’s duct. Parotid glands have zymogen granules.

b. Submandibular / submaxilla gland: it produces 70% of salivary secretions. It is innervated by

facial nerve. Secretions are mainly seromucous. Saliva secreted by this gland is emptied into
the oral cavity via Wharton’s duct. They have translucent granules

c. Sublingual glands: it produces 5% of salivary secretions. It is innervated by facial nerve.

Secretions are mainly mucous. Saliva secreted by this gland is emptied into the oral cavity by
Rivinus ducts.

Note: name of gland, percentage, innervation, type of secretion, duct (npisd is a mnemonic you can
use)

MECHANISM OF ANS IN DETERMINING SALIVA SECRETION

Initially, the sympathetic nervous system encourages salivary secretion. But, due to its
vasoconstrictive property, it inhibits salivary secretion.

The Glossopharyngeal nerve is therefore responsible for the parotid gland; while the facial nerve is
responsible for innervation of both submandibular gland and sublingual gland.
NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

COMPOSITION OF SALIVA

About 800-1500 mls of saliva is produced daily. At rest, 0.5 mls of saliva is produced per minute.

It is made up of organic and inorganic components.

Inorganic components; water(99%)

Ions: Major ions like Na+, K+, Cl-, CO 32-. Minor ions like PO42-, Ca2+

Organic components;

Enzymes

Ptyalin – alpha-amylase responsible for carbohydrate digestion. Optimum pH ideal for ptyaline
enzyme is 6.7.

Lingual lipase- produced by Epner’s gland. Helps with about 30% of lipid, fat digestion in the
mouth.

Other include; peroxidases, acid phosphatase, kallikrain. Note; initial saliva contains kallikrain.
Kallikrain encourages more saliva to be produced. Kallikrain contains bradykinin which stimulates
saliva secretion.

Mucin

It mixes with water to form mucous. The mucous helps with the following

1. Lubrication of food. 2. Saves oral cavity from excoriation or drying up. 3. Binds food particles
together for effective swallowing. 4. Mucous covering serves as a protective layer. 5. Mucin is
amphoteric and therefore helps with buffering of pH

Immunoglobulin (Ig)

Ig can be found on mucosal surfaces such as the mouth.

Lysoenzymes

They make use of water for hydrolysis. Work with thioganate to destroy invaders.

Lactoferrin

It binds to iron and it is bacteriostatic.

NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

Proline- rich proteins

They maintain the integrity of enamel.

Other organic components include urea, blood group antigens.

FUNCTIONS OF SALIVA

1. Swallowing
2. Keep mouth wet
3. Acts as solvent for molecules that stimulate taste buds
4. It maintains oral pH
5. Aids in speech
6. Keeps mouth clean
7. Neutralize gastric acid

MECHANISM OF SALIVA SECRETION

The initial saliva produced by acinar cells is called Primary Salivary secretion. It is an ultrafiltrate of
plasma and it has the same ionic concentration with ECF.

As saliva trickles down the duct, ductal modification occurs. Aldosterone plays a role in this
process.

There is reabsorption of Na+ by the ductal cells. There is also secretion of K+ into the lumen.

The reabsorption of Na+ by ductal cells happens more than K+ is expelled; this creates an
electronegativity of -70mV which draws Cl- into the cells.

HCO3 is also reabsorbed by the lumen.

The final saliva will have HCO3 and k+.

Regulation of salivary secretion

It is regulated by neuronal mechanism (ANS and PNS)

NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

Salivation

Salivation is a conditioned reflex.

Factors that encourage salivation

1. Food with sour taste

2. Smooth objects in the mouth
3. Smell, taste, sight, thought of flavoured food.

Disorders associated with salivation

Hypo-salivation: associated with dryness of mouth (xerostomia)

Causes include: Fear, fever dehydration, lesions of salivary gland.

It also occurs during Bell’s palsy which is associated with paralysis of facial nerve.

Hyper-salivation: associated with excess saliva secretion

Causes include: tooth decay, pregnancy, cerebral palsy, esophagitis and gastritis.

Oesophageal secretions

The proximal regions contain mucus-producing glands.

NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

GASTRIC SECRETIONS

Glands in the stomach include:

a. Gastric glands
b. Pyloric glands

GASTRIC GLANDS contribute to about 80% gastric secretion through oxyntic cells.

These are deep tubular-like glands. They are also called oxyntic glands.

Gastric glands consist of cells including:

a. Mucus neck cells

b. Oxyntic cells/ parietal cells
c. Peptic cells/ chief cells

Mucus neck cells: they produce mucus. Mucus produced is as thick as 1mm. it lines the stomach
preventing it from being destroyed by gastric acid.

Oxyntic cells: they produce HCl. They also produce Intrinsic Factor (IF). It contributes to about 80%
of HCl secretion. In a day, about 2-3L of HCL is secreted. On secretion, the pH is 0.8. Eventually, it
becomes 1-3.5. Oxyntic cells are found in the inner surface of stomach body and fundus. There are
receptors found on oxyntic cells; including muscarinic, histamine, gastrin receptors. Importance of
oxyntic cells: the IF produced helps in the reabsorption of cobalamin (vit b12) at the distal ileum.
Without cobalamin, red blood cells will not grow resulting in Pernicious anaemia.

NB: someone with stomach cancer who will have part of stomach removed cannot produce IF.

Peptic cells: produce pepsinogen (inactivated form of pepsin. NB: pepsin helps to digest collagen).
Pepsinogen forms pepsin in the presence of HCl. The pepsin breaks down proteins into peptides.
Pepsin is optimal at pH of 1.8-3.5. NB: at pH greater than 5, pepsin is inactivated.

PYLORIC GLANDS

They are found in the pyloric and antral regions of the stomach/ distal 20% of the stomach. It
controls 20% HCl secretion.

Nb: 1. It has both mucus neck cells and peptic cells. But the mucus neck cells are more in number.
That means it produces both mucus and pepsinogen.

2. It produces gastrin.
3. There are no oxyntic cells therefore it does not produce IF and HCl.
NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

COMPOSITION OF GASTRIC SECRETIONS

ORGANIC ONES INCLUDE;

a. Pepsin : begins protein digestion

b. Gelatinase : liquefies meat / digests gelatin found in meat.
c. Gastric lipase : breaks down fat in stomach
d. Gastric alpha-amylase: it has very little role to play. It is not very important.
e. IF
f. Mucus

DEFENCE MECHANISM FOR PROTECTIN STOMACH AGAINST GASTRIC ACID

1. Mucus layer
2. Surface membrane of mucus layer that seems impermeable to acid
3. Tight junctions that are impermeable to H+.

Nb: Prostaglandins increase mucus secretion

substances that destroy mucosal surfaces include:

a. NSAIDs (Non-Steroidal Anti-Inflammatory Drugs): they destroy the mechanism that allows
for production of prostaglandins
b. Ethanol
c. Vinegar
d. Aspirin
e. Helicobacter pylori infection ( this is always seen during peptic ulcer)

PEPTIC ULCER

It is a disease characterized by ulcer in the wall of the stomach and duodenum caused by digestive
action of HCl.

Recurrent Epigastric Pain: it is a burning pain that also radiates to the back. It is relieved by eating or
by vomiting. It is more common in blood group O+ persons.

Causes of peptic ulcer

1. Destruction of some mucosal barrier by some substances like NSAIDs, vinegar, bile salts.
2. Prolonged secretion of gastric acid: seen in Zollinger Ellison Syndrome

Treatment

1. Antibiotics eg clarithromycin, amoxicillin.

2. Enhancing mucosal defence with the use of Prostaglandins, sucralfate
3. Inhibiting acid secretion using antacids like gestid, gastol.
4. Proton-pump inhibitors eg omeprazole (act against H+/K+ ATPase)
5. Muscarinic blockers eg atropine (target Acetylcholine receptors)
6. Surgery by vagotomy and removal of gastrin secreting antral mucosa
NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

7. Histamine receptor antagonists eg cimetidine, ranitidine (they block histamine receptors of

oxyntic cells)

MECHANISM OF GASTRIC ACID SECRETION

(Draw diagram)

The process begins from within the oxyntic cells. First, water reacts with CO2 to form carbonic acid,
catalysed by carbonic anhrdrase.

The co2 enters the cell either by duffision or by metabolism of the cell.

The carbonic acid is dissociated to HCO3 and H+.

The H+ leave the cell into the ductal lumen through the H+/K+ ATPase located on the apical
membrane of the oxyntic cell.

The HCO3 is transported back into the ECF in exchange for Cl- with the help of HCO3/Cl- ATPase on
the basolateral membrane. This raises the pH of venous blood; alkaline tide.

Na+/K+ ATPase also helps to exchange Na for K.

The K+ and Cl- within the cell exit the cell into the ductal lumen via their respective ion channels.

There is now Cl-, Na+, H+, K+ in the lumen. HCl salt is formed. KCl and NaCl is formed in minute
amounts.

The increased osmotic pressure leads to water flow into the lumen thereby forming the gastric acid.

Functions of Gastric Acid

1. Helps kill bacteria

2. Helps to activated pepsin from pepsinogen
3. Increases flow of bile and pancreatic juice
4. Denatures proteins

Regulation of HCl Secretion

HCl secretion is regulated by both hormonal and neuronal mechanisms.

1. NEURONAL CONTROL: is via Enteric Nervous System and Peripheral Nervous system. The
PNS acts via the acetylcholine receptors on the oxyntic cells.

2. HORMONAL CONTROL: Gastrin stimulates enterochromaffin cells to release histamine.

Histamine binds to the histamine receptors of the oxyntic cells bringing about gastric acid

secretion. The gastrin is either G17 (the more abundant and has 17 amino acid) or G34.
NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

PHASES OF GASTRIC ACID SECRETION

1. Cephalic phase
2. Gastric phase
3. Intestinal phase

1. Cephalic phase: accounts for 20% gastric acid secretion. Sight, smell, thought of favourite
food stimulates gastric secretion. Emotional factors such as anger that increases gastric acid
secretion, fear and depression that decreases gastric acid secretion. Urogenic signals are
sent from the cerebral cortex via vagus nerve to stomach.

2. Gastric phase: contributes about 70% gastric secretions. Stimulus is presence of food in the
stomach. This phase is controlled by vagovagal reflex, myenteric reflex. It is also mediated
via gastrin hormone.

3. Intestinal phase: this accounts for 10% gastric acid secretion.

a. It is inhibitory
b. Stimulus is food in the intestine. It sends signals to the stomach to stop the production
of HCl.
c. Irritation and distension of intestine and the breakdown of products of protein
decreases gastric secretion through enterogastric reflex.
d. Hormones like secretin, CCK, VIP, GIP, somatostatin also decrease gastric acid secretion.
NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

PANCREATIC SECRETION

Pancreas has both endocrine and exocrine functions.

Exocrine: it contains acini that branch into ducts that empty into the ampulla of vater. The acini cells
are sites for production of pancreatic digestive enzyme. The ducts are responsible for production of
watery secretion containing HCO3-.

Endocrine: the pancreas is responsible for release of some hormones like somatostatin, insulin and
glucagon. They are produced by islet of Langerhans cells. The cells are made of A cells (that produce
glucagon), B cells (that produce insulin) and D cells (that produce somatostatin)

Components of pancreatic juice

About 0.5-1.5 L/day of pancreatic juice is produced. The pH is 8-9.

Organic components:

a. Pancreatic amylase: it hydrolyzes starch, glycogen and most carbohydrates to form

disaccharides. It doesn’t digest cellulose.
b. Trypsin, chymotrypsin and carboxypolypeptidase.
i. Trypsin which is the most abundant out of the three enzymes is produced in its
inactive form called trypsinogen. The inactive form of carboxypolypeptidase is
procarboxypolypeptidase; while that of chymotrypsin is chymotrypsinogen.
ii. CCk encourages the secretion of enterokinase from the brush border of small
intestine.
iii. Enterokinase activates trypsinogen to form trypsin.
iv. Trypsin stimulates the release of more trypsinogen and the activation of
procarboxypolypeptidase and chymotrypsin.
v. Only Carboxypolypeptidase can release individual amino acids.

c. Pancreatic lipase: hydrolyses neutral fats into 2 fatty acids and 2-Monoacylglycerol.
d. Cholesteryl esterase: hydrolyses cholesterol esters into cholesterol and fatty acids.
e. Phospholipase: splits fatty acids from phospholipids.
f. Elastase: it is activated from its inactive form; proelastase by trypsin. It digests elastic fibres
in meat.
g. Deoxyribonuclease: DNA breakdown
h. Ribonuclease: RNA breakdown
i. Procolipase: it is activated by trypsin to form colipase. It exposes the active site of pancreatic
lipase.

NB: the pancreas prevents self-digestion by making a specific inhibitor, a protein called pancreatic
trypsin inhibitor.

Inorganic components:

H2O
NTO UCHENNA OKORE’S NOTE (MBBS 024 CLASSREP)

Ions (HCO3-, Na+, Mg2+, Ca2+, K+, Cl-, SO42-, H2PO4)

SECRETION OF BICARBONATE IONS BY PANCREAS

The concentration of pancreas is about 145mEq/L which is 5times normal concentration of HCO3
plasma.

In the pancreatic ductal cell, there is reaction between water and CO2 under the influence of
carbonic anhydrase. Carbonic acid is formed and it dissociates to form HCO3 and H+.

The H+ leaves the cell through the Na+/H+ ATPase located at the basolateral membrane of the cell.
The H+ enters the blood vessel resulting in acidic tide.

HCO3 is pumped out alongside Na+ into the ductal lumen.

Copious amount of pancreatic juice rich in bicarbonate ion is formed.

It washes down the pancreatic enzymes into the larger ducts.

REGULATION OF PANCREATIC SECRETION

There are three basic stimuli;

a. Acetylcholine: released from PNS vagus nerve endings and from other cholinergic nerves in
the ENS.
b. Cholecystokinin: produced by I-cells of the duodenum and jejenum. Has 33 amino acids and
is secreted in response to presence of proteases, peptones and fatty acids in the duodenum.
It stimulates contraction of gall bladder.

Nb: ACH and CCK only affect pancreatic acini. That is, it only leads to production of digestive
enzyme that is very deficient in water

They act via phospholipase C to make acini cells discharge enzymes. (2 nd messenger system)

c. Secretin: has 27 amino acids. It is produced by S-cells of duodenum and jejenum. It is

secreted as prostatin. Stimulus is when HCl in acid chyme reaches the intestine.
Secretin stimulates ductal cells to release copious amount of pancreatic juice rich in
bicarbonate ions.
Secretin acts via cyclic AMP.
It also stimulates bile secretion.

Phases of pancreatic secretion.

1. Cephalic phase:
Nervous stimuli stimulates PNS. ACH is released, acini cells are stimulated to release
pancreatic enzyme. It is responsible for 20% of total pancreatic enzyme secretion. There
is little or no juice. It occurs when food is in the mouth.
2. Gastric phase:
Nervous stimuli stimulates the same effect as the cephalic phase. It is for 5-10% of
enzyme production. Occurs when food is in the stomach. There is little or no copious
juice.
3. Intestinal phase: responsible for 70% enzyme secretion. There is lots of copious juice
produced.