Digestion 2x PDF
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Eastern Mediterranean University
Dr. Hızır Kurtel
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The document provides a detailed account of various aspects of digestive physiology, including the regulation of hunger, appetite, and satiety. It covers short and long-term feedback mechanisms. Additional sections describe the structure and function of salivary glands and their nervous control.
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EATING: SALIVATION, MASTICATION AND DEGLUTITION Dr. Hızır Kurtel PHYSIOLOGY OF HUNGER : HUNGER: Craving for food. Associated with a series of objective sensations such as hunger pangs and include salivation and increased food-searching behavior APPPETITE: Attitudes toward...
EATING: SALIVATION, MASTICATION AND DEGLUTITION Dr. Hızır Kurtel PHYSIOLOGY OF HUNGER : HUNGER: Craving for food. Associated with a series of objective sensations such as hunger pangs and include salivation and increased food-searching behavior APPPETITE: Attitudes toward different types of food. May persist even hunger has been appeased. SATIETY: Lack of a desire to eat that occurs after ingestion of food ANOREXIA: Aversion to eating despite an existing stimulus for hunger CENTRAL CONTROL Higher centres: involving prefrontal cortex and amygdala (involved in habit and conditioning) Hypothalamus: appetite is regulated by interaction between two areas within the hypothalamus: Ventromedial nucleus Ventrolateral nucleus These centres have rich supply of receptors, whose neurotransmiters mediate: Promotion of feeding: neuropeptide Y (activation of Y5 receptor), GABA, orexin Inhibition of feeding: Serotonin, norepinephrine, POMC, CRH FEEDBACK CONTROL FEEDBACK CONTROL Why do you feel full when you Short-term or alimentary feedback chew gam ? Oral activity: salivation, chewing, taste swallowing (inhibits feeding centre approximately 30 min) Stomach or duodenal distention: Vagal afferents inhibit the feeding centre Chemical component of the food (inhibit food intake): GI hormones and humoral factors stimulate the release of : CCK, GRH, GLP-1, somatostatin Insulin and glucagon FEEDBACK CONTROL Long-term or nutritional feedback Temperature: Interaction between the hypothalamus and temperature-regulating systems Cold: stimulates feeding Heat: inhibits feeding centre Blood concentration of nutrients (aa, glucose, lipids): Low concentration of any of above stimulates an increase in feeding Hypothalamic glucoreceptors monitor glucose (glucostat theory); high concentrations stimulate the satiety centre, low concentrations stimulate feeding centre The amount of white adipose tissue (stored energy): Negative feedback via leptin. High concentrations of leptin indicate obesity. Stimulation of leptin receptors in hypothalamus increases substances inhibiting food intake REGULATION OF FLUID INTAKE THIRST: Angiotensin II acts on specific areas of the hypothalamus which, in turn activate the thirst center. Hemorrhage leads to increased drinking despite an unchanged extracellular fluid osmolality. Which statment is correct regarding slaviry glands ? SALIVARY GLANDS: 1- Secretory Structures: The PAROTID GLANDS which are histologically serous type (largest glands) The SUBMANDIBULAR and SUBLINGUAL GLANDS which are both of the mixed serous and mucous type. The many small buccal and labial glands are also of the mixed type. Major flow in unstimulated phase comes from submandibular. Major flow in stimulated phase comes from parotid gland Salivary Glands Minor Major Buccal Lingual Labial Superior Salivary Nucleus Inf. Salivary Nucleus CN-VII CN-IX n glion glio n Gan Ga Subma Otic ndibular SUBMANDIBULAR SUBLINGUAL PAROTID 75% 5% 20% of Saliva Mixed Serous 2- Anatomy and Innervation: The secretory unit of salivary glands (asinus) is a blind end of a branching duct system and is made up of a group of cells called acinar cells. Aciner cells secrete the initial salivary fluid. The salivary glands receive a high blood flow proportional to their weight. Capillaries are very permeable, allowing rapid movement of water and other molecules across their basement membrane. 3- Co mposition: a- Daily volume: 1000-1500 ml b- pH: Ranges from 6.0-7.4, it is generally near 7.0 c- Major Characteristics Large volume relative to the mass of the tissue High potassium concentration Low osmolarity Contains specialized organic mat erial d- Ionic Composition: Electrolyte concentration and osmolality vary with secretion rate, but generally, in co mparison with plasma, saliva contains higher concentrations of potassium (K +) and bicarbonate + (HCO 3 ) and lower concentrations of sodium (Na and - chloride (Cl ) The degree of hypotonicity and the electrolyte composition of saliva are dependent upon the rate of salivary secretion. At low secretion rates (0.5 ml/min) the movement of the primary secretion within the ducts is slow enough to allow the ductal transport processes to decrease the osmolality of the primary secretion by 70 per cent or to 88 mOsm per liter. As secretion rate is increased, the reduced time of exposure of the primary secretion to the ductal epithelium limits the amount of electrolytes which can be removed (sodium) or added (potassium). Thus, at higher secretion rates the tonicity of the saliva approaches that of the primary secretion. e- Organic Composition: Saliva contains proteins in concentrations ranging between 100 to 300 mg/dl. Salivary proteins can be divided into two classes, 1- Those specifically secreted by salivary epithelium 2- Those which gain access to saliva via filtration (plasma proteins). Those specifically secreted by salivary epithelium Alpha-amylase (ptyalin), quantitatively the most important, almost entirely derived by parotid gland Lingual lipase Ribonuclease, Antibacterial agents such as muramidase (lysozyme), Immunoglobulin (chiefly LgA), Lactoferrin, Mucoproteins, which include mucins (formed primarily in the sublingual and submandibular glands. Mucin is the primary determinant of salivary viscosity). The ABO blood group substances. R-protein which binds dietary vitamin B12 (protect cobalamin (Vitamin B12) from acid degradation in the stomach by producing a complex) Epidermal growth factor (stimulates gastric mucosal growth). Amylase is synthesized and stored in the serous (acinar) cells of the salivary gland (primarily parotids) in the form of zymogen granules. These granules are located in the apical portion of the cell, and their contents are discharged by exocytosis into the lumen in response to certain secretagogues. The steps involved in the release of mucin from mucous cells are poorly understood. Stored droplets of mucin in the apical portion of the cell are probably discharged by exocytosis, and it is likely that events similar to those in the serous cell link the stimulus to secretion. f - Salivary Oxidants: It has been known for some time that the peroxidases found in exocrine secretions such as saliva, tears and - colostrum will oxidize SCN (thiocyanate) in the presence of H 2 02 to yield hypothiocyanous acid (HOSCN). peroxidase - + H 2 02 + SCN + H HOSCN + H 2 0 Human saliva, tears and milk have relatively high - concentrations of peroxidase, SCN and H2 Q2. In addition, the parotid gland possesses the ability to concentrate SCN (x 1000 times). powerful sympathetic stimulation because it will cause constriction of blood vessels cannot be associated with high saliva output but under normal 4- Regulation of Salivary Secretion circumstances sympathetic system also contributes to a- Nervous Control of Salivary Gland Function: saliva output but when once stimulated saliva output The primary physiological control of the decreases salivary glands is by the autonomic nervous system. Stimulation of either sympathetic or parasympathetic nerves to the salivary glands stimulates salivary secretion, but the effects of the parasympathetic nerves are stronger and more long lasting. Comparison of Sympathetic and Parasympathetic influences on Salivary Secretion Responses Sympathetic Parasympathetic Saliva ouput scant copious Temporal response transient sustained Composition of Protein rich Protein poor secretions high K and HC03 lower K~ and HCO~ Response to decreased decreased denervation secretion, secretion glandular atrophy Para-Otic Parasympathetic nervous regulation Medulla has 4 important centers CVS Respiratory Swallowing Vomiting What causes the dryness of “morning mouth” ? Ordinarily, a constant flow of saliva flushes out the mouth and keeps the papillae on the tongue short. But salivation is reduced during sleep, and the papillae grow longer, trapping food and bacteria and producing “morning mouth” Why do dental procedures stimulate salivation? Manipulative activities in the mouth stimulate pressoreceptors that activate salivation by the Unconditioned salivary reflex The generalised increase in sympathetic activity associated with anxiety, fear and stress causes dryness of the mouth, often to such a degree that person is unable to speak clearly, if at all. This has particular significance for patients who are being fasted prior to anesthesia. The combination of fear and certain amount of dehydration may cause a distressingly dry mouth. Drugs such as atropine that block the effect of A patient visits ER with acetylcholine on the salivary glands, and therefore reduce person sympathetic nervous system secretions, are used in premedication before intubation of hyperactivity however since the patient is in coma there inhalation anaesthesia. This reduces the danger of is a necessity for intubation which would of secretions trickling down into the trachea the statement below is correct regarding the b- Hormonal Regulation: In contrast to neural influences which affect all elements of the salivary functions, some hormones such as aldosterone and antidiuretic hormone (ADH) exert their effects only on the ductal epithelium. Hormonal influences do not alter salivary secretion rate, yet they do modify the ionic composition of saliva. Aldosterone acts directly on the ducts to increase both sodium absorption and potassium secretion. Adrenocortical insufficiency is characterized by an increased salivary sodium concentration rn saliva. ADH reduces the sodium concentration of saliva, presumably by enhancing sodium absorption in the ducts. The physiologic role of hormones in the regulation of salivary secretion is far less important than that of neural influences. a- The protective functions of saliva: The human mouth is populated by a wide spectrum of pathogenic bacteria, which can cause dental caries and inflammation of the oral mucosa in the absence of saliva. The antibacterial action of saliva can be attributed to the presence of lactoferrin and muramidase (lysozyme). The iron-binding protein, lactoferrin, which is found in a number of exoerine secretions, including milk and pancreatic juice, exerts its action by depriving microorganisms of nutrient iron. Lysozyme is a glycoprotein which hydrolyses the constituents of bacterial cell wall polysaccharides, thus destroying the microorganism. immunoglobulins, which are capable of binding with antigenic components of the bacterial cell wall Bicarbonate, a major ionic constituent of saliva, plays an important role in the neutralization of acid in the mouth. The two major sources of acid in the mouth are ingested materials and the products of bacterial metabolism. Acid released by bacteria plays an important role in the formation of dental caries (by dissolving enamel and dentine). Tooth Decay: Bacteria that cause dental caries produce a gluelike enzyme called glucosyl transferase (GTF) that converts ordinary sugar into dextran, a sticky substance that clings to the tooth’s enamel GFT also helps the bacteria adhere to the enamel. Dextran is involved in the formation of plaque, a destructive film that builds up on teeth. Once plaque is formed the bacteria on the teeth produce another enzyme that promotes erosion of the enamel (incidentially apples may keep the doctor away, but not the dendist. They contain more than 10 percent fermentable carbohydrate, a potent producer of tooth decay). b- Digestive and lubricative properties: The presence of mucins in saliva facilitates Sjögren mastication and deglutition. Keratoconjunctivitis Sicca (Dry eyes) Patients with inadequate salivary flows have difficulty in swallowing dry foods, (XEROSTOMIA - DRY MOUTH eg Medications such as Nidazol). Sjögren Sjögren Salivary amylase hydrolyses alpha-1, 4 Syndrome glycosidic bonds of polysaccharides such as starch. Xerostomia Inflammatory In the overall digestion of carbohydrates in man, Arthritis salivary amylase plays only a minor role, owing to limited time that the enzyme has to act under condition close to its optimal pH (approximately 7.0). Although salivary bicarbonate help in achieving the optimal pH, rapid entry of food into the acid environment of the stomach inactivates the enzyme. However, when food is chewed for an extended period of time, up to 75 per cent of the starch can be digested to the disaccharide stage by amylase in the mouth. Facilitation of speech, oral comfort, and taste, and modification of the temperature of ingested food are other important functions of saliva. These are essential for oral comfort and clear speech. Saliva also facilitates taste sensation. MASTICATION AND SWALLOWING (Deglutition): a- Functions of Chewing. To crush and break food into a size suitable for swallowing Lat Pterygoid Mandibular depressor Med Pterygoid CN-V (Trigeminal) Masseter Mandibular elevator Temporalis To break apart otherwise undigestible cellulose coatings on plant foods, allowing later digestion of the nutrients To increase the surface areas of all food products To mix the food with saliva To stimulate taste buds and release odors which stimulate the olfactory receptors b- Swallowing: In general, swallowing can be divided into three stages 1- The voluntary stage, When the food is ready for swallowing, it is voluntarily squeezed or rolled posteriorly into the pharynx by pressure of the tongue upward and backward against the palate (intrinsic and extrinsic muscles of tongue CN-XII). From squeezed backward towards the pharynx and here on, the process of swallowing becomes entirely, or touches the wall of pharynx and tonsillar almost entirely, automatic and ordinarily cannot be pillars reflex activity begins and now from now stopped. on swallowing process is involuntary and can almost never be initiated spontaneously 2- The pharyngeal stage: Involuntary and constitutes the passage of food through the pharynx into the esophagus. As the bolus of food enters the pharynx, it stimulates swallowing receptor areas all around the opening of the pharynx, especially on the tonsillar pillars, and impulses from these pass to the brain stem to initiate a series of automatic pharyngeal muscular contractions that pushes the material into the esophagus. ins tem Inhibition of respiration and glottic closure are part of the he Bra CN-IX (Action potensials from here arrive to CNS through sensory branches and synapses reflex response. with other cranial nerves) ot T OVERALL FUNCTIONS INCLUDE Prevent bolus from going into nasopharnynx (Soft palate will close it «levator veli palatini, tensör veli palatini) Prevent bolus from going into larinyx Ensure bolus going into pharynx UES Relaxation (M. Cricopharyngeus) The successive stage of swallowing are automatically controlled in orderly sequence by neuronal areas distributed throughout the reticular substance of the medulla and lower portion of the pons. The areas in the medulla and lower pons that control swallowing are collectively called the deglutition or swallowing center. The pharyngeal stage of swallowing is principally a reflex arc. It is almost never initiated by direct stimuli to the swallowing center from higher regions of the central nervous system. Instead it is almost always initiated by voluntary movement of food into the back of the mouth, which, in turn, elicits the swallowing center. 3- The esophageal stage: Another involuntary phase that promotes passage of food from the pharynx to the stomach. At the pharyngoesophageal junction, there is a 3 cm segment of esophagus in which the resting wall tension is high. (Upper esaphageal sphincter = UES) UES which is formed by cricopharyngeal muscle relaxes reflexly upon swallowing, permitting the swallowed material to enter the body of the esophagus. A ring contraction of the esophageal muscle forms behind the material, which is then swept down the esophagus by a peristaltic wave at a speed of approximately 4 cm/s. The excitatory neurotransmitter released by the vagal nerves innervating the striated muscle and enteric nerves is acetylcholine (ACh). The excitatory and inhibitory neurotransmitters released by the enteric nerves innervating the smooth muscle are less well characterized. There is evidence for ACh and the tachykinins serving as excitatory transmitters and for nitric oxide, VIP, and ATP, serving as inhibitory transmitters. Esophagial Manometry Normally the esophagus exhibits two types of peristaltic movements: Primary peristalsis is simply a continuation of the peristaltic wave that begins in the pharynx and spreads into the esophagus during the pharyngeal stage of swallowing. This wave passes all the way from the pharynx to the stomach in approximately 8 to 10 seconds. Secondary peristalsis: If the primary peristaltic wave fails to move all the food that has entered the esophagus into the stomach, secondary peristaltic wave result from distention of the esophagus by the retained food, and they continue until all the food has emptied into the stomach. These secondary waves are initiated partly by intrinsic neural circuits in the esophageal enteric nervous system and partly by reflexes that are transmitted through vagal afferent fibers from the esophagus to the medulla and then back again to the esophagus through vagal efferent fibers. The event is limited to the smooth muscle component of the esophagus and is the result of activation of enteric nerves. Initiation of secondary peristalsis does not involve extrinsic neural reflexes and, thus, is not accompanied by the oral-pharyngeal phase of swallowing At the lower end of esophagus, extending from about 2 to 5 cm above its juncture with the stomach, the esophageal circular muscle is slightly thickened and functions as a lower esophageal sphincter (LES) or gastroesophageal sphincter. Yet when a peristaltic swallowing wave passes down the esophagus, “receptive relaxation” relaxes the lower esophageal sphincter ahead of the peristaltic wave and allows easy propulsion of the swallowed food into the stomach. The stomach contents are highly acidic and contain many proteolytic enzymes. The esophageal mucosa, except in the lower eighth of the esophagus, is not capable of resisting for long the digestive action of gastric secretions. Fortunately, the tonic constriction of the lower esophageal sphincter helps to prevent significant reflux of stomach contents into the esophagus except under abnornal conditions. Agents and Conditions Affecting Lower Esophageal Sphincter Pressure Increase Decrease Protein meal Chocolate Coffee Alcohol Alkali Peppermint Gastrin Smoking Motilin Gastric acidification Prostaglandins Secretin Metoclopramide Glucagort Methacholine Cholecystokinin Bethariechol Isoproterenol Betazole Atropine d- Motor Disorders of the Esophagus: ACHALASIA sia ala Achalasia is a condition in which food Ach accumulates in the esophagus and the Trypanasoma Cruzi (Chagas Disease) organ becomes massively dilated. It is due to increased resting lower Cardiomyopathy Megacolon esophageal tension, incomplete Mechanism (may be idiopathic) relaxation of this sphincter on swallowing, and weak esophageal peristalsis. Myenteric Plexus Motility of Mid-Distal There are lesions in the vagus nerves and Esophagus NO/VIP lower esophageal sphincter. The condition can be treated by pneumatic LES tone dilation of the sphincter or incision of the esophageal muscle (myotomy). The opposite condition is lower MECHANISMS OF GERD CAUSES esophageal sphincter incompetence, LES Tone Smoking Alcohol, Caffeine (GERD) which permits reflux of Hiatal Hernia Sliding Hernia gastric acid contents into the Intragastric Pressure Pregnancy, Obesity, esophagus. Meals, Gastroparesis(delayed emptying, (DM) This causes heartburn and HCl Production NSAIDs, Alcohol, esophagitis and can lead to Smoking ulceration and stricture due to scarring. The condition can be treated by avoiding irritating foods or surgically, by making a fold of gastric tissue (fundoplication). In infants, antireflux mechanisms i.e., LES function and secondary peristalsis, do not exist, explaining why infants regurgitate so readily, The diaphragm may play a relatively greater role in the prevention of gastroesophageal reflux in infants.