The colon moves contents through two types of movements: 1. Mixing or segmentation movements which cause the colonic wall to bulge and mix contents. 2. Propulsive or mass movements which push stool towards the rectum and initiate defecation. When stool enters the rectum, stretch receptors trigger a parasympathetic reflex that causes colon contractions and internal anal sphincter relaxation to initiate defecation.

1. Gastrointestinal physiology
Transport & mixing of food (Cont).
Dr.M.A.M.Shaikhani.

2. Colonic movements(Ms):
• 2 types:
• 1.Mixing or segmentation movements(SMs);
• Same as in SI .
• Large circular constriction contractions scattered along colon.
• Caused by the combined contraction of circular muscles (about
2.5 cms) & longitudinal muscle fibers( which are arranged into 3
longitudinal strips called (Tenae coli) cause the colonic wall to
bulge outside into baglike sacs causing the appearance of
haustrations .
• Help in mixing colonic contents & absorbing water & electrolytes
from the wall so concentrating it to semifluid, mush, semimush,
solid & finally hard food residues called stool.
• 2.Propulsive or mass Ms:
• · Forward Ms. Help to push stool towards the rectum & initiating
the defecation reflex.
• More abundant in the transverse & sigmoid colon, stimulated by
distention or irritation of colon.

3. HAUSTRAL CONTRACTIONS
Food
residue
Haustra

4. MASS MOVEMENTS
Food residue
Rectum

5. Defecation reflex:
· The rectum is usually empty.
· When the stool enters the rectum
· The sensation of its presence is transmitted to
the myenteric plexus & through
parasympathetic pelvic afferent nerves to the
spinal cord to initiate colonic contractions
through parasympathetic efferent nerves .
· External sphincter relaxation occur through
skeletal motor nerves starting defecation when
the situation is proper as there is higher centers
control from conscious cortex over the whole
defecation reflex.

7. Figure 24.25
The Defecation Reflex

8. Figure 24.25
Stretch
receptors
Sensory
neurone
Anal
sphincters
Parasympathetic
neurone
Somatic
neurone
DEFECATION
REFLEX
Rectum

9. Reflexes in the colon and rectum
Mass
movements+
+
Food in
stomach
Food
in
duodenum
Faeces
Defaecation reflex
Colon
rectum
anus
Ach
Spinalcord
IAS
EAS
FAECES
+
Distention
-
VIP
ATP
+
-
Pudendal
nerve

10. The Defecation Reflex: Summary
Removes undigested faeces from the body.
Stretch receptors in GIT wall detect distension of rectum.
Parasympathetic reflex causes contractions of the sigmoid colon &
rectum + relaxation of internal anal sphincter.
External anal sphincter (under voluntary control) consciously
relaxed if appropriate.

11. The peristaltic movement of the colon is called:
A. Constriction movement.
B. Segmentation movement.
C. Mass movements.
D. Propulsive movements.
E. Mixing movements.

12. Defectaion:
A. Is a reflex act.
B. Has no conscious control.
C. Is completely a reflex act in neoborns.
D. Involve autonomic & skeletal nerves.
E. Both Internal& external anal sphincters are involved.

13. Mixing colonic movements:
A. Cause colonic segmentation.
B. Lead to haustral appearing colon.
C. More distally than proximally.
D. Involve only longitudinal muscles.
E. Similar to those of small intestine.

14. Neurotransmitters that partcipate in defecation
inclde:
A. Gastrin.
B. Acetylcholine.
C. Vasoactive intestinal peptide.
D. Adenosine diphosphate.
E. CCK.

15. Secretary functions of GIT:
•Of 2 types:
•1.Enzymes helping digestion.
•2.Mucous for lubrication & protection of GIT mucosal surfaces
from excoriation.
• Anatomical types of secretary glands:
•1.Mucous glands: 2 types:
•a.single cell (goblet cells).
•b.complex cell mucous glands.
•2.Crypts of Liberkhan: deeper & contains specialized secretary
cells.
•3.Deep tubular glands in stomach & upper duodenum secreting
acid & pepsinogen.
•4.Complex glands like salivary ,pancreatic & hepatic glands.

16. 3Mechanisms of stimulation of GIT glands:
• 1.Local contact of food with GIT mucosal surfaces activating
enteric nervous system through:
• A.Chemical irritation.
• B. Tactile irritation.
• C.Distension.
• 2.Autonomic stimulation:
• Specially through the parasympathetics (vagi & other cranial
parasymp. Nerves) stimulating eso.,stomach,pancreas, Brunner
glands in duodenum & glands of distal colon,while secretion in the
remainder of SI & 1st
2/3 of large intestine(LI) is stimulated by
local myenteric nerves & hormones locally in each segment.
• The sympathetics also slightly increase the glandular secretion
but through vascular constriction reduces secretion as an overall
effect.

17. Secretion of saliva:
• Daily secretion is 1 liter in a rate of 0.5 ml/min.
during day & very little during sleep.
• It contain 2 major types of secretions:
• 1.Serous secretion containing ptyalin ,an alpha-
amylase for digesting starch.
• 2.Mucous secretion for lubrication.

18. Secretion of saliva:
• Salivary glands consist of acini & ducts ,in the
acini there is primary secretion of
ptyalin,mucous & extracellular fluid while in the
ducts there is K+ & HCO3- secretion & active
Na+ reabsorbtion & passive Cl- reabsorbtion,so
as a result there is high K+ & HCO3- & low Na+
& Cl- in the saliva.

19. Secretion of saliva:
Functions of saliva:
• 1.Digesting starch by ptyalin.
• 2.Maintaining oral hygiene /Preventing dental
caries, through:
• A.Washing away pathogenic bacteria & food
particles.
• B.it has bactericidal activity through its
thiocyanate , proteolytic enzymes as lysozyme &
protein antibodies contents.
• In sjogren syndrome when there is inflammation
of salivary /lacrimal glands there is dry
eyes/mouth with premature & severe dental
caries.

20. Nervous regulation of salivary secretion:
• Stemulation through parasympathetic NS(PNS) from
salivary nuclei located at the brain ponto-medulary
junction excited by taste(specially sour) & tactile
stimuli(as presence of smooth objects in mouth)& smell.
• Inhibited or stimulated by higher centers specially the
appetite center located close to PNS center in the
anterior hypothalamus which function in response to
signals from taste & smell areas of the cerebral cortex or
amygdala.
• Salivation also occurs in response to reflexes in the
stomach& upper intestine by the presence of irritating
food or nausea since saliva has diluting & acid
neutralizing effect.
.

21. Esophageal secretions:
No enzymes , only mucous secreted by simple &
complex mucous glands.

22. CONTROL OF SALIVARY SECRETION
cerebral cortex
salivary centre
in medulla
autonomic nerves
salivary glands
↑ salivary secretion
pressure receptors
and chemoreceptors
in the mouth
other inputs:smell& taste
centers
conditioned
reflex
simple
reflex

23. • Gastric secretions:
3 types of secretary glands
• 1.Oxyntic(parietal) glands :in the body & fundus of S ,80% of
Stomach glands ,secret Hcl,pepsinogen,intrinsic factor & small
amount of mucous .It contains 3 types of cells:
• a.Mucous neck cells secreting mucous.
• b.Peptic or chief cells secreting pepsinogen.
• c.Parietal or oxyntic cells secreting Hcl& intrinsic factor essential
for vitamin B12 absorption.
• 2.Pyeloric glands : in antrum ,secret mainly mucous & very
important hormone called Gastrin & small amounts of
pepsinogen .
• 3.Numerous mucous glands:between the above 2 main glands
• Secret large amounts of mucous which covers & protects the S
wall by a protective layer from digestion by acid-pepsin.

24. • Gastric secretions:
less important enzymes include
gastric lipase,amylase & gelatinase.

26. HCl
Gastrin
Histamine
Pepsinogen

27. Activation of pepsinogen to pepsin:
• Done by Hcl as it is inactive in an alkaline medium.
Regulation of gastric acid secretion:
• Stimulated by 3 hormones:ACH(PNS),gastrin & Histamine:
• 1.PNS (vagus) stimulation :secreting ACH which can be blocked
by anticholinergic drugs pirenzepen used for peptic ulcer(PU)
therapy.
• 2.Gastrin release from antral glands which can be blocked by
proglumide.
• 3.Histamine release stimulating H2 receptors which can be
blocked by H2 blockers as cimetidin(Tagamet).
• The 3 above hormones secret Hcl through activation of the proton
pump(H+-K+ ATPase)which is the final common pathway in acid
secretion which can be blocked by omperazole ,an effective
therapy for peptic ulceration & hyperacidity.

28. Figure 24.14
The Secretions of Hydrochloric Acid

30. GASTRIN
histamine
Parietal
cell
ECL cell
Chief cell
D-cell
somatostatin
-
+
noradrenaline,
CCK, VIP & CGRP
Ach
H+
-
+
+
Gland lumen
+
THE CONTROL OF ACID SECRETION

31. Acid inhibitory therapy
H2 receptor
antagonists
Histamine
Parietal cell
H2 receptor
H+
/K+
ATPase
(the proton
pump)
H+
K+
Proton pump
inhibitors
Peptic ulcer
reflux oesophagitis
“heart burn”
Tagamet,
Zantac,
Pepcid AC
Omeprazole
(Losec/Nexium)
Gastrin:
Proglumide
Vagus:
pirenzepine

32. Inhibition of gastric acid secretion:
By:
· 1.Acid feed back(FB) inhibition in the presence of excess acid
when the S (PH) becomes 3 or less.
In patients with (PU) this (FB) inhibition is abnormal so Hcl
continue to be secreted in spite of very high acid& low PH in the
stomach leading to PU.
· 2.Through the enterogastric reflex in the presence of excess
acid,fat & protein breakdown products,hyperosmolar fluid
,distention or any irritating factor in the upper SI which cause the
release of several inhibitory intestinal hormones as
secretin,CCK,Gastrin inhibitory peptide & somatostatin.
· 3.Interdigestive period: in this period between meals the S
secrets few mls. Of gastric juice containing little enzymes, more
mucous & moderate amounts of HCO3 called non-oxyntic type of
secretion .This interdigestive type of secretion may change with
high enzyme-acid content in patients with PU & those with
emotional upsets.

33. G. Phases of gastric secretion:
Consists of 3 phases;
1.cephalic phase :
· 1/5 of gastric secretion associated with eating a meal.
occurs before or while the food is eaten.It is stimulated
centrally.
2.Gastric phase:
· 2/3 of total acid secretion associated with eating a mael.
· Occurs when the food enters the S stimulated by long
vagovagal reflexes,local enteric & gastrin mechanisms.
3.Intestinal phase:
· acid secretion in response to presence of food in upper intestine
specially the duodenum
due to small amounts of gastrin released by duodenal mucosa in
response to distention & chemical irritation.

34. 1. CEPHALIC PHASE
Sight, smell or
thought of food
- Parasympathetic activation
of gastric motility & gastric juice secretion
Vagus
nerve

35. Food arrival causes
muscular reflexes &
gastrin secretion by
G cells.
Gastrin stimulates secretion from both chief &
parietal cells.
2. GASTRIC PHASE
Gastrin
GOGO
FOODFOOD

36. Arrival of food in duodenum
triggers release of hormones
that inhibit gastric motility &
secretions.
3. INTESTINAL PHASE
Circulation
Secretin &
Cholecystokinin (CCK)

37. 1. Taste sense.
2. Smell sense.
3. Appetite.
4. Gastric irritation.
5. Fear.
The following can stimulate saliva:

38. 1. Parasympathetic stimulation.
2. Sympathetic stimulation.
3. Gastrin.
4. CCK.
5. Somatostatin.
The following stimulate gastric acid secretion:

39. 1. Dental caries.
2. Dry mouth.
3. Impaired overall digestion.
4. Impaired carbohydrate digestion in the mouth.
5. Dysphagia.
Impaired salivary secretion can cause:

40. 1. Histamine receptors.
2. Gastrin receptors.
3. H-K ATPase receptors.
4. Ach receptors.
5. Sympathetic receptors.
The final common pathway in gastric acid secretion is:

41. 1. Gastric phase.
2. Cephalic phase.
3. Intestine phase.
4. Cephalic & intestinal phase.
5. None of the above.
Most of the gastric acid secretion occur in: