1. Dr. Shamanthakamani Narendran
MD (Pead), Ph.D. (Yoga Science)

2. SALIVA
 A clear, tasteless, odorless, slightly acid (pH
6.8) viscid fluid, consisting of the secretion
from the parotid, sublingual, and submandibular
salivary glands and the mucous glands of the
oral cavity.
 Its function is to keep the mucous membrane of
the mouth moist, to lubricate the food during
mastication, and, in a measure, to convert starch
into maltose, the latter action being effected by
a diastatic enzyme, ptyalin.

3. Composition of saliva
 Total amount = 1000 to 1500 mL/day.
 More after meals and relatively less during
sleep.
Under resting condition % of Total Output
Submandibular gland  70 .
Parotid gland  25 .
Sublingual gland  5 .
 The volume depends on the ability of salivary
glands to secrete water.
 Specific gravity 1.002 to 1.012
 pH slightly acidic 6.0 to 7.4

4. CONSTITUENTS OF SALIVA
Water
99.5%
Solids 0.5%Gases
CO2, O2, N2
Cellular
constituents
 Yeast cells
 Bacteria
 Protozoa
 Polymorphonuclear
leucocytes
 Desquamated
epithelial cells
Organic
0.3%
Inorganic 0.2%
 NaCl
 KCl
 CaCO3
 Calcium Phosphate
 Potassium thiocyanate
 Acidic & Alkaline sodium
phosphate

5.  It is the continuous secretion of saliva even
when there are no stimulating factors.
 This helps to keep the mucous membranes of
mouth and pharynx moist.
 This is possibly because of small amounts of
Acetylcholine being secreted continuously in
the glands.
Spontaneous secretion

6.  Conditioned or Acquired Reflex, Cephalic
phase – Stimulation of some special sense
organ other than taste, eg, smell, sight or
hearing or thinking about food.
 Unconditioned or Inherent reflex – in this,
food should be actually given or taken.
(1) Reflex from the mouth; chief place for the
normal unconditioned stimulus.
(2) Esophogo-salivary reflex; sensory stimulus
arise from esophagus.
Secretion due to stimulus

7.  Gastrointestinal Phase – It occurs when food
has been swallowed and reflexes originate in
the stomach & upper intestine especially when
irritating food is swallowed.
It is also seen in many irritating conditions of
stomach for instance, gastritis, gastric cancer,
etc.
Increased salivation before vomiting is a typical
example.

8. NOTE
 It is possible that stimulus for salivation may arise
in other viscera also. For instance, in pregnancy
increased salivation occurs. It is believed that the
sensory stimulus arises from distended uterus.
 As the food is chewed, the contraction of the
muscles of mastication help to push out the saliva
accumulated in the ducts and acini of the glands.
Mastication acts not as a real stimulus but through
its mechanical effect.
 Nausea & disagreeable substance also cause
salivary secretion.
 There is no hormonal regulation.

9. Preparation of food for swallowing
 Mucin acts as a good lubricant for swallowing.
 Mucin softens the mass of food.
 Saliva moistens the mouth and facilitates
chewing & mixing of food and thus in bolus
formation & deglutition.
Solvent actions
 Taste is a chemical sensation.
 Unless the substance be in solution the taste
buds cannot be stimulated.
 Saliva acts as a solvent.
Function of saliva

10. Antibacterial or cleansing action
 Constant flow of saliva removes bacteria from any area
where bacteria can grow.
 Saliva contains several factors that can destroy bacteria
like several proteolytic enzymes like lysozyme,
thiocyanate ions.
 Saliva often contains significant amount of protein
antibodies that can destroy oral bacteria including
those that cause dental caries.
Speech
 Moistening of lips and mucous membranes by saliva
aids in speech.
 Decrease in salivary secretion cause impairment of
speech.

11. Digestive function
Boiled starch
Amylase and M
altase
Breakdown of beta-1, 4
glucosidic linkages
Maltotriose and some glucose

12. Excretory function
 Many substances both organic and inorganic are
secreted to saliva.
 In diabetes mellitus, glucose is secreted.
 In Nephritis, urea is secreted
 Viruses of rabies and poliomyelitis
 Alkaloids like morphine and antibiotics
 Alcohol content of saliva has been used for
medicolegal purpose (alcohol test)
 Smoker’s saliva contain thiocyanates.

13. Regulation of water balance
 When liquid is lost from the body salivary glands are
subjected to dehydration effect. This arouses a sense of
thirst.
Helps in heat loss
 Frothing found in animals (dog, sheep, etc.)
Removes irritating factor
 Saliva helps to remove the irritating factor by diluting or
neutralising it. It thus prevents injury to mucous
membranes.
Applied
 Decrease or absence of salivary secretion  Xerostomia
 Excessive salivary secretion  Sialorrhea (seen in
patients with cancer of esophagus)

14. GASTRIC SECRETION,
GASTRIC ANALYSIS
 Gastric analysis measurement of pH and acid
output of stomach contents;
 Basal acid output can be determined by
collecting the overnight gastric secretion or by a
1-hr collection;
 Maximal acid output is determined following
injection of histamine;
 Output is measured by titration with a strong
base.

15. Composition of gastric secretion
 Volume = 1500 to 2000 mL/day (depending
upon diet)
 pH 0.5 to 1.5
 Gastric juice is Isotonic to blood

16. CONSTITUENTS OF GASTRIC JUICE
Water 99.45% Solids 0.55%
Organic 0.40%
 Pepsinogen (Pepsin I, II, III)
 Mucin
 Gelatinase, Urease, Carbonic
anhydrase
 Cathepsin, Gastricsin
 Gastric Renin
 Intrinsic factor
 Lysozyme
Inorganic 0.15%
 HCL
 NACL
 KCL
 CACL2
 Calcium Phosphate
 Magnesium Phosphate
 Bicarbonates

17. Function (in short)
 The enzyme pepsin, with HCL digests protein
upon the stage of peptone
 Renin coagulates caseinogen of milk
 Gastric lipase digests fat to some degree
 HCL acts as antiseptic and causes some
hydrolysis of all the foodstuffs
 Excretion  toxin, heavy metal, certain
alkaloids, etc.
Regulation of gastric secretion
 It is a coordinated neurohormonal control.

18. Cephalic phase
 There is reflex activity: Afferent formed by
sensory pathways arising from retina (sight),
tongue (taste), ear, etc. Efferent through vagus.
 Since food is actually present in mouth, the
gastric juice released in this phase is called
Psychic or Appetite juice.
 It reaches its peak within 1 hour & may persist
for 3 hours.
 The juice is highly acidic & rich in pepsin
 Appetite juice is abolished by Atropinization or
sectioning of vagi.

19. Gastric phase
 In this presence of food in the stomach causes
gastric secretion.
 It is brought about by
(1) Nervous stimulation
(2) GI Hormones (Gastrin)
 The gastric juice is released after a latent period
of 30-60 minutes, the response lasts for 2 hours.

20. Gastric glands
Nervous stimulation
Long reflex or vagovagal reflex
Presence of food in stomach
Mucous membrane of stomach is stimulated
Afferents go via the vagus
Medullary centre
Efferents come via vagus
Synapse in the intrinsic plexuses
Release of gastric juice
(Gastrin) G-cells
in pyloric glands

21. Gastric glands
Nervous stimulation
Short reflex or Intramural reflex
Distension of stomach by food
Mucous membrane of stomach is stimulated
Afferents go to internal plexus
Efferents from internal plexus
Release of gastric juice
Gastrin cells in
pyloric glands

22. Gastrin
 Produced by G-cells in the walls of the glands
 G-cells are flask shaped with a broad base
containing many gastric granules and a narrow
apex that reaches the surface. Microvilli project
from the apical end into the lumen.
Molecular forms of gastrin are
1. G17 or little gastrin containing 17 amino acid
residues
2. G37 or big gastrin containing 37 amino acid
residues
 G17 is more abundant but both are important.

23. All gastrins occur as
 Sulphated form (gastrin I)
 Non-sulphated form (gastrin II)
 Gastrin is inactivated in kidneys & small
intestine.

24. Action of gastrin
 Stimulation of gastric acid secretion rich in HCL
and pepsin.
 Stimulation of growth of gastric mucosa
 Insulin & Glucagon secretion only after a protein
meal.
 Increase GI Motility
 Contraction of gastroesophageal junction
 Increase release of
(a) Succus Entericus,
(b) Bicarbonates, enzymes in bile and
pancreatic juice.

25. Factors affecting gastrin secretion
Stimuli that increase secretion Stimuli that decrease
secretion
Luminal: Protein digestion product
Distension of Lumen
Luminal: Acid
Blood Borne: Calcium,
Epinephrine
Blood Borne:
Secretin, GIP, VIP,
Glucagon, Calcitonin
Neural: Vagovagal reflexes,
Intramural reflexes

26. Regulation of gastrin secretion
More gastrin secretion
More acid released in antrum
Acid feeds back to inhibit gastric secretion
(-ve Feedback)

27. Intestinal Phase
 Presence of gastric chyme in the upper part of
small intestine cause release of gastric juice
 Latent period in 2 to 3 hours. Lasts for 8 hours.
Accounts for less than 20% of total acid
secreted in the stomach.
 An intestinal hormone, Entro-oxyntin is
responsible for this phase.
Inter-Digestive Phase
 Even after prolonged fast, HCL is found in
gastric juice of man which occurs in an
intermittent fashion & cause is unknown.

28. Other factors
 Which increase secretion
(a) Hypoglycemia,
(b) Alcohol & caffeine.
 Which decrease secretion
(a) Emotions, fear, grief, panic.
(b) High level of [H+] in the pyloric antrum or proximal
duodenum.
(c) Presence of fat in duodenum
(d) Presence of hyperosmolar concentration in
duodenum.
(e) Hormones from intestine namely GIP,
Enteroglucagon, VIP, Secretin, Enterogastrone,

29. Clinical assessment of Gastric Secretion
[Gastric Analysis or Fractional Test Meal]
Procedure
 The subject is asked to take light diet previous
night & is called fasting next morning.
 Ryles tube is introduced upon the second mark.
 Fasting juice is collected, so as to completely
empty the stomach. Juice collected is placed in a
separate flask for analysis.
 Any one test meal is given. There are certain
standard test meals (a) 7% 50mL alcohol,
(b) 300mL oat meal gruel, (c) Dry toast with a
cup of tea.

30.  After giving a test meal, gastric samples are
collected every 15 minutes for 3 hours. Each
time about 10mL of the contents are aspirated.
Each sample is placed in a separate flask for
analysis.

31. Each sample is analysed as follow:
 Free acid: It is titrated with standard alkali (0.1
N NaOH) till pH 3.5 is obtained. Acidity is
expressed in clinical units in terms of number of
milliliters of standard alkali required to titrate
100 mL of gastric sample to pH 3.5.
 Total acid: Sample is further titrated with the
alkali till pH 8.5 is obtained. It is expressed in
clinical units as a amount of standard alkali
required to titrate 100mL of gastric sample to
pH 8.5.

32.  Combined acid: It includes chloride of HCL
Combined HCL Combined HCL inorganic chloride
etc.
 Strach & Sugar: Presence indicates that stomach is
not yet emptied.
 Bile: It regurgitates from duodenum. Presence
indicates that pyloric sphincter is open & the
stomach has started emptying.
 Blood: Presence in first one or two samples may be
due to injury caused during the passage of Ryles
tube, otherwise blood is not the normal constituent.
It’s presence in all the samples indicates that there is
hemorrhage which may be due to gastric ulcer or
gastric cancer.

33.  Lactic acid: It is product of fermentation &
therefore it is high when acid secretion is less
 Mucus: Normally, some amount is present.
Excess indicates that there is irritation of
stomach mucosa.
 Pepsin: Its presence indicates that peptic cells
are functional
 Tubeless gastric analysis: Cation exchange
resin is given by mouth. This is dissociated in
stomach by HCL. The liberated cations are
absorbed & are excreted in urine. The amount
of cations excreted in urine indicates the
amount of acid secreted.

34.  Insulin test: Instead of standard test meal, 7
units of insulin is injected subcutaneously. This
produces hypoglycemia, which stimulates
Vagus nerve & causes secretion of gastric juice.
 Secretion depends on integrity of Vagus nerve.
Therefore the test is done after vagotomy
operation which is done for treating peptic
ulcer, to judge whether all vagal fibers to the
stomach are cut or not.

35. PANCREATIC SECRETION
 An elongated lobulated retroperitoneal gland,
devoid of capsule, extending from the concavity
of the duodenum to the spleen;
 It consists of a flattened head (caput) within the
duodenal concavity, an elongated three-sided
body extending transversely across the
abdomen, and a tail in contact with the spleen.
 The gland secretes from its exocrine part
pancreatic juice that is discharged into the
intestine and from the its endocrine part the
internal secretions, insulin and glucagon.

36. Composition & function of pancreatic juice
 Daily output is about 2.5 liters.
 pH is alkaline 7.5 to 8.5
 Inorganic components are Na+, HCO3-, Cl-,
etc
 Organic components are the various digestive
enzymes
1. Proteolytic enzymes:
(a) Trypsinogen
(b) Chymotrypsinogen
(c) Procarboxypeptidase
(d) Proelastase.

37. 2. Amylolytic enzyme
(a) Pancreatic amylase
3. Lipolytic enzyme
(a) Pancreatic lipase
(b) Cholesterol esterase
(c) Phospholipase A & B
(d) Colipase
4. Nucleic acid splitting enzyme
(a) Ribonuclease
(b) Deoxyribonuclease.

38.  Trypsin Inhibitor: It is secreted by acinar
cells & prevents the activation of Trypsinogen
to Trypsin & thus prevents autodigestion of
pancreas.
 The enzymes are secreted into the second part
of duodenum in their inactive forms.
 When gastric chyme enters the duodenum, it
causes secretion of Enterokinase by duodenal
cells which converts trypsinogen to trypsin.

39. Blood Vessel Ductal Cell Lumen
Na+
Na+
Na+
K+
K+
Active
Transport K+
HCO3
-
Cl-
Cl-
Active
-
(CA – Carbonic Anhydrase)
H2O+CO2
CA
H+
+HCO3-
HCO3
-
ATPase
Na+
-K+
ATPase
Na+
-K+
Pump

40. HCO3
-
Cause
 Alkaline pH by neutralising the acidity of
gastric chyme thus activates pancreatic
enzymes.
 Stops the action of gastric pepsin.
Regulation :
1. Cephalic phase :
Thought, slight or smell of food  Centers in
the medulla via associated pathways in the brain
 Pancreas to release juice rich in enzymes 
Efferent via vagus.

41. 2. Gastric phase
Food in stomach  Distension of stomach 
Vagovagal reflex  Pancreatic secretion rich
in enzymes.
3. Intestinal phase
When food reaches the Intestine,
(a) The acidity of chyme cause secretion of
Secretin.
(b) Fatty acids & protein digestion products cause
secretion of Cholecystokinin (CCK-Pz)
These two hormones are absorbed & carried to
liver by portal circulation.

42. Applied physiology
 Acute pancreatitis
Block in one of pancreatic duct
Accumulation of enzymes in pancreas
Trypsin inhibitor efficacy lost
Accumulation of pancreatic enzyme in pancreas
Conversion of enzyme into active forms in pancreas
Autodigestion of pancreas.

43. Applied physiology
 Cystic fibrosis
Acini become fibrosed
No secretion of enzyme
Pancreatic insufficiency

44. Pancreatic sufficiency test
 Small fraction of Pancreatic enzymes enter the
blood either via lymphatics or directly.
 When there is a block in the pancreatic duct, the
enzymes in the acini are reabsorbed & their
blood concentration becomes higher.
 Serum Amylase Activity: 60 to 180 Somogyi
units.

45.  In Acute Pancreatitis, this value becomes 500
Somogyi units.
 Normal urine contains small traces of amylase
which rise in Acute Pancreatitis.
 Fecal fat content: In Pancreatic insufficiency.
Pancreatic lipase is absent. Triglycerides are not
broken down & therefore heavy amount of fat
in stool, ie, Steatorrhea.
 Normal action of CCK-Pz and Secretin is lost in
Pancreatitis.

46. BILE
The yellowish brown or green
fluid secreted by the liver and
discharged into the duodenum
where it aids in the
emulsification of fats, increases
peristalsis, and retards
putrefaction; contains sodium
glycocholate and sodium
taurocholate, cholesterol,
biliverdin and bilirubin, mucus,
fat, lecithin, and cells and
cellular debris.

47.  Bile from hepatocytes  hepatic ducts 
Liver Bile
 Bile evacuated from gallbladder and delivered
into the duodenum via common bile duct is
called Gall Bladder Bile.
 Daily output of bile is 0.5 to 1 litre.
 Osmolarity of bile is 300 millosmole/liter, ie,
same as of plasma & isotonic with blood.

48. Liver Bile Gallbladder Bile
1. Specific gravity 1.010 to 1.011 1.026 to 1.040
2. pH definitely
alkaline
8.0 to 8.6
slightly alkaline or
slightly acidic
6.8 to 7.6
3. Water 98% 89%
4. Organic constituents in gm%
a. Bile salts
b. Bilirubin
c. Cholesterol
d. Lecithin
e. Fatty acids
1.1
0.04
0.1
0.04
0.12
0.6
0.3
0.3 to 0.9
0.3
0.3 to 1.2

49. Liver Bile Gallbladder Bile
5. Inorganic constituents in mEq/lit
a. Na+
b. K+
c. HCO3
-
d. Cl-
e. Ca++
145
5
28
100
5
130
12
10
25
23

50. Bile acids via blood
stimulate
parenchymal
secretion
Vagal stimulation
causes weak
contraction of
gallbladder
Cholecystokinin via blood stream causes
1. Gallbladder contraction
2. Relaxation of sphincter of Oddi
Bile stored and
concentrated up to 15
times in gallbladder
Secretin via
blood stream
stimulates liver
ductal secretion

51. Most of the bile synthesized in hepatocytes are
recycled by means of Enterohepatic Circulation.
Bile enters the second part of duodenum through common bile
duct and proceeds downwards
For the upper small intestine  Bile is absorbed by diffusion
From ileum & upper colon  Bile is absorbed by active
transport.
Into portal venous  to liver sinusoids  picked up by
hepatocytes  into bile canaliculi  Bilary tree
Again to duodenum

52.  80-90% of bile salts are absorbed from the
small intestine.
 10-20% enter the colon & are converted to salts
of lithocholic acid & deoxycholic acid which
are excreted in stool.
 The total bile acid pool [3.5g] recycles via
Enterohepatic Circulation & the entire pool
recycles twice/meal and 6-8 times/day.

53. Bile acids
 Synthesized by the hepatocytes from cholesterol.
 2 types (a)Primary Bile acids  Cholic acid &
Chenodeoxycholic acid; (b)Secondary Bile acids
 Deoxycholic acid & Lithocholic acid
 Primary bile acids are converted bile acids by the
action of bacteria in ileum & colon by removal of
the hydroxyl group.
 Secondary bile acid reenters the portal circulation
and the liver & are again excreted via
Enterohepatic Circulation by liver as secondary
bile acid only.

54. Bile salts:
 Bile acids are conjugated with either taurine or
glycine and in our body these acids are present
either as sodium taurocholate or as sodium
glycocholate which are therefore known as bile
salts.
Micellar formation:
 When bile acid concentration reaches 2-5
millmoles/lit, bile salts tend to form Micelles
 The concentration of bile salts at which they
form micelles is called Critical Micellar
Concentration.

55.  Micelles are Amphipathic, ie, they have both
hydrophilic & hydrophobic parts.
 In a micelle, the bile salts are present like
spades of a bicycle while phospholipids
interdigitate.
 The hydrophilic polar side of the bile salts &
phospholipid are in the peripheral side while the
hydrophobic nonpolar ends are present in
central region.
 Such a micelle can carry cholesterol &
triglycerides which go to occupy central
region.

56.  Cholesterol & triglycerides are water insoluble
but when they are within the micelle they are
water soluble because micelle is water soluble.
Cholesterol
Bile salts
Phospholipid
Triglyceride

57. Bile Lipid : Bile acid + cholesterol
 Bile pigments: Bilirubin [Major] & Biliverdin
 Bilirubin formed from the hem portion of
hemoglobin.
 In the liver, bilirubin is conjugated with
glucuronic acid to form Bilirubin Glucuronide
& is secreted in the bile.

58. Control of bile secretion
 Bile acid dependent flow (BADF)
Bile formed in liver  Bile stored in
gallbladder  Gallbladder contracts  Bile
enters duodenum  80-90% bile salts
reabsorbed from small intestine  Carried to
liver through blood stream  Bile salts
stimulates liver  More bile formed  Bile
enters duodenum.
 Bile acid independent flow (BAIF)
Some flow of bile occurs from liver without the
effect of bile acid.

59.  Ductular secretion: Ductules of biliary tree
secrete H2O & HCO3
-
Amount of bile from common bile duct = BADF
+ BAIF + Ductular secretion
 Influence of foodstuff: Fats & proteins stimulate
bile secretion. Carbohydrate have no such effect.
 Secretin: Increases bile flow, so it is suggested
that Hepatocrinin may be a specific liver
hormone present in intestine released by the
action of food.
 It has been noted that bile secretion increases
about 1 hour after meal, remains high for about 2-
5 hours and then declines.

60. Function of bile
Bile is essential for life
 Digestion: Bile is essential for the complete
digestion of fats and to some extent of proteins
and carbohydrates. This action is due to the
presence of bile salts, which act in the following
ways. (a) By reducing surface tension, (b)
Activating action, & (c) Solvent action
 Absorption: bile helps in the absorption of
various substances. This is also due to presence
of bile salts. (a) Fats – (1) Hydrotropic action, (2)
Bile salts reduce the surface tension of the
absorbing epithelium; (b) Iron, calcium, & (c)
Vitamin A, D, E, & K

61.  Excretion. Certain substances are excreted
through bile, for instance (a) Some metals like
copper, zinc, mercury, etc., (b) Toxins, bacteria,
etc., (c) Bile pigments, (d) cholesterol and
lecithin are probably chief excretory products.
 Laxative action. Bile salts stimulate peristalsis.
When introduced directly into the colon it
stimulates peristalsis of these parts.
 Cholagogue action. Bile acts as its own
stimulant.
 Bile helps to maintain a suitable pH of the
duodenal contents and thus helps the action of all
enzymes.

62.  Lecithin and cholesterol, present in bile, also
help in some ways.
 Mucin of bile acts as a buffer and a lubricant.
 Regurgitation of bile in the stomach helps to
neutralize gastric acidity and thus prevents the
injurious effect of acids on gastric mucosa.
 From the above functions it is evident that bile
is important not only as digestive juice but also
for various other purposes.

63. GASTROINTESTINAL HORMONES
 They are hormonally active polypeptides that
play a role in regulation of gastrointestinal
secretion & motility.
 Few of these hormones act as neurotransmitters
in the intrinsic plexus of nerves of GIT.
 They are also found in the brain where they act
as neurotransmitters, hence they are called Gut
Brain Peptides.

64. Sources:
 The GI hormones are secreted by the APUD
cells.
 APUD cells (amine precursor uptake &
decarboxylation) mainly take up amine
precursor & decarboxylation them to give GI
hormones.
 APUD cells are of neural crest origin.
 Also found in hypothalamus, islets of
langerhans, lung, etc.

66. The GI hormones are:
 Gastrin
 Gastric Releasing
Peptide
 Glicentin
 Serotonin
 Somatostatin
 Bombesin
 Neurotensin
 Vasoactive Intestinal
Peptide (VIP)
 Gastric Inhibitory
Peptide (GIP)
 Glucagon
 Secretin
 Substance P
 Cholecystokinin-
Pancreozymin
(CCK-Pz)
 Motilin
 Opiod Peptides

67. Classification:
 Gastrin family  Primary members are
Gastrin & CCK-Pz.
 Secretin family  Primary members are
Secretin, Glucagon, Glicentin, VIP, GIP
1. Gastrin  Chemistry:
Macroheterogenic forms
34 Amino acids (G-24)
17 Amino acids (G-17)
14 Amino acids (G-14)
Microheterogenic forms
C-terminal tetrapeptide
N- terminal tetrapeptide
Sulphated & nonsulphated forms
Amidated & nonamidated forms
G17 is the principal form

68. 2. Cholecystokinin – Pancreozymin (CCK-Pz or
CCK)
Macroheterogenic forms
CCK-58 (58 amino acids)
CCK-39
CCK-33
CCK-12
CCK-8
C-terminal tetrapeptide
Microheterogenic forms
Sulphated form (7th
amino acid
residue is sulphated)
Amidated form (C-terminal
amidated)

69. Factors
 Luminal factors
 Positive feedback effect of bile and pancreatic
juice
 Secretin

70. DEGLUTITION
 Deglutition or swallowing is a complicated
mechanism, principally because most of the
time the pharynx subserves several other
functions besides swallowing & is converted
only for a few seconds at a time into a tract
from propulsion of food.

71.  Deglutition or swallowing: To pass anything
through the fauces, pharynx, and esophagus into
the stomach; to perform deglutition.

72. About 2400 swallows/day
 It is divided into 3 stages
Oral
 Voluntary
 It initiates swallowing
Pharyngeal
 Involuntary
 It involves passage of food from pharynx to esophagus
Esophageal
 Involuntary
 It promotes passage of food from the esophagus to
stomach

73. Nervous control of pharyngeal stage
Afferent
Ring of nerve plexus of pharyngeal opening with greatest
sensitivity in the tonsillar pillar via Trigeminal,
Glossopharyngeal, Vagus
Nucleus
 Tractus Solitarius
 Nucleus ambiguous
Efferent
To pharyngeal musculature & tongue via 5the, 9th
, 10th
,
12th
cranial nerves & even a few of superior cervical
nerves.

74.  The areas in the medulla & lower pons that
control swallowing or deglutition are
collectively called swallowing or deglutition
centers.
 Deglutition apnea is the inhibition of
respiration during act of deglutition in the
pharyngeal stage lasting for 1 or 2 seconds.
The centers of respiration & deglutition are
situated close by in the medulla. The
swallowing enter specifically inhibits the
respiratory center of medulla during this time,
halting respiration at any point in its cycle to
allow swallowing to proceed.

75. Receptive relaxation of stomach:
 As the food in the esophagus reaches the lower
end of esophagus due to the esophageal
peristaltic wave passing towards the stomach, a
wave of relaxation transmitted through
myenteric Inhibitory neurons precedes the
constriction.
 Furthermore, the entire stomach and to lesser
extent, even the duodenum becomes relaxed as
the wave of relaxation reaches the lower end of
esophagus and thus are prepared ahead of time
to receive the food propelled down the
esophagus during swallowing act.

76. Nervous control:
 Peristaltic waves are initiated by vagal reflexes
that are a part of the overall swallowing
mechanism.
 Lower Esophageal Sphincter (LOS):
 The lower end of esophagus, extending from
about 2 to 5 cm above its junction with the
stomach is thickened & functions as a LOS or
Gastroesophageal Sphincter.
 Physiologically, it remains tonically contracted in
contrast to the middle and upper part of
esophagus which normally remains completely
relaxed.

77.  When a peristaltic swallowing wave passes down
the esophagus, Receptive relaxation relaxes the
LOS ahead of peristaltic wave & allows easy
propulsion of swallowed food into stomach.
 The stomach contents are highly acidic & contain
many proteolytic enzymes.
 The esophageal mucosa, except in the lower 1/8th
of the esophagus is not capable of resisting for
long the digestive action or gastric secretion.
Fortunately, the tonic constriction of the LOS
helps to prevent significant reflux of stomach
contents into the esophagus except in abnormal
conditions.

81. Applied
 Achalasia cardia: Failure of LOS to relax or
dysphagia.
 Heartburn: Reflex of gastric contents into the
esophagus giving rise to burning sensation at
the lower end of esophagus.
 Belching: The voiding of gas or of a small
quantity of acid fluid from the stomach through
the mouth.
 Paralysis of muscle of Palate: Failure to seal
off the nasopharynx from the buccal cavity.

82. Methods of study
 Barium swallow [Rat-tail appearance of
Achalasia cardia].
 Intraluminal pressure measurement by balloons.
 Open tipped tubes  transducers.
 Esophagoscopy.

83. MOVEMENTS OF SMALL INTESTINE
The types of movements of small intestine are
 Mixing contraction or Segmentation contraction
 Propulsive or peristaltic contraction
 Pendulous contraction
 Movements of villi.

84. Mixing contraction
 When a portion of the small intestine becomes
distended with chyme, the stretch of the intestinal
wall elicits localized concentric or ring-like
contractions spaced at intervals along the intestine
 The segments between these contraction may be 1
cm in length
 Contracted part relaxes & the ballooned up relaxed
part forms a concentric contracted ring.
 Each time a new set of contraction develops at a
different point.
 Development & rate (frequency) of these
contractions is based on basic electric rhythm or
electrical changes in the intestinal muscles.

86. Mixing contraction - Functions
 It helps in digestion due to proper mixing of
food with enzymes of digestive juices
 In absorption due to constantly changing the
layer of fluid in contact with mucosa and
pressure
 In improvement of intestinal circulation
It is slightly propulsive in nature also and are
reflex response related to local myenteric
plexus.

87. Peristaltic contraction
 Peristalsis is described to be a composite wave,
consisting of a wave of relaxation followed by a
wave of constriction. It is a translatory
movement and travels down the gut in an aboral
direction.
 Bayliss & Starling or Law of Intestine or
Myentric Reflex.
 Peristaltic & rhythmic segmenting are present
simultaneously.
 Rush Wave or Peristaltic Rush.
 Gradient of rhythirsicity.

89. Peristaltic contraction - Causes
 Stimulation of vagus increases and that of
sympathetic inhibits peristalsis
 Vagotomy on the other hand decreases the
peristaltic activity only to a minor extent.
 The local nerve plexus (Auerbach’s plexus)
helps in coordination of peristaltic movement.
 Distention of the intestine, normally caused by
presence of food, movements due to a stretch
reflex – Myentric reflex
 Reflex inhibition of whole of the small
intestine may take place due to stretching of
lower part of small intestine.

90.  These inhibitions may be removed by stimulation
of splanchnic nerves.
 Presence of local nerve plexus are required for this
& the afferent receptors of which are present in the
mucous membrane of intestine.
 Liberation of 5-Hydroxytryptamine (Serotonin)
from the enterochromaffin cells is possible
mediator in this reflex action.
 Role of a basic polypeptide substance P as a
mediator has also been suggested.
 Role of endocrines: Pituitrin excites the
movements.
 Gastroileal reflex.

91. Peristaltic contraction - Functions
 Chief function is propagation of the food.
 Other functions are same as of segmentation
movement.

92. Pendular contraction
 2 important movement of intestine are mixing
and propulsions.
 End segment of intestine show side-to-side
movement called pendular movement
 They facilitate progress of chyme & also help in
mixing digestive juices with food and
increasing blood flow to intestine which enables
maximum absorption.

93. Movements of Villi
 Side-to-side movement – Help admixture &
absorption.
 Pumping movement – Help in increase flow of
blood and lymph
 Protecting action due to the contraction of
muscularis mucosa.

94. THE SMALL INTESTINE –
Evoked Movement & Evoked Digestive Process
Duodenum
 Evoked Movement: Non-propulsive
peristalsis (contraction with no preliminary
relaxation) and rhythmic segmenting
movements involve the circular muscle and are
regulated by the myenteric plexus. Pendular
(swaying) movements alternate with the above,
and involve the longitudinal muscle. These
movements thoroughly mix the chyme with
intestinal, pancreatic & hepatic secretions.

95. Duodenum
 Evoked Digestive Process: Secretion and
Breakdown. Food contacts mucous membranes
lining intestine, activating release of secretin +
cholesystokinin. These, along with vagal
activation, trigger release into duodenum of 1)
pancreatic enzymes via pancreatic duct; 2) bile
from gall bladder via hepatic duct. Breakdown
of protein, fat and carbohydrates into amino
acids, monosaccharides and fatty acids is
carried out.

96. Jejunum
 Evoked Movement: Propulsive peristalsis
(contraction preceded by relaxation) is
regulated by the myenteric plexus acting on
both circular and longitudinal muscle. This
moves the contents toward ileum.
 Evoked Digestive Process: Absorption.
Breakdown products are actively transported
from intestinal lumen to blood and lymph
vessels by epithelial cells in the luminal brush
border.

97. Ileum
 Evoked Movement: Propulsive peristalsis
same as above Reflex relaxation of the
ileocecal valve, contents pushed into cecum of
large intestine.
 Evoked Digestive Process: Absorption.
Similar, but less as chyme moves toward
cecum.
Remember: Ilium has fewer/lower plicae
circularis, and more/shorter vasa recta than does
jejunum.

98. GI WALL CROSS SECTION

99. Ileocecal valve & ileocecal sphincter
 Principal function of ileocecal valve is to
prevent back flow of fecal contents from the
colon into small intestine.
 The lips of the ileocecal valve protrude into the
lumen of the cecum and therefore are forcefully
closed when excess pressure builds up in cecum
& tries to push the cecal contents backward
against the lips.
 The valve usually can resist reverse pressure
50-60 cm of water.

100.  The wall of the ileum from several centimeters
immediately preceding the ileocecal valve has a
thickened muscular coat called the ileocecal
sphincter.
 This sphincter normally remains mildly constricted
and slows the emptying of ileal contents into
cecum except immediately after a meal, when a
gastroileal reflex intensifies the peristalsis in the
ileum.
 The resistance of emptying at the ileocecal valve
prolongs the stay of chyme in the ileum and
thereby facilitates absorption. Only about 1500 mm
of chyme empty into the cecum each day.

101. Feedback control of the ileocecal sphincter:
 Whenever cecum is distended, the contraction of
the ileocecal sphincter is intensified and heal
peristalsis inhibited which greatly delays emptying
of additional chyme from the ileum.
 Any irritant in the cecum delays emptying for
instance, an inflamed appendix can cause such
intense spasm of the ileocecal sphincter and
paralysis of the ileum that they block emptying of
the ileum.
 These reflexes are mediated both by the way of the
myenteric plexus in the gut wall itself and through
extrinsic nerves especially reflexes by way of the
prevertebral sympathetic ganglia.

102. GASTRIC EMPTYING
 Food entering stomach is a mixture of solids &
liquids but as it passes through pylorus, it is
liquid chyme.
 Gastric emptying depends on
(a) Balance between force & frequency of
gastric peristalsis.
(b) Pyloric resistance.

103. Factors influencing gastric emptying
 Distension of stomach
 Effects of composition of chyme
 Osmolarity of chyme
 Effect of fat
 Effect of acid
 Products of protein digestion
 Effect vagal stimulation
 Hormones

104. MASTICATION
 The process of chewing food in preparation for
deglutition and digestion; the act of grinding or
comminuting with the teeth.
 It is the rhythmic movement of the Jaws,
tongue, & lips when the food is in the mouth.
 It takes place at temperomandibular joint
 It is the first mechanical process to which the
food subjected to in its progress though the
GIT.
 Incisors for cutting, Molars for grinding

105. Chewing reflex
 The presence of bolus of food in mouth causes
reflex inhibition of muscles of mastication &
the lower jaw drops down.
 The initiates the stretch reflex of the jaw
muscles that leads to rebound contraction.
 This automatically leads to closure of teeth, but
it alos compresses the bolus of food against the
lining of mouth, which inhibits the jaw muscles
once again, allowing the jaw to drop & to
rebound.

106. Saliva: It assists in mastication as follows:
 By dissolving some of readily soluble food
components.
 By partly digesting starch in the food by action
of enzyme alpha-amylase (Ptyalin)
 It softens the mass of food
 By converting the bolus with mucus to make it
move about easily.

107. Muscles of mastication :
 Masseter, temporalis, medial & lateral
Pterygoids supplied by mandibular nerve.
 Buccinator supplied by facial nerve.
Centres of mastication :
 Areas of reticular formation
 Hypothalamus & Amygdaloid
 Lower part of postcentral gyrus.

108. Importance of mastication :
 It adds to the pleasure of eating tasty food and
gives a sense of contentment and satisfaction.
 Prolonged stimulation of taste sensation may
increase the secretion of digestive juices.
 Chewing of fruits & vegetables is important as
the cellulose covering around the nutrient part
must be broken before swallowing.

109.  Digestive enzyme act only on the surface area
& the rate of digestion highly depends on the
total surface area of food particles exposed to
the digestive secretion.
 The smaller size of food particles increase the
ease with which food is emptied from stomach
into the intestine.

110. FUNCTIONS OF LARGE INTESTINE
 Absorption of water & electrolytes and
important nutrient substances except fatty acid.
 Acts as a temporary storage space for waste
products of digestion.
 Acts as an incubator for various bacteria which
synthesize certain vitamins like Vit K & Vit B
complex & contribute to overall nutritional
status of individual.

111.  During its prolonged stay in colon, water is
absorbed from chyme so that 1000-1200 mL of
chyme which enters the cecum per day is
transformed to semisolid mass called feces
which is 150-200 mL/day
 Movements of large intestine are comparatively
slower and may be due to the poor development
of myenteric plexus and it is scanty extrinsic
innervation by vagus.

112.  Mucus in large intestine has – prevents
excoriation, provides adherent qualities for
holding fecal matter together, protects intestinal
wall from great amount of bacterial activity
occurring in feces, alkalinity of mucus secretion
provides a barrier to prevent acids formed deep
in feces from attacking intestinal wall.
 Secretion of water & electrolytes in response to
irritation.
 Absorption of sodium

113. THE LARGE INTESTINE –
Evoked Movement & Function
Cecum
 Evoked Movement: Pulls valve edges
together, closing it.
 Function: Contents prevented from reflux into
ileum.

114. Ascending, transverse, and descending colon
 Evoked Movement: Rhythmic, segmenting
movements (under control of myenteric plexus and
circular muscle) are weak due to low intrinsic and
extrinsic (vagal & pelvic splanhnic) innervation.
Peristaltic movements are strong, under control of
myenteric plexus; the longitudinal muscle (=teniae
coli), shortens and widens the colon; and the
circular muscle pushes the colonic contents
caudally.
 Function: Contents exposed to mucosal surface,
and water is reabsorbed, leaving the waste products
of digestion. Empty the contents of one section into
the next.

115. Rectum
 Evoked Movement: Involuntary reflex.
Stretching causes opening (i.e. inhibition) of the
internal anal sphincter (circular smooth
muscle). Autonomic innervation (via
parasympathetic preganglionics of the sacral
cord, and postganglionics of the myenteric
plexus) aids inhibition.
Voluntary control. Somatic motor neurons in
the sacral cord inhibit contraction of the
external anal sphincter (striated muscle) via the
pudendal nerves.

116.  Function: Fecal contents accumulate, gradually
raising pressure on the external anal sphincter.
Fecal contents expelled.

117. DEFECATION

118. BASAL METABOLIC RATE
 Oxygen utilization of an individual during
minimal physiologic activity while awake; an
obsolete test determined by measuring oxygen
consumption of a fasting subject at complete
bodily and mental rest and a room temperature
of 20°C.
 Energy, in terms of heat, produced as a by-
product of total cellular metabolism is essential
for the maintenance of life of the organism.

119.  The amount of energy, required for any
individual varies directly with the degree of
activity and environmental condition, but the
rate of energy production in an individual by
it’s overall cellular metabolism is more or less
constant under some standard condition known
as Basal Metabolism.
 The rate of its energy production at basal
condition per hour & per sq. meter of body
surface area is known as Basal Metabolic
Rate.

120. The basal conditions
 The person should be awake but at complete
rest, both physical & mental.
 The person should remain in normal condition
of environment, ie, at normal temp, pressure,
humidity.
 The person should be without food at least for
12-18 hours, ie, in the postabsorptive state.
 The person should be without food at least for
12-18 hours, ie, in the postabsorptive state.

121.  The BMR may be defined as the amount of heat
given out by a subject who, though awake, is
lying in a state of maximum physical & mental
rest under comfortable physical & mental rest
under comfortable conditions of temperature,
pressure, & humidity, 12-18 hours
(postabsorptive) after meal.
 BMR is expressed as the heat production per sq
metre of body surface per hour.
 In adult male – normal BMR = 40
calories/m2
/hr.
 In adult female – normal BMR = 37
calories/m2
/hr.

122. BMR Determination
 Direct calorimetry.
 Indirect calorimetry.
 Benedict-Roth Spirometer (only BMR)
 Douglas Bag (BMR & Metabolic Rate)

123. Measurement
 Measure the oxygen consumption of the subject
using Benedict-Roth apparatus.
 O2 consumption per hour is determined & it is
then multiplied with 4.825 cal to obtain the heat
production per hour. Obtained value is then
divided by the surface area – of the person, to
get the final result.
 BMR 
Total heat production / hour
Body surface area (m2
)

124.  Comparing the BMR of the subject with that of
normal person is expressed as % Difference =
Difference in BMR x 100 / Normal BMR
Reads formula: Bedside method
 BMR = 0.75 [PR + 0.74 x 99] –72
 PR = Pulse Rate, PP = Pulse Pressure

125. Factor affecting BMR
 Surface area & BMR are inversely related.
 Age: BMR is low in newborn; but it is higher in
small children and is maximum at 5-6 yrs. It then
gradually decreases with age advancement
 Sex:BMR of males is higher than females of same
built & age.
 Season: BMR decreases in summer months, but
increases in winter.
 Racial variations of BMR are also observed.
 Sleep: BMR decreases by 10-15% in sleep.
 Drugs: Caffeine, benzedrine, etc. increase the
BMR. The reverse in observed by anesthetics.

126.  Hormones: Thyroid hormone, growth hormone.
Epinephrine etc. increase BMR of many tissues
of our body.
 Habit: Trained athletes and manual workers have
a slightly higher BMR than persons leading a
sedentary life.
 Diet: Prolonged undernutrition lowers the
metabolic rate.
 Pregnancy: BMR of pregnant woman is the
sumtotal of her own metabolism as in her non-
pregnant state & combined with that of the fetus.
 Body temperature: BMR increases by about
12% with the rise of 10
C [such as fever]

127. Conditions increasing BMR
 Hyperthyroidism
 Fever
 Cardiorenal disease with dyspnea [25-50%]
 Leukemia [21-80%]
 Polycythemia [10-40%], etc.

128. Conditions decreasing BMR
 Starvation & undernutrition
 Hypothyroidism
 Addition’s disease
 Lipid nephrosis, etc.
Importance of nothing BMR
 For prescribing a diet of adequate caloric value.
 For the diagnosis of various pathological
conditions specially in hypothyroidism &
hyperthyroidism.
 To note the effect of different types of food & drug
on BMR.

129. BALANCED DIET
 A diet is the kinds of food on which a person or
group lives.
 A balanced diet is defined as one which
contains variety of foods in such quantities and
proportions that the need for energy, amino
acids, vitamins, minerals, fats, carbohydrates,
and other nutrients is adequately met for
maintaining health, vitality and general well
being and also makes a small provision for
extra nutrients to withstand short duration of
leanness.

130.  The dietary pattern varies widely in different
parts of the world.
 It is generally developed around the kinds of
good produced depending upon the climatic
conditions of the region, economic capacity,
religion, customs, taboos, tastes and habits of
the people.

131. Nutrients Main functions
Carbohydrates Energy
Fats Energy
Proteins Energy
Protection against infection
Growth and repair
Minerals &
Water
Growth repair
Regulation of tissue infection
Vitamins Protection against infection
Regulation of tissue function

132. Dietary goals recommended by WHO are as below
 Dietary fat should be limited to approximately 20-
30% of total daily intake.
 Saturated fats should contribute no more than
10% of the total energy intake. Unsaturated
vegetable oils should be substituted for remaining
fat requirement.
 Protein should constitute approximately 15-20% of
the daily intake.
 Carbohydrates rich in natural fibre should
constitute the remaining food energy. Excessive
consumption of refined carbohydrates should be
avoided.

133.  Sources rich in energy such as fats and alcohol
should be restricted.
 Salt intake should be reduced to an average of
not more than 5 g per day.
 Junk foods such as colas, ketchups and other
foods that supply empty calories should be
reduced.
 The diet should be adapted to special needs of
growth, pregnancy, lactation, physical activity,
medical disorders (eg. Diabetes)

134. The dietary sources of energy are
 Proteins  4 kcal/g
 Fats  9 kcal/g
 Carbohydrates  4 kcal/g
Broadly the total energy requirement of an
individual is made up of 3 components
 Energy required for Basal Metabolism
 Energy required for daily activities – walking,
sitting, standing, dressing. Etc.
 Energy expenditure for occupational work –
light work, moderate work, heavy work.

135. Nutritional problems in public health
 Low birth weight
 Protein energy malnutrition. Clinical forms –
Kwashiorkor and Marasmus
 Vitamin deficiencies – Xerophthalmia (dry eye)
refers to all the ocular manifestations of vitamin
A deficiency
 Nutritional anemia
 Iodine deficiency disorders
 Endemic fluorosis seen in many parts of world
where drinking water contains excessive
amounts of fluorine (3-5 mg/l)

136. Nutritional factors important in selected diseases
 Cardiovascular disease
 Diabetes
 Obesity
 Cancer
Conclusion
 A balanced Diet has become an accepted means
to safeguard a population from nutritional
deficiencies.