Physio git 5 & 6.
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Transcript of Physio git 5 & 6.
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Gastrointestinal physiology Transport & mixing of food (Cont).
Dr.M.A.M.Shaikhani.
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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.
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HAUSTRAL CONTRACTIONS
Foodresidue
Haustra
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MASS MOVEMENTS
Food residue
Rectum
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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.
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Figure 24.25
The Defecation Reflex
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Figure 24.25
Stretchreceptors
Sensoryneurone
Analsphincters
Parasympatheticneurone
Somaticneurone
DEFECATIONREFLEX
Rectum
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Reflexes in the colon and rectum
Mass movements+
+
Food in stomach
Food in
duodenum
Faeces
Defaecation reflex
Colonrectum
anus
Ach
Sp
inal co
rd
IAS
EAS
FAECES
+Distention
-
VIPATP
+
-Pudendal
nerve
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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.
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The peristaltic movement of the colon is called:
A. Constriction movement.B. Segmentation movement.C. Mass movements.D. Propulsive movements.E. Mixing movements.
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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.
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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.
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Neurotransmitters that partcipate in defecation inclde:
A. Gastrin.B. Acetylcholine.C. Vasoactive intestinal peptide.D. Adenosine diphosphate.E. CCK.
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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.
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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.
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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.
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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.
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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.
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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.
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Esophageal secretions:No enzymes , only mucous secreted by simple &
complex mucous glands.
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CONTROL OF SALIVARY SECRETION
cerebral cortex
salivary centrein medulla
autonomic nerves
salivary glands
salivary secretion
pressure receptorsand chemoreceptors
in the mouth
other inputs:smell& taste centers
conditionedreflex
simplereflex
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• 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.
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• Gastric secretions:
less important enzymes include gastric lipase,amylase & gelatinase.
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HCl
Gastrin
Histamine
Pepsinogen
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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.
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Figure 24.14
The Secretions of Hydrochloric Acid
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GASTRIN
histamine
Parietal cell
ECL cell
Chief cell
D-cell
somatostatin -
+
noradrenaline,
CCK, VIP & CGRP
Ach
H+
-
+
+
Gland lumen
+
THE CONTROL OF ACID SECRETION
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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
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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.
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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 duodenumdue to small amounts of gastrin released by duodenal mucosa in response to
distention & chemical irritation.
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1. CEPHALIC PHASE
Sight, smell orthought of food
- Parasympathetic activationof gastric motility & gastric juice secretion
Vagusnerve
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Food arrival causes muscular reflexes & gastrin secretion byG cells.
Gastrin stimulates secretion from both chief &parietal cells.
2. GASTRIC PHASE
Gastrin
GOGOFOODFOOD
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Arrival of food in duodenum triggers release of hormonesthat inhibit gastric motility &secretions.
3. INTESTINAL PHASE
Circulation
Secretin &Cholecystokinin (CCK)
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1. Taste sense.2. Smell sense.3. Appetite.4. Gastric irritation.5. Fear.
The following can stimulate saliva:
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1. Parasympathetic stimulation.2. Sympathetic stimulation.3. Gastrin.4. CCK.5. Somatostatin.
The following stimulate gastric acid secretion:
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1. Dental caries.2. Dry mouth.3. Impaired overall digestion.4. Impaired carbohydrate digestion in the mouth.5. Dysphagia.
Impaired salivary secretion can cause:
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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:
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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: