GI Physiology Lectures 46-51 PDF

GI PHYSIOLOGY -- LECTURES 46-51 =============================== **[Lecture 46 - GI Structure & Function]** - Differentiate importance of sympathetic and enteric nervous systems in digestive function. *(Listed twice)* - SNS -- Decreases digestive processes due to fight and flight,...

GI PHYSIOLOGY -- LECTURES 46-51 =============================== **[Lecture 46 - GI Structure & Function]** - Differentiate importance of sympathetic and enteric nervous systems in digestive function. *(Listed twice)* - SNS -- Decreases digestive processes due to fight and flight, has a net inhibitory effect (indirectly by vasoconstriction); (Secretions and sensory) - ENS -- Direct all contractile, secretory, and endocrine GI functions in the absence of extrinsic innervation. Referred to as the second brain. - Myenteric (Auerbach) -- rhythmic contractions, gut motility - Submucosal (Meissner) - secretions and sensory function - Distinguish regional innervation of the esophagus. - Vagus nerve (CN X) innervates the upper GI tract, including the striated muscle of the upper third of the esophagus; parasympathetic - Sympathetic innervation of the proximal esophagus is derived primarily from the cervical and upper thoracic paravertebral ganglia, whereas the lower esophageal sphincter is derived from the celiac ganglion **[Lecture 47 - GI Motility]** - Recognize dysphagia and recall regulatory mechanisms of lower esophageal sphincter opening. - Dysphagia -- Difficulty swallowing - Innervation of the lower esophageal sphincter is derived from the celiac ganglion - Esophageal Spasms -- Esophageal body is primarily involved - Diffuse -- contractions are uncoordinated - Nutcracker -- amplitude is excessive - Achalasia -- Lower esophageal sphincter and esophageal body are both involved - Failure of normal relaxation of lower esophageal sphincter associated with uncoordinated contractions of the thoracic esophagus - Treatment -- calcium channel blockers and nitrates, Myotomy (procedure to cut muscle to help with obstruction), botox - Distinguish between inhibitory and stimulatory innervations in GI motility. - SNS is inhibitory and mediated by norepinephrine - PNS is stimulatory and mediated by acetylcholine - ENS -- Direct all contractile, secretory, and endocrine GI functions in the absence of extrinsic innervation. Referred to as the second brain. - Myenteric (Auerbach) -- rhythmic contractions, gut motility - Submucosal (Meissner) - secretions and sensory function - Motor neurons in the myenteric plexus release Ach and Substance P, which cause smooth muscle contraction - Inhibitory motor neurons release vasoactive intestinal peptide (VIP) and nitric oxide (NO), which cause smooth muscle relaxation - Distinguish ionic basis of slow wave potentials in GI motility. - Slow waves originate in the Interstitial Cells of Cajal (ICC), which is the pacemaker - ICC membrane depolarization is due to Ca^2+^ influx and is up to 10K times higher than extracellularly - Repolarization is due to K^+^ channels opening and efflux **[\ ]** **[Lecture 48 - GI Salivary and Gastric Secretions]** - Determine likely cause of GI symptoms and role of somatostatin in alleviation of those symptoms. - Somatostatin is inhibitory and produced from the D cells regulation of gastrin secretion (inhibits acid) - Inhibits parietal cells, histamine, and gastrin - Peptic ulcers -- over acidity in the stomach - Achlorhydria -- autoimmune condition of parietal cells resulting in decreased acid production - Predict effect of vagus associated compounds on gastrin release. - Gastrin is from the G cells - Vagus nerve gastrin-releasing peptide (GRP) / bombesin G cells parietal cell H^+^ release and gastric mucosa growth (trophic influence) - Indirectly: Vagal stimulation also increases the release of histamine from enterochromaffin-like (ECL) cells in the stomach. Histamine, in turn, binds to H₂ receptors on parietal cells, stimulating the production of gastric acid. - Acidic environment has negative feedback on G-cell release of gastrin. - Somatostatin inhibits G cell gastrin secretion **[Lecture 49 - GI Accessory Secretory Organs I]** - Recall pancreatic fluid synthesis and sequence for aqueous component. - Enzymes are secreted by the acinar cells, which aqueous components are secreted by the centroacinar cells, which is then modified by ductal cells - ACh and CCK act on ductal cells - Provides rapid neutralization of acidic chyme - See PPT - Recall ionic composition of pancreatic fluid and how it is affected by flow rate. - A diagram of a fluid composition Description automatically generated **[\ ]** **[Lecture 50 - GI Accessory Secretory Organs II]** - Understand the bilirubin breakdown pathway. - Most breakdown is in the spleen, the rest in the RES, including the liver - Recognize biliary cancer symptoms and causes. - Biliary cancer (cholangiocarcinoma) is a rare but aggressive cancer of the bile ducts, and it typically presents with jaundice, abdominal pain, fatigue, and weight loss. Early detection is difficult due to the lack of specific symptoms in the early stages. Several risk factors, including chronic bile duct inflammation, PSC, cirrhosis, and parasitic infections, can increase the risk of biliary cancer. Treatment is often limited to surgical resection in early stages, with chemotherapy and palliative care options for advanced disease. **[Lecture 51 -]** **[When Things Go Wrong]** - Recall the role of the arcuate nucleus in appetite regulation and which neuropeptides are present. - The arcuate nucleus is central to appetite regulation, and its neurons are influenced by a variety of neuropeptides and hormones. NPY and AgRP promote hunger and increase food intake, while POMC, α-MSH, and CART suppress appetite. The arcuate nucleus integrates signals from peripheral hormones like leptin, insulin, and ghrelin to maintain energy homeostasis, ensuring that food intake is balanced with the body\'s energy needs. - AgRP is most potent and long lasting - Basis of IBS-D diagnostic antibody test. - Two antibodies - If either are elevated, the test is considered positive and patient can be diagnosed with IBS-D or IBS-M - Antibodies are Anti-CdtB and Anti-Vinculin - If both are not elevated, the test is considered negative [**Unknown Lecture -** **GI Digestion and Absorption**] - Distinguish between CCK, VIP and bicarbonate with respect to roles in gastric motility to determine source of symptoms/presentation. - CCK plays a critical role in regulating gastric motility by slowing gastric emptying and stimulating gallbladder contraction, leading to symptoms like nausea, bloating, and right upper quadrant pain in cases of gallbladder dysfunction. - VIP generally promotes gastric motility through smooth muscle relaxation, but an excessive VIP (as in a VIPoma) leads to watery diarrhea, hypokalemia, and achlorhydria. - Bicarbonate helps to neutralize stomach acid and protect the gastric lining. Problems with bicarbonate secretion (e.g., in conditions like pancreatitis) lead to gastritis or peptic ulcers, while excess bicarbonate can result in alkalosis and digestive discomfort. - Thus, understanding the roles of these substances allows clinicians to distinguish between different gastrointestinal conditions based on the pattern of symptoms, contributing to accurate diagnosis and treatment. GI PHYSIOLOGY -- LECTURES 46-51 =============================== **[Lecture 46 - GI Structure & Function]** - Differentiate importance of sympathetic and enteric nervous systems in digestive function. *(Listed twice)* - SNS -- Decreases digestive processes due to fight and flight, has a net inhibitory effect (indirectly by vasoconstriction); (Secretions and sensory) - ENS -- Direct all contractile, secretory, and endocrine GI functions in the absence of extrinsic innervation. Referred to as the second brain. - Myenteric (Auerbach) -- rhythmic contractions, gut motility - Submucosal (Meissner) - secretions and sensory function - Distinguish regional innervation of the esophagus. - Vagus nerve (CN X) innervates the upper GI tract, including the striated muscle of the upper third of the esophagus; parasympathetic - Sympathetic innervation of the proximal esophagus is derived primarily from the cervical and upper thoracic paravertebral ganglia, whereas the lower esophageal sphincter is derived from the celiac ganglion **[Lecture 47 - GI Motility]** - Recognize dysphagia and recall regulatory mechanisms of lower esophageal sphincter opening. - Dysphagia -- Difficulty swallowing - Innervation of the lower esophageal sphincter is derived from the celiac ganglion - Esophageal Spasms -- Esophageal body is primarily involved - Diffuse -- contractions are uncoordinated - Nutcracker -- amplitude is excessive - Achalasia -- Lower esophageal sphincter and esophageal body are both involved - Failure of normal relaxation of lower esophageal sphincter associated with uncoordinated contractions of the thoracic esophagus - Treatment -- calcium channel blockers and nitrates, Myotomy (procedure to cut muscle to help with obstruction), botox - Distinguish between inhibitory and stimulatory innervations in GI motility. - SNS is inhibitory and mediated by norepinephrine - PNS is stimulatory and mediated by acetylcholine - ENS -- Direct all contractile, secretory, and endocrine GI functions in the absence of extrinsic innervation. Referred to as the second brain. - Myenteric (Auerbach) -- rhythmic contractions, gut motility - Submucosal (Meissner) - secretions and sensory function - Motor neurons in the myenteric plexus release Ach and Substance P, which cause smooth muscle contraction - Inhibitory motor neurons release vasoactive intestinal peptide (VIP) and nitric oxide (NO), which cause smooth muscle relaxation - Distinguish ionic basis of slow wave potentials in GI motility. - Slow waves originate in the Interstitial Cells of Cajal (ICC), which is the pacemaker - ICC membrane depolarization is due to Ca^2+^ influx and is up to 10K times higher than extracellularly - Repolarization is due to K^+^ channels opening and efflux **[\ ]** **[Lecture 48 - GI Salivary and Gastric Secretions]** - Determine likely cause of GI symptoms and role of somatostatin in alleviation of those symptoms. - Somatostatin is inhibitory and produced from the D cells regulation of gastrin secretion (inhibits acid) - Inhibits parietal cells, histamine, and gastrin - Peptic ulcers -- over acidity in the stomach - Achlorhydria -- autoimmune condition of parietal cells resulting in decreased acid production - Predict effect of vagus associated compounds on gastrin release. - Gastrin is from the G cells - Vagus nerve gastrin-releasing peptide (GRP) / bombesin G cells parietal cell H^+^ release and gastric mucosa growth (trophic influence) - Indirectly: Vagal stimulation also increases the release of histamine from enterochromaffin-like (ECL) cells in the stomach. Histamine, in turn, binds to H₂ receptors on parietal cells, stimulating the production of gastric acid. - Acidic environment has negative feedback on G-cell release of gastrin. - Somatostatin inhibits G cell gastrin secretion **[Lecture 49 - GI Accessory Secretory Organs I]** - Recall pancreatic fluid synthesis and sequence for aqueous component. - Enzymes are secreted by the acinar cells, which aqueous components are secreted by the centroacinar cells, which is then modified by ductal cells - ACh and CCK act on ductal cells - Provides rapid neutralization of acidic chyme - See PPT - Recall ionic composition of pancreatic fluid and how it is affected by flow rate. - A diagram of a fluid composition Description automatically generated **[\ ]** **[Lecture 50 - GI Accessory Secretory Organs II]** - Understand the bilirubin breakdown pathway. - Most breakdown is in the spleen, the rest in the RES, including the liver - Recognize biliary cancer symptoms and causes. - Biliary cancer (cholangiocarcinoma) is a rare but aggressive cancer of the bile ducts, and it typically presents with jaundice, abdominal pain, fatigue, and weight loss. Early detection is difficult due to the lack of specific symptoms in the early stages. Several risk factors, including chronic bile duct inflammation, PSC, cirrhosis, and parasitic infections, can increase the risk of biliary cancer. Treatment is often limited to surgical resection in early stages, with chemotherapy and palliative care options for advanced disease. **[Lecture 51 -]** **[When Things Go Wrong]** - Recall the role of the arcuate nucleus in appetite regulation and which neuropeptides are present. - The arcuate nucleus is central to appetite regulation, and its neurons are influenced by a variety of neuropeptides and hormones. NPY and AgRP promote hunger and increase food intake, while POMC, α-MSH, and CART suppress appetite. The arcuate nucleus integrates signals from peripheral hormones like leptin, insulin, and ghrelin to maintain energy homeostasis, ensuring that food intake is balanced with the body\'s energy needs. - AgRP is most potent and long lasting - Basis of IBS-D diagnostic antibody test. - Two antibodies - If either are elevated, the test is considered positive and patient can be diagnosed with IBS-D or IBS-M - Antibodies are Anti-CdtB and Anti-Vinculin - If both are not elevated, the test is considered negative [**Unknown Lecture -** **GI Digestion and Absorption**] - Distinguish between CCK, VIP and bicarbonate with respect to roles in gastric motility to determine source of symptoms/presentation. - CCK plays a critical role in regulating gastric motility by slowing gastric emptying and stimulating gallbladder contraction, leading to symptoms like nausea, bloating, and right upper quadrant pain in cases of gallbladder dysfunction. - VIP generally promotes gastric motility through smooth muscle relaxation, but an excessive VIP (as in a VIPoma) leads to watery diarrhea, hypokalemia, and achlorhydria. - Bicarbonate helps to neutralize stomach acid and protect the gastric lining. Problems with bicarbonate secretion (e.g., in conditions like pancreatitis) lead to gastritis or peptic ulcers, while excess bicarbonate can result in alkalosis and digestive discomfort. - Thus, understanding the roles of these substances allows clinicians to distinguish between different gastrointestinal conditions based on the pattern of symptoms, contributing to accurate diagnosis and treatment.