GIT 1: Upper GIT with Accessory Organs 2024 PDF

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WorthwhileClematis

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University of the East Ramon Magsaysay Memorial Medical Center

Carolina C. Jerez, MD

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physiology gastrointestinal tract digestive system anatomy

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This document appears to be lecture notes for a physiology course, focusing on the upper gastrointestinal (GIT) tract and accessory organs. It covers topics such as eating, glands, secretions, and control mechanisms in the digestive system.

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PHYSIOLOGY LECTURE | TRANS #1 LE GIT 1: Upper GIT with Accessory Organs CAROLINA C. JEREZ, MD | 01/15/2024 |...

PHYSIOLOGY LECTURE | TRANS #1 LE GIT 1: Upper GIT with Accessory Organs CAROLINA C. JEREZ, MD | 01/15/2024 | Version #1 04 OUTLINE A. GHRELIN I. Eating X. Abdominal Pain Produced mainly by the stomach; small amounts are released by A. Ghrelin F. Vomiting (Emesis) the brain, small intestines, and pancreas B. Leptin G. Diarrhea One of the two hormones in humans that control eating habits II. Gastrointestinal Tract H. Dyspepsia → Signals the brain that the stomach is empty and that it is time A. Glands/Cells in the (Indigestion) to eat III.Small Intestine I. Non-Abdominal Stimulates the pituitary gland to release growth hormone IV.Control Mechanisms in Conditions Storage of fat Digestive System XI. Physical Assessment May be associated with psychiatric conditions such as anorexia A. Neural Control A. Inspection nervosa B. Hormonal Control B. Percussion B. LEPTIN C. Myogenic Control C. Palpation A protein hormone made by adipocytes V. Movement in the Gut XII. Difficulty Swallowing Other hormone in humans that control eating habits VI. Secretions in the Gut A. Normal Swallowing → Influences appetite satiety VII. Oral Cavity B. Swallowing Control Its primary role is to regulate long term energy balance A. Teeth Pathways → Its goal is to maintain energy reserves B. Tongue C. Substances that affects VIII. Swallowing / Swallowing LES Contraction II. GASTROINTESTINAL TRACT Reflex XIII. Gastroesophageal Reflux Starts from the mouth and ends at the anal cavity IX. Stomach Disease A tube-like organ that works with the gallbladder, pancreas, and A. Gastric Emptying Process A. Phases of Gastric associated glands (e.g. salivary glands) A. Factors Affecting Gastric Secretion Has similar histology throughout Emptying B. Proton Pump → Peculiarities: B. Secretory Cells in the C. Protective Mechanisms ▪ Esophagus: lined by stratified squamous epithelium to Stomach of the Gastric Mucosa prevent erosion due to the food being taken in C. Regulation of Acid D. Other preventive − Upper ⅓ is made up of striated muscle. Hence, it is Secretion mechanisms voluntary D. HCL Secretion E. Gastroesophageal Reflux − Lower ⅓ is made up of smooth muscle Process/Proton Pump Disease (GERD) A. GLANDS/CELLS IN THE STOMACH F. Reduction of Gastric Acid Surface Mucous Cells and Mucous Neck Cells - secrete mucus Secretion and bicarbonate XIV. Review Questions Parietal Cells - secrete hydrochloric acid and intrinsic factor Chief Cells - secrete pepsinogen and gastric lipase Must Lecturer Book Previous Youtube G Cells - secrete gastrin ❗️ Know 💬 📖 📋 Trans 🔺 Video III. SMALL INTESTINE Contains Plicae Circulares with Villi that functions to: SUMMARY OF ABBREVIATIONS → Increase the surface area of the small intestine → Help the food mix with the chyme ANS Autonomic Nervous System → Facilitate absorption of nutrients ICC Interstitial Cells of Cajal LES Lower Esophageal Sphincter UES Upper Esophageal Sphincter IV. CONTROL MECHANISMS IN DIGESTIVE FUNCTION ACh Acetylcholine A. NEURAL CONTROL HCl Hydrochloric Acid VIP Vasoactive INtestinal Peptide NO Nitric Oxide HCO3- Bicarbonate K+ Potassium Na+ Sodium LEARNING OBJECTIVES ✔ Describe the anatomy of the Gastrointestinal Tract ✔ Enumerate the functions of the gastrointestinal system ✔ Describe control mechanisms in the different portions of GIT ✔ Describe activities of the different parts of the GIT in relation to its digestive process ✔ Correlate some clinical conditions to the different GIT process NOTE: The above mentioned learning objectives were lifted from Batch 2025 Trans of the same topic as Dr. Jerez was not able to Figure 1. Nervous Control of the GIT[Lecturer’s PPT] list learning objectives during her synchronous and The digestive system has its own nervous system or the Enteric asynchronous lecture for this topic. Nervous System → Can function autonomously I. EATING A vital part for survival of the living organism. Hence, each living organism must eat at certain times of their lives LE 4 TG 7 | Gallego, Galolo, Gante, Garcia, E.N., Garcia, TE | Gallego, Garcia, G.J. AVPAA |J. Enriquez, T. Guzman PAGE 1 of TRANS 1 G.J, Garcia, R.M., Garcia, C.J. 10 PHYSIOLOGY | LE4 Upper GIT with Accessory Organs | Carolina C. Jerez, MD MYENTERIC PLEXUS OR AUERBACH’S PLEXUS Table 1. Hormonal Mediators in the GIT Found in between the Inner Circular and Outer Longitudinal layers HORMONAL MEDIATORS IN THE GIT of the Muscularis of the Stomach Mainly controls the movements of the digestive system (muscular activity) Ghrelin Glucagon Causes increased rhythm and rate of contractions of the gut wall Leptin Pancreatic Polypeptide → increased peristalsis Gastrin GLP-1 Sends inhibitory signals to control sphincter muscles Cholecystokinin GLP-2 Secretin PYY3-36 SUBMUCOSAL PLEXUS OR MEISSNER’S PLEXUS Insulin Found in between the Muscularis and Submucosa of the Stomach Controls the gastrointestinal secretions, absorption, and local C. MYOGENIC CONTROL blood flow (secretory activity) The intrinsic rhythm of the GI muscle occurring as a slow wave set Controls the local contraction of the submucosa (infolding) by the pacemaker activity of the Interstitial Cells of Cajal (ICC) CENTRAL NERVOUS SYSTEM (cell types found in the circular muscle) Both the Myenteric and Submucosal Plexuses have neuronal Slow Waves - rhythmical changes in membrane potential caused connections from the Sympathetic and Parasympathetic Nervous by variations in sodium conductance Systems (ANS) through which the brain and spinal cord synapse → Unique to GI muscle to cells in the GIT → Intensity usually varies between 5 to 15 mv There are also sensory neurons in the intestinal epithelium that → Frequency ranges in different parts of the human GIT between pass messages from the Myenteric and Submucosal Plexuses to 3 to 12 mins the CNS → Caused by complex interactions among the smooth muscle Factors that can stimulate sensory neurons in the GIT cells → Irritation of gut mucosa → Move as a syncytium for more effective activity → Distention of the gut → Presence of certain chemicals PARASYMPATHETIC NS Stimulates the activity of the Enteric NS Increases most of the GIT activities SYMPATHETIC NS Works opposite the Parasympathetic NS Inhibits most of the GIT activities Strong stimulation of the Sympathetic NS can block the movement of food through the gut REFLEXES Reflexes managed by the Enteric NS → Stimulus originates from the mucosa → Controls GIT secretion and peristalsis Figure 3. Graph of Slow Waves[Lecturer’s PPT] Reflexes that originate from the gut → prevertebral ganglia → gut → Gastrocolic Reflex Spike Bursts - true action potentials → Enterogastric Reflex If the area of the GIT with the slow waves is stimulated → Colonoileal Reflex (mechanical/nervous/chemical) and reaches threshold potential, Reflexes that originate from the gut → CNS → gut spike bursts are activated → Through the vagus nerve → Pain Reflex GENERAL PATTERNS OF MOTILITY → Defecation Reflex Migrating Motor Complexes (MMC) → Cycles of motor activity migrate from stomach to ileum B. HORMONAL CONTROL → Occurs during fasting between periods of digestion (3 phases) → Initiated by Motilin → Migrate aborally (away from the mouth) (5cm/min), occuring every 90 mins. → Increases gastric, pancreatic, and bile secretion → Clears the stomach and intestine of luminal contents for the next meal → Eating stops MMC, inhibits Motilin, and resumes peristalsis and BER GI SMOOTH MUSCLES Function as a syncytium → Gap junctions between the muscle cells make the muscle contract in unison leading to a more effective activity Types: → Unitary/Single-unit → Multi-unit Note: Please review smooth muscle contraction! Figure 2. Hormonal Control of the GIT[University of Waikato] PHYSIOLOGY Upper GIT with Accessory Organs PAGE 2 of 10 PHYSIOLOGY | LE4 Upper GIT with Accessory Organs | Carolina C. Jerez, MD V. MOVEMENT IN THE GUT Figure 6. Daily Secretion of Intestinal Juices[Lecturer’s PPT] CASE SCENARIO: MUMPS/PAROTITIS Usually happens in childhood There is an infection of the parotid glands → affecting salivary secretion VII. ORAL CAVITY Figure 4. Peristalsis vs Segmentation[Lecturer’s PPT] A. TEETH Peristaltic Movement - aboral direction; movement of the bolus of food towards the anal cavity; entails muscular contraction and relaxation of the circular and longitudinal muscles of the GIT Segmentation - non-adjacent segments of the GIT contract and relax for a to-and-fro/forward-backward movement in order to mix the bolus of food with the secretions of the GIT Haustration - Division of the colon into segments called haustra Haustral Contraction - These are slow, segmenting, and uncoordinated movement in the haustra of the large intestine (Occurs every 25 minutes) Mass Movements - modified peristalsis found only in the large intestines (transverse and sigmoid colons) → Slow persistent haustral contractions that propel the chyme through the transverse colon making it fecal in nature (semi-liquid to semi-solid form) Figure 7. Types of Teeth[Lecturer’s PPT] VI. SECRETIONS IN THE GUT Saliva - secreted by the salivary glands (parotid, submandibular, Works in mechanical digestion and sublingual) Temporary teeth (20) - normally start to erupt at 6 months → Secretion is stimulated by the ANS Permanent teeth (32) ▪ Parasympathetic: CN VII, CN IX, and Acetylcholine increase B. TONGUE salivary secretion Contains taste buds ▪ Sympathetic: T1-T3 and Norepinephrine through β → Help in nutrition by stimulating appetite through taste of the receptors increase salivary secretion food → Secreted from the acinar cells → Replaced every 10 days, especially when one eats very hot ▪ Primary secretion contains: Ptyalin, Mucus, Extracellular food Fluid VIII. SWALLOWING / SWALLOWING REFLEX → Goes down into the canals Roughly divided into the oral phase, oral propulsive phase, ▪ Exchange between Na+ (absorbed) and K+ (secreted) pharyngeal phase, and esophageal phase ▪ Passive Cl- absorption The bolus of food is moved toward the back of the oral cavity by ▪ HCO3- secretion the action of the tongue pushing against the hard palate → Functions: → The bolus of food is positioned at the initial part of the ▪ Digestion esophagus, at the upper esophageal sphincter ❗️ ▪ Anti-bacterial/viral/fungal ▪ Composed of striated muscles and is therefore, voluntary in ▪ Lubrication nature → Receptors in the area are stimulated, causing them to open, marking the initiation of the peristaltic movement. It is also referred to as the primary peristaltic movement, which pushes food down the esophagus The nasopharynx is sealed off to prevent entry of air during swallowing, the larynx is elevated, and the pharynx enlarged to accommodate the entry of food Pharyngeal sphincters contract sequentially, squeezing the food down the esophagus through peristaltic movement → The epiglottis closes the trachea as food passes down the esophagus There is an increasing pressure as the food goes down the esophagus until the lower esophageal sphincter (LES) opens, which causes a subsequent drop in pressure as food enters the stomach Figure 5. Functions of Saliva[Lecturer’s PPT] PHYSIOLOGY Upper GIT with Accessory Organs PAGE 3 of 10 PHYSIOLOGY | LE4 Upper GIT with Accessory Organs | Carolina C. Jerez, MD → The lower esophageal sphincter has a phasic contraction, where it may open when the LES tone is decreased, or closed when the LES tone is increased → See Table 2 for factors affecting LES tone → Innervated by ganglion cells which secrete inhibitory neurotransmitters such as Nitric oxide and VIP When there is still food left in the esophagus, it stimulates a secondary peristaltic movement that helps clear the esophagus of the remaining bolus Table 2. Factors affecting LES tone FACTORS THAT INCREASE FACTORS THAT DECREASE LES TONE LES TONE Acetylcholine Nitric Oxide Increased Vasoactive intestinal intraabdominal and peptide (VIP) intragastric pressure Cholecystokinin [Lecturer’s PPT] Gastrin (CKK) Figure 8. Gastric Emptying Sequence Motilin Gastric inhibitory Protein rich food peptide (GIP) Mixing waves (Pink Arrows) are generated by inward stomach Beta adrenergic contractions, pushing the more fluid chyme (Blue Arrows) toward receptor agonists the pyloric sphincter Secretin More solid chyme squeezes past the peristaltic constriction to flow Progesterone back toward the fundus while still remaining in the body of the Prostaglandin E stomach for further breakdown (Orange Arrows) Peristaltic waves (Purple Arrows) are also present, similar in direction to mixing waves, but with greater contraction IX. STOMACH → Contraction strength increases as it goes down in order to An expandable muscular sac, with a rough volume of 50 mL when crush food into finer pieces, allowing for only a few milliliters of empty and can expand up to 4L when full the most fluid chyme through the pyloric opening into the → an empty stomach has an inner surface with multiple folds duodenum (Small red arrows) called rugae which flatten when the stomach is full → More solid portions of the chyme in the pyloric region then Has 4 regions, each with different gastric secretions undergo retropulsive movement to return to the body of the → Cardia - located in the immediate surrounding after the LES stomach for further segmentation and processing (Yellow → Fundus - most superior region of the stomach; proximal to the arrows) cardia B. FACTORS AFFECTING GASTRIC EMPTYING → Body - inside the body are folds/rugae Volume of meal- the stomach takes longer to empty on larger → Antrum meals → Pylorus - region closest to the pyloric sphincter, which leads to Composition of meal- Carbohydrates are the easiest to empty, the small intestine followed by proteins, and then fats The stomach wall has 4 layers Physical state/Viscosity of meal- more liquid chyme empty more → Mucosa, lined with surface epithelium, folds into the underlying easily than more solid/viscous chyme connective tissue of the lamina propria, forming gastric pits Temperature of meal- temperatures that are too high or too low that contain the various gastric glands of the stomach slows gastric emptying → Submucosa Gastrointestinal pH- gastric emptying is slow at low pH, Higher at → Muscularis externa (also has 3 sub layers) alkaline pH ▪ Longitudinal layer ▪ Circular layer C.SECRETORY CELLS IN THE STOMACH ▪ Oblique layer − Present only in the stomach compared to other digestive organs, enables the churning motion used in mechanical digestion → Serosa Receives boluses of food from esophagus and turns it into chyme, a semi-liquid mass of partially digested food Mechanically breaks up food and partially digests protein, while absorbing only very little Serves as a temporary storage that releases only a small amount of chyme into the intestine at a time, allowing the intestines to have adequate time to digest and absorb nutrients A. GASTRIC EMPTYING PROCESS Food from the esophagus that enters the stomach is first forced Figure 9. Gastric Secretory Cells [Lecturer’s PPT] into the fundus Mucous cells- secretes alkaline mucus which prevents the → Pressure in the fundus decreases as the stomach volume stomach from digesting itself increases, it is referred to as receptive relaxation/ → Tight junctions are located between the epithelium, accommodation preventing gastric juices from seeping into the underlying → As the stomach volume increases, food trickles down the body tissue of the stomach where peristaltic movement and segmentation → Injured cells are rapidly replaced within a span of 3-6 days mixes the food with stomach secretions Mucous neck cells- secretes mucus and bicarbonates Parietal cells- secretes hydrochloric acid and intrinsic factor (for Vitamin B12 absorption in the intestines) PHYSIOLOGY Upper GIT with Accessory Organs PAGE 4 of 10 PHYSIOLOGY | LE4 Upper GIT with Accessory Organs | Carolina C. Jerez, MD → breaks up food → denatures proteins → kills ingested bacteria → activates pepsin through conversion of pepsinogen to pepsin, which digests proteins Chief cells- secretes pepsinogen (inactive form of pepsin) and gastric lipase (in infants) Enteroendocrine cells such as: → G cells- Located in the pylorus, secretes gastrin which increases gastric secretions, promotes gastric emptying, and intestinal motility → D cells- Located in the pylorus, secretes somatostatin which reduces gastric secretions and motility while also inhibiting other hormones → ECL-like cells- Located in the fundus, secretes histamine which increases gastric acid production of parietal cells D. REGULATION OF ACID SECRETION Gastric activity is under both neural and hormonal control, falling under 3 phases (which can occur simultaneously), the cephalic, gastric, and intestinal phases Cephalic phase is where 30% of HCl secretion occurs ❗️ Figure 10. Interactions of regulatory mechanisms for acid secretion [Lecturer’s PPT] Stimulators of acid release: ACh, gastrin, histamines → Can be triggered by thought, smell, taste or conditioning inputs Inhibitors of acid release: Somatostatin, prostaglandins → Inputs act on hypothalamus, which relays the information to E. HCL SECRETION PROCESS / PROTON PUMP the medulla, vagus nerve fibers from the medulla then Carbonic acid within gastric parietal cells is dissociated with the stimulates the enteric nervous system to prepare for catalysis of carbonic anhydrase, forming hydrogen ions and digestion bicarbonate (HCO3-) → Vagus nerve signaling may stimulate parietal cells to secrete → When parietal cells are stimulated by ACh, the ff occur: HCl ▪ Using Hydrogen-Potassium ATPase pump, hydrogen ions ▪ may stimulate the release of gastrin, which then elicits the are extruded into the lumen of the stomach in exchange for release of HCl from the parietal cells potassium ions, Chloride (Cl-) is released separately into Gastric phase is where 60% of HCl secretion occurs the lumen, which then forms HCl with the H ions → Stretch receptors in the stomach activate the parasympathetic ▪ On the circulatory end, Sodium-Potassium ATPase nervous system (vagovagal reflex) to release ACh, pumps take up K+ in the bloodstream in exchange for → In distension of stomach: releasing Na+, Cl- is taken up in exchange for HCO3- ▪ Vagus nerve signals parietal cells to release HCl without the use of ATP ▪ Vagus nerve signals the release of gastrin which then ▪ HCO3- is released into the bloodstream, it is also referred to stimulates parietal cells as the alkaline tide → In distension of antrum: ▪ As mediated by the myenteric plexus, a local reflex is triggered, which results in gastrin release, resulting in X. ABDOMINAL PAIN subsequent parietal cell stimulation Types of abdominal pain: → When stimulated by amino acids/small peptides: → Sudden ▪ Gastrin is released in response to the partially digested → Persistent proteins and rising pH, which stimulates the parietal cells → Stabbing → Negative feedback is present in this phase, winding it down in → Generalized response to excessive presence of HCl as the stomach is → Localized emptying Abdominal pain can be accompanied by: Intestinal phase is triggered by arrival of chyme in the duodenum → Vomiting or Emesis → Initially, stretching and presence of partially digested food in the → Diarrhea duodenum triggers the parasympathetic (vagovagal reflex), → Dyspepsia or Indigestion which stimulates the release of intestinal gastrin → Non-abdominal conditions → Next, prolonged distension of the duodenum triggers the enterogastric reflex and release of intestinal hormones such as cholecystokinin (CCK), secretin, and gastric inhibitory peptide which all serve to inhibit gastric activity to allow the intestines to process chyme [Lecturer’s PPT] Figure 11. Fever and Abdominal Pain PHYSIOLOGY Upper GIT with Accessory Organs PAGE 5 of 10 PHYSIOLOGY | LE4 Upper GIT with Accessory Organs | Carolina C. Jerez, MD A. VOMITING (EMESIS) D. NON-ABDOMINAL CONDITIONS Three phases of vomiting Congestive heart failure 1. Prodrome Heart stroke 2. Retching Pneumonia 3. Vomiting Pulmonary embolism Factors that can lead to vomiting Endometriosis → Motion Sickness XI. PHYSICAL ASSESSMENT → Problems with vision Four Basic Skills: → Problems in emotional centers 1. Inspection → Administration of drugs 2. Auscultation → Toxins 3. Percussion 4. Palpation Table 3. Physical assessment of Abdomen NORMAL DEVIATION FROM ABDOMEN FINDINGS NORMAL Perform light No tenderness, Tenderness and palpation followed relaxed abdomen hypersensitivity by deep palpation with smooth of all four consistent tension. Superficial masses quadrants Tenderness maybe Localized areas of present near the increased tension xiphoid process over cecum and Generalized or sigmoid colon localized area of tenderness Mobile or fixed masses Bowel Sounds → Gurgling sounds [Lecturer’s PPT] ▪ Movement of gas and fluid via peristalsis Figure 12. Pathway for Vomiting ▪ Normal bowel sound B. DIARRHEA → Borborygmi Passage of 3 or more loose of liquid stools per day or more ▪ Loud rumbling sounds due to movement of air within the gut frequently than normal ▪ Normal bowel sound Loose stools → Hypoactive → appear softer than normal ▪ Diminished or absent bowel sounds → watery, mush, and shapeless ▪ Peritonitis → may have a foul odor ▪ Proximal obstruction → usually occurs after eating something ▪ Ileus Causes of Diarrhea and Chronic diarrhea ▪ Ischemia → Parasitic infection → Hyperactive → Viral infection ▪ Extremely increased bowel sounds → Bacterial infection ▪ Gastroenteritis → Food intolerance ▪ Laxatives → Food allergy ▪ Inflammatory bowel disease (IBD) → Medications ▪ Bowel obstruction → Intestinal diseases → Hollow, high-pitched tinkles → Gallbladder or stomach surgery ▪ Similar to rain on a tin roof, due to liquid and gas under → Some type of cancer pressure within dilated gut → Diabetes ▪ Small bowel obstruction → Unsuitable lifestyle and diet A. INSPECTION Large intestine Table 4. Abdominal Inspection → responsible for absorption of water, vitamins, electrolytes NORMAL DEVIATION FROM → stool formation and excretion (which do not happen when you PROCEDURE FINDINGS NORMAL have diarrhea, because water stays inside the large intestine Skin: 1- Pale, with white 1- Dark bluish which produces watery stools) 1- Color striae striae is seen in C. DYSPEPSIA (INDIGESTION) 2- Integrity 2- No rashes or cushing syndrome, Pain in the upper abdomen 3- Venous pattern lesions redness in Feeling of fullness 3- Fine veins inflammation Discomfort observable 2- Rashes or Increase sensitivity of the mucosa to the acidity and stretching lesions Overeating 3- Engorged veins Eating too fast Umbilicus 1- Sunken, 1- Deviation from Too much caffeine spicy, fatty food or carbonated drinks 1- Position centrally located midline with mass, Anxiety 2- Color 2- Pinkish hernia, everted Smoking 3- Presence of distension umbilical hernia 2- Bluish PHYSIOLOGY Upper GIT with Accessory Organs PAGE 6 of 10 PHYSIOLOGY | LE4 Upper GIT with Accessory Organs | Carolina C. Jerez, MD B. PERCUSSION Tympany over air-filled structures → When a patient has colic Dullness over fluid or solid organs [Lecturer’s PPT] Figure 13. Percussion Sound ORGANS TO PERCUSS ON THE ABDOMEN Organs to percuss include liver and spleen → The liver is located on the right side, and the spleen is located on the left side → These organs are percussed to determine whether they are enlarged or normal [Lecturer’s PPT] Figure 15. Palpation Procedure XII. DIFFICULTY SWALLOWING A. EVENTS HAPPENING IN A NORMAL [Lecturer’s PPT] SWALLOWING REFLEX Figure 14. Organs to Percuss on the Abdomen 3 phases of swallowing reflex C. PALPATION → Voluntary phase Table 5. Palpation Normal Findings vs. Deviation from Normal ▪ The initial phase NORMAL DEVIATION FROM ▪ You are able to remove the food you have taken in ABDOMEN → Pharyngeal phase FINDINGS NORMAL Perform light No tenderness, Tenderness, and → Esophageal phase palpation followed relaxed abdomen hypersensitivity. Swallowing center by deep palpation with smooth, → Extravagal nuclei of all four consistent tension. Superficial masses. → Nucleus ambiguus quadrants → Dorsal motor nucleus Tenderness may be Localized areas of Cervical ganglia present near the increased tension → Anatomically, the upper portion of the esophagus is composed xiphoid process, of striated muscle. Therefore, voluntary in nature over the cecum, Generalized or Swallowing is initiated voluntarily in the mouth consisting of 3 and sigmoid colon localized areas of different phases tenderness → Oral phase: initiates the swallowing reflex. Food bolus is pushed back activating receptors that initiate the reflex Mobile or fixed → Pharyngeal phase: includes relaxation of the upper masses. esophageal sphincter (UES) ▪ The receptors in the pharynx are stimulated, sending impulses for the UES to relax → Esophageal phase: includes the initial primary peristaltic wave which includes the series of movements of contractions and relaxation. When the esophagus is not cleared of the previously swallowed food a second wave of movements will occur, which is the secondary peristaltic movement ▪ At rest the lower esophageal sphincter (LES) is contracted. Relaxation is mediated by postganglionic parasympathetic, which are inhibitory releasing vasoactive intestinal peptide (VIP) and nitric oxide (NO) ▪ LES is phasically contracting. There are times that it will open, and there are times it will close. PHYSIOLOGY Upper GIT with Accessory Organs PAGE 7 of 10 PHYSIOLOGY | LE4 Upper GIT with Accessory Organs | Carolina C. Jerez, MD [Lecturer’s PPT] Figure 18. Pressure Measurements C. SUBSTANCES THAT AFFECTS THE [Lecturer’s PPT] Figure 14. Swallowing Center LES CONTRACTION Table 6. Substances that Affects the LES Contraction INCREASE LES DECREASE LES CONTRACTION CONTRACTION Hormones Gastrin, motilin, Secretin, substance P cholecystokinin, glucagon, gastric inhibitory peptide, vasoactive intestinal polypeptide, Figure 16. Swallowing Reflex Phases [Lecturer’s PPT] progesterone Neural Alpha-adrenergic Alpha-adrenergic B. SWALLOWING CONTROL PATHWAYS agents agonists, antagonists, Oropharyngeal swallowing is controlled by the brainstem and beta-adrenergic beta-adrenergic affected by skeletal muscle. antagonists, agonists, cholinergic The enteric nervous system controls esophageal swallowing cholinergic agonists antagonists, serotonin with smooth muscle effectors. Medications Metoclopramide, Nitrates, calcium Disorders in oropharyngeal and esophageal swallowing may have domperidone, channel blockers, similar or different causes. prostaglandin F2α, theophylline, There is the spinal cord because as mentioned, striated muscles cisapride morphine, are present on the upper portions of the esophagus meperidine, diazepam, barbiturates Foods Protein Fat, chocolate, ethanol, peppermint XIII. GASTROESOPHAGEAL REFLUX DISEASE A. PHASES OF GASTRIC SECRETION Cephalic Phase → The sight or smell of food will increase gastric secretion → Excitatory events include ▪ Sight or thought of food ▪ Stimulation of taste or smell receptors → Inhibitory events include ▪ Loss of appetite or depression ▪ Decrease in stimulation of parasympathetic division Gastric Phase → The food is already in the stomach Intestinal phase [Lecturer’s PPT] Figure 17. Swallowing Control Pathways → Begins as partially digested food enters the duodenum → Stretch receptors and chemoreceptors in the duodenum Pressure measurements are especially useful to evaluate stimulate reflex pathways through the medulla that initially lead functional disorders with no reliable anatomic correlates. to more gastric secretion, gastric motility, and emptying of the There is also increasing pressure from the UES. As it opens, there stomach. is a decrease in pressure. → But later release of hormones inhibits the rate of gastric The pressure will increase as it goes down the esophagus, and secretion. eventually decrease the pressure because of the opening of the LES to allow the food bolus to go into the stomach. PHYSIOLOGY Upper GIT with Accessory Organs PAGE 8 of 10 PHYSIOLOGY | LE4 Upper GIT with Accessory Organs | Carolina C. Jerez, MD [Lecturer’s PPT] Figure 19. Gastric Secretion Phases [Lecturer’s PPT] Figure 22. Histology of the Stomach [Lecturer’s PPT] Figure 23. Gastric Mucosa [Lecturer’s PPT] Figure 20. Intestinal Phase Mucus/bicarbonate barrier on the surface of the gastric B. PROTON PUMP epithelium → the mucus is very important Proton pump will increase the acid inside the stomach Secreted by mucus cells creating a pH which is near neutral → If you want to decrease acid secretion, use proton pump Production of prostaglandins inhibitors → modulates acid secretion by blocking histamine stimulated In the luminal side, there is Potassium-Hydrogen ATPase increase in cyclic AMP within the parietal cells → Dissociation of carbonic acid in the presence of carbonic When taking the history of the patient, you ask the patient whether anhydrase will secrete hydrogen ion and bicarbonate. they are taking any medications that could affect the activity of the → The bicarbonate will be brought to the blood in exchange for protective mechanisms chloride → For instance, when the patient is taking medications that → The hydrogen that is secreted in the lumen of the stomach will prevent prostaglandin secretion, resulting in gastric acid join with chloride producing hydrochloric acid (HCl) secretion due to histamine In the circulation side, there is Sodium-Potassium ATPase D. OTHER PROTECTIVE MECHANISMS Local microcirculation is important in maintaining surface epithelial metabolic integrity and interstitial fluid bicarbonate Restitution: process by which the gastric epithelium is able to repair rapidly any mucosal damage E. GASTROESOPHAGEAL REFLUX DISEASE (GERD) When there is a repeated reflux of the acidic contents of the stomach to the esophagus causing irritation of the mucosa causing a feeling of discomfort to the individual. → The LES is not closing properly causing a reflux of the acidic chyme back into the esophagus. This ruins the mucosa of the esophagus. Delayed gastric emptying → The food stays longer in the stomach and cannot be processed properly because of some other reasons. → This will delay the passage of food from the stomach to the small intestine [Lecturer’s PPT] Figure 21. Proton Pump → The longer it is delayed, the more irritation it will cause to the C. PROTECTIVE MECHANISMS OF THE GASTRIC mucosa MUCOSA The stomach lumen with the pH of 2, mucus layer, neck cells and the mucus cells secreting the mucus together with the bicarbonate and prostaglandins → These mechanisms can protect the gastric mucosa from high acidity in these areas PHYSIOLOGY Upper GIT with Accessory Organs PAGE 9 of 10 PHYSIOLOGY | LE4 Upper GIT with Accessory Organs | Carolina C. Jerez, MD Artificial Sweeteners Herbs and Spices Trans Fats Raw Foods Alcohol Clean Water (adding lemon Coffee to it will make it more Soda alkaline) Energy drinks Green Juices LIFESTYLE: LIFESTYLE: Smoking Relaxation + Deep Stress breathing Lack of Exercise Laughter Poor Sleep Exercise Lack of Pleasure (fun, joy, Lots of quality sleep happiness) Connection with Others Drugs Love XIV. REVIEW QUESTIONS 1. Movement of the bolus of food towards the anal cavity. It entails muscular contraction and relaxation of the circular and longitudinal muscles of the GIT a. Segmentation b. Mass Movements c. Peristaltic movement 2. The following are phases of swallowing/swallowing reflex [Lecturer’s PPT] except: Figure 24. Gastroesophageal Reflux Disease (GERD) a. Cephalic Phase F. REDUCTION OF GASTRIC ACID SECRETION b. Oral Phase Acetylcholine, histamine, and gastrin will stimulate gastric acid c. Pharyngeal Phase secretion d. Oral Propulsive Phase e. Esophageal Phase 3. All of the following bowel sounds are normal except: a. Gurgling sounds b. Borborygmi c. Hollow, High pitched tinkles 4. This feature of the small intestine is responsible for increasing its surface area, helps with food mixing with chyme, and helps with facilitation of absorption of nutrients: a. Surface Mucous Cells b. Parietal Cells c. Plicae Circulares with Villi d. Muscularis layer 5. Which of the following DOES NOT stimulate gastric acid secretion? a. Hydrochloric Acid b. Acetylcholine c. Histamine d. Gastrin ANS: 1. C. Peristaltic Movement - peristaltic movement is the contraction and relaxation of the muscles in the GIT that produces aboral direction, which moves the bolus away from the mouth towards the anal cavity. 2. A. Cephalic Phase - cephalic phase is a phase in gastric secretion in which a sight or smell of food will increase gastric secretion, thus increasing the appetite. 3. C. Hollow, high pitched inkles - Both A and B are normal bowel sounds. Hollow, high pitched inkles may indicate that you have small bowel obstruction. 4. C. Plicae Circulares with Villi - Both A and B are cells present in the stomach and secrete substances such as mucus and bicarbonate (Surface Mucous Cells) and Hydrochloric Acid and Intrinsic Factor (Parietal Cells). D [Lecturer’s PPT] Figure 25. Mechanism of Gastric Acid Secretion is a layer of the stomach. 5. A. Hydrochloric Acid - This substance is secreted by Parietal Cells in the Table 7. Acid-forming vs. Alkaline-forming Stomach and does not have anything to do with stimulation of gastric acid Acid-forming in the body Alkaline-forming in the body secretion. B,C,and D are the main stimulators. DIET: DIET: V. REFERENCES Animal products (e.g. meat, Most Fruits Canvas Asynchronous Materials provided by Dr. Carolina C. Jerez fish, poultry, dairy) Most Vegetables Grains (e.g. wheat, rye, Leafy Greens corn) Wheatgrass Legumes Sea Vegetables (e.g. Processed Carbohydrates seaweed) Refined Sugar Nuts and Seeds PHYSIOLOGY Upper GIT with Accessory Organs PAGE 10 of 10

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