Introduction to Gastrointestinal Physiology
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ojames03 Plus on March 28, 2012
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Math / Symbols | English |
|---|---|
 Symptom vs Sign | 1)Symptom --> What patient complains of 2)Sign --> What you ellicit on the patient |
| Central Signs & symptoms of GI Disorders | **See slide 2 for details** |
| Portal Hypertension | -->Can lead to hematemesis |
| Melena | -->Passing of dark stools -->Seen in 2 conditions: 1)Bleeding in upper GI track 2)Iron supplementation |
| Hematochezia | -->Passing fresh red blood into the stools |
| Focal tenderness over abdomen | -->Painful palpatation over the abdomen (Ex. tender hepatomegaly) |
| Steatorrhea (passing fat into the stools) | -->Seen in: 1)gallbladder stones 2)hyperbilirubemia 3)pancreatitis 4)Bile Salt Deficiency |
| 4 Fxn's of the GI Tract | 1)Ingestion 2)Digestion 3)Absorption 4)Egestion (Excretion) -- -->these 4 processes are aided by 2 processes in the GIT: 1)Gastrointestinal Motility : Causes **mechanical breakdown of the food** & propulsion of food through the gut 2)Gastrointestinal Secretions -->regulated by hormones & nerves |
| 2 Components of the GI Tract | 1)Intrinsic component 2)extrinsic component |
| Intrinsic Component | -->Represents the **Enteric NS** -->The Enteric NS consists of 2 Plexuses: 1)Submucosal (Meissner's) Plexus 2)Myenteric (Auerbachs Plexus) -->Represent neurons & synapses located within the wall of the GI tract -- NOTE: -->It can operate **independently, but is REGULATED by the ANS* |
| Extrinsic Componentt | -->Represents the sympathetic & parasympathetic innervation of the autonomic NS |
| Circular & Longitudinal Muscle | -->Represnets the **motility* of the GI tract |
| Submucosal Plexus | -->Located btwn the submucosa & circular muscle -->Fxn: **Secretory fxn of GIT** |
| Myenteric Plexus | -->Located btwn the inner circular & outer longitudinal muscle layer -->Fxn:**Motor fxn of GIT** |
| If the sympathetic & parasympathetic nerves to the gut are CUT | -->Many motor & secretory activities continue b/c these processes are directly controlled by the *enteric nervous system* |
| Chemoreceptor vs Mechanoreceptor | 1)Chemoreceptor (senses changes in the chemical enviornment) 2)Mechanoreceptors (sense the distention of the GI tract) |
| Secretion & Absorption | **Occurs through the plasma** |
| Parasympathetic NS | -->Stimulates motility & secretions of GI Tract |
| Gastric Juice | -->Is stimulated by food |
| Features of Parasympathetic Nerve Supply | -->Occurs through the **vagus (CN10) & pelvic nerves (S2-S4)** 1)Vagus nerve innervates the upper part of the GI tract (*cutoff is ascending colon**) 2)Pelvic nerve innervates the lower part of the GI Tract (from the tranverse colon & downward) |
| Functions of the Parasympathetic NS | 1)Efferent parasymp. NS is usually **excitatory** (incr. GI secretions & motility) 2)Mechanoreceptors & Chemoreceptors in GI mucosa relay **afferent* signals to the CNS 3)**Relaxes the sphnicters** (ONLY NONSTIMULATORY FUNCTION) |
| Features of Sympathetic NS | -->Originates from the lateral horn cells of spinal cord (T5-L2) |
| Functions of Sympathetic NS | 1)Efferent sympathetic NS is usually INHIBITORY (decr. GI secretions) 2)Mechanoreceptors & Chemoreceptors in GI mucosa relay **afferent* signals to the CNS 3)**Contracts the sphnicters** (only NONINHIBITORY FUNCTION) |
| Review of Differences of adrenergic vs. cholinergic innervation & diff types of neurons in the peripheral NS | **See phyiology notes for a review**(& notes drawn out) |
| Features of the Extrinsic Sympathetic & Parasympatheic nervous system | -->Connect to both the myenteric & submucosal plexus -->although the enteric NS can function independently of these extrinsic nerve, stim.by the parasymp & symp systems can greatly enhance or inhibit GI fxn -->Sensory nerve endings that ORIGINATE in the GI epithelium or gut wall send AFFERENT fibers to both plexuses of the enteric system, as well to: 1)Sympathetic (Ex. prevertebral) ganglia of the symp. NS 2)Spinal Cord 3)in the Vagus Nerves all the way to the brain stem -->Sensory nerves: 1)Can elicit local reflexes within the gut wall itself OR Other reflexes that are relayed to the gut from either the prevetebral gangli or basal regions of the brain |
| Stimulus of constipation | -->Any mechanism that **blocks GI secretion & motility of the parasympathetic NS* (or stimulates sympathetic activity) -->Example is *atropine* (muscarinic receptor blocker --> blocks the action of Ach) |
| Stimulus of diarrhea | -->Any mechanism that **enhances GI secretion & motility of the parasympatic NS* (or inhibits sympathetic activity) -->Major example is **organophosphates**(or organophosphate poisoning --> blocks the action of NE) |
| Examples of Organophosphates (Acetylcholinesterase Inhibitors) | 1)Diaxinon (chemical agent in warfare & terror) 2)Cloropyrifos (Dursban) 3)Sarin (Isopropyl Methylfluorophosphonate) (nerve agent) 4)Diisopropylfluorophosphate (DFP) |
| 3 regulatory functions of GIT functions | 1)Hormones (or endocrine hormones 2)Neurocrines 3)Paracrines |
| Regulatory functions | 1)Contraction/relaxation of smooth muscle 2)Secretion of digestive enzymes & electrolytes 3)Trophic (**growth**) effects on GI tissues |
| Consequences of overactivity of parasympathetic system | -->Major symptoms inclu |
| SLUDGE symtomes of overstimulation of muscarinic receptors | **Salivation, Lacrimation, Urination, Defecation, Gastritis, Emesis** |
| Stools | -->Epithelium cells as well as food |
| Features of hormones (or endocrines) | -->Are peptides secreted into the portal circulation, pass through the liver, & enter the systemic circulation -->4 Major GI Hormones: 1)Gastrin --> part of gastrin-CCK family 2)Cholecystokinin (CCK) --> part of gastrin-CKK family 3)Secretin --> part of secretin-glucagon family 4)Gastric Inhibitory Peptide (GIP) --> part of secretin family |
| Gastrin | -->Secreted by G Cells in **antrum of the stomach* -->Physioligical Actions: 1)Increase H+ secretion by gastric parietal cells (** in the body of the stomach**) 2)Stimulates growth of GASTRIC MUCOSA (rich in parietal cells) |
| Positive regulation of gastin secretion | 1)Distention of the stomach following a meal 2)Production of digestion (ex. peptides & amino acids) acids 3)Release of Gastrin Releasing Peptide (GRP) --> induces vagal stimulations |
| Negative regulation gastrin secretion | -->***Incr. H+ (via negative feedback) |
| Gastrin Releasing Peptide (GRP) | -->Increases Gastrin secretion |
| Neural Pathway leading to the release of gastrin | Distention --> + mechanoreceptors --> afferents to CNS --> Integration --> Efferents containing parasympathetic nerve --> release of gastrin-releasing peptide (GRP) --> + release of gastrin |
| Gastrinoma | -->A tumor in the pancreas that secretes excess of gastrin leading to ulceration in the duodenum, stomach and the small intestine -->**does not respond to negative feedbac** -->Can come from non-beta cell of the pancrease OR duodenum -- -->Increase in gastrin --> incr. in HDl --> Hypertrophy of the mucosa --> incr in gastric juice -->**ulceration** -- -->Can also result in inactivation of enzymes by low pH in stomach, leading of the stearrhea |
| Tumor of parietal cells | 1)Increases in H+ (decr. in pH), leading to an ULCER 2)Stimulates the growth of the gastric mucosa by stimulation protein synthesis |
| Parietal cells | -->For parietal cells: secretes HCl -->Chief Cells: secretes pepsinogen |
| The reason why atropine (an Ach blocker) CANNOT blocks vagally mediated gastrin secretion (despite vagal stim. being a stimulus for its release) | -->B/c the mediator of vagally induced Gastrin secretion is GASTRIN RELEASING PEPTIDE(GRP) (**not acetlylcholine**) |
| Zollinger-Ellison (ZE) Syndrome | -->Caused by *Gastrin-Secreting Tumor* (Gastrinoma) |
| Signs of Zollinger-Ellison Syndrome | 1)Hypertrophy of the gastric mucosa (due to gastrin stimulation of the growth of gastric mucosa by stimulating protein synthesis) 2)Duodenal Ulcers (due to incr. secretion of H+) 3)**Steatorrhea* (Incr. H+ secretion inactivates pancreatic lipase)(characterized by *greasy, foul smelling, CLAY COLORED STOOL that floats**) |
| Note about duodenal ulcers | -->May present with gastric ulcers |
| Symptoms of ZE Syndrome | 1)*Abdominal Pain* 2)Diarrhea (due to lack of absorption/breakdwon of food --> leads to incr. in osmotic diarrhea) 3)Steatorrhea 4)Heartburn |
| Diagnosis of ZE Syndrome | 1)Incr. Gastrin levells in the blood (incr. in gastric juice due to the errosion of gastric mucosa) 2)Peptic Ulcer |
| Increase H+ ions secretion (↓pH) | -->Inactivates all pancreatic enzymes, including pancreatic lipids |
| Treatment of Zollinger-Ellison Syndrome | 1)Administration of H2 receptor-blocking drugs on **parietal cells** -->Examples are "-tidine" drugs: **Cimetidine, Ranitidine, Famotidine** 2)Administration of Proton Pump inhibitors (H+/K+ Antiporter) -->Examples are "-prazole drugs": Omeprazole, Lanzaprozole, Pantoprazole, Esmoprazol 3)Surgical removal of the tumor |
| Cholecystokinin (CCK) | -->Secreted by **I cells of the duodenal & jujunal mucosa* -->Promotes fat digestion & absorption -->Is stimulated in response to **FATS & AMINO ACIDS ENTERING THE DUODENUM** |
| Major Functions of CCK | 1)Contraction of gall bladder WITH relaxation of sphincter of Oddi -->Ejects bile into small intestinal lumen for digestion of the lipids 2)Secretion of Pancreatic Enzymes such as ***Pancreatic amylase, Pancreatic Proteases & Pancreatic Lipase (enzyme rich pancreatic secretion) 3)Low amount of secretion of **HCO3** from pancreas relative to pancreatic enzyme secretion (Secretin has this role) 4)**Moderately slows down gastric emptying** (ensures adequate time for intesintal digestion & abosroption) |
| Patients with ***Gallstone Disease*** (with pain after eating a meal) | -->MUST AVOID FATTY FOODS, due to the contraction of the gallbladder via stimulus of CCK |
| Stimulus causing CCK release | 1)Partially digested fats & proteins in duodenum & jujunum (+ stimulates secretion of CCK) 2)MAG & Fatty Acids 3)Peptides & Amino Acids -- -->***TAG's DO NOT stimulate the release of CCK b/c TAG's cannot cross the INTESTINAL CELL MEMBRANE |
| Secretin ("Natures Antacid") | -->Secreted by the *S* Cells of the duodenum |
| Stimulus that incr. secretin secretion | 1)H+ concentration into the lumen of the duodenum (**most important reason**) 2)FA's in the lumen of duodenum 3)A pH < than 4.5 |
| pH of gastric juice | 2-2.5 -- -->If it reaches the range of .5 to 1 (then gastrin is released in to lumen of stomach |
| Physiological Actions of Secretin | 1)Stimulates secretion of HCO3- from the pancrease & into the bile (neutralizes H+ and incr. pH of intestinal contents; the neutralization is essential for fat digestion b/c pancreatic lipases activated at *alkaline pH*) 2)Inhibits H+ secretion from the STOMACH 3)INHIBITS growth effects of gastrin on GASTRIC MUCOSA |
| Gastric Inhibitory Peptide (GIP) or Glucose Dependent Insulinotropic peptide | -->Secreted by *K Cells* of the duodenal & jejunal mucosa |
| Physiological Action of GIP | 1)Stimulates insulin secretion by Beta Cells of pancreas (**represents the most common form of HYPOGLYCEMIA**) 2)Inhibits H+ Secretion from the stomach |
| Oral Glucose | -->A powerful stimulant for insulin secretion (vs. intravenous glucose) |
| Stimulus of the secretion of GIP from the duodenal/jejunal mucosa | 1)Oral glucose 2)Proteins 3)FA's -- NOTE: ***Is the only hormone that requires ALL 3 to be released |
| Regulation of GIP Secretin | -->Secretion in response to END PRODUCTS of digestion of all nutrients (esp. glucose, amino acids, & fatty acids) |
| Features of Pacracrines in the GIT | -->Act locally within the SAME TISSUE that secretes -->Diffuse a small distance to reach target cells/tissue -->2 major paracrines in GIT: 1)Somatostatin 2)Histamine |
| Major Features of Somatostains | -->Secreted by the **D Cells* of the GI mucosa (*not by the pancrease**) -->Is stimulated by the LOW pH in the stomach -->Acts on the parietal cell to decr. acid secretion -->Contains INHIBITORY ACTIONS of the GIT to decr. GI motility |
| Major Features of Histamine | -->*Is secreted by *ECLs** (Enterochromaffin -Like Cells of the antral region of the STOMACH -->Helps to **stimulate H+ secretion by gastric parietal cells** in the antrum of the stomach |
| Stimulators of Gastric Acid Secretion | 1)Gastrin (directly on parietal cells) 2)AcH (" " " ") 3)Histamine (" " " ") |
| Inhibitors of GastricAcid Secretion | 1)Somatostatin 2)Prostaglandin (E2) 3)H+ in the stomach 4)Chyme in the duodenum 5)Atropine 6)Cimetidine (or other H2-Receptos Antagonists for gastric parietal cell) 7)Omprazole (or other H+/K+ ATPase pump inhibitor) |
| Features of Neurocrines in the GIT | -->Are synthesized in the neurons of the GIT, and are released by **action potenitals** -->They diffuse across the synapse & act on target cells (either neurons or non-neuronal cells) -->Major Examples include: 1)Ach 2)NE 3)Vasoactive Intestinal Peptide (VIP) 4)Gastrin Releasing Peptide (GRP) 5)NO |
| Features of VIP | 1)Relaxes of smooth muscles (& **sphincters** 2)Increases intestinal & pancreatic secretions) 3)Causes ***secretatory diahhrea (due to intesinal infections such as CHOLERA; Cholera is caused by excessive chloride secretion by the enerocytes |
| Features of Gastrin-Releasing peptide (GERP) | 1)Relaxes smooth muscle 2)**increases secretions in the small intestine & pancrease*) |
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