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GI Course
GI Motility
| Question | Answer |
|---|---|
| Where is striated muscle located? | pharynx and upper esophagus, and the external anal sphincter |
| Phasic muscle contractions | rapid, contract, found in busy regions such as esophagus antral stomach and small intestine |
| Tonic muscle contractions | slow, sustained contractions. minutes to hours. found in non busy regions like sphincters, orad stomach |
| How does single-unit smooth muscle contract in the small intestines? | Autonomic neuron vericosities receive a signal which cause them to release neurotransmitters. These attach to receptors on the smooth muscle and cause the entire muscle to contact. (gap junctions) |
| Propulsion | Occurs by peristalsis. The propulsive segment of the tract produces a contraction of circular muscle and a relaxation of longitudinal muscle. The Receiving segment occurs by contraction of longitudinal muscle and inhibition of circular muscle. |
| Mixing | Segmentation. |
| Motility patterns of the GI tract are programmed by which nervous system? | The enteric nervous system. |
| Physiologic Ileus | The absence of motility along the intestine in which motor function is neurally programmed to stop. (normal). |
| Trituration | crushing and grinding of food in the stomach |
| What does Activating an inhibitory nucleus do to smooth muscle in the GI tract? To the LES? | The inhibitory neurons will cause a physiological ileus when active. This action on the LES will cause the sphincter to relax and food to pass through. |
| What are the phases of swallowing? | Oral, Pharyngeal, Esophageal, Gastric |
| Where is the esophageal pressure less than zero? | In the middle, when it passes through the thoracic cavity. |
| Muscle and Nerve of the Upper esophageal sphincter? | striated muscle and innervated by excitatory somatic nerves (travel in the vagus). |
| Nerve of the Lower Esophageal Sphincter? | Innervated by parallel sets of parasympathetic excitatory AND inhibitory pathways. |
| What causes contraction of the Lower Esophageal Sphincter? | Myogenic, cholinergic regulation, and Humoral (gastrin). |
| Primary Peristalsis | the first swallow that follows the oral-pharyngeal phase. |
| Secondary Peristalsis | When the first swallow does not take down all of the food. Distention of the esophagus leads to this. |
| The swallowing Center is made up of: | Nonvagal nuclei, Nucleus ambiguous, Dorsal motor nucleus. |
| Nucleus ambiguous | Somatic Nerve, activates muscles of the pharynx and striated areas of the esophagus. |
| Dorsal motor nucleus | Vagus Nerve. Areas of smooth muscle are activated. |
| Muscle and Nerve distribution of the upper esophagus. | Extrinsic nerves and striated muscle. |
| Muscle and Nerve distribution of the lower esophagus. | extrinsic AND enteric nerves. as well as smooth muscle. |
| What would happen with diseases of a myoneuronal juction? | This would cause difficulties in swallowing in the pharynx and upper esophagus. |
| What would a disease of enteric nerves and/or smooth muscle present as? | Problems with the lower peristalsis and tone of lower esophageal sphincter. |
| What causes the activation of enteric inhibitory nerves? | Distention and the vagus nerve. |
| Which hormone can relax the LES? | CCK |
| Achalasia | defective enteric INHIBITORY neurons (loss of intramural neurons). Makes the active neurons have a stronger effect therefore contracting and keeping food from passing down the esophagus. |
| How is achalasia treated? | Treated surgically by opening the LES. Patient must also be perscribed anti acid reflux meds. |
| The stomach is innervated by: | sympathetic and parasympathetic nerves. |
| Receptive Relaxation: Vagovagal reflex | opening of sphincter also causes the orad area of stomach to relax. |
| Adaptive Relaxation (Gastric Accommodation) | distention in stomach triggers; then vago-vagal reflex with efferents going to inhibitory ENS neurons. Probably also some local reflex. |
| Feedback Relaxation | Receptors in small intestine. Involves both local reflex as well as hormones from gastric endocrine cells that interact with the gastric ENS. Followed by low amplitude tone. |
| What occurs in the orad stomach as gastric contents are emptied. | There is a low amplitude contraction in the muscles that decreases stomach size and thus accommodates the remaining contents and helps deliver chyme to the distal stomach. |
| How often are contractions in the Caudad Stomach | 3-5 cycles per minute |
| GI motility during the Fed or Digestive State: | peristaltic contractions that begin at mid-stomach and move downward toward the pyloris. (3-5 per min). This is so forceful that only a small portion of the bolus goes through the sphincter. Remainder gets shoved back to orad stomach. |
| Retropulsion | Occurs in the stomach during the fed/digestive state. Muscle contractions at mid stomach push the bolus forcefully towards the pyloric sphincter. The bolus is pushed back up towards the orad and only a small amount gets through. Breaks up the bolus. |
| Muscle Contractions during Fasted or interdigestive state: | Periodic bursts of high amplitude contractions called the migrating motor complex (MMC). These sweep the stomach clean. |
| Interstitial cells of Cajal | Govern the rhythm of contractions in stomach and small intestines. 3-5 per minute. Pace makers. |
| Slow Waves | Do not cause contractions except possibly in stomach. Always present whether or not there are contractions; and their frequency is stable in each region. Determines the cycle of contractions. |
| What can increase the frequency of slow waves? | temperature and metabolic activity |
| What do nerves and hormones do to slow waves? | They can affect the height of the plateau or whether or not the spike potential occurs. frequency is NOT altered. |
| How does the Vagus affect the slow waves? | increases contractions |
| How do the sympathetics affect slow waves? | decreases contractions |
| Hormones that increase contractions of slow waves? | ACH, gastrin and CCK |
| If fat slows gastric emptying, what hormone is probably involved? | CCK |
| What is the primary site for digestion and absorption? | small intestines. |
| MMC (Migrating motor complex) | Housekeeper of the gut. problems with this will lead to bacterial overgrowth. |
| Small Intestine motility in the Interdigestive state (2-3 hrs after meal) | Few or no contractions. Migrating motor complex. |
| Where does interdigestive state motility in small intestine begin and end? | begins in stomach, ends at the terminal ileum |
| what is the cycle of small intestine motility during interdigestive state? | cycles every 90 minutes DURING FASTING |
| What initiates motility in small intestines during interdigestive state? | probably motilin. |
| What stops motility of small intestine during interdigestive state? | Food in the stomach. may be mediated by hormones. IV injection of gastrin and CCK will terminate the MMC Neural mechanisms (vagus). |
| Contractions in the small intestine depend on what? | slow waves and spike potentials. contractions require a spike potential. |
| Peristaltic Reflex | law of the intestines. not important in healthy people. depends on enteric. Can sweep the entire length of the small intestine. |
| Intestino-intestinal reflex | If area of bowel is grossly distended, contractile activity in the rest of the bowel is inhibited. Depends on extrinsic. |
| Power propulsion | Long, large contractions in response to noxious stimuli. Causes vomiting in retrograde direction and explosive diarrhea in orthograde direction. |
| Gastro-ileal reflex | Food in stomach causes causes a reflex in ileal-cecal sphincter and contraction of ileum. Mediated by CCK, Gastrin, extrinsic. |
| Potential mediators of Gastro-ileal reflex | CCK, Gastrin, and Extrinsic |
| Ileal-Brake | Occurs when lipids and/or carbs are infused in the ileum in amounts that cause malabsorption. Cause the inhibition of gastric and pancreatic secretion and motility. Retrograde signals via neurohumoral signals. GLP-1 mediated. |
| What mediates the Ileal Brake reflex? | GLP-1 (glucagon-like peptide) |
| Relationship of sphincter and colonic distention. | This causes the ileocolic sphincter to close up (creating a positive pressure). Mediated by enteric NS. |
| Haustrations | Move a bolus through the large intestine through small movements. Contracts and reabsorbs H2O. Shown via barium swallow. |
| What is the main movement through the large intestine? | Haustrations and mass movements. |
| Gastrocholic Reflex | Food in the stomach causes an increase in motility and mass movements in the large intestine. |
| What is gastrocholic reflex regulated by? | CCK, Gastrin, and Parasymp NS. |
| Hirschspring's (Agamglionic megacolon) | Loss of ganglia that regulate large intestine Haustrations. Loss of inhibiting neurons. |
| Describe the Rectosphincter Reflex (recto-anal reflex) | Pressure passively increases as it gets filled. Contraction will actively increase pressure and thus relax the internal and contract the external. This allows receptors to sense the contents. Inc pressure will relax internal and contract external more. |
| Transit time through the stomach after a meal? | 0-5 hours |
| Transit time after ingestion of meal in the Duodenum? | approximately 2-7 hours. Highest average at 2. |
| Transit Time through the colon. | gone within 24 hours after entry into colon. |
| Continence of a bowel movemtn requires: | Contraction of puborectalis, Maintenance of anorectal angle, Normal rectal sensation, contraction of the sphincter. |
| Defecation requires: | Relaxation of puborectalis, straightening of anorectal angle, relaxation of sphincter. |
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