Propulsion and Mixing of Food in the Alimentary Tract Chapter 63: Propulsion and Mixing of Food in the Alimentary Tract

Motility Chewing and Swallowing Esophageal Motility Gastric Motility Small Intestinal Motility Large Intestinal Motility

Chewing (mastication) Purpose of Chewing - Breaks cells - breaks apart undigestible cellulose Increases surface area - decreases particle size Mixes food with saliva - Begins digestion of starches (-amylase, lingual lipase) Lubricates food for swallowing

Nervous Control of Chewing Innervation - 5th cranial nerve innervates muscles of mastication Controlled by nuclei in brain stem Reflex mechanism - Food in mouth  muscles of mastication relax  jaw drops  stretch reflex  rebound contraction  pushes food against lining of mouth  repeat

Swallowing (deglutination) Three stages - Voluntary - initiates swallowing process Pharyngeal - passage of food through pharynx into esophagus Esophageal - passage of food from pharnyx to stomach

Pharyngeal Stage of Swallowing Reflex controlled by brain stem - 1. Food in pharynx - tactile stimulation 2. Soft palate pulled upward 3. Palatopharyngeal folds (“sizer”) pulled together 4. Trachea is closed (respiration inhibited) - Vocal cords approximated - Larynx raises and epiglottis covers larynx 5. Relaxation of UES 6. Peristaltic contraction of pharnyx

Nervous Control of Swallowing Swallowing Center - medulla Sensory input from pharnyx and esophagus Coordinates activity from vagal nuclei with other centers (e.g., inhibits respiratory center) Pharyngeal Phase - Food in pharynx  afferent sensory input via vagus / glossopharyngeal N.  swallowing center  brain stem nuclei  efferent input to pharynx. Figure 63-1; Guyton & Hall

Esophageal Stage of Swallowing Primary peristalsis - continuation of pharyngeal peristalsis Secondary peristalsis - Induced by distention Repeats until bolus is cleared Upper esophagus - upper 1/3 is striated muscle Lower esophagus - lower 2/3 is SM

Nervous Control of Esophageal Phase Primary peristalsis - Continuation of pharyngeal peristalsis Coordinated by swallowing center Cannot occur after vagotomy (striated muscle) Secondary peristalsis - Stretch related afferent sensory input to ENS and swallowing center are both involved Can occur after vagotomy (SM)

Esophageal Pressures Between Swallows During Swallowing High pressure at sphincters Pressure in esophageal body  intrapleural pressure During Swallowing UES relaxes - (low pressure) Peristaltic wave - (high pressure) LES and fundus relax - receptive relaxation (low pressure). Vagal input is inhibitory. VIP is transmitter for receptive relaxation.

Esophageal Sphincters - Purpose Purpose of high resting pressures in UES and LES UES - keeps air from entering esophagus LES - prevents acid reflux into esophagus

Disorders of Swallowing (Dysphagia) CVA (stroke) / cranial nerves damage Aspiration - UES and pharyngeal contractions are not coordinated Secondary peristalsis is still functional Muscular diseases - myasthenia gravis, polio, botulism Anesthesia - aspiration of stomach contents.

Gastroesophageal Reflux Disease (GERD) Heartburn / acid indigestion (1/10 people) Backwash of acid, pepsin, and bile into esophagus Can lead to - stricture of esophagus (scar tissue) asthma (aspiration) chronic sinus infection (reflux into throat) Barrett’s esophagus

Achalasia and Megaesophagus What is the cause / characteristics? Motility disorder affecting lower 2/3 of esophagus - LES fails to relax - LES pressure is high - Organized peristaltic contractions are absent Neurological problem with ENS (myenteric plexus) After months/years - megaesophagus develops - can hold > 1 liter of food Esophageal ulceration, rupture, and death can occur

Achalasia and Megaesophagus What are the symptoms? Difficulty swallowing liquids and solids Regurgitation of undigested food Weight loss, halitosis, excessive belching, heartburn

Achalasia and Megaesophagus What is the treatment? (1) Anti-spasmotic drugs that relax smooth muscle (2) Pneumatic dilator (stiff balloon) (3) Surgical myotomy

Gastric Motility Functions of gastric smooth muscle - Relaxes to accommodate food - orad area (receptive relaxation) Mixes food with gastric juice - caudad area (retropulsion) Propels chyme into duodenum - caudad area (antral pump)

Physiologic anatomy of the stomach Figure 63-2; Guyton & Hall

Motility of the Orad Area Contractile activity - Low amplitude contractions occur as meal empties Receptive relaxation - (VIP is neurotransmitter) Vagovagal reflex - vagal aff. carry impulses to CNS - vagal eff. carry impulses from CNS to stomach Vagotomy abolishes reflex Gastric distensibility - CCK increases (decreases gastric emptying) Gastrin effect not physiologic

Motility of the Caudad Area Peristalsis is the primary contractile event Pressure tracings show - Increased magnitude of contraction on approach to antrum Decreased phase lag on approach to antrum Decreased phase lag causes increased velocity of peristaltic wave

Electrical and Mechanical Events Relationship between slow wave and muscle tension in caudad area - Slow wave depolarization can elicit contraction of SM (without spikes) - stomach only Slow wave plateau must reach threshold to cause SM contraction Larger slow waves that have spike potentials cause increased strength of SM contraction

Regulation of Gastric Emptying Chyme must enter duodenum at proper rate pH must be optimal (high) for enzyme function Slow enough for nutrient absorption Immediately after meal - emptying does not occur before onset of gastric contractions Conditions favor emptying - (a) Increased tone of orad stomach (b) Forceful peristaltic contractions (c) Decreased tone of pylorus (d) Absence of segmental contractions in intestine

Gastric Emptying is Accomplished by Coordinated Activities of Stomach, Pylorus, and Small Intestine Immediately after a meal Conditions favor emptying Intestinal receptors activated

Regulation of Gastric Emptying Activation of receptors in intestinal mucosa initiates enterogastric reflexes. This decreases gastric emptying by - (a) Relaxation of orad stomach (b) Decreased force of peristaltic contractions (c) Segmentation contractions in intestine

Intestinal Receptors - Gastric Emptying Intestinal mucosa receptors - stimulated by high or low osmolarity, acid, fat, and protein Receptors trigger enterogastric reflexes Fat/proteins - CCK release increases gastric distensibility which decreases gastric emptying Acid - decreases gastric emptying (in 20-40s) via intrinsic neural reflex Involvement of other hormones - probably not physiologic

Small Intestinal Motility Small intestinal motility contributes to digestion and absorption by - Mixing chyme - with digestive enzymes and other secretions Circulation of chyme - to achieve optimal exposure to mucosa Propulsion of chyme - in an aboral direction

Small Intestinal Motility Two types of movements in small intestine following a meal - Peristalsis - a propulsive movement recall “Law of Gut.” Segmentation - a mixing movement

Role of Slow Waves Contraction is controlled by slow wave activity - Slow wave frequency- 12/min duodenum, 10 jejunum, 8 ileum Contraction frequency - limited by slow wave frequency Spike potentials necessary - Unlike stomach, contractions do not occur in absence of spike potentials

Slow Wave Frequencies Along Small Intestine Slow waves measured at six points along small intestine - Slow wave phase lag - - promotes propagation of contractions (peristalsis) Slow wave frequency - - decreases at distal portions of small intestine (5 and 6 are distal)

Migrating Motility Complexes (MMC) Purpose - (housekeeping function). Sweeps undigested residue toward colon to maintain low bacterial counts in upper intestine. Most coordinated, rapid peristalsis. Occurs between meals. Characteristics - Periods of intense peristaltic contractions Takes ~90 min to go from stomach to colon Mediated by motilin and ENS

Control of Small Intestinal Motility Whether spike potentials and hence contractions occur depends upon neural and hormonal input - Nervous factors - (PNS - stimulates / SNS - Inhibits) Peristaltic reflex - (Law of the Gut) - Mediated by ENS. Intestino-intestinal reflex - severe distention inhibits bowel. Extrinsic nerves. Gastroileal reflex - Meal stimulates. Ileocecal sphincter relaxes, ileal peristalsis increases. (gastrin, CCK, extrinsic nerves, ??).

Control of Small Intestinal Motility Whether spike potentials and hence contractions occur depends upon neural and hormonal input - Hormonal factors - Epinephrine - released from adrenals - inhibits motility Motilin - mediates migratory motor complexes Serotonin and prostaglandins - there are large quantities in small intestine that can stimulate motility Other hormones. Gastrin, CCK, and insulin stimulate contractions. Secretin and glucagon inhibit contraction. The roles of these are uncertain.

Ileocecal Junction Functions as a valve and a sphincter - Valvular function - - prevents backflow into small intestine mechanically Sphincter function - - regulates movement of ileal contents into large intestine. ENS and extrinsic nerves.

Emptying at the ileocecal valve Figure 63-4; Guyton & Hall

Motility of Large Intestine Functions of large intestine smooth muscle - Mixes chyme – enhances fluid / electrolyte absorption (haustral contractions) Propels fecal material - (mass movements)

Absorptive and storage functions of the large intestine Figure 63-5; Guyton & Hall

Musculature of Large Intestine Longitudinal SM - 3 groups (teneae coli) Circular SM - continuous to anus Internal anal sphincter - a thickening of circular SM External anal sphincter - striated muscle, surrounds internal anal sphincter Haustra (haustrations) - not fixed, appear and disappear

Innervation of Large Intestine Myenteric plexus - concentrated beneath teneae Parasympathetic input - Vagus innervates proximal colon Pelvic nerves (S2-S4 ) - distal colon, rectum / anus Sympathetic input - T10-L2 CG and SMG - proximal colon IMG - distal colon Hypogastric plexus - rectum and anal canal External anal sphincter - pudendal nerves

Haustral Contractions Purpose - Mixing movements facilitate fluid and electrolyte absorption (minimal propulsion) Structural and functional basis - They appear and disappear every 30-60s Require contraction of longitudinal and circular SM Circular SM is concentrated in some areas

Mass Movements Propulsive movements (modified peristalsis) Purpose - move feces to rectum / stimulate defecation reflex Distance - transverse colon to sigmoid colon or rectum Occurrence - After meals, series lasting 10-30 min. (1-2 min each) Reflexes - gastrocolic reflex (distention of stomach) - duodenocolic reflex (distention of duo)

Control of Defecation There are three levels of control - Intrinsic reflex Spinal cord reflex Involvement of higher centers

Intrinsic Defecation Reflex Intrinsic reflex mediated entirely by ENS is initiated when feces enters rectum via mass movements Rectal distention initiates afferent signals that spread through myenteric plexus to descending and sigmoid colon, and rectum. This causes contractions that force feces toward anus. Internal anal sphincter relaxes and if external anal sphincter is voluntarily relaxed, defecation occurs.

Defecation Reflex - Spinal Cord Parasympathetic cord reflex greatly intensifies intrinsic reflex (but is not different qualitatively) Rectal distention also initiates cord reflex. Afferent signals go to sacral cord and then back to descending and sigmoid colon, and rectum by way of parasympathetic fibers in pelvic nerves. The lower neurons S2-S4 provide sensory and motor fibers for defecation reflex. They are intact when spinal cord is injured at higher levels.

Afferent and efferent pathways of the parasympathetic mechanism for enhancing the defecation reflex Figure 63-6; Guyton & Hall

Defecation Reflex - Higher Centers Afferent signals entering spinal cord initiate other effects that require intact spinal cord. deep breath, closure of glottis, and increased abdominal pressure all work to move fecal contents downward Spinal transection or injury can make defecation a difficult process cord defecation reflex can be excited (either digitally or with enema)

Colon Motility Disorders Paralysis of defecation reflexes in spinal cord injuries - Destruction of conus medularis (only intrinsic reflex is functional) Destruction between conus medularis and brain (intrinsic reflex and local cord reflex are functional) Function of external anal sphincter?

List of Sphincters Upper esophageal sphincter (pharyngoesophageal) Lower esophageal sphincter (gastroesophageal) Pyloric sphincter (gastroduodenal) Ileocecal valve / sphincter Internal anal sphincter External anal sphincter

List of Reflexes - gastric distention relaxes ileocecal sphincter Peristaltic Reflex: - stretch bowel, proximal contraction, distal relaxation Enterogastric Reflex: - from duodenum to regulate gastric emptying Gastroileal Reflex (gastroenteric) - gastric distention relaxes ileocecal sphincter

List of Reflexes (cont’d) Intestino-intestinal Reflex: - over-distention or injury of bowel segment causes entire bowel to relax Gastro- and Duodenocolic Reflexes: - distention of stomach / duodenum initiates mass movements Defecation Reflex (rectosphincteric) - rectal distention initiates defecation