GIT 1: Physiology of the Upper and Lower GIT PDF

PHYSIO LEC: LE 4 | TRANS 1 GIT 1: Physiology of the Upper and Lower GIT CAROLINA C. JEREZ, MD | 01/06/2024 OUTLINE ​ Long-term Regulation...

PHYSIO LEC: LE 4 | TRANS 1 GIT 1: Physiology of the Upper and Lower GIT CAROLINA C. JEREZ, MD | 01/06/2024 OUTLINE ​ Long-term Regulation →​Maintains normal quantities of energy stores in the form I.​ Regulation of Energy VIII. Bristol Stool Chart of fat in the body Homeostasis IX. Secretion in the GIT →​Regulates food intake and energy balance through A.​ Systems of Food A.​ Salivary Glands Intake Regulation B.​ Hunger and B.​ Gastric Glands C.​ Intestinal Glands regulators ❗️ insulin and leptin, the two most important long-term Appetite a.​ Small Intestine B. HUNGER AND APPETITE HORMONES Hormones Secretion ​ Both Ghrelin and Leptin send signals to the a.​ Ghrelin b.​ Large hypothalamus for regulation of appetite b.​ Leptin Intestine →​Ghrelin: II.​ Introduction to the GIT Secretion ▪​ Increases appetite A.​ Germ Layers of X. Gastrointestinal Tract in ▪​ Found in the stomach the GIT Turmoil →​Leptin B.​ Embryological A.​ Abdominal ▪​ Decreases appetite defects Examination ▪​ Found in adipose tissue C.​ Functional B.​ Abdominal GHRELIN Anatomy Regions D.​ Levels of control of C.​ Referred Pain & ​ 28-amino-acid peptide hormone, first described in 1999 as GIT functions Radiating Pain the endogenous ligand of the growth hormone III. GIT motility D.​ Abdominal Sounds secretagogue receptor (GHSR; ghrelin receptor) →​Stimulates the pituitary gland to release growth hormone [2027 Trans📋] A.​ Types of E.​ GIT Problems Movement F.​ Gastroparesis B.​ Mastication G.​ GERD ​ Produced by endocrine cells lining the stomach and C.​ Movements in the H.​ Diarrhea proximal small intestine. esophagus I.​ Constipation →​Endocrine cells are the source of most of the ghrelin IV. Stomach J.​ Bloating that circulates the blood V. Intestines K.​ Nausea and →​Other cells that secrete ghrelin include P/D1 cells A.​ Small intestine Vomiting located in the fundus (upper part of the stomach) B.​ Large intestine XI. Esophagus ​ Ghrelin increases when the stomach is empty causing VI. Control of Defecation VII. Defecation Reflex A.​ Esophageal Dysphagia is full causing appetite to decrease →​Empty stomach: ↑ Ghrelin = ↑ Appetite ❗️ appetite to increase, and decreases when the stomach A.​ Intrinsic B.​ Achalasia →​Full stomach: ↓ Ghrelin = ↓ Appetite ​ Storage of fat [2027 Trans📋] Defecation Reflex XII. Review Questions B.​ Integrated XIII.​References ​ Associated with psychiatric conditions such as anorexia nervosa [2027 Trans📋] Defecation Reflex SUMMARY OF ABBREVIATIONS ACTIONS OF GHRELIN GIT Gastrointestinal Tract ​ Regulates blood glucose through reduced insulin GHSR Growth Hormone Secretagogue Receptor secretion and by regulating the synthesis and breakdown ❗️ 📣 📖 📋 Must know Lecturer Book Previous Trans of glucose and glycogen ​ Reduces heat production to conserve energy ​ Reduces sympathetic activity LEARNING OBJECTIVES ​ Promotes differentiation and fusion of muscle fibers ✔​ Understand the hormones controlling our desire to eat ​ Regulates bone growth through osteoblast differentiation ✔​ Understand the functional anatomy of the and proliferation gastrointestinal tract ​ Protects bone ✔​ Understand the control mechanisms of ​ Opposes leptin in bone metabolism gastrointestinal activity ​ Highly expressed in metastatic cancer cells ✔​ Understand gastrointestinal motility and secretions ✔​ Review smooth muscle contractions including basal LEPTIN electrical rhythm/ migrating myoelectric complex ​ Protein hormone made by adipocytes [2027 Trans📋] ✔​ Understand some gastrointestinal reflexes ​ Sends signals toward the hypothalamus to indicate that a person has “eaten enough”, boosts metabolism and makes I. REGULATION OF ENERGY HOMEOSTASIS a person burn more calories than normal A. SYSTEMS OF FOOD INTAKE REGULATION ​ ↑ leptin levels = ↑ adipose tissue size, which ​ Short-term regulation communicates energy storage status to the brain →​Prevention of overeating during each meal ​ Leptin expression and circulating levels show circadian →​Involves signaling that arises from the gastrointestinal fluctuations and change with nutritional state tract (GIT) as well as the liver LE 4 TRANS 1 VER 3 TG-1&2: I. Doble, J. Dollano, D. Dolosa, JA. Doringo, IJ. TE: T. Dy, D. Emralino-Casin AVPAA: J. Flores Page 1 of 20 Doringo, J. Dos Remedios, D. Duro, A. Eming, A. Enrico, L. Eralino, N. Escobar, T. Esguerra  ​ Fasting decreases circulating leptin levels while feeding or obesity increases leptin levels ❗️ C. ANATOMY OF THE GIT GROSS ANATOMY Figure 1. The pattern of impulses of non-hypothalamus brain areas towards the hypothalamus and pituitary gland [Lecturer’s PPT] FUNCTIONS OF LEPTIN ​ Long-term regulation of body weight and as an adaptive response to fasting and starvation ​ Mutations in leptin or leptin receptor genes can case abnormalities in the following: →​Obesity →​Hematopoiesis Figure 2. Outline of the GIT [Lecturer’s PPT] →​Immunity →​Reproduction ​ The main parts of the GIT include the following: →​Bone metabolism →​Mouth →​Blood pressure →​Esophagus ​ Deficiencies in leptin can be caused by obesity (caused by →​Stomach leptin-related gene mutations), hypothalamic amenorrhea, →​Small intestine and lipoatrophy. This deficiency may result in the following: →​Large intestine →​Profound obesity →​Anus →​Diabetes mellitus ​ Accessory organs - these organs secrete substances →​Delay in puberty which can lead to Infertility that are utilized for digestion and absorption of food and →​Reduction in immune system response nutrients →​Decrease in sympathetic nervous system activity →​Liver →​Decrease blood pressure →​Pancreas →​Reduction in bone density →​Gallbladder II. INTRODUCTION TO THE GIT A. GERM LAYERS OF THE GIT ​ The gastrointestinal tract (GIT) evolves from 3 germinal layers: →​Mesoderm →​Ectoderm →​Endoderm ​ Gastrulation of the GIT starts at the 3rd week of gestation and ends at the 32nd week of gestation B. EMBRYOLOGICAL DEFECTS ​ Atresia - a condition in which an orifice or passage in the body is closed or absent →​Esophageal Atresia →​Duodenal Atresia →​Jejunal and Ileal Atresia ​ Hypertrophy/Pyloric Stenosis - a condition wherein a tract fails to develop; thickening or narrowing of the pylorus ​ Omphalocele - specific part of the GIT fails to close, causing abdominal contents to fail to return to the abdomen and protrude outside the abdominal cavity while being protected by the peritoneum ​ GI atresia - refers to a condition wherein a part of the GIT fails to develop ​ Meconium Ileus - first stool blocks the last part of the baby’s small intestine PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 2 of 20  Figure 4. Tonic and Phasic Responses in Neuronal Action Potential Generation [Lecturer’s PPT] ​ Tonic Contractions - sustained amounts of calcium allows sustained contractions even in the absence of basal 📣 stimuli 📣 →​ No time for the sphincters to relax 📣 →​ Observed in smooth muscles and sphincters →​ Prevents bolus from moving backward ​ Phasic Contractions - separate rhythmic contractions that Figure 3. Arterial Supply, Venous Drainage, and Lymphatic Vessels of the GIT [Lecturer’s PPT] →​📣 occur at intrinsic frequencies Lasts only for a few minutes (e.g. opening of the ​ Arterial supply of the GIT includes the following: →​Celiac artery →​Hepatic arteries →​📣esophageal sphincter) Peristaltic movements move the food bolus forward (e.g. food will go down to the stomach from the →​Cystic arteries esophagus) →​Gastric arteries HISTOLOGY [2025 Trans 📋] →​Splenic arteries ​ Venous drainage of the GIT includes the following: →​Inferior vena cava →​Hepatic veins →​Renal veins →​Testicular veins ​ Unlike other organ systems of the body, venous drainage from the GI tract does not return directly to the heart but first enters the portal circulation leading to the liver [Berne & Levy, 7th ed 📖] ​ There are sphincters that divide the GIT into several areas. They are usually made up of smooth muscles →​Gastroesophageal sphincters →​Pyloric sphincters →​Ileocecal sphincters →​Internal anal sphincters *space left intentionally blank* Figure 5. Cross Section of GI Tract Tunics [Lecturer’s PPT] Layers (innermost to outermost): ​ Mucosa →​Innermost layer of the GIT PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 3 of 20  →​Parts of the mucosa: information to provide outputs that control movements and ▪​ Epithelium fluid exchange between the gut and the lumen −​ Absorptive enterocytes Table 1.Components of Intrinsic Control [2025 Trans 📋] ◦​ Most abundant type of cell in this layer ◦​ For digestion and absorption Intrinsic (Enteric Nervous System) −​ Columnar epithelial cells are linked by tight Myenteric/ Submucosal/ junctions Aueerbach’s plexus Meissner’s plexus −​ Villi & crypts: Found in the surface area ​ Located between the ​ Found in between the ▪​ Lamina propria circular and longitudinal Muscularis and −​ Composed of loose connective tissue muscle layers [Berne & Levy, Submucosa of the −​ Contains glands, lymph vessels and nodules, 7th ed 📖] Stomach capillaries, and nerve fibers ​ Primarily controls the ​ Innervates the ▪​ Muscularis Mucosa −​ Folds and ridges are formed due to contractions which affect the surface area motility of the GI smooth muscle ​ Secretes ❗️ submucosal layer [Berne & Levy, 7th ed ​ Receives 📖] sensory ◦​ Secretion and absorption is also affected neurotransmitters that information from ​ Submucosa inhibit motility chemoreceptors and →​Composed of loose connective tissue ​ Upon stimulation, it mechanoreceptors in GI →​Contains the following: increases tract ▪​ Submucosa glands ​ Controls the ▪​ Blood vessels ▪​ Tonic contraction of gastrointestinal ▪​ Nerves the gut secretions, absorption, →​Contains the Submucosa/Meissner’s plexus ​ Muscularis externa →​Muscular layers (ICOL): ▪​ Intensity of contraction and local blood flow (secretory activity) ❗️ ▪​ Inner circular layer ▪​ Rate and rapidness −​ Upon contraction, it decreases the diameter of the lumen of contraction ▪​ Outer longitudinal layer −​ Upon contraction, it shortens the length of the digestive system →​Contains the Myenteric/Auerbach’s plexus ▪​ Located between the two muscle layers ▪​ Also part of the ENS ▪​ For motor activity (ex: peristalsis) ​ Serosa/Adventitia →​Outermost layer →​Composed of: ▪​ Serosa −​ Composed of simple squamous epithelium −​ Present in organs suspended in the body wall ▪​ Adventitia −​ No mesothelium −​ Replaces the serosa parts that are not suspended by the mesentery D. LEVELS OF CONTROL OF GIT FUNCTIONS NERVOUS CONTROL ​ Autonomic Nervous System →​Sympathetic →​Parasympathetic ​ Enteric Nervous System →​Myenteric Figure 6. Submucosal and Myenteric Plexus [Lecturer’s PPT] →​Submucosal ENTERIC NERVOUS SYSTEM [2025 Trans 📋] ​ Preganglionic and Postganglionic Fibers of ANS: allows adjustment of activity of enteric plexuses ​ Aka “the second brain” and the Intrinsic Control ​ Interneurons Mechanism ​ Visceral Afferents →​Controls motility and secretions without any direct connections in the CNS →​Serves as the control command center of the GIT so that information gathered may be processed in these areas so that there is a specific output for every input which may affect the muscle, glands and the blood vessels ​ Found in the lining of the digestive tract ​ It contains a complete reflex circuit that is able to detect the physiologic condition of the GIT, then it integrates this PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 4 of 20  AUTONOMIC NERVOUS SYSTEM [2025 Trans 📋] Table 2.Components of Extrinsic Control [2025 Trans 📋] Extrinsic (Autonomic Nervous System) Parasympathetic NS Sympathetic NS ​ Comes from ​ Comes from the craniosacral outflow thoracolumbar outflow ​ Stimulates the activity of ​ Works opposite the the Enteric NS Parasympathetic NS (excitatory) ​ Inhibits most of the GIT ​ Increases most of the activities (inhibitory) GIT activities ​ Strong stimulation of the ​ NT: Acetylcholine Sympathetic NS can (Cholinergic) block the movement of Figure 7. Spike potentials in GIT food through the gut ​ NT: Epinephrine (Adrenergic) ​ 📣 Spike potentials are superimposed on Basal Electrical ​ 📣 The bigger upstroke and downstroke would be that Rhythm 📣 excitatory while Sympathetic stimulation is inhibitory ❗️ RECALL: Parasympathetic stimulation in the GIT is of the Basal Electrical Complex which can be seen all ​ 📣 Muscular tension occurs during spike potentials throughout the GI tract HORMONAL CONTROL [2025 Trans 📋] →​ True action potentials ​ Gastrin →​One of the stimuli: stretch in one area of GIT which may →​From G cells of antrum, duodenum, and jejunum. reach threshold will produce spike potentials →​Increases acid secretion →​Other conditionals include: parasympathetic ​ Cholecystokinin (CCK) stimulation →​From the duodenum (I cells) →​Causes gallbladder contraction and pancreatic secretion 📣 RECALL ​ Two types of smooth muscle: multifiber smooth →​It Inhibits gastric emptying ​ Secretin muscle and unitary smooth muscle →​From S cells of duodenum, jejunum, and ileum →​Inhibits acid secretion and stimulates pancreatic HCO3 secretion ​ Gastric Inhibitory Peptide (GIP) →​ From K cells of duodenum and jejunum →​ Reduces gastric motility and stimulates insulin secretion. ​ Motilin →​ From M cells of duodenum and jejunum Figure 8. Smooth Muscle →​ Increases GIT motility and stimulates the production of pepsin MYOGENIC CONTROL [2027 Trans 📋] ​ The intrinsic rhythm of the GI muscle occurring as a slow wave set by the pacemaker activity of the Interstitial Cells of Cajal (ICC) (cell types found in the circular muscle) ​ Slow Waves - rhythmical changes in membrane potential caused by variations in sodium conductance → Unique to GI muscle → Intensity usually varies between 5 to 15 mv → Frequency ranges in different parts of the human GIT between 3 to 12 mins → Caused by complex interactions among the smooth muscle cells → Move as a syncytium for more effective activity Figure 9. Mechanism of Muscle Contraction *space left intentionally blank* PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 5 of 20  MIGRATING MYOELECTRIC COMPLEX ❗️ Masseter Maxilla Angle and Elevates Mandibular Table 3. Migrating Myoelectric Complex (Masseter= and ramus of Mandible, division of chewer) zygomatic Mandible as in Trigeminal Phase Comments Duration arch closing (V) nerve mouth Phase 1 Quiescent period with rare 30-60 min contractions Temporalis Temporal Coronoid Elevates Mandibular (tempor- = bone process and division of Phase 2 Intermittent action potentials and 20-40 min time or and retracts Trigeminal contraction that gradually increase in temples) ramus of Mandible (V) nerve intensity and frequency as the phase Mandible progresses Medial Medial Angle and Elevates Mandibular Phase 3 Short periods of intense, large, 10-20 min pterygoid surface of ramus of and division of regular contractions. This phase is (medial= the lateral Mandible protracts Trigeminal termed as “housekeeper wave” as it closer to portion of (protrude) (V) nerve enables all undigested materials to midline; pterygoid Mandible be swept pterygoid= process of and 📣 These phases occur during the interdigestive activity winglike) sphenoid bone; moves Mandible 📣 of the GIT Maxilla from side Housekeeper wave: the one that cleans the GIT of the to side previous digestive activity, so that the GIT is again ready for another bulk of activity III. GIT MOTILITY →​ 📣 ​ Move the food From more proximal to more distal portion of GIT ​ Mix and grind ​ Store the foodstuff in its current location A.​ TYPES OF MOVEMENTS ​ Peristalsis [2026 Trans 📋] →​Constriction above the bolus of food by stimulation of acetylcholine and relaxation distal to food bolus by release of nitric oxide and vasoactive intestinal peptides →​Involuntary contraction and relaxation of the smooth muscles both longitudinal and circular muscles allowing Figure 10. Teeth [Lecturer’s PPT] the propulsion of food from the pharynx to the anus →​Adjacent segments of the alimentary canal organs 📣 Teeth help masticate/chew food ​ There are two sets of teeth: Temporary/Milk Teeth and alternatively contrast and contract →​Food is moved distally along the tract Permanent Teeth →​May be primary or secondary ​ Aside from the teeth, the tongue also helps in pushing the ​ Segmentation [2026 Trans 📋] food to the pharynx and esophagus. It is also responsible →​Nonadjacent segments of the alimentary canal organs for the chemical senses (taste). contract SWALLOWING REFLEX →​Mixing movement of the muscles ​ Requires a sequential contraction of the tongue, →​Observed in the small intestine ​ Haustral contractions [2026 Trans 📋] pharyngeal and laryngeal muscles to propel food to the esophagus →​Observed in large intestine →​Movement causing the segments of the large intestine to contract at regular intervals (churning movement Esophageal Phase ❗️ ​ Three phases: Oral Phase, Pharyngeal Phase, and every 25 mins) →​Churning movements help refine the bolus of the food into smaller particles to ease the digestion and absorption of food ​ Mass Movement [2026 Trans 📋] →​Occurs once or twice a day only →​Uniform contractions from the transverse colon moving the contents towards the rectum ​ Sphincter contraction and relaxation ​ Mastication B.​ MASTICATION Table 4. Muscles that move the Mandible Muscle Origin Insertion Action Innervation Figure 11. Swallowing and the structures involved [Lecturer’s PPT] PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 6 of 20  📣 The area where you have the common pathway for respiration and digestion is being closed so that there will be ​ Fundus →​Part of the stomach which receives food that has been no food going to your respiratory system brought through the esophagus →​Where the lower esophageal sphincter is located, which closes after the food enters the stomach →​Accomodation ​ Accommodates a large portion of food without increasing pressure ​ Food can stay in the fundic area for at least an hour →​Fundic emptying ​ Peristaltic movement may also occur aside from accommodation when the fundus is filled up with food ​ Body or Pacemaker Region →​Peristaltic movement that mixes food with secretions containing different enzymes coming from the gastric glands and moves food to the more distal part of the stomach which will then start digestion →​Segmentation ​ Several areas of the stomach are contracting to further mix and make the food finer before it will be delivered to the small intestine ​ It is only the stomach that has an additional muscle layer [Guyton and Hall 14th ed] which is the oblique muscle layer, which is necessary for Figure 12. Swallowing mechanism the churning of food inside the stomach for further refinement of the food C.​ MOVEMENTS IN THE ESOPHAGUS ​ As the food particles are now fine and mixed with different gastric fluids, there will be delivery of the these food PRIMARY PERISTALSIS ​ Swallow-induced [2026 Trans 📋] particles into the antral portion ​ Due to the peristaltic movement and increasing pressure in ​ Occurs after the upper esophageal sphincter opens the area, there will be dilation of the pyloric sphincter ​ Brings down the food from the mouth/ throat down the line where the food can go down–food is now known as chyme to the esophagus and then to the stomach. SECONDARY PERISTALSIS ​ Retropulsive movement ​ Stretch-induced [2026 Trans 📋] →​As it enters the pylorus or the first part of the small ​ If there is food stuck in the esophagus, this area will intestine, there will be resistance since not all food that be stimulated due to stretch. The stretch will incite the has been taken in are fine enough to enter and meet the secondary peristaltic movement. activities in the small intestine →​As a result, chyme will return to the antral area, which further processing will occur until it is fine enough In the esophagus, there are both primary and secondary to be transferred to the small intestine peristalsis III. STOMACH Figure 14. Segmentation of the stomach [Lecturer’s PPT] VI. INTESTINES A. SMALL INTESTINES HISTOLOGY ​ All parts of the GIT may look the same. However, there are some modifications present to have a different function from other portions of the GIT. ​ Movements will still include both peristaltic waves and segmentation Figure 13. Physiological anatomy of the stomach [Guyton and Hall 14th ed] ​ Villi →​Also known as “Absorptive epithelium” PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 7 of 20  →​Increases the absorptive surface for digested nutrients →​Irregularly spaced contractions so that it can be used by the body →​Weak regularly spaced contractions ​ Peristaltic rush →​Powerful and rapid peristalsis which is initiated partly by the autonomic nervous system and partly by the enteric nervous system ​ Ileocecal valve →​Prevents the backflow of the fecal contents from the cecum to the ileum ​ The presence of valves, which are thickened circular muscles, prolongs the stay of chyme into the ileum B. LARGE INTESTINES HISTOLOGY ​ The histology of the large intestine is different from the small intestines, although there are still goblet cells and a columnar type of epithelium, which are absorptive cells. Therefore, absorption of water and minerals can occur in Figure 15. Histology of the Small Intestine [Lecturer’s PPT] this portion of the GIT. ​ Structure of the small intestine →​It is made up of 4 layers ▪​ Peritoneum ▪​ Muscular layer ▪​ Mucosa ▪​ Submucosa →​It consists of columnar epithelial cells, or enterocytes, with tiny microvilli (1 μm long) on their free border. →​Goblet cells that secrete mucus →​These epithelial cells enclose a network of blood and lymph capillaries. →​The lymph capillaries are called lacteals because absorbed fats give the lymph a milky appearance ​ Villi →​The surface area of the small intestine mucosa is greatly increased by permanent circular folds, villi, and microvilli →​The villi are tiny finger-like projections, 0.5 to 1 mm long Figure 17. Histology of the Large Intestine [Lecturer’s PPT] →​They are large and numerous in the duodenum and jejunum, but are smaller and fewer in the ileum COLON SMALL AND LARGE INTESTINAL MOTILITY 📣 ​ First part of the large intestine ​ Functions: →​Absorption of water and electrolytes ​ The chyme becomes more solid and dry →​Changes the chyme to solid feces ❗️ →​For storage of fecal material before its expulsion ​ More absorption of water and minerals can occur before feces is expelled Figure 16. Types of intestinal segmentation movements ​ Segmentation movements of both small and large intestines moving the bolus down the line to more latter portions of the GIT ​ Types of intestinal motility include the following: →​Peristalsis or Regularly spaced peristalsis Figure 18. Segmental contractions in the colon [Lecturer’s PPT] →​Isolated contractions PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 8 of 20  ​ 📣 Unlike peristaltic movements that move fecal material there are segmental contractions only ❗️ from a proximal to a distal segment in the GIT, in the colon, →​Responsible for mixing, not propulsion ​ 📣 Mixing the contents of the large intestine →​No net forward movement →​Occur in the cecum and proximal colon ​ Contractions are associated with sac-like structures called haustra ​ Movements are called haustrations Figure 20. Control of defecation [Lecturer’s PPT] VII. DEFECATION REFLEX A. INTRINSIC DEFECATION REFLEX Table 5. Intrinsic Defecation Reflex ENS MYENTERIC PLEXUS Stimulus Feces enter the rectum - Distention of rectal wall Receptors Stretch receptors in the rectal wall Afferents Sensory fibers terminating in the myenteric plexus Center Myenteric plexus Figure 19. Parts of the human colon. [Lecturer’s PPT] Efferents Motor signals to smooth muscles Effectors Smooth muscle cells of descending colon, →​Mass movements, where several parts of the large sigmoid colon, and rectum intestines are contracting at the same time, move the Response Peristaltic waves forcing feces towards contents 2-3x a day over long distances rectum - Relaxation of internal anal →​There is slow movement of semisolid material to allow sphincter absorption of water in the distal colon →​As rectum fills with fecal material, the smooth muscles B. INTEGRATED DEFECATION REFLEXES of the wall of the rectum contracts →​The internal sphincter will start to relax →​The external anal sphincter is contracted ​ No expulsion of fecal material as long as the external sphincter is contracted ​ Made up of skeletal muscles and is therefore under voluntary control ​ 📣 VI. CONTROL OF DEFECATION Conscious and voluntary control ​ Parasympathetic pathways →​Excitatory to GI function ​ Internal and external sphincters must be relaxed for feces to exit the large intestine *space left intentionally blank* Figure 21. Integrated defecation reflexes [Lecturer’s PPT] PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 9 of 20  ​ 📣 Mass movements are seen in the stimulation of local defecation reflexes →​Stimulation of parasympathetic control of the defecation reflex →​Causes relaxation of external anal sphincter ​ Both internal and external are now relaxed to evacuate the formed feces VIII. BRISTOL STOOL CHART Figure 23. Salivary glands [Lecturer’s PPT] SALIVA PRODUCTION Figure 22. Bristol stool chart [Lecturer’s PPT] Table 6. Stool types BRISTOL STOOL CHART: STOOL TYPES Type 1 Separate hard lumps Severe constipation Type 2 Lumpy and sausage-like Mild constipation Type 3 A sausage shape with cracks in the surface Figure 24. Salivary Gland Production Stages [Lecturer’s PPT] Normal ​ Two stages Type 4 Like a smooth, soft sausage or snake →​Stage 1: Fluid Secretion Normal ▪​ Plasma-like, NaCl-rich fluid Type 5 Soft blobs with clear-cut edges →​Stage 2: NaCl Reabsorption and K+ Secretion Lacking fiber ▪​ Exchange of Na and K Type 6 Mushy consistency with ragged edges ▪​ K-rich, NaCL-poor Mild diarrhea Type 7 Liquid consistency with no solid pieces Severe diarrhea ​ 📣▪​ Hypotonic fluid Initially, the saliva that is made is Na-rich and plasma-like, but when it starts to be secreted, it becomes K-rich and hypotonic. IX. SECRETIONS IN THE GIT Table 7. Types of saliva from each salivary gland A. SALIVARY GLANDS Percentage of Acinar Whole ​ 3 pairs Gland Viscosity Unstimulated Type →​Parotid gland Daily Saliva →​Submandibular gland Parotid Serous Watery 25 →​Sublingual gland Submandibular MIxed Semi 71 ​ Secrete saliva (mix of mucus and serous fluid) into the Viscous mouth Sublingual Mucous Viscous 3-4 →​Moistens food into a mass called bolus Minors Mucous Viscous Trace →​Contains salivary amylase which begins starch breakdown →​Has lysozymes and antibodies that kill bacteria ​ ​ ❗️ 📣 1.5L-2L of saliva are made per day. Condition affecting salivary production: Parotitis →​Example: Endemic parotitis, a.k.a mumps B. GASTRIC GLANDS ​ Different secretions of the cells in the gastric glands found in the stomach PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 10 of 20  Table 10. Major Gastrointestinal Hormones ❗️ Stimuli for Hormone Location Major Activity Release Antral G cells in the distension, vagal Gastric acid and Gastrin antrum of the stimulation, pepsinogen stomach peptides, amino secretion acids Inhibits gastrin and HCl release Inhibits D cells in the pancreatic and antrum of the Duodenal Somatostatin gastric stomach, acidification secretions pancreatic islets Decreases Figure 25. Gastric glands [Lecturer’s PPT] gastrointestinal transit Decreases Amino acids, gastric acid Gastric glucose, acid in K cells in the secretion Inhibitory duodenum, and duodenum peptide long-chain fatty Increases insulin acids release Gallbladder contraction and I cells in the sphincter of Amino acids, Cholecysto- duodenum and Oddi relaxation fatty acids, kinin proximal proteins jejunum Pancreatic enzyme secretion Pancreatic Figure 26. Gastric glands [Lecturer’s PPT] secretion of Table 8. Secretory products of cells in the gastric gland Gastric Gland Cells Secretory Product ❗️ Secretin S cells in duodenum and Acid, fat, or bile proximal in the duodenum water and bicarbonate jejunum Surface mucous cells Mucin in an alkaline fluid Alkalization of Mucous neck cells Mucin in an acidic fluid bile Parietal cells HCl and intrinsic factor Increases intestinal Chief cells Pepsinogen and lipase secretion of G cells/Enteroendocrine Gastrin water and cells Acetylcholine Vasoactive Neuroendocrine electrolytes (Vagal Table 9. Phases of Gastric Secretion Phase ❗️ Action Intestinal Peptide cells throughout the GI tract mediated) and fat Increases motility The sight, taste, smell, or thought of Inhibits gastrin food triggers parasympathetic release Cephalic Phase Acid reflexes. Gastric juice is secreted in Increases response. environment, motility by Duodenum and vagal Motilin activating the Jejunum stimulation, Food in the stomach chemically and migrating motor gastrin-releasing mechanically stimulates the release of complex peptide gastrin, which, in turn, stimulates the Triggers growth Gastric Phase secretion of gastric juice; reflex hormone release responses also stimulate gastric juice Ghrelin Stomach Fasting state secretion. Believed to mediate hunger Stimulates As food enters the small intestine, it Gastrin- release of most stimulates intestinal cells to release Releasing Stomach and Postprandial GI hormones intestinal gastrin, which, in turn, briefly Peptide small bowel state Intestinal Phase promotes the secretion of gastric juice (Bombesin) Believed to from the stomach wall. This phase mediate satiety primarily inhibits gastric juice secretion. ​ PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 11 of 20  →​Water →​Mucus →​Mineral salts →​Enzyme: Enterokinase (enteropeptidase). ​ The enzymes involved in completing the chemical digestion of food in the enterocytes of the villi are: →​Peptidases →​Lipase →​Sucrase, maltase, and lactase Figure 27. Mechanism of HCl secretion by gastric parietal cells [Lecturer’s PPT] ​ Hydrochloric acid secretion in parietal cells is driven by the hydrogen-potassium ATPase pump (H⁺-K⁺ ATPase). →​H⁺ Secretion: H⁺ ions are actively exchanged for K⁺ via the H⁺-K⁺ ATPase, with K⁺ recycled. Na⁺-K⁺ ATPase on Figure 29. Function of Digestive Secretions [Lecturer’s PPT] the basolateral membrane supports this process. →​HCO₃⁻ Formation: OH⁻ reacts with CO₂ to form HCO₃⁻ (via carbonic anhydrase), exchanged for Cl⁻, which LARGE INTESTINAL SECRETIONS combines with H⁺ to form HCl in the canaliculus. →​Final Secretion: Water follows osmotically, resulting in secretion of HCl, KCl, and NaCl into the gland lumen. C. INTESTINAL GLANDS OR CRYPTS OF LIEBERKÜHN ​ Situated below the surface between the villi ​ The glands and intestinal villi are covered by epithelium which contains multiple types of cells. →​Enterocytes - Absorbing water, electrolytes →​Goblet Cells - Secreting mucus →​Enteroendocrine Cell - Secreting hormones →​Paneth Cells - Secreting antimicrobial peptides Figure 30. Large Intestinal Secretions [Lecturer’s PPT] ​ This is stimulated by →​Vagus nerve →​Secretin →​Local Irritation X. GASTROINTESTINAL TRACT IN TURMOIL ​ Common signs and symptoms include: Figure 28. Crypts of Lieberkühn in the small intestine →​Abdominal pain [Lecturer’s PPT] →​Nausea SMALL INTESTINE SECRETIONS →​Vomiting (SUCCUS ENTERICUS) →​Bloating ​ Secretion from the small intestine is called succus →​Diarrhea entericus →​Constipation ​ Volume: 1800 mL/day →​Dysphagia ​ The principal constituents of intestinal secretions are: →​Heartburn PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 12 of 20  A. ABDOMINAL EXAMINATION ​ Crucial for diagnosis of abdominal conditions ​ It decreases the need for imaging and facilities diagnosis when performed correctly ​ Briefly explains the purpose of the different steps to the patient ​ Parts of the examination include: →​Visual assessment →​Auscultation →​Percussion →​Palpation →​Digital rectal examination B. ABDOMINAL REGIONS ​ Different abdominal regions: →​Epigastric region →​Left & Right Hypochondrium →​Umbilical region →​Left & Right Lumbar →​Hypogastrium Figure 33. A Map of different etiological origins of referred pain [Lecturer’s PPT] →​Left & Right Iliac region ​ Radiating Pain →​Pain that spreads from one area of the body to another. →​ 📣 Initially confined in a small area. It would then be radiating or going to some other places in your body Table 11. Summary of Referred and Radiating Pain REFERRED VS. RADIATING PAIN Referred Pain Radiating Pain Presents as somatic pain Pain that spreads from one area to another Initially confined to a small Various patterns of distribution area Autonomic nerve afferent - traveling with somatic nerves Figure 31. Abdominal Regions [Lecturer’s PPT] Well-defined dermatomal 📣 - pattern Possible organs that may have pathology looking at the different areas D. ABDOMINAL SOUNDS ​ From the video shown in the PowerPoint: →​There are multiple bowel sounds on the four quadrants of the lower torso ​ Bowel sounds heard in the lecture: →​Borborygmus →​Diarrhea →​Hyperactive →​Irritable bowel syndrome →​Normal →​Post-op →​Ulcerative colitis Figure 32. Potential abdominal areas & organs to cause abdominal E. GIT PROBLEMS pain [Lecturer’s PPT] ​ Motility Problems →​Term that affects the different parts of the GIT C. REFERRED PAIN & RADIATING PAIN →​Problems may arise due to dysfunction in nerves or ​ Referred Pain muscles which may lead to dysfunction in GIT →​Occurs when visceral pain sensation presents as contraction or relaxation. somatic pain →​There is inability of the GIT contents to be propelled in →​Various patterns of distribution the absence of mechanical obstruction. →​Due to autonomic nerve afferent traveling with somatic 📣 nerves, which have a well-defined dermatomal pattern Sometimes it is not in the area where you have the pain but rather, far from the area where you have the actual CASE #1: WHAT IS WRONG WITH LOLO? A 54 year old male presented himself to his physician because of difficulty swallowing of 3 months duration for pathology. solid and liquid foods. This was associated with nausea and vomiting with associated weight loss. After PE and PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 13 of 20  laboratory examinations, a diagnosis of Achalasia was considered. ​ Recall: Swallowing Reflex ​ Different Stages of Swallowing: ▪​📣 →​Oral Preparatory stage Food is still in the mouth and you’re chewing →​Oropharyngeal stage →​Pharyngeal stage →​Esophageal stage F. GASTROPARESIS ​ There is a delay of the stomach contents to empty into the small intestines ​ Factors affecting gastric emptying: →​Volume of the food →​Type of meal (Fatty) →​Osmotic pressure →​Physical states of gastric contents Figure 36. Anatomy of Gastroesophageal Reflux Disease [Lecturer’s PPT] →​Viscosity ​ In Figure 36, the Lower esophageal sphincter and the →​Body position flap valve remain open so there is regurgitation of food materials (food previously swallowed) back into the esophagus. ​ Common Symptoms of GERD: →​ Chest pain →​ Painful burning sensation in the throat or chest →​ Trouble swallowing or eating normally Developing a sour taste in the mouth (due to the backflow of the acid from the stomach) →​ Wheezing, asthma symptoms, chronic coughing, and difficulty breathing →​ Excessively salivating (occurs in order to maintain Figure 34. Different etiology for gastroparesis.[Lecturer’s PPT] the acidity of the stomach within that secretion. It helps prevent different signs and symptoms with G. GERD (GASTROESOPHAGEAL REFLUX DISEASE) GERD) ​ GERD is a problem in the gastrointestinal tract due to the →​ Tooth erosion inability of the Lower Gastroesophageal Sphincter to →​ Belching close effectively, the contents of the stomach go back (reflux of materials) into the esophagus. Therefore, there will be erosion which will hurt the mucosa in the esophagus and there will be inflammatory changes in the lower part of the esophagus. ​ Otherwise known as: →​ Heartburn →​ Regurgitation →​ Dysphagia →​ Chronic cough Figure 37. Common Symptoms of Gastroesophageal Reflux Disease Figure 35. Mechanism of Gastroesophageal Reflux Disease [Lecturer’s PPT] PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 14 of 20  STEPS TO RELIEVE ACID REFLUX ​ Lifestyle changes ​ Maintaining healthy weight →​Overweight individuals often experience stomach night when lying down. ​ Quit smoking 📣 contents refluxing into the esophagus, especially at ​ Elevate the head of your bed →​Lie down in a semirecumbent position ​ Don’t lie down shortly after a meal 📣 ​ Slowly eat food and chew thoroughly ​ Avoid trigger foods (fried and fatty foods) ​ Avoid carbonated drinks ​ Avoid tight-fitted clothing Figure 39. Types 1 and 2 on the Bristol Stool Chart can indicate constipation. [Lecturer’s PPT] ​ 10 Causes of Constipation → Not eating enough fiber → Not drinking enough water → Out-of-balance gut bacteria → Certain medications → Too much supplemental Calcium or Iron → Eating too much dairy → Eating too much sugar and unhealthy fats Figure 38. Pathophysiology, Pathogenesis, and management of Gastric disorders [Lecturer’s PPT] 📣 → Depression ​ The gastrointestinal tract and the microbiota are interconnected H. DIARRHEA ​ Depression may alter the eating habits of an individual causing them to either eat less or more ​ Loose, watery stools more than 3x a day than they usually do, which may result to ​ You may also have cramps, nausea, and an urgent need to constipation have a bowel movement. → Lack of physical activity ​ Normal Bowel Functions → Laxative abuse → 3 bowel movements per day to 3 per week ​ The use of laxatives habitually or frequently higher → No blood (even under microscope) than the recommended dose to stimulate bowel → Easily passed without pain or cramping movements. → Well-formed ​ Consequences: dehydration, electrolyte imbalance, Table 12. Types of Diarrhea Type of Diarrhea Cause ​ 📣 and laxative dependence. Excessive use of laxatives may be prevented by eating the right proportions of different foods Vibrio cholerae, viral Secretory gastroenteritis Table 13. Types of Laxatives Lactose intolerance, congenital Type of Laxatives Examples Osmotic metabolic disease, drugs, or Ispaghula husk supplements Bulk-forming Laxatives Methylcellulose Bacterial dysentery (EHEC, Bran Shigella), chemotherapy, Inflammatory Senna radiation, inflammatory bowel Bisacodyl disease Stimulant Laxatives Sodium picosulfate Hypermotility, diagnosis of Glycerin suppositories Motility exclusion Lactulose Osmotic Laxatives Magnesium sulfate I. CONSTIPATION Phosphate enema CASE #3: Docusate sodium Fecal Softeners Liquid Paraffin This is a 12-year-old male presenting with a history of chronic Arachis Oil constipation. Mother cannot remember when he first passed meconium. She does not report the use of glycerin Prucalopride Prokinetic Agents suppositories in infancy. Attempted toilet training at 3 years of Tegaserod age. Fecal incontinence began around 4–5 years of age. ​ It is the decrease in the frequency of stool ​ Less than one stool in 3 days ​ Type 1 and 2 in the Bristol Stool Chart PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 15 of 20  J. BLOATING ​ Cerebral Cortex ​ GIT/Vestibular Nuclei ​ Chemoreceptor Trigger Zone (CTZ) ​ Mechanism of Vomiting →​Heaving, increased salivation, and retching. →​Relaxation of the pyloric sphincter causes the retropulsive movement of stomach contents upwards. The increased peristaltic movement toward the 📣 esophagus propels these contents further up the tract →​Increase in abdominal pressure with a decrease in chest and thoracic pressure →​Contraction of the abdominal muscles expelling stomach contents Figure 40. Mechanism of Bloating and Distension [Lecturer’s PPT] →​ Stages of Vomiting: Pre-ejection, Retching, and ​ Rapid enlargement of the abdominal area ​ Causes of Bloating 📣 Expulsion of Vomitus XI. ESOPHAGUS ​ Once there is an increase in the pressure in the upper esophageal sphincters, it will stimulate the peristaltic movement down the line and it will open your lower esophageal sphincter to allow the food taken in to your stomach. ​ In your upper esophageal sphincter, some of the muscles are not smooth muscles, but rather striated muscles →​Striated Muscles: Innervated by your somatic nerves. →​Smooth muscles: Innervated by the enteric nervous system and autonomic nervous system. ​ The gastrointestinal tract is divided by sphincters, in the esophagus, there are upper and lower esophageal sphincters. Figure 41. The Five “F’s” of Bloating [Lecturer’s PPT] →​They are necessary, as they allow the backflow of the food that has been taken in from one part to another, in → Gas ​ 📣 Talking while eating and improper chewing of this case, from the stomach back to the esophagus. ​ The major cause of bloating ​ ❗️ food may cause gas to accumulate in the stomach 📣 This may be very painful since the pain may ​ What movements are observed in the esophagus during swallowing? →​Primary Peristaltic Movement migrate to different abdominal regions as air passes ▪​ It is stimulated by swallowing through the GI tract ▪​ This helps bring the food to the stomach. → Urinary Retention → Pregnancy → Constipation ▪​📣 →​Secondary Peristaltic Movement This is due to the food particles that may not go down the stomach, therefore another peristalsis may → Obstruction be initiated. ​ 📣 → Gastroparesis Absence of GI tract movement which slows down the movement of food throughout the tract ​ Are the gastroesophageal sphincters contracted or relaxed during swallowing? →​Lower gastroesophageal sphincters will be phasically contracting 📣 K. NAUSEA AND VOMITING ​ Chief indicator of GIT abnormality ​ Nausea comes first before vomiting ❗️ →​The opening of the sphincters will only last for a few minutes so that the movement of food will go down to your stomach. ​ The emetic stimulus may be: →​Toxins in food (e.g. norovirus, vomitoxin, staphylococcal enterotoxin, brevetoxin, domoic acid) CASE #2: JERRY’S FIERY FEELING →​Abnormal motion sickness Jerry is a 45-year old male weighing 270lbs; 6ft with a BMI →​Disease (e.g. gastroparesis, chronic unexplained of 35.6 who reported to his doctor that he was having a nausea & vomiting, kidney failure) fiery, burning sensation in his chest which was worse at →​Side effect of therapy (e.g. cytotoxic drugs, surgery and night so that he had to sleep in an upright anesthesia, radiation, opioid analgesics, dopamine D2 (semi-recumbent) position. He reported that he has a agonists) feeling in his throat which made swallowing difficult. ​ Nausea is an unpleasant sensation that causes learned aversion, leading to learned avoidance. An upper GI endoscopy was done which showed ​ Vomiting is a reflexive response to nausea that causes inflammation of the lower part of the esophagus. An food and toxins to be expelled from the upper gut lumen. increase in salivary secretion was also noted– a symptom ​ Neural Pathways for Nausea and Vomiting commonly associated with gastric acid regurgitation. →​Afferent Pathways to the Vomiting Center PHYSIOLOGY GIT 1: Physiology of the Upper and Lower GIT Page 16 of 20  ​ Decreases gastric Recall: secretions Gastric Glands - there are several types of cells that can ​ Strongly decreases secrete several products gastric motility Cholecystokinin Duodenum ​ Increases gallbladder contraction ​ Increases pancreatic enzyme secretion ​ Gastrin, acetylcholine and histamine - increases gastric acid secretions A.​ PROBLEMS IN THE ESOPHAGUS ESOPHAGEAL DYSPHAGIA ​ Difficulty of swallowing (dysphagia) food through the esophagus ​ Causes of Esophageal Dysphagia →​Achalasia →​Spasms →​Esophageal Narrowing →​Esophageal Cancer →​Esophageal Blockage Figure 42. Gastric Glands [Lecturer’s PPT] →​Esophagitis →​Scleroderma Table 14. Cells of the gastric glands and their secretory products →​Radiation Treatment Cells of the Gastric Glands Secretory Products ​ Possible treatment: Esophageal Dilation Surface Mucous Cells Mucin in an alk