Mastication and Deglutition PDF

MASTICATION AND DEGLUTITION BY Dr. Oguntola R.A  Introduction Significances of Mastication Masticatory Movements Muscles of Mastication and actions Role of Tongue Control of Mastication  INTRODUCTION Mastication or chewing is th...

MASTICATION AND DEGLUTITION BY Dr. Oguntola R.A  Introduction Significances of Mastication Masticatory Movements Muscles of Mastication and actions Role of Tongue Control of Mastication  INTRODUCTION Mastication or chewing is the first mechanical process in the gastrointestinal (GI) tract, by which the food substances are torn or cut into small particles and crushed or ground into a soft bolus. Mastication of food is the initial stage in the process of digestion. Large pieces of food are reduced for swallowing. The food is broken apart, and the surface area increased for the efficient action of digestive enzymes and to facilitate solubilization of food substances in the saliva to stimulate taste receptors.  SIGNIFICANCES OF MASTICATION 1. Breakdown of foodstuffs into smaller particles 2. Mixing of saliva with food substances thoroughly 3. Lubrication and moistening of dry food by saliva, so that the bolus can be easily swallowed 4. Appreciation of taste of the food.  MASTICATORY MOVEMENTS The jaw moves rhythmically, opening and closing in a series of cyclical movements. 4 Phases  ROLE OF TONGUE Help in positioning of food between occlusal surfaces of teeth.  MUSCLES OF MASTICATION AND ACTIONS PRIMARY MUSCLES 1. Masseter muscle 2. Temporal muscle 3. Pterygoid muscles 4. Buccinator muscle. SEECONDARY MUSCLE 1. Digastric 2. Mylohyoid 3. Geniohyoid  ACTIONS OF MUSCLES DURING MASTICATORY MOVEMENTS Opening/ Depressor jaw muscles: mylohyoid, digastric, lateral pterygoid. Closing/Elevator jaw muscles: medial pterygoid, masseter, tempolaris. Closing muscles are usually inactive during jaw opening, when jaw opening muscles are very active. Jaw closing muscles activity: - Starts at the beginning of jaw closing - Increases slowly as the teeth begin to interdigitate - More active on the side where food is crushed.  Action of mastication is mostly a reflex process. It is carried out voluntarily also. The center for mastication is situated in medulla and cerebral cortex. Muscles of mastication are supplied by mandibular division of 5th cranial (trigeminal) nerve.  Interconnected neural circuits form a neural oscillatory network that is capable of generating the pattern of masticatory movements. Cyclical movements generated and controlled at the level of brainstem. Complex interactions between several motor nuclei and sensory input from oral cavity, terminating primarily in the trigeminal sensory and mesencephalic nuclei. Final pattern of mastication is interaction at the brainstem and peripheral sensory input. DEEGLUTITION/ SWALLOWING  OUTLINE Introduction Stages of deglutition Phases Deglutition reflex Applied physiology  INTRODUCTION Deglutition or swallowing is the process of passing food from the mouth into the esophagus where itt is transported to the stomach so that the main iprocesses of digestion and nutrient absorption can commence. Reflex sequence of muscle contractions that propel ingested materials and pooled saliva from mouth to the stomach. Over a period of 24 hours, swallowing occurs as many as 1000 times. Swallowing frequency is highest during easting, least during sleep and occurs at a rate of about once per minute at other times. STAGES OF DEGLUTITION Deglutition or swallowing is probably a reflex phenomenon. Higher centers facilitate this reflex. Once initiated, the swallowing centers in the medulla evokes the complete act of swallowing by discharge through six nuclei and the motor neurons. This reflex act occurs in three stages: 1. First stage or oral stage 2. Second stage or pharyngeal stage, and 3. Third stage or oesophageal stage. FIRST STAGE OR ORAL STAGE The first stage consists of the passage of material through the oral cavity into the pharynx which is under voluntary control. Due to the contraction of the mylohyoid, styloglossus and hypoglossus muscles, upward and backward movements of the tongue occur and the bolus of food which remains on the upper surface of the tongue is thrown back through the pillars of the fauces into the pharynx. During this phase mastication ceases and respiration is inhibited reflexly. SECOND STAGE OR PHARYNGEAL STAGE It consists of passage of bolus from the pharynx into the oesophagus which is reflex process and known as swallowing reflex. Key events in second stage include: 1. The contact of food material with the pharyngeal and peripharyngeal structures initiates and completes reflexly the second as well as third stage of deglutition. These reflexes are inhibited and abolished by cocainisation. 2. The soft palate is elevated and the nasopharynx is closed off from the rest of the pharynx. 3. There are elevation and forward movements of the larynx along with the elevation of the hyoid bone. 4. The vocal cords are adducted and there is momentary stoppage of respiration and speech. With the entrance of bolus in the pharynx, contraction of superior pharyngeal constrictor occur inducing rapid pharyngeal peristaltic wave (primary peristaltic wave) which moves down the pharynx, propelling the bolus in front of it. The wall and structure of hypopharynx are elevated to engulf the oncoming bolus. 5. The oesophagus, which was kept closed, until now by the contraction of cricopharyngeus muscle, relaxes as the bolus approaches the oesophagus and thus the bolus enters the oesophagus and the pharynx reopens. Mechanism of Protection of Airway during the Passage of Food through the Pharyngeal Crossroads There are four possible outlets from the oral pharynx through which food may be expelled: a) Back into the mouth, b) up into the nasopharynx, c) forward into the larynx, and d) downward into the oesophagus. The swallowing reflex is so coordinated that food passes only in one of these possible paths, namely into the oesophagus. Return in the mouth is prevented by the high pressure (even 100 cm of H20) developed in this area (posterior half of oral cavity) due to forceful contraction of the tongue against hard and soft palates. Combined actions of tensor veli palatini and levator veli palatini muscles stiffen the soft palate which presses against posterior pharyngeal wall and passage into nasopharynx is prevented. Entrance of food into the respiratory tract is prevented by inhibition of respiration.  THIRD STAGE OR OESOPHAGEAL STAGE Esophageal stage is also an involuntary stage. In this stage, food from esophagus enters the stomach. The terminal part of the second stage and the first part of third stage cannot be differentiated, because both are same and one. The upper oesophageal sphincteric mechanism is dealt here along with remaining portion of the third stage. Esophagus forms the passage for movement of bolus from pharynx to the stomach. Movements of esophagus are specifically organized for this function and the movements are called peristaltic waves  Peristalsis means a wave of contraction, followed by the wave of relaxation of muscle fibers of GI tract, which travel in aboral direction (away from mouth). By this type of movement, the contents are propelled down along the GI tract. When bolus reaches the esophagus, the peristaltic waves are initiated. Usually, two types of peristaltic contractions are produced in esophagus. 1. Primary peristaltic contractions 2. Secondary peristaltic contractions.  Primary Peristaltic Contractions When bolus reaches the upper part of esophagus, the peristalsis starts this is known as primary peristalsis. After origin, the peristaltic contractions pass down through the rest of the esophagus, propelling the bolus towards stomach. Pressure developed during the primary peristaltic contractions is important to propel the bolus. Initially, the pressure becomes negative in the upper part of esophagus. This is due to the stretching of the closed esophagus by the elevation of larynx. But immediately, the pressure becomes positive and increases up to 10 to 15 cm of H2O. Secondary Peristaltic Contractions If the primary peristaltic contractions are unable to propel the bolus into the stomach, the secondary peristaltic contractions appear and push the bolus into stomach. Secondary peristaltic contractions are induced by the distention of upper esophagus by the bolus. After origin, these contractions pass down like the primary contractions, producing a positive pressure. Role of Lower Esophageal Sphincter Distal 2 to 5 cm of esophagus acts like a sphincter and it is called lower esophageal sphincter. It is constricted always. When bolus enters this part of the esophagus, this sphincter relaxes so that the contents enter the stomach. After the entry of bolus into the stomach, the sphincter constricts and closes the lower end of esophagus. The relaxation and constriction of sphincter occur in sequence with the arrival of peristaltic contractions of esophagus.  DEGLUTITION REFLEX Though the beginning of swallowing is a voluntary act, later it becomes involuntary and is carried out by a reflex action called deglutition reflex. It occurs during the pharyngeal and esophageal stages. Stimulus When the bolus enters the oropharyngeal region, the receptors present in this region are stimulated. Afferent Fibers Afferent impulses from the oropharyngeal receptors pass via the glossopharyngeal nerve fibers to the deglutition center. Center Deglutition center is at the floor of the fourth ventricle in medulla oblongata of brain. Efferent Fibers Impulses from deglutition center travel through glossopharyngeal and vagus nerves (parasympathetic motor fibers) and reach soft palate, pharynx and esophagus. The glossopharyngeal nerve is concerned with pharyngeal stage of swallowing. The vagus nerve is concerned with esophageal stage. Response The reflex causes upward movement of soft palate, to close nasopharynx and upward movement of larynx, to close respiratory passage so that bolus enters the esophagus. Now the peristalsis occurs in esophagus, pushing the bolus into stomach.  APPLIED PHYSIOLOGY Common Disturbances in the Swallowing 1. In the first stage: Inflammation of any oral structure, paralysis of tongue and congenital defects of oral structure result difficulty of swallowing. 2. In the second stage: Acute pharyngitis, tonsillitis, poliomyelitis, diphtheria result difficulty in deglutition. 3. In the third stage: Diffuse spasm in the oesophagus producing dysphagia and cardiac pain, achalasia (lower sphincter does not relax), scleroderma (lower part of oesophagus generally in spam), chalasia (lower sphincter remains relaxed condition, inducing gastro-oesophageal reflux), Gastroesophageal Reflux Disease (GERD), Achalasia cardia. MOVEMENT OF THE GIT, MOTILITY, MASS MOVEMENT, AND STOMACH EMPTYING ANATOMICAL AND FUNCTIONAL DIVISIONS OF THE STOMACH  MOVEMENTS OF THE STOMACH Gastric Relaxation: Fundus and Body (gastric reservoir) relax to accommodate and store the volume of the meal. Peristalsis waves of contraction (Mixing and Grinding): Antral peristalsis to grind the meal into small particles and mix with secretions.  Gastric Relaxation Three kinds of gastric relaxation can be differentiated: a receptive, an adaptive and a feedback-relaxation of the gastric reservoir. Gastric relaxation increases compliance, so that luminal pressure changes very little between the empty state (50 mL volume) and filled state (1500 mL volume). The process is termed as gastric accommodation.  The receptive relaxation consists of a brief relaxation during chewing and swallowing. The stimulation of mechano-receptors in the mouth and pharynx induces vago-vagal ref le xes which cause a relaxation of the gastric reservoir. By this rec eptive relaxation the stom ac h is prepared to receive a bolus of food.  Adaptive relaxation: When the stomach is f illed with food digesta/bolus, mechano- and/or chemoreceptors are stimulated which elicit gastro-gastric ref lexes that further relax the gastric reservoir. This regulation provides a prolonged storage of the digesta until they are suf ficiently broken down for emptying into the duodenum. Gastrin and the presence of certain nutrients in the small intestine additionally cause relaxation of the gastric reservoir.  The feedback-relaxation of the stomach ensures that gastric emptying is adapted to the process of digestion and absorption of nutrients in the small intestine. The receptive, adaptive and feedback-relaxation of the stomach are mediated by nonadrenergic, non-cholinergic mechanisms (called NANC-inhibition). Mediators for NANC inhibition are nitric oxide (NO), Pituitary adenylate cyclase activating peptide (PACAP), vasoactive intestinal peptide (VIP) and adenosine triphophate (ATP), all of which are released from motor pathways in the enteric nervous system.  Regulation of stomach activity
a. Cephalic Phase The taste or smell or even thoughts of food stimulate the medulla oblongata. Parasympathetic action potentials are carried by the vagus nerves to the stomach Postganglionic neurons stimulate secretion by parietal and chief cells (HCl and pepsin) and stimulate the secretion of the hormone gastrin and histamine. Gastrin is carried through the circulation back to the stomach where it and histamine stimulate further secretion of HCl and pepsin. b. Gastric Phase  c. Intestinal Phase -Chyme in the duodenum with a pH less than 2 or containing lipids inhibits gastric secretions by three mechanisms -Sensory input to the medulla from the duodenum inhibits the motor input from the medulla to the stomach. Stops secretion of pepsin and HCl. -Local reflexes inhibit gastric secretion - enterogastric reflex, Secretin and cholecystokinin produced by the duodenum decrease gastric secretions in the stomach.  PERISTALSIS CONTRACTION (MIXING AND GRINDING) The main feature of the gastric pump is the peristaltic wave. Pacemaker cells in the stomach body induces slow waves on which the spike potentials that initiate the peristalsis contraction are superimposed The peristaltic waves are propagated from the body to the antrum, which eventually closes the pyloric sphincter.  In the region of the gastric body the peristaltic waves are shallow; When the peristaltic wave reaches the antrum, the waves becomes deeper. The peristaltic contraction of the antrum can be divided into three phases: 1) a phase of propulsion, 2) a phase of emptying and mixing, and 3) a phase of retropulsion and grinding. Due to the regularly occurring pacemaker potentials these phases occur cyclically. When the peristaltic wave moves over the proximal antrum the previously contracting terminal antrum relaxes. Therefore chyme is propelled into the distal (or terminal) antrum (phase of propulsion).  When the peristaltic wave moves over the middle of the antrum the pylorus opens and duodenal contractions are inhibited; thus, small amounts of gastric chyme are delivered across the pylorus into the duodenum. During this phase of emptying and mixing the peristaltic waves are relatively far away from the pylorus, i.e. the gastric chyme is not forced into the duodenum by pressure but is swept into the small intestine by the peristaltic wave. This mechanism of the antral pump is associated with a sieving effect. Because liquids f lo w more rapidly than viscous and solid materials liquids with small suspended particles are swept across the pylorus into the duodenum whereas the viscous and solid mass of the chyme are retained in the stomach  Usually, the peristaltic waves do not occlude the lumen of the middle antrum. Therefore, parts of the chyme f low across the central opening of the peristaltic wave retrograde into the relaxing proximal antrum. In this way the phase of emptying is associated with mixing of the gastric chyme. At the same time the subsequent peristaltic wave proceeds along the gastric body sweeping chyme into the proximal antrum. Thus chyme of the gastric body and chyme of the middle antrum accumulate in the relaxed proximal antrum During the contraction of the terminal antrum the pylorus closes and the transpyloric flow is stopped.  The chyme present in the terminal antrum is forced retrograde across the central opening of the peristaltic wave into the relaxing middle antrum. This jet-like retropulsion causes a forceful mixing of the chyme associated with grinding of particles Therefore the contraction of the terminal antrum represents the phase of retropulsion and grinding. SMALL INTESTINE Site of greatest amount of digestion and absorption of nutrients and water Divisions Duodenum- first 25 cm beyond the pyloric sphincter. Jejunum- 2.5 m Ileum- 3.5 m. Peyer’s patches or lymph nodules  MOVEMENT IN THE SMALL INTESTINE 1. Segmental contractions mix 2. Peristalsis propels 3. Ileocecal sphincter remains slightly contracted until peristaltic waves reach it; it relaxes, allowing chyme to move into cecum 4. Cecal distention causes local reflex and ileocecal valve constricts Prevents more chyme from entering cecum Increases digestion and absorption in small intestine by slowing progress of chyme Prevents backflow  MOVEMENT OF THE SMALL INTESTINE Chyme transverse the length of the small intestine 3-5hours Movements of small intestine are essential for mixing the chyme with digestive juices, propulsion of food and absorption. A. Mixing movements: i. Stationary contractions ii. Clusters of contractions. B. Propulsive movements: i. Peristaltic movements ii. Giant aboral contractions C. Peristalsis in fasting – migrating motor complex (MMC). MMC is a cyclic recurring motility pattern that occurs in the stomach and small bowel during fasting STATIONARY CONTRACTIONS Occur isolated at single sites without a strict spatiotemporal relation They occlude the intestinal lumen pushing the chyme orally and aborally and separating it into segments. Therefore, these contractions are also called “segmenting contractions”. The stationary segmenting contractions cause mixing of the luminal contents  CLUSTERS OF CONTRACTIONS Clustered contractions are characterised by several repetitive contractions The contractions represent short peristaltic waves pushing the chyme a few centimetres aborally followed by a partial back-flow during the period of relaxation. (pendullar movement) Thereby the chyme is mixed. When the repetitive short peristaltic waves of the clustered contractions move over the same intestinal segment, the clustered contractions are stationary. In contrast, when each subsequent peristaltic wave starts and ends a few millimetres further aborally, the clustered contractions slowly migrate distally. short intestinal segment. Both stationary and migrating clusters of contractions frequently occur after a fat meal.  PERISTALSIS Peristaltic waves are circular constrictions propagating aborally. Due to reflexes initiated by the enteric nervous system they are associated with an aboral relaxation or inhibition of the muscle, respectively. After a non-caloric meal peristaltic waves are the dominant feature The peristaltic waves produce an aboral transport of chyme. The propagation velocity of the peristaltic waves is determined by the proximal to distal propagation of the slow waves in the smooth muscle syncitium.  THE GIANT CONTRACTIONS Contractions are characterised by a large amplitude and a long duration In physiological conditions they were observed at the ileum during the interdigestive period in humans. The giant contractions completely occlude the intestinal lumen and propagate slowly in an aboral direction pushing the luminal contents distally and cleaning the intestine. In respect to this procedure they are also called “stripping wave”. The propagation velocity of the giant contractions is usually slower than that of the peristaltic waves Aboral giant contractions of the small intestine are the typical contractile pattern in diarrhoea. They can be induced by infections with Cholera toxin or Trichinella spiralis, by radiation, by oral administration of acetic acid or by chemical drugs like Erythromycin  MIGRATING MOTOR COMPLEX Migrating motor complex is a type of peristaltic contraction, which occurs in stomach and small intestine during the periods of fasting for several hours. It is different from the regular peristalsis because, a large portion of stomach or intestine is involved in the contraction. It starts as a moderately active peristalsis in the body of stomach and runs through the entire length of small intestine The contraction extends to about 20 to 30 cm of stomach or intestine. This type of movement occurs once in every 1½ to 2 hours. It travels at a velocity of 6 to 12 cm/min.  Migrating motor complex sweeps the excess digestive secretions into the colon and prevents the accumulation of the secretions in stomach and intestine. It also sweeps the residual indigested materials into colon.  LARGE INTESTINE Extends from ileocecal junction to anus Consists of cecum, colon, rectum, anal canal Movements sluggish (18-24 hours); chyme converted to feces. Absorption of water and salts, secretion of mucus, extensive action of microorganisms. 1500 mL chyme enter the cecum, 90% of volume reabsorbed yielding 80-150 mL of feces  ANATOMY OF THE LARGE INTESTINE 1. Cecum Blind sac, vermiform appendix attached. 2. Colon Ascending, transverse, descending, sigmoid Circular muscle layer complete; longitudinal incomplete (three teniae coli). Contractions of teniae form pouches called haustra. Mucosa has numerous straight tubular glands called crypts. Goblet cells predominate, but
there are also absorptive and granular cells as in the small intestine  3. Rectum Straight muscular tube, thick muscular tunic 4. Anal canal- superior epithelium is simple columnar; inferior epithelium is stratified squamous Internal anal sphincter (smooth muscle) External anal sphincter (skeletal muscle) Hemorrhoids: Vein enlargement or inflammation 24-72  MOVEMENT IN THE LARGE INTESTINE Mass movements Common after meals Integrated by the enteric plexus Local reflexes instigated by the presence of food in the stomach and duodenum Gastrocolic: initiated by stomach Duodenocolic: initiated by duodenum Defecation Defecation reflex: distension of the rectal wall by feces Parasympathetic stimulation Usually accompanied by voluntary movements to expel feces. Abdominal cavity pressure caused by inspiration and by contraction of muscles of abdominal wall. MOVEMENT IN THE LARGE INTESTINE 24-74  VOMITING Vomiting or emesis is def ined as the forceful expulsion of gastrointestinal contents through the mouth“. Vomiting represents a defence reaction to protect the body against the intake of dangerous agents. VARIOUS CAUSES: antibiotics, Analgesics, narcotics, cancer chemotherapy, mechanical obstruction, radiation injury, gastroparesis, functional bowel disorders, intraperitoneal inf lammation, increased intracranial pressure, Emotional responses, psychiatric conditions, tumors, labyrinthine disorders, pregnancy, uremica, diabetic ketoacidosis, viral or bacterial gastroenteritis  MECHANISM OF VOMITING Anorexia Nausea Copious salivation (water brash) Vasoconstriction with pallor, sweating, dizziness and tachycardia Retrograde giant contraction precedes vomiting. It originates in the proximal jejunum, propagates orally towards the stomach and moves up to the proximal antrum. The retrograde giant contraction forces the chyme of the proximal small intestine across the widely opened pylorus into the relaxed gastric body. Some minutes later retching and vomiting occurs  Closure of glottis Upward and forward movement of larynx and hyoid bone Elevation of soft palate RETCHING BEGINS Rhythmic inspiratory movements against a closed glottis produce negative oscillations in intrathoracic pressure and concomitant contractions of the abdominal muscles and the diaphragm cause an increase in intra-abdominal pressure Compression of the stomach between diaphragm and abdominal wall leading to rise in intragastric pressure  The distal part of the esophagus containing smooth muscle cells relaxes whereas the proximal striated esophagus contracts resulting in a funnel-like opening of the cardia and the distal esophagus. These rhythmic events during retching cause a repetitive flow of gastric chyme into the esophagus followed by an immediate backflow.  VOMITING OCCURS Vomiting is associated with a contraction of the intercostal muscles and Simultaneous relaxation of lower esophageal sphincter, esophagus and upper esophageal sphincter An increase in the intrathoracic pressure so that the chyme is forced into the mouth and expelled. Thus during retching and vomiting ejection of gastric contents is not produced by contractions of the stomach but by contractions of skeletal muscles.  INTERNAL AND ETERNAL SPHINCTERS OF THE ANAL CANAL The internal sphincter is thickened terminal of the circular smooth muscle of the rectum. It is tonically contracted It is innervated by sympathetic fibres from the pelvic plexus It is reflexly relaxed transiently when the rectum or the retrosigmoid part of the colon is distended During prolonged distention, the stretch receptors in the rectal wall adapt and the sphincter regains its contracted state. The External Sphincter is a cuff of voluntary striated muscle around the anal canal distally overlapping the internal sphincter. It is innervated by a branch of the pudendal nerve It is tonically contracted as a result of a sacral reflex.  DEFECATION Voiding of feces is known as defecation. Defecation involves a series of coordinated motor activities. The rectum has two primary functions: (1) to serve as a storage site for feces and (2) to expel feces during defecation. Thus, the rectum must have the ability to accommodate a certain volume of stool. When this capacity is exceeded intramural stretch receptors are activated, making the individual aware of the urgency of the forthcoming event and relax the internal anal sphincter (Usually, the desire for defecation is elicited by an increase in the intrarectal pressure to about 20 to 25 cm H2O)  The individual then increases intra-abdominal pressure by forcing air against the closed glottis (Valsalva maneuver) and relaxes the external anal sphincter, which is made of skeletal muscle. The individual can inhibit defecation by voluntarily Increasing the tone of external anal sphincter, which transiently increases internal sphincter tone. However, as rectal pressure builds, the urge to defecate increases and the above processes are again initiated.  DEFECATION REFLEXES (DF) Classified into two (2): - Intrinsic and extrinsic Intrinsic DF is mediated through the myenteric plexus The distention of the rectal wall by the arriving faeces initiates peristaltic waves spread through a local circuit in the descending & sigmoid colon and the rectum. The waves forces the faeces towards the anus. As the faeces arrived at the anus, the internal anal sphincter relaxes. At this period if the external anal sphincter is open, there will be defeacation of the feaces to the external environment. Intrinsic DF usually produced weak contractions and needs reinforcement by contractions mediated by the Extrinsic DF. Extrinsic DF is a parasympathetic DF because it involves nerves in the sacral segment of the spinal cord.

 Distension of the rectum causes afferent parasympathetic impulses to be transmitted into the spinal cord At the spinal cord, the afferent impulses are integrated and efferent impulses are conducted through the efferent parasympathetic nerve back to the descending colon. sigmoid colon, rectum and anus. Contractions produced by this reflex augment the weak contractions produced by intrinsic DF Defecation can only occur if the circumstance is socially acceptable for the it. Defecation can therefore be voluntarily delayed through the voluntary contraction of the external anal sphincter. The voluntary contraction of this sphincter is sufficient enough to override series of contraction produced by the intrinsic and extrinsic DF. Defecation act begins with relaxation of the external anal sphincter and followed by increased intrabdominal pressure to aid the expulsion of the feaces. ASSIGNMENT 1. List the GI tract sphincters and their locations 2. Write short note on MMC THANK YOU 89