Unit

Digestive System
4
Physiological Anatomy of GIT (Fig. 4.1)
Pharynx Salivary Glands
Parotid

n
Oral Cavity Sublingual
Submandibular
Uvula

i
Tongue

a
Oesophagus

J
Liver
Stomach
Gallbladder

.
Pancreas
Pancreatic
Common duct
bile duct

K
Colon
Small Intestine

.
Transverse colon
Duodenum
Ascending colon Jejunum
Descending colon

A
Ileum
Caecum
Appendix
Rectum

Anus
Fig. 4.1 The digestive system
1. Length 10 m (30 feet).
2. Organisation (layers) of GIT outside to inwards: (Fig. 4.2)

Myenteric Mesentery
nerve plexus
(Auerbach’s
plexus) Serous layer (1)
Submucous Longitudinal
nerve plexus smooth muscle
(Meissner’s layer (2)
plexus)
Villi Circular smooth
Lymphatic Lumen muscle layer (3)
nodule
Submucous layer (4)

Muscularis mucosa (5)

Lamina propria (6)

Mucous layer
with glands
Brunner’s gland
Fig. 4.2 Cross-section of GIT, showing the different layers of its wall
2

3. Innervation (Enteric Nervous System: Little brain) – two divisions

(i) Intrinsic innervation (Fig. 4.3)
(a) Myenteric plexus (Auerbach’s plexus) – Motor
(b) Submucous plexus (Meissner’s plexus) – sensory

Enteric nervous system To ANS

and CNS
Myenteric plexus neurons

Interneuron

Submucosal

n
plexus

i
Sensory neuron
Motor Motor (function as chemo
neuron neuron and stretch receptors)

a
Longitudinal and circular
smooth muscle layers of Mucosal epithelium

J
the muscularis mucosa

Fig. 4.3 Organisation of the enteric nervous system

.
(ii) Extrinsic innervation
Parasympathetic (cholinergic) nerves Sympathetic (adrenergic) nerves

K
(i) ↑s motility and tone (i) ↓s motility and tone

.
(ii) Relaxation of sphincters (ii) Contraction of sphincters
(iii) ↑s secretions from the stomach and intestine (iii) Inhibit secretions
4. Structure of small intestine (Fig. 4.4)

A
(i) 20–40 villi/mm2; contain microvilli →↑s absorptive surface area.
(ii) Each villus contains:
(a) a lymph vessel (lacteal)
(b) an arteriole and venule; and
(c) a nerve net.
  4: Digestive System ❑ 3

Cell shedding Microvilli

Intestinal gland cell

Cell
Direction of cell
migration
migration
and
maturation

i n
Mucosa

a
Globet cell

Argentaffin (or
enterochromaffin) cell

J
Crypt of Lieberkuhn
(site of cell birth)

.
Paneth cell

Artery

K
Vein

.
Lymph vessel

Fig. 4.4 Arrangement of vascular supply in small intestine

A
(iii) Crypts of Lieberkuhn (intestinal glands)
(a) Show active mitosis → cell sloughing upto (30 g/day).
(b) Contain:
– Goblet cells → secrete mucus
–A rgentaffin (or enterochromaffin) cells → secretin and 5-HT
–P aneth cells → secrete defensins
(iv) Epithelial cells and paneth cells produce:
(a) digestive enzymes (for proteins, carbohydrates & fats)
(b) enterokinase – activates trypsinogen
(v) Brunner’s glands (in duodenum) → thick alkaline mucous secretion (to protect duodenal mucosa
from the gastric acid).
(vi) Jejunum i.e. upper 40%: maximum mucosa folding (plica circulares)
(vii) Ileum i.e. lower 60%: goblet cells are maximum; contains Peyer’s patches.
5. Structure of large intestine (colon)
(i) mucosal surface is smooth (no villi)
(ii) there are no plica circulares
(iii) abundant tubular glands and goblet cells
(iv) shows sacculation and haustra.
4

Salivary Secretion
Salivary Glands (Fig. 4.5)
% contribution to Parasympathetic
Type Histology
salivary secretion nerve supply via
1. Parotid Contains pure serous cells 25% IX nerve
2. Submandibular or submaxillary Serous: mucous cells : : 4:1 70% VII nerve
3. Sublingual Serous : mucous cells : : 1:4 5% VII nerve

i n
Parotid gland
Parotid duct

a
Submandibular
duct Sublingual duct
Submandibular Sublingual gland

J
gland

Fig. 4.5 Salivary glands

.
Serous versus mucous salivary gland

K
Serous cells Mucous cells

.
Forms a thin watery secretion containing ‘ptyalin’ Forms a viscous secretion containing ‘mucin’,
(“salivary α-amylase”) → digestion of starch to (lubricant for food and protecting the oral mucosa).
maltose.

A
Composition of Saliva
Daily secretion: 1500 mL/day.
Enzymes:
1. Ptyalin (salivary α-amylase)
2. Lysozymes (bactericidal)
3. Lingual lipase
Mucin
IgA: → local protection against bacteria and viruses.
Electrolytes – cations: Na+, K+, Ca2+;
Anions: Cl–, HCO3–
pH: 7.0 (resting states); 8.0 (during active states)

Functions of Saliva
1. Ptyalin (salivary α-amylase)
(i) digest starch to α-limiting dextrin and maltose (optimal action at pH 6.5)
(ii) readily inactivated at pH ≤ 4.0.
2. Mucin
(i) lubricates the food, facilitates swallowing
(ii) protects oral mucosa
(iii) aids speech
3. Serves as a solvent → activate taste buds.
4. Prevents dental caries (contains lysozymes, IgA and lactoferrin-bacteriostatic).
5. Maintains oral pH at 7.0 → protects tooth enamel.
  4: Digestive System ❑ 5

Note: Acidic oral pH → loss of calcium from the teeth.

Mechanism of salivary secretion (Fig. 4.6)

H 2O H 2O

secretion of a primary isotonic

NaCl NaCl

First secretory step:

fluid rich in NaCl

Acinar lumen

i n
NaCl Primary NaCl
H 2O isotonic
fluid H 2O
NaCl

a
NaCl
H 2O H 2O

J
NaCl

. secretion of K+ and HCO3

reabsorption of NaCl and
Second secretory step:
–
K+
–
HCO3
Ductal cells

NaCl

K
K+
–
HCO3

.
NaCl

A
Passive
Final hypotonic
Active
saliva
Fig. 4.6 Mechanism of salivary secretion ( Aquaporin-5)

Control of Salivary Secretion

1. Acinar cells →
(i) primary secretion (isotonic);
(ii) final salivary secretion hypotonic. (Rich in K+ and HCO3–)
160 Saliva Plasma
Na+ : 145

120
Concentration

Cl.– : 110
Na+ : 80-90
(mEq/L)

HCO3– : 27

80
HCO3– : >50
: 5

40
Cl.– : 50
K.+

K+ : 15-20
0
0 20 40 60 80 100

Secretory rate (mg/gm of gland/min)

Fig. 4.7 Effect of secretory rate on the electrolyte

composition of saliva
6

2. As salivary flow increases, Na+, Cl– and HCO3– concentration ↑s, K+ concentration ↓s → isotonic
final salivary secretion. (Fig. 4.7)
3. Stimulation of parasympathetic nerves → profuse watery saliva (Atropine ↓s salivary secretion).
4. Stimulation of sympathetic nerve → secretion of small amounts of saliva rich in organic constituents
and mucus.
5. Increases by:
(i) taste of food (inborn reflex)
(ii) by sight, smell or thought of food (psychic or conditioned reflex)
(iii) dry food
6. Aptyalism (xerostomia)

n
Causes: anxiety, fear, fever, duct obstruction
7. Sialorrhoea

i
Causes: pregnancy, tumour, VII CN damage
8. Aldosterone: ↑ [K+] and ↓ [Na+] of saliva.

a
In Addison’s disease → high salivary Na+/K+ ratio.

Mouth and Oesophagus

. J
Swallowing (Deglutition); Stages:
Stage I : Oral stage – voluntary stage.
Stage II : Pharyngeal stage – Involuntary (reflex) stage; duration: 1-2 secs.

K
Stage III : Oesophageal stage – Involuntary (reflex) stage; duration: 1-2 secs (for liquids) and 10 secs (for

.
dry food).

Oesophageal Sphincters

A
Upper oesophageal sphincter Lower oesophageal (cardiac) sphincter
1. Formed by: cricopharyngeal muscle (a true Formed by oesophagus walls in apposition.
sphincter)
2. Possesses high resting tone and is under vagus Possesses high resting tone and kept in close
control. position.
(i) relaxed by vagus; NO, VIP and secretin;
(ii) constricted by gastrin.
3. Function: Prevents swallowing of air during Prevents regurgitation of food, gastric juice and air.
respiration.

Types of oesophageal peristalsis

Primary Secondary
1. Initiated by: swallowing (when food passes 1. Presence of food within oesophagus.
into oesophagus)
2. Coordination by: vagal fibers 2. Intrinsic nervous system of oesophagus due to
stimulation of mechanical or irritant receptors.

Important Note: Each act of swallowing → arrest of respiration (deglutition apnoea).

Disorders of Swallowing
1. Deglutition reflex if abolished → regurgitation of food into the nose or aspiration of food into
larynx.
2. Aerophagia:
  4: Digestive System ❑ 7

3. Achalasia cardia: (Fig. 4.8)

Dilatation of proximal
segment of oesophagus

i n
a
Lower oesophageal
(cardiac) sphincter Stomach
constricted

J
Fig. 4.8 Achalasia cardia

.
4. Dysphagia
5. Incompetence of lower oesophageal sphincter → gastroesophageal reflex disease–GERD.

Stomach

K
Physiological Anatomy (Fig. 4.9)

.
1. Gastric mucous membrane: Contains 3 types of gastric glands.
A. Main gastric glands

A
(i) Chief (or peptic) cells→secrete pepsinogen.
Functions:
HCl (optimum
pH = 2)
(a) pepsinogen pepsin
  (inactive) (active)
(b) digests proteins to polypeptides (optimal pH < 4.0; gets inactivated at pH > 5.0)
(c) curdles milk
Oesophagus

Fundus
Cardia II. (cardiac tubular glands)
Pacemaker
soluble mucus cells

Body
Lesser curvature
Incisura angularis

1st part of
duodenum Greater
curvature
2nd part of
duodenum Pyloric canal Fundus and Body
Pyloric antrum I. (Main gastric glands)
Pylorus
(pyloric sphincter) 1. Parietal (oxyntic) cells
(i) HCl; (ii) I.F.
2. Chief (peptic) cells
III. Pyloric (Antral) glands pepsinogen
(i) G-cells gastrin 3. Surface epithelium
(ii) Soluble mucus visible mucus

Fg. 4.9 Structure of the stomach and function of types of glands (I, II & III) in it
8

(ii) Parietal (or oxyntic) cells → secrete HCl & IF

Functions of HCl
(a) Activates pepsinogen to pepsin
(b) Kills ingested bacteria.
(c) Converts Fe3+ → Fe2+
(iii) Mucus cells of surface epithelium → secrete visible mucus and HCO3–; → mucosal bicarbonate
barrier → prevent damage to the mucosa. (Fig. 4.10)

Mucous
layer
HCO3 HCO3

n
Mucosal surface-pH 7

i
Mucus
droplets
Mucous

a
cells

Interstitial Fluid
Capillary

J
Fig. 4.10 Mucosal bicarbonate barrier

.
B. Cardiac tubular glands: Secrete soluble mucus.
C. Pyloric (antral) glands:

K
(i) Contain G-cells → secrete gastrin.
(ii) Secrete soluble mucus.

.
Differences between visible and soluble mucus
Visible mucus Soluble mucus

A
(i) Secreted by: surface epithelium (i) Pyloric and cardiac tubular glands
(ii) A gel like substance, alkaline in nature (ii) A sticky secretion
(iii) Lubricates the food and prevents damage (iii) Lubricates the surface over which ‘chyme’ moves
to gastric mucosa by acid-pepsin digestion.

Gastrin
HCl or products of digestion
(i) Secreted as progastrin (inactive) gastrin (active).
(ii) Forms: G34, G17 (main form) and G14.
(iii) Functions
(a) Stimulate gastric acid and pepsin secretion.
(b) Stimulate the growth of mucosa of GIT.
(c) Stimulate gastric motility and gastric emptying.
(d) Contraction of gall bladder.
(iv) Gastrinoma: occur in stomach or duodenum or pancreatic tumour of δ-cells (Zollinger-Ellison
Syndrome) → secrete large amounts of gastrin →↑ HCl secretion → peptic ulcer.
(v) Factors affecting gastrin secretion
Increase Decrease
(i) Products of protein digestion. (i) Acid in the antrum.
(ii) Distension of pyloric antrum. (ii) GIT hormones: Secretin; GIP; VIP; glucagon
(iii) Increased vagal discharge → GRP. and calcitonin.
(iv) Ca2+ and epinephrine

2. Functions of the stomach

(i) Storage:
(ii) Digestion:
  4: Digestive System ❑ 9

(iii) HCl
(iv) IF → absorption of vitamin B12
(v) Controlled release of food
(vi) Secretes gastrin

Composition and Functions of Gastric Juice

Daily secretion: 2.5-3 L/day, isotonic.
pH: 1-2 (acidic).
Electrolytes: Cations (Na+, K+, H+, Mg2+);
Anions (Cl–, HCO3–, HPO42–, SO42–).

n
Enzymes
HCl

i
1. Pepsinogen pepsin
optimal pH = 2
(inactive)         (active)

a

2. Rennin (in infants) → curdles milk
3. Gastric lipase – weak fat splitting enzyme

J
4. Lysozymes: bactericidal
5. Carbonic anhydrase in small amounts.

.
Mucus: Soluble and visible.
Intrinsic factor

K
Water

.
Mechanism of HCl secretion (Fig. 4.11)
Interstitial fluid Gastric lumen
(plasma)

A
Basolateral
membrane
H 2O H 2O
Na+ Parietal
H 2O (oxyntic)
K+ cell
K+
Cell metabolism
CO2 + H2O K+

CA H+ HCl Secretion
  
H2CO3 into stomach
Cl.–
Apical
H+ Cl.– membrane
HCO3– HCO3 –
Canaliculus
Cl.–

Mucus neck
cell

Fig. 4.11 HCl secretion by parietal cells in the stomach. (H+ is secreted
into the lumen of the canaliculi in exchange for K+ by H+ – K+
ATPase, i.e. proton pump); CA: carbonic anhydrase
10

Regulation of HCl secretion (Fig. 4.12)

PGE2

Gi
Gastrin
Cyclic
AC G
AMP
ECL a
H2 s
ATP H+ t
GS Protein r
Histamine H+ – K+ ATPase
kinase i

n
K+
c
↑I/C

i
GR l
Gastrin free Ca2+
u
m
M3 e

a
Parietal
Acetyl (oxyntic) n
cell
choline

J
Stimulation

.
Inhibition

Fig. 4.12 Agents → Regulation of HCl secretion by the parietal cell and their mode of action
↓ by: PGE2 ↑ by: histamine, A-ch, gastrin;

K
(M3 : M3 muscarinic receptor; GR : gastrin receptor;

.
AC : adenylate cyclase; ECL : Enterochromaffin like cells;
Gs and Gi protien: ‘s’ and ‘i’ denotes stimulatory and inhibitory actions respectively)

A
Factors affecting HCl secretion: [(–): inhibition; (+): Stimulation]

⇒ (+) Antral gastrin (–) ⇐ Secretin;

Vagal stimulation
(–) Products of digestion GIP; VIP; glucagon;
⇓ (–) calcitonin
Distension of stomach
Ca2+; Epinephrine (+) ⇑

Parietal Cell
Histamine; A-ch ⇒ (+) Acid secretion (–) ⇐ PGE2

⇓ (–)
(+) ⇑
Acid entering The Duodenum

Notes:
1. Pure parietal cell secretion contain 0.17N HCl with pH 0.87.
2. After an overnight fast the basal acid output (BAO): 10 mEq of H+ per hour.
3. Maximal acid output (MAO): 25-27 mEq of H+ per hour. (after inj-histamine or gastrin)
4. MAO values:
(a) normal in healthy and patients with gastric ulcer,
(b) increase with duodenal ulcer.
5. Post-prandial alkaline tide, is associated with:
(a) alkaline urine
(b) slight depression of breathing.
  4: Digestive System ❑ 11

Regulation of Secretion of Gastric Juice

1. Nervous regulation: Vagus is secretomotor nerve to stomach → (vagal juice).
Mechanism
(i) release of GRP → ↑ gastrin secretion → ↑ acid secretion.
(ii) release of A-ch → ↑ acid and pepsinogen secretion.
2. Humoral regulation: Psychic stimuli, food in stomach → (+) vagus nerve → release of gastrin →
↑ gastric juice secretion.

Note: Nervous and humoral mechanisms are markedly synergistic.

Phases of gastric juice secretion (Fig. 4.13)

n
Cephalic Phase Gastric Phase Intestinal Phase

i
1. Cause: Psychic stimulation 1. Stretching of the receptors in stomach 1. It occurs when food
(called appetite juice). wall (mechanical stimulus), and products enters the duodenum.

a
of digestion (chemical stimulus).
2. Mediated by: Vagus. 2. ‘Local reflex’ responses and ‘gastrin’. 2. ‘Reflex’ and ‘hormonal
feedback’ effects from

J
small intestine.

.
3. Contribution to the total 3. 50-60%. 3. Much less.
secretion: 30–50%.

K
Sight
Smell
of food

.
Taste
Thought
1
Cephalic phase
(30–50%)

A
Vagus nerves
Food in stomach stimulates stimulate
secretion of hormone secretion of
gastric juice

Blood- GASTRIN
Secretin and
2 stream
GASTRIN cholecystokinin
Gastric in blood in blood reduce gastric 3
phase stimulates motility and secretion Intestinal
(50–60%) secretion of of gastric juice phase
gastric juice (10%)
Secretin and
cholecystokinin
Food in duodenum stimulates
secretion of hormones

Fig. 4.13 The three phases of secretion of gastric juice.

Gastric Motility (Fig. 4.14)

1. Peristaltic contractions coordinated by BER or gastric slow wave initiated by pacemaker cells; occur
every 3/min; most marked in the distal half of the stomach (called antral systole).
2. Factors affecting
Agents that stimulate Agents that inhibit
(i) gastrin (i) enterogastrone (i.e. CCK plus secretin)
(ii) histamine (ii) Ep.
(iii) A-ch, nicotine (iii) NE
(iv) barium (iv) atropine
(v) K+ (v) Ca2+
 12

–15 [A] [B]

Electrical
recording Spike potentials
(Membrane mV Acetylcholine Epinephrine
potential)
–50 BER

10 s
10 s
Mechanical
recording 1.5 g
(tension)

Fig. 4.14 Electrical (Basic electrical rhythm or gastric slow wave) and Mechanical response of GIT smooth muscle (A);
and effect of chemical agents on them (B).

n
Notes

i
1. Action potential fires when slow wave potential rises above threshold.
2. The force and duration of muscle contraction are directly related to the amplitude and frequency of action potential.

a
Gastric Emptying

J
(Duration: 2½ - 3 hours on a mixed diet)

.
1. Food in the stomach → (+) stretch receptors → (+) vasovagal reflex → receptive relaxation (to
accommodate 1–2 litres of food).
2. Begins as soon as chyme pass through the pylorus.

K
3. Directly proportional to force of gastric peristalsis.
4. Mechanism: Antrum pyloric region and duodenum all these three function as a unit.

.
5. Regurgitation from duodenum is prevented because:
(i) contraction duration of pyloric segment > duodenum
(ii) CCK-PZ and secretin → contraction of pyloric sphincter.

A
6. Factors affecting
Inhibited by Stimulated by
(i) Increase in amount of the chyme. (i) Small amount of chyme in the stomach.
(ii) Products of protein digestion and acid in the stomach (ii) Alkalinity.
(via neural mediated enterogastric reflex).
(iii) Hypo-osmolar chyme. → distension of duodenal (iii) Hyperosmolar chyme. → shrinkage of
osmoreceptors. duodenal osmoreceptors.
(iv) Fat and protein rich food. (iv) Carbohydrate rich food.
(v) CCK-PZ, secretin, fear. (v) Gastrin, excitement.

Note: Alcohol intoxication can be avoided after ingestion of fats.

Migrating Motor Complexes (MMC)

1. Modified pattern of electrical and motor activity in the smooth muscles of the GIT.
2. Migrate from the stomach to the distal ileum @ 5 cm/min during fasting.
3. Each cycle has 3 phases: (Fig. 4.15)
4. Completely inhibited by a meal and resumed 90–120 minutes after a meal.
5. Each MMC →↑ secretion of liver bile, gastric juice and pancreatic juice.
6. Significance: Help clear the GIT.
  4: Digestive System ❑ 13

III
Phases of MMC (a) (b) (c)
Phase I – No electrical spike Antrnum
potentials or mechanical
Duodenum
activity (no contractions)
Proximal jejunum
Phase II – Irregular electrical and Distal jejunum
mechanical activity Proximal ileum
II
Distal ileum
Phasae III – Regular electrical and
mechanical activity I 1 2 3
Hours
(A) (B)

Fig. 4.15 (A) Phases of migrating motor complexes (MMC);

(B) Pattern of MMC: (a) Phase-I (30–60 min); (b) Phase-II (20–40 min); (c) Phase-III (10–25 min)

i n
Gastric function tests
1. Fractional test meal

a
2. Histamine test
3. Augumented histamine test

J
4. Pentogastrin test
5. Insulin test

.
6. Barium meal
7. Blood and urine pepsinogen
8. IF secretion

. K
Applied:
Total Gastrectomy
1. Deficiency of I.F. → pernicious anaemia.

A
2. Protein digestion normal.
3. Iron deficiency anaemia
4. Rapid absorption of glucose → hyperglycemia → abrupt rise in insulin secretion → hypoglycemia.
5. Dumping Syndrome: Weakness, dizziness and sweating after meals:

Note: Bariatric surgery → loss of reservoir function of the stomach.

Peptic Ulcer (Fig. 4.16)

1. Definition:
2. Pathogenesis
(i) Mucosal-bicarbonate barrier disruption with bacteria Helicobacter pylori inf. or ↑ acid secretion.
(ii) Hypersecretion of gastric acid → ulcers of duodenum and pre-pyloric portion of the stomach.
(iii) ↑ sensitivity to gastrin.

Oesophagus

Lower oesophageal
sphincter

Duodenal ulcer
Stomach

Gastric
(or stomach)
Duodenum ulcer

Fig. 4.16 Peptic ulcer disease

14

Note: Increased pepsinogen I levels→↑gastric acid secretion→5 fold increase in incidence of peptic ulcer.

Pancreas
Physiological Anatomy (Fig. 4.17)
1. A double function organ containing both exocrine as well as endocrine cells.
2. Secretory acini and duct cells → perform exocrine function. (Fig. 4.18)

n
Liver
Hepatic duct

i
Cystic duct
Common bile

a
duct

J
Gall bladder

.
Duct of Santorini Pancreas
(accessory
pancreatic duct) Duct of Wirsung
(Major pancreatic
Sphincter of duct)

K
Oddi
Ampulla of
Duodenal papilla
Vater

.
Duodenum

Fig. 4.17 Pancreas and its structure

A
Intercalated
Acinar duct
cells
Centroacinar
cells
Nuclei

Fig. 4.18 Secretory acini and duct cells of pancreas

Composition and Functions of Pancreatic Juice

Daily secretion: 1200-1500 mL, isotonic.
– –
pH: 7.8-8.4; markedly alkaline (high HCO3 ) –[HCO3 ] increases and [Cl–] decreases with increase in
secretory rate (Fig. 4.19)
 ation: Na+, K+, Ca2+, Mg2+, Zn2+
Electrolytes: C
– 2– 2–
Anion: HCO3 , Cl–, SO4 , HPO4
  4: Digestive System ❑ 15

Pancreatic juice Plasma

160 Na+
Na+ 151.5

Concentration (mEq/L)
120 HCO3– Cl.– 110

80

40
HCO3– 26.0
Cl.–
K+ 5.38
K+
0

n
0 0.4 0.8 1.2 1.6 2.0
Secretary rate (mL/min) Electrolytes (mEq/L)

i
Fig. 41.9 Relation between the rate of secretion and electrolyte concentration
in the pancreatic juice

a
Enzymes:
1. Pancreatic α-amylase: Stable at pH 4-11; digests starch to maltose.

J
2. Pancreatic lipase: pH range of activity 7-9; hydrolyses neutral fats to glycerol and fatty acids.
3. Proteolytic enzymes

.
enterokinase and
(i) Trypsinogen trypsin (digests proteins to small polypeptides).
trypsin (autocatalyst)
(inactive)          (active);

K
trypsin
(ii) Chymotrypsinogen chymotrypsin (digests proteins to small polypeptides).

.
(inactive)      (active)
enterokinase
and trypsin
(iii) Procarboxypeptidase A and B carboxypeptidase A and B. (Converts polypeptides

A
to AA).
(iv) Ribonuclease and deoxyribonuclease, (split nucleic acids to nucleotides).
4. Trypsin inhibitor – protects the pancreas from autodigestion.

Regulation of Pancreatic Juice Secretion

A. Nervous regulation
1. Vagus nerve stimultion → release of A-ch → Enzyme rich viscous pancreatic juice secretion.
2. Amount of lipase increases with diet rich in fats; amylase with carbohydrate rich diet and trypsin
with protein rich diet.
3. Reflex stimulation of vagus nerve is seen with:
(i) Conditioned reflexes: Sight and smell of food
(ii) Unconditioned reflexes: Chewing and swallowing of food

B. Humoral regulation (Fig. 4.20)

1. Role of Secretin –

CCK-PZ
Acinar Enzyme rich
cell pancreatic juice

Duct Secretin Alkaline (HCO3– rich)

cells watery pancreatic juice

Fig. 4.20 Sites of action and effects of secretin and cholecytokinin-

pancreozymin (CCK-PZ) on pancreatic juice secretion
16

(i) Produced by: argentaffin cells in crypts of mucosa of duodenum and jejunum.
(ii) Secretion:
HCl and fatty acids
prosecretin secretin
(inactive)           (active).
(iii) Actions:
(a) Secrete alkaline watery pancreatic juice.
(b) Stimulates bile secretion and potentiates the effects of CCK-PZ on pancreas.
(c) Along with CCK-PZ → contraction of pyloric sphincter and delays gastric emptying.
(d) Feedback control
Secretion of secretin ⎯⎯→ secretion of alkaline
pancreatic juice in

n
duodenum

i
Inhibits Neutralizes the acid
from the stomach

a
2. Role of Cholecystokinin-Pancreozymin

J
(CCK-PZ)
(i) Produced by mucosal cells of duodenum and jejunum.

.
(ii) Actions
(a) Causes contraction of gall bladder → releases bile.
(b) Causes secretion of pancreatic juice rich in enzymes.

K
(c) ↑s secretion of enterokinase from duodenum.
(d) ↑s motility of small and large intestine.

.
(e) ↑s pancreas growth (trophic effect).
(iii) Positive feedback control
   Products of digestion (in small intestine)

A
  
stimulate
           increase ‘CCK-PZ’ secretion
  
      increase bile and pancreatic juice secretion

Note: Secretin and CCK-PZ, potentiates the action of each other.

Factors which increase secretin and CCK-PZ release

1. Acid in the duodenum.
2. Products of carbohydrates, fats and proteins digestion in small intestine.

Pancreatic Exocrine Function Tests

1. Estimation of serum amylase level: Normal: 50-120 units/L (↑s in acute pancreatitis).
2. Faecal fat excretion test
(i) Normal 5-6 g/day on diet containing 100 g of fat/day.
(ii) In pancreatic exocrine insufficiency ↑s to 40-50 g/day.
3. Secretin and CCK-PZ stimulation test (Fig. 4.21)
(i) With normal pancreatic functions
(a) Secretin → mainly ↑ [HCO3–]; and
(b) CCK-PZ → ↑ flow of pancreatic juice rich in enzymes.
(ii) Pancreatitis → pancreatic juice which is:
(a) low in volume
(b) low HCO3– levels, and
(c) normal or low enzyme levels.
  4: Digestive System ❑ 17

12 (Volume) 150 (HCO3–) 24

(Enzyme)

Concentration (mEq/L)
10 125

Amylase (µ/mL)
Flow (mL/min)
(—) Secretin
8 100 16
(---) CCK-PZ
6 75

4 50 8

2 2

0 0 0
0 20 40 60 80 0 20 40 60 80 0 20 40 60 80
Time (min) Time (min) Time (min)

n
Injection Injection Injection

i
Fig. 4.21 Effect of administration of secretin and CCK-PZ on the composition
and volume of the pancreatic juice in humans

a
Total Removal of Pancreas
1. Diabetes mellitus

J
2. Digestive disturbances
(i) Increase in faecal fat contents → steatorrhoea.

.
(ii) No abnormality of carbohydrate digestion and absorption.

Liver and Gall Bladder

. K
General
1. Hepatic blood flow: 1500 mL/min.: 2 0% by hepatic artery;
80% by portal vein.

A
2. Hepatic O2 consumption: 60 mL/min.
3. Mean pressure in hepatic and portal system
(i) hepatic arterial pressure : 100 mHg
(ii) portal vein pressure : 7 mmHg
(iii) hepatic vein pressure : 5 mmHg

Important Notes:
1. Resistance of blood flow through the liver is low.
2. 8 0% of the liver tissue can be removed → restoration of original liver mass
3. Liver efficiency ↓s when it is loaded with fats and ↑s when its stores of carbohydrates and proteins are
plentiful.

Functions of the Liver and Signs of Liver Insufficiency

Functions of the Liver Signs of Liver insufficiency (or damage)
I. Synthetic: Liver synthesizes
1. All plasma proteins (specially albumin) 1. Hypoproteinaemia → oedema.
2. Clotting factors: I, II, V, VII, IX and X. 2. Haemorrhagic disorders.
3. Enzymes: SGOT, SGPT and SICD. 3. Increase in concentration of these enzymes
4. Urea from ammonia. 4. (i) Blood urea ↓s (N: 20–40 mg/dL).
(ii) Blood ammonia ↑s (N: 20–80 µg/dL).
5. Cholesterol from active acetate. 5. S. cholesterol ↓s (N: 120–200 mg/dL).
18

Functions of the Liver Signs of Liver insufficiency (or damage)

II. Metabolic
1. On carbohydrate metabolism: synthesis, storage 1. Hypoglycemia → muscle weakness, tremors,
and release of glucose. slurred speech, convulsions and coma (Pre-
hepatic coma) → death.
2. On protein metabolism: Synthesizes plasma 2. Aminoaciduria
proteins, clotting factors, enzymes, urea and (Normal: S. amino acid level - 30–65 mg/dL).
lipoprotein
3. On fat metabolism: Synthesizes lipoproteins, 3. Fatty Liver (fat laden liver) → hepatomegaly;
fatty acids, cholesterol and phopholipids. ascites, portal hypertension; piles, oesophageal

n
varices.
III. Bile Secretion which helps in:

i
Activation of lipase; and emulsification of fats. Steatorrhoea; hepatic jaundice.
IV. D
 etoxification and protection against unwanted Foetid breath (like smell of a dead body)

a
substances.
V. Miscellaneous

J
1. Storage of glycogen, fat, protein, vit. (A and 1. Deficiency symptoms of these substances.
B12).

.
2. Hormone inactivation: cortisol, aldosterone, 2. Blood level of these hormones increases.
insulin, glucagon, testosterone and
thyroxine.

K
3. Site of formation and destruction of RBCs. 3. Anaemia.

.
The Bile
Liver bile Gall bladder bile

A
1. Colour Light golden yellow Almost black
2. Consistency Watery Thicker
3. pH 7.8-8.6 (isotonic) 7.0-7.4
4. Water 97% 89%
5. Solids 2-4% More; 10-12%
6. Bile salts/bile acids 120-180 mg/dL More by 5-6 times
7. Bile pigments 50 mg/dL More by 5-6 times
8. Cholesterol 60-170 mg/dL More by 5-6 times
9. Electrolytes
(i) Na+ and K+ Less More by 2 times
(ii) Cl– and HCO3 – More Less by 5-6 times
10. Daily secretion 500-1000 mL Gall bladder storage capacity : 60 mL

Bile Salts
1. Sodium and potassium salts of bile acids.
2. Liver → secretes primary bile acids (cholic acid & chenodeoxycholic acid) hich by colonic bacteria
form secondary bile acids (deoxycholic acid & lithocholic acid)
3. Of the total bile salts which enter the duodenum, 90-95% are reabsorbed actively from terminal ileum
in portal vein and return to the liver (Entero-hepatic circulation). (Fig. 4.22)
4. Normal rate of bile salts synthesis: 0.2-0.4 g/day with 3.5 g as the total pool of circulating bile salts.
The entire pool recycle twice per meal and 6-8 times/day.
5. Actions
(i) Hydrotropic action
(ii) Activates lipases in the intestine.
  4: Digestive System ❑ 19

Hepatic Bile salts

portal vein
Synthesis 5%
(0.2 gm/day)
Bile salts
(pool
Liver 3.5 gm)

Common
Cystic bile duct
duct
Portal
circulation
Gall (95% per
bladder day)

n
Duodenum

Bile salts
(0.2 gm/day)

a
Bile salts

i
J
Ileum

.
Small intestine

Bile salts 50%

lost in feces

K
Fig. 4.22 Entero-hepatic circulation of bile salts

.
Bile Pigments: Bilirubin and biliverdin
1. Formed from haem (after RBCs destruction in R-E system).

A
2. → golden yellow colour of liver bile.
3. Only excretory products; (no digestive function).

Functions of bile
1. Bile salts:
(i) digestion and absorption of fats.
(ii) absorption of fat soluble vitamins.
2. Neutralization of the acid chyme from the stomach.
3. Excretion of drugs and toxins.
4. Solubility of cholesterol.

Control of bile secretion

1. Nervous regulation: Vagal stimulation →↑ bile secretion.
Mechanism
(i) Contraction of gall bladder, and
(ii) Relaxation of sphincter of Oddi.
2. Humoral regulation
(i) Acid, products of carbohydrates, fats and protein digestion in stomach and small intestine → ↑
secretin and CCK-PZ from the duodenum → contraction of gall bladder → ↑ biliary secretion.
(ii) Choleretic: Increase biliary secretion from the liver e.g., bile salts and bile acids.
(iii) Cholagogues: Cause contraction of gall bladder by release of CCK-PZ from duodenum e.g., fatty
acids; acid in small intestine, products of protein digestion and Ca2+.
20

Functions of Gall Bladder

1. Storage of bile: Capacity: 60 mL.
2. Control of flow of bile following a meal.
3. Reduces the alkalinity of stored bile
4. Regulates equalization of pressure in biliary system.
5. Secretes mucin → makes the bile thick.
Cholecystectomy Features:
1. Fat indigestion.
2. Bile ducts become dilated.

n
3. Dribbling of bile in intestine → wastage of bile.

i
Gall Stones: (Cholelithiasis).
Causes:

a
1. Presence of abnormal substances in the bile.
2. Change in relative composition of the bile.

J
Types: (Fig. 4.23)
1. 85% cholesterol stones

.
(i) Normal: Bile cholesterol : bile salts : : 1 : 20 or 1 : 30; if falls below 1 : 13 → precipitation of cholesterol.
(ii) Radiolucent
2. 15% pigment stones: mainly of calcium bilirubinate; radiopaque.

K
(A) (B)

A . Fig. 4.23 Gall stones (A) Cholesterol and (B) pigment stones

Small Intestine
Intestinal Juice–Succus Entericus (secreted by Crypts of Lieberkuhn)
Composition and functions
Daily secretion : 3 litres
pH : 7.6
Water : 98.5%
Solids : 1.5%
(i) inorganic (cations and anions): 0.7%
(ii) organic (enzymes): 0.8%
Enzymes
1. Enterokinase (enteropeptidase) → activates trypsinogen.
2. Proteolytic enzymes: Erepsin; nucleotidase and nucleosidase.
3. Enzymes for splitting disaccharides into monosaccharides e.g., invertase (sucrose); maltase; lactase.
4. Intestinal lipase.
5. Cholesterol esterase: converts cholesterol esters to free cholesterol.
6. Alkaline phosphatase: converts organic phosphate to free phosphate.
  4: Digestive System ❑ 21

Control of secretion
1. Ingestion of meal → secretion of intestinal juice (markedly increased in the 3rd hour).
2. Mechanical stimulation (distension) via local myenteric reflex → ↑ volume and total enzymes.
3. Local irritants → increases the volume of the juice rich in mucus content.

Digestion in the Small Intestine

1. Carbohydrate digestion:
invertase (pH: 5-7)
(i) Sucrose Glucose & fructose
maltase (pH: 5.8-6.2)
(ii) Maltose 2 molecules of glucose

n
lactase (pH: 5.4-6.0)
(iii) Lactose Glucose & galactose

i
α-limiting
dextrinase
(iv) α-limiting dextrins dextrins, Glucose

a
Note: Low lactase levels → lactose intolence.

J
2. Fat digestion:

.
lipase lipase lipase
Fats Triglycerides Diglyceride Monoglyceride
FA FA
3. Protein digestion

K
Erepsin
(i) Peptones and polypeptides Amino

.
                    acids
nuclease
(ii) Nucleic acids nucleotides and

A
nucleotidase
nucleoside purines+pyrimidines
nucleosidase

Malabsorption Syndrome
Definition
Causes
1. Resection of small intestine.

Notes: Ileal resection → greater degree of malabsorption than the jejunum resection

2. Gastrocolic fistula
3. Sprue
4. Coeliac disease (or Gluten enteropathy)
(i) Congenital absence of enzyme gluten hydrolase → formation of gliadin from gluten
(ii) Gliadin → inflammatory allergic response → flattens microvilli.

Movements of Small Intestine (Fig. 4.24)

A. Rhythmic segmental (or pendular) movements

1. Appear at regular intervals involving a localised segment of 1-2 cm.
2. Concerned with:
(i) mixing function
(ii) churning action
3. Frequency of contractions: highest in the duodenum (12/min) and lowest in the ileum (9/min).
22

4. Controlled by pacemaker cells in the IInd part of duodenum

(i) frequency of contractions α frequency of BER of slow waves;
(ii) strength of contraction α to the frequency of spike generated by the slow waves;
(iii) slow wave amplitude:
(a) increased by GIT hormones e.g., gastrin, CCK-PZ and motilin;
(b) decreased by secretin and glucagon.
Peristalsis

Food

n
Ringlike

i
peristaltic
contractions
sweep food

a
along the GI
tract

J
Segmentation

K .
.
Circular muscles … until chyme is

A
contract, breaking thoroughly mixed
chyme into ever with digestive
smaller pieces… juices

Fig. 4.24 Movements of small intestine

B. Peristalsis (or wormicular movements)

1. A coordinated reaction in which a wave of contraction preceded (come before) by a wave of
relaxation which passes down a hollow viscus.
2. Polarity of the intestine or law of the gut.
3. Function: propel the intestinal contents towards ileocaecal valve (few cms per wave).
4. Usual stimulus for peristalsis is: distension → wave pass @ 2 to 25 cm/sec. Mechanism: Local
stretch → release 5HT → activate myenteric plexus (Myenteric reflex).

Notes:
1. A-ch and substance P → circular contraction above the point of stimulus; and
2. Nitric oxide, VIP and ATP → relaxation below the point of stimulus.

5. Role of extrinsic innervation:

(i) Strong emotion → activate vagus nerve → ↑ muscular contraction and ↑s the tone of small
intestine; and
(ii) Anger, fear and pain → activate sympathetic component → ↓s muscular contraction and ↓ s tone
of the small intestine.
  4: Digestive System ❑ 23

Applied
1. Peristaltic rush
2. Gastro-ileal reflex
3. Paralytic (or adynamic) ileus

Large Intestine (Colon)

Movements
A. Segmental (or haustration) contractions
Type I Type II

n
1. Small amplitude waves which occur @ 1. Larger waves, occur @ 1-2/min and last for

i
10‑12/ min and are of 5 sec duration. approx. 30 sec.
2. Aid mixing of contents. 2. Aid mixing and facilitate absorption.

a
B. Peristaltic contractions
Type III Type IV: Mass action contraction

J
1. Very small pressure waves of prolonged Simultaneous contractions occurring at the
duration. same time over a large portion of the colon →

.
2. Propel the contents towards the rectum. defecation.

Note: Distention of the stomach by the food initiates contraction of the rectum and frequently a desire to

K
defecate, called gastro colic reflex. Defecation after meals is the rule in children.

.
Transit time in the GIT (Fig. 4.25)

A Mouth
1 minute

Oesophagus
4–8 seconds

Stomach
2–4 hours

Hepatic flexure
6 hours
Splenic flexure
Small intestine 9 hours
3–5 hours
Pelvic colon
10 hours to
several days
Fig. 4.25 Transit time in GIT

Note: Emotional disturbances → via ANS → Irritable bowel syndrome (IBS)

may occur during periods of stress.
24

Hirschsprung’s Disease (Aganglionic Megacolon) (Fig. 4.26)

1. Commonly in children.

Normal Area affected by

sigmoid colon Hirschprung’s

n
and rectum disease

i
Fig. 4.26 Hirschprung’s disease (Inset: Clinical picture)

2. Causes:

a
(i) Congenital absence of ganglionic cells in both the plexuses (Myenteric and submucous) or
(ii) degeneration of Myenteric plexus.
3. Site of involvement: Usually colon and pelvic – rectal junction.

J
4. Child defecates only once every 3 weeks.

.
Beneficial effects of colonic bacterial flora (Fig. 4.27)
1. Synthesis of vitamin K, B-complex vitamins and folic acid.
2. Production of flatus (CO2, H2S, hydrogen & methane) In some persons, gas in the intestine →

K
cramps, borborygmi (rumbling noises) and abdominal discomfort.

.
3. Responsible for the acidic reactions of the stools (pH 5 to 7).
4. Forms indole and skatole → odour of the faeces.
5. Forms pigments from the bile pigments → brown colour of the stools.

A
6. Decreases plasma cholesterol and LDL levels.
Acts as immunomodulators

Produce nutrients e.g. B-group vitamins, Inhibit growth of harmful

folic acid, digestive enzymes bacteria and yeasts

Structural functions Lowers blood fats

Immune system development

Metabolic functions Improve mineral absorption

Control of epithelial cell differentiation
and proliferation

Restore normal intestinal flora Reduce food intolerances

Reduce liver toxins

Fig. 4.27 Beneficial effects of clonic bacteria

Note: At birth, colon is sterile but colonic bacterial flora becomes established early in life.

Dietary Fibers
1. Examples: Cellulose, hemicellulose, lignin, algal polysaccharides and pectic substances. In humans:
no appreciable digestion of these fibers.
  4: Digestive System ❑ 25

2. Physiological significance
(i) Stimulates intestinal peristalsis → prevents constipation.
(ii) Reducing meal (postprandial hyperglycemia).
(iii) Reduces blood cholesterol level; helps controlling obesity, atherosclerosis and DM.
(iv) Decreases the incidence of colon cancer

Absorption in the GIT

Absorption of carbohydrates
1. Main Site: Jejunum and upper ileum.

n
2. Process of absorption

i
(i) Simple diffusion
(ii) Active transport (Fig. 4.28) 2 steps
(a) Sodium-dependent glucose transporter-1 (SGLT-1)

a
(b) Glucose transporter-2 (GLUT-2)
Apical surface Basal surface

J
Intestinal Blood
lumen

.
Microvilli 2 K+

K
3 Na+
2 Na+

.
SGLT-1 Na+ K+
ATPase

Glucose
Glucose

A Na+ glucose symporter

(driven by high extracellular [Na+])
Glucose uniporter GLUT-2
(facilitates downhill efflux)

Fig. 4.28 Mechanism of glucose absorption across intestinal

epithelium (SGLT-1: Sodium dependent glucose transporter-1;
GLUT-2: Glucose transporter-2)

3. Rate of absorption: 120 g/hour.

4. Factors affecting glucose absorption from GIT
(i) Decrease. Causes:
(a) Abnormal mucous membrane (enteritis, coeliac disease);
(b) Intestinal hurry (diarrhoea, gastrocolic fistula);
(c) Adrenal cortex deficiency → ↓ Na+ concentration.
(ii) Increase cause: thyroxine.

Note: Insulin has no effect on absorption of glucose from the GIT.

5. Alimentary glycosuria

Absorption of Fats (Fig. 4.29)

1. Pancreatic electrolytes + monoglycerides + fatty acids + bile salts → Micelles (water soluble
complexes).
26

2. Micelles are passively absorbed along their concentration gradient in the ileum.
(i) Monoglycerides and fatty acids with >14C are re-esterified → triglycerides and then coated with
a layer of β-lipoprotein, cholesterol and phospholipids → chylomicrons (called esterified fatty
acids) → enter lymphatics and via thoracic duct → blood stream.

Bile salts Triglycerides (TG)

Triglycerides Fatty Acids (FAs)

Short chain FAs Long chain FAs

n
(< 12-14 C atoms) (> 14 C atoms)
Pancreatic
lipase uptake

i
Diglycerides FAs FAs

a
esterification

Monoglycerides

J
Fatty acids
Reabsorbed

.
from ileum
Micelles
Chylomicron
formation

. K
Chylomicrons FAs
in lymph

A
To portal vein
(A) (B) To lymphatics

Fig. 4.29 Intraluminal events during fat digestion and absorption (A); absorption of fat by intestinal mucosal cells (B)

(ii) Short chain fatty acids <12-14C atoms pass directly from mucosal cell into the villus blood
capillaries (as free fatty acids or non-esterified fatty acids – NEFA).
3. Absorption: Greatest in the upper part of small intestine; from the ileum.
4. On a moderate fat intake only 5-6% is excreted in stools.
5. Fat stores – It is stored in adipose tissues (white and brown).
White adipose tissue/White fat depot Brown adipose tissue/Brown fat depot
(i) Form 10–15% of body weight. (i) Makes up small percentage of total body fat.
(ii) Represents the biggest stores of energy in (ii) More abundant in infants between the
the body and helps in maintenance of NEFA scapulas, around the neck, behind sternum
concentration in the blood. and around the kidney; represents small
percentage of total body fat. (Fig. 4.30)

(iii) Oxygen consumption is low. (iii) High.

(iv) It is under hormonal control: growth (iv) Under rich sympathetic control.
hormone, insulin and catecholamines.
(v) Main role: maintenance of FFA concentration. (v) Responsible for heat production.
  4: Digestive System ❑ 27

Sympathetic nerve varicosity

Nor-epinephrine Adenylyl
cyclase

G-protein
β3-agrenergic
receptor cAMP
ATP

n
protein kinase C

i
Hormone sensitive lipase
Brown fat

a
cell Triglycerides Free fatty acids

Mitochondria

J
Heat
Fig. 4.30 The metabolism of a brown fat cell

.
(Activation of β3-adrenergic receptors on the cell surface leads to signal chain that results in an increased breakdown of triglycerides. These
are metabolized in the mitochondria to generate heat.) (Inset: Location of brown fat in infants)

K
Absorption of Amino-acids

.
1. Coupled to Na+ transport
2. Rapid in the duodenum and jejunum but slow in ileum.
3. Of the total proteins digested: 50% come from ingested food; 25% from digestive juices, and 25%

A
from desquamated mucosal cells.
4. Only 2-5% of the proteins in the small intestine escape digestion and absorption.
5. Proteins in stool come from bacterial and cellular debris.
6. Absorption decreases with age.
7. Absorption of foreign proteins from the GIT may → allergic symptoms (food allergy).

Overall Water Balance in the GIT (Fig. 4.31)

Total Input (9000 mL/day) Reabsorbed 8800 mL/day)
1. Ingested – 2000 mL 1. Jejunum >60% : 5500 mL
2. Endogenous secretion – 7000 mL 2. Ileum 20-25% : 2000 mL
(i) Salivary glands : 1500 mL 3. Colon 10-15% : 1300 mL
(ii) Stomach : 2500 mL
(iii) Bile : 750 mL
(iv) Pancreas : 750 mL
(v) Intestine : 1500 mL
Balance in stools, <5%: 200 mL/day.
28

Ingests Saliva
2000 mL/day 1500 mL/day

Gastric juice
2500 mL/day

n
Bile

i
750 mL/day
Small instestine
Pancreatic juice absorbs
750 mL/day 7500 mL/day

a
Intestinal secretions
1500 mL/day

J
Colon absorbs

.
1300 mL/day

Balance in stool
(< 5%) 200 mL/day

K
Fig. 4.31 The overall balance between secretion and absorption of

.
water in the GIT

GIT Hormones

A
1.Gastrin
2.CCK-PZ
3.Secretin
4.GIP: Gastric inhibitory polypeptide
(i) Produced by: duodenum and jejunum in response to glucose and fat.
(ii) Actions: inhibit gastric juice secretion and its motility.
5. VIP: Vasoactive intestinal peptide
(i) Released from jejunum in response to fatty meals.
(ii) Actions:
(a) +++↑s intestinal secretions of electrolytes and water;
(b) relaxes intestinal smooth muscles and sphincters;
(c) inhibits gastric acid secretion; and
(d) dilates peripheral blood vessels.
6. Glucagon
(i) Secreted by stomach, duodenum and α-pancreatic islet cells.
(ii) Plays important role in hyperglycemia of diabetes mellitus.
7. Motilin
(i) Secreted by stomach, duodenum and colon mucosa.
(ii) Actions:
(a) contraction of intestinal smooth muscles;
(b) regulates intestinal motility during inter-digestive phase.
8. Substance P
(i) Found in the endocrine cells and nerve cells in the GIT.
(ii) ↑s motility of small intestine.
  4: Digestive System ❑ 29

9. GRP: Gastrin releasing peptide

(i) Present in the vagal nerve endings that terminate on gastrin cells.
(ii) Act as a neurotransmitter → ↑ gastrin secretion.
10. Somatostatin (GHIH)
(i) Produced by δ-cells in the pancreatic islets and in GIT mucosa; secretion is increased by acid in
the stomach.
(ii) Actions:
(a) inhibits secretion of gastrin, VIP, GIP, secretin and motilin
(b) inhibits pancreatic juice secretion
(c) inhibits gastric acid secretion and motility

n
(d) inhibits gall bladder contraction

i
(e) inhibits absorption of glucose, amino acids and triglycerides.
11. Ghrelin

a
(i) Secreted by the stomach.
(ii) Controls food intake.
(iii) Secretion is increased by fasting and decreased after ingestion of food.

J
(iv) Stimulates GH secretion.

.
GIT Reflexes
1. Deglutition reflex

K
2. Receptive relaxation
3. Enterogastric reflex

.
4. Myenteric reflex
5. Gastroileal reflex

A
6. Gastrocolic reflex
7. Peristaltic rush