REVISION FOR GASTROINTESTINAL PHYSIOLOGY AP Dr Swe Swe Win Basic goal of GIT regulation is to provide optimal condition for

efficient digestion and maximal absorption of nutrients.

SUMMARY OF MOTILITY (M), SECRETION (S), DIGESTION (D), ABSORPTION (A) & OTHER FUNCTIONS (OF) IN DIFFERENT REGIONS OF GIT
ORAL CAVITY & OESOPHAGUS M- chewing, swallowing (peristalsis), S- saliva, mucus, lipase, amylase, salt, water D-carbohydrates (polysaccharides), fats (minimal) A- drugs (antiangina) OF- lubrication, moistens

STOMACH M- receptive relaxation, gastric slow waves (BER), peristaltic mixing & propulsion, regulate emptying of dissolved food small intestine S- Hcl, intrinsic factor (oxyntic cell), pepsinogen, gastric lipase (cheif cells) mucus & HCO3 (surface musus cells) gastrin (Gcells) histamine (ECl cells) somatostatin (Dcells) serotonin (gastric S cells) D- Proteins (pepsin), fat (gastric lipase), CH (salivary amylase (pH inhibition) A- lipid soluble substances e.g alcohol, asprin OF- storage, dissolve, sterilization (kill bacteria), protect surface epithelial cells, conversion of ferric ferrous, slow emptying into duodenum proper time for digestion & absorption by small intestine.

SMALL INTESTINE M- mixing ad propulsion mainly Electrical- small bowel slow waves, migrating motor complexes Mechanical- peristalsis - segmentation contraction tonic contraction - movement of villi movement of ileocaecal valve - peristaltic rush S- enzymes, HCO3 and salt & water, mucus (goblet cells) - enzymes (pancreas) - bile, HCO3 (liver) - secretin (duodenal S cells) - CCK (lining cells of duodenum) - GIP (duo. & jejunum mucosal cells) - motilin (duo. & jejunum mucosal M cells) - VIP (jejunum) - substance P (endothelial cells of GI) - gastrin release peptide (GRP) wide spread distribution D- carbohydrates, fat, polypeptides, nucleic acids A- peptides by active transport - amino acids, glucose & fructose by secondary actve transport - fats by simple diffusion - water by osmosis - ions, minerals & vitamins by active transport OF- maintains fluidity of intestinal content - lubrication, neutralize HCl entering small intestine - hydrolytic function- aqueous component of succus entericus provide water & thus help in all hydrolytic of enzyme reactions of digestion of various food particles.

LARGE INTESTINE M- segmental mixing, mass movement for propulsion S- mucus (goblet cells) D- none (except by bacteria) A- ions, water, minerals, vitamins, small organic molecules produced by bacteria, salts, glucose alcohol, drugs (anaesthetic agents, sedatives, steroids) OFstorage& concentration of ingested matter. lubrication, synthesis & absorb folic acid, vitamin B12, vitamin K by bacteria flora excretion of heavy metal (mercury), lead, bismuth, arsenic. defecation

1. INNERVATIONS OF GIT Purpose- motility - secretion i. Autonomic nervous system extrinsic NS (extrinsic regulation). Afferent- carry sensory from chemoreceptors, mechenoreceptors in GIT spinal cord, brain stem. Efferent- carry information from spinal cord, brain stem GIT Parasympathetic o GI motility & secretion o through vagus & pelvic nerves o preganglionic fibers enteric nervous system Sympathetic o GI motility & secretion o postganglionic nerves GIT Enteric nervous system (ENS) intrinsic NS known as little brain. regulation is by negative feedback control by release of a variety of GI hormones. Myenteric (Auerbachs) plexus Submucous (meissners) plexus Along entire length of gut. Located in submucosa between lies between longi & circular layers of ms circular muscle & muscularis mucosa provides motor innervations to 2 ms layers Best developed in submucosa Present in striated ms portion of oesophagus-Innervates glandular epithelium,muscularis mucosa, submucosal blood vessels, intestinal endocrine cells.

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2. SPHINCTERS Some are tonically contracted to close off the GIT from outside world & to keep materials from passing freely from one section of the tract to another. They are or selective retention of solutes / chime in specific sites to promote optimal digestion & absorption. i. Upper oesophageal sphincter o True sphincter o Formed by cricopharyngeal muscle (striated) o Prevent entry of air into oesophagus during normal respiration. ii. Lower oesophageal sphincter o also known as cardiac sphincter. o situated at distal 2 cm of oesophagus o is a functional/ physiological sphincter. o principle function is to prevents regurgitation of gastric contents into oesophagus when the intragastric pressure is markedly raised (after a heavy meal or ingestion of carbonated drinks) , the resistance of LES is overcome and air escapes into the mouth (belching). o gastrin increases the tone of LES. Pyloric sphincter o separates storage component of GIT (stomach) from the digestive and absorptive components (small & large intestine) duodenum. o regulated gastric emptying and prevents duodenal-gastric reflux. o secretin, CCK causes contraction delay gastric emptying. Ileocaecal sphincter o separates ileum from caecum. o regulates ileal flow into the colon. o distension of ileum relaxation of sphincter o distension of colon contraction of sphincter o under control of vagus, sympathetic, ENS. Sphincter of Oddi o regulates the movements of contents of the common bile duct into the duodenum. Internal & external anal sphincters o Internal is formed by both the longitudinal & circular smooth muscle . o under involuntary control. o External sphincter (contain striated muscle), under both voluntary & involuntary control.

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MOTILITY 1. Motility moves food from mouth to anus and mechanically mixes food. 2. GI smooth muscles are composed of single unit smooth muscle (with the exception of pharynx, upper 1/3 oesophagus, external anal sphincter- all of which are striated muscle)and electrically connected by gap junction. 3. Different regions exhibit different types of contraction. Some segments are tonically contracted but others exhibit phasic contraction. 4. Phasic contractions occur in oesophagus, gastric antrum, small intestine which contract & relax periodically. 5. Tonic contraction occurs in sphincters. 6. Intestinal muscles exhibit spontaneous slow wave potentials. When slow wave reaches threshold, it fires action potential & contract. 7. Slow waves originate in the interstitial cells of Cajal. 8. Between meals, migrationg motor complex (MMC) moves food remnants from upper GIT to lower regions (house-keeping). 9. Peristaltic contractions are progressive waves of contraction. Peristalsis is mediated by the ENS and altered by hormones, paracrine signals, meuropeptides. 10. Segmental contractions are primarily mixing contractions. 11. Depolarisation of circular muscle leads to contraction of ring of smooth muscle diameter of that segment. 12. Depolarisation of longitudinal muscle leads to contraction in longitudinal direction length of that segment.

PERISTALTIC CONTRACTIONS create forward movement stimuluswhen the wall is stretched (the response is called myogenic reflex. are most important in oesophagus in normal digestion periods they are limited to short distances a deep contraction (peristaltic wave) from behind the point of stimulation and passes along the intestine towards the rectum at rates varying 2-25cm/sec with varying intensities when there is obstructionperistaltic rushes (very intense peristaltic waves) occur.

SEGMENTATION CONTRACTION ring-like contractions that appear at fairly regular intervals along the gut, then disappears and are replaced by another set of ring contractions in the segments between the previous contractions in the contracting segment, circular muscles contract while longitudinal muscles relax. these contractions may occur randomly along the intestine or at regular intervals. Alternating segmental contractions chum the intestinal content, mixing them with various secretions of intestine & keeping them in contact with absorptive epithelium. no net forward movement.

TONIC CONTRACTIONS relatively prolonged contractions that in effect isolate one segment of intestine from another. slow transit permit longer contact of the chime with the enterocytes & promotes absorption.

PHYSIOLOGY OF SWALLOWING Food Stimulus

Swallowing receptor areas of pharynx (especially on tonsillar pillars)

Receptors

Sensory portions of trigeminal and glossopharyngeal nerves

Afferents

Deglutition or swallowing center in the medulla and lower pons

Center

Respiratory center

Motor impulses

Deglutition apnoea
(respiration inhibited)

V,IX, XI, XII cranial nerves

+

Efferents

Few superior cranial nerves

Series of automatic pharyngeal muscle contractions

Effects
&

Responses Sequence of events in swallowing

(Entire process takes 1-2 seconds)

1. Tongue sweeps hard palate moving food backward into oropharynx (Oral/buccal phase- voluntary). 2. Nasopharynx closes (superior pharyngeal sphincters)(pharyngeal phaseinvoluntary.) 3. Respiration inhibited. 4. Laryngeal muscle contract to close glottis and elevate larynx. 5. Peristalsis initiated by superior pharyngeal constriction and continued by middle and inferior pharyngeals. 6. Upper oesopharyngeal sphincter (UES) relaxes(oesopharyngeal phase- involuntary) 7. Peristaltic wave proceeds down oesophagus. 8. Receptive relaxation occurs in the stomach. 9. Lower oesophageal sphincter (LES) dilates just prior to contraction wave.

DISORDERS OF SWALLOWING
1. Abolition of deglutition reflex It causes regurgitation of food into the nose or aspiration into the larynx and trachea. It may occur when Ix or X nerve is paralysed in lesions of medulla when pharynx is anaesthetised with cocaine (deglutition reflex is abolished temporarily) 2. Aerophagia It refers to unavoidable swallowing of air along with the swallowing of food bolus and liquids. It usually occurs in nervous individuals having low tone of the upper oesophageal sphincter (UES). Some of the gases present in the air swallowed are absorbed, partly the air is regurgitated into the oral cavity and out in the atmosphere (belching), and majority of air passes on the colon and is then expelled as flatus through the anus. 3. Cardiac achalasia

It is a neuromuscular disorder of the lower two-thirds of oesophagus. It is characterised by failure of the lower oesophageal sphincter (LES) to relax 4.
during swallowing and food accumulates in the oesophagus. Gastroesophageal reflux disease (GRD) There is incompetence of LES causing reflux of acidic gastric contents into oesophagus. oesophageal pain (heart burn) irritation of oesophagus or bronchioles (due to aspiration). Conditions associated with GRD Conditions in which emptying of the stomach is not normal (e.g. pyloric sphincter disease) When the gastric contents are pushed up against the oesophagus (e.g When the patient is lying down). when the LES is forced through the diaphragm into the thoracic cavity (e.g. hiatal hernia)
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during pregnancy, the growing foetus may push the top of the stomach into the thorax. The low intra-thoracic pressure (compare to the higher intra-abdominal pressure) causes the LES to expand, allowing reflux to occur. conditions in which LES fails to contract between swallows. Dysphagia It is a term used to denote difficulty in swallowing due to any cause.

GASTRIC MOTILITY 1. Receptive relaxation (storage function, accormodation) is a vaso-vagal reflex is initiated by distension of stomach abolished by vagotomy. The oral portion of stomach relaxes to accormodate the ingested food. The inhibitory neurotransmitter is either VIP or nitric oxide 2. Mixing and digestion The caudal region (distal body & antral part) contracts to m.ix food with gastric secretions and begin the process of digestion. The size of the particle is reduced. (a) Gastric Slow waves GSW (Basal Electrical Rhythm BER) o represents a wave of depolarisation of stomach cells initiated by pacemaker cells from the circular muscles of fundus on the greater curvature to pyloric sphincter. o consist of upstroke and plateau phase (rate 3-4 waves/min) o electrophysiologically unknown. o assumed that upstroke & plateau are due to influx of sodium & calcium. o in stomach, Ach increases contractile activity (produces peristalsis)by increasing the amplitude & duration of plateau phase. Thus frequency of slow waves set the maximal frequency of contraction. o other agents that initiate contraction of gastric smooth muscle are gastrin, nicotine, barium, potassium. o agents that inhibit the activity are enterogastrone, E, NE, atropine & calcium. (b) Migrating Motor Complexes (house-keeping) o are propulsive movements initiated during fasting. o begin in the stomach and move undigested material from the stomach and small intestine into the colon. o housekeeping function that sweeps food remnants and bacteria out of the upper GI into large intestine. o repeats every 90-120 min during fasting. o correlates with high levels of motilin.

3. Gastric Emptying (GE) The caudal region of the stomach contracts to propel. The rate of GE is fastest when stomach contents are isotonic. If hypotonic or hypotonic GE slowed. fats inhibit GE (delayed GE time) by stimulating release of CCK. H+ in duodenum inhibits GE via direct neural reflexes. (via interneurons in the GI plexus). GE results from a progressive wave of forceful contractions which sequentially involves antrum, pylorus, proximal duodenum all 3 functions as a unit. Chyme is pumped in a small at a time into small bits- the peristaltic waves which provide this pumping action is known as pyloric pump. The factors regulating GE 1. Fluidity of the chime Liquids empty faster than solids 2. Gastric factors Volume of food in the stomach o Greater volume greater stretching distension long vagal mediated & short intrinsic neural plexus mediate reflexes strong peristalsis rate of GE Gastrin o Presence of meat in stomach release gastrin activity of pyloric pump GE Type of food ingested o Carbohydrate rich food rapid GE o Protein rich food slow GE o Fat rich food slowest GE 3. Duodenal factors Enterogastric reflex o Neurally mediated reflex o Initiated by generation of receptors in duodenal mucosa o Important stimuli are distension of duodenum acidity of stomach content (pH <4) high or low osmolarity of chime presence of fat & protein digestion product in chyme Enterogastric hormones o CCK, Secretin, GIP 4. Other factors Emotions o Anger, aggresion G motility o Depression & fear G motility Vagotomy o decreases the magnitude or coordination of stomach contraction slow emptying

MOTILITY OF SMALL INTESTINE 1. Electrical movements Small bowel slow waves Migrating motor complexes 2. Mechanical Peristalsis Segmentation contraction Tonic contraction Movement of villi Movement of ileocaecal valve Peristaltic rush

MOTILITY OF LARGE INTESTINE 1. Haustal shultting Similar to segmentation contraction. 2. Peristalsis 3. Mass movement 4. Defecation

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SECRETION SALIVARY SECRETION Almost entirely under the control of parasympathetic system (promotes secretion). Initial fluid formation in the acinus is via a chloride pump, & electrolyte composition is similar to interstitial fluid. NaCl is reabsorbed in the ducts making the secretions hypotonic. Composition o Low sodium, chloride because of reabsorption. o High in potassium , bicarbonate because of secretion. o amylase secreted in the active form & begins the digestion of carbohydrates. o Low tonicity: because of reabsorption of NaCl and impermeablity of ducts to water.

GASTRIC SECRETIONS Cell Type Substance secreted mucous Stimulus for release Function of secretion

Mucous neck cell

Tonic secretion with irritation of mucosa Secreted with mucus

Physical barrier between lumen & epithelium Buffers gastric acid to prevent damage to epithelium

Bicarbonate

Parietal cells

Gastric acid intrinsic factor

Ach, gastrin, histamine

Activate pepsin, kills bacteria complexes with vitamin B12 to permit absorption Stimulate gastric acid secretion

Enterochromaffin like cells (ECL) Chief cells

Histamine

Ach, gastrin

Pepsin (ogen) Gastric lipase Somatostatin Gastrin

Ach, acid, secretin

Digest protein Digest fats Inhibit gastric acid secretion Stimulates gastric acid secretion

D cells G cells

Acid in the stomach Ach, peptides & amino acid

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MECHANISM OF GASTRIC ACID SECRETION BY PARIETAL (OXYNTIC) CELL

RECEPTORS & SIGNAL TRANSDUCTION PATHWAYS IN THE PARIETAL ECLL

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REGULATION OF GASTRIC- ACID SECRETION

Regulation of gastric-acid secretion. In the corpus of the stomach, the vagus nerve not only stimulates the parietal cell directly by releasing ACh, it also stimulates both ECL and D cells. Vagal stimulation of the ECL cells enhances gastric-acid secretion via increased histamine release. Vagal stimulation of the D cells also promotes gastric-acid secretion by inhibiting the release of somatostatin, which would otherwise inhibit-by paracrine mechanisms-the release of histamine from ECL cells and the secretion of acid by parietal cells. In the antrum of the stomach, the vagus stimulates both G cells and D cells. The vagus stimulates the G cells via GRP (gastrin-releasing peptide), promoting gastrin release. This gastrin promotes gastric-acid secretion by two endocrine mechanisms: directly via the parietal cell and indirectly via the ECL cell, which releases histamine. The vagal stimulation of D cells via ACh inhibits the release of somatostatin, which would otherwise inhibit-by paracrine mechanisms-the release of gastrin from G cells and-by an endocrine mechanism-acid secretion by parietal cells. Luminal H+ directly stimulates the D cells to release somatostatin, which inhibits gastrin release from the G cells, thereby reducing gastric-acid secretion (negative feedback). In addition, products of protein digestion (i.e., peptides and amino acids) directly stimulate the G cells to release gastrin, which stimulates gastric-acid secretion (positive feedback). ACh, acetylcholine; CCK b, cholecystokinin B; ECL, enterochromaffin-like; ENS, enteric nervous system.

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SUMMARY OF DIGESTION & ABSORPTION OF CARBOHYDRATE, PROTEIN & FAT

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SUMMARY OF DIGESTION AND ABSORPTION OF NUTRIENTS

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