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Phys4 GI Lect4

Phys4 GI Motility I

2 different types of contractions seen in the GI 1.Phasic (Rapid contract/relax. 2.Tonic (slow sustained contractions lasting minutes to hours). **These are regional things.
where would you see Phasic contractions in the GI BUSY regions. 1.Esophagus. 2.Antral Stomach. 3.Small Intestine.
Where would you see Tonic contractions in the GI? NON-BUSY regions: 1.Sphincters. 2.Orad Stomach.
What type of Smooth muscle is found in the GI? Unitary smooth muscle (Cells are connected via gap junctions, there is a uniform contraction as a unit).
What programs ALL motility patterns? Enteric NS. Including the "absence of motility". **Hormones, SNS, PNS all influence as well.
GI Propulsion (Movement down the GI tract). Enteric motor program: Paristalsis. Alternating contracting and relaxing of the longitudinal & circular muscle.
Which muscle layer contracts infront of the bolus during paristalsis? Longitudinal muscle. Circular relaxes
Which muscle layer contracts behind the bolus during paristalsis? Circular muscle. Longitudinal relaxes
GI Mixing (mixing in the small intestine). Enteric motor program: Segmentation. **Is coupled with propulsion, a segment mixes and then propulsion occurs.
GI Parking (no motility). Enteric motor program: Physiologic Ileus (planned rest, the enteric NS sends out inhibitory signals). **NORMAL, quiescnece of motor function is neurally programmed.
What happens to GI motility when you block the enteric NS with anesthetics or pathological condition Disorganized, nonpropulsive contractile behavior occuring continuously.
GI Trituration Crushing & Grinding of food in the stomach.
How do inhibitory neurons affect the contractility of smooth muscle in the GI? Inh motor neurons must be turned off for circular muscle contraction. **They are normally ACTIVE (physiological Ileus, until a mixing/propulsion program comes to inactivate them, allowing the contraction.
What is the Normal activity of inhibitory neurons at the lower esophageal sphincter? INACTIVE (so the sphincter remains CLOSED). **Must be turned on for sphincter relaxation.
When are the inhibitory neurons activated in the lower esophageal sphincter? During swallowing. **Remember sphincters are opposite of tract muscle in that they Inh neurons are usually inactive instead of active.
Contraction wave during vomiting The contraction starts in the small intestine with an inactive Inh nueron wave and moves orally.
4 Phases of swallowing 1.Oral (food propelled into pharynx by tongue). 2.Pharyngeal. 3.Esophageal (bolus propelled into stomach via paristalic motion). 4.Gastric (Orad Stomach).
Is swallowing voluntary or involuntary? Voluntary until it reaches the back of the throat.
2 protective mechanisms during swallowing? 1.Upper constrictors contract to close off the nasopharynx from oropharynx. 2.Epiglottis moves down, glottis moves up to prevent food entry into trachea.
What pressures influence the pressure seen in the body of the esophagus? 1.Intrathoracic. 2.Intraabdominal.
What pressures influence the pressure seen in the stomach? 1.Intraabdominal. 2.tonic contraction of the fundus.
What is manometeric recording using for? diagnosing dysphagia (difficulty swallowing)
Pressures in the Lower Esophageal sphincter and fundus during swallowing While the body of the esophagus experiences a rise in pressure during swallowing, the usually higher pressure in LES and fundus decrease b/c the sphincter is relaxing.
Innervation of Upper and Lower Esophageal sphincter 1.Upper: innervted by excitatory (ACh & Substance P) somatic nerves that travel on the vagus. 2.Lower: parallel sets of PNS excitatory (ACh & Substance P) and inhibitory pathways (VIP & NO).
What is occuring in the Esophagus DURING swallowing? 1.UES relaxes/opens (suppression of neural impulse). 2.Larynx displaced. 3.Primary Peristalsis (follows Oral pharyngeal phase, initiated by distention). 4.Secondary paristalsis (only if primary can't move bolus down). 5.Activation of Enteric Inh N on
What cuases the activation of Enteric Inhibitory neurons on the LES 1.Vagus N. 2.Distention. 3.CCK. 4.Belch reflex (Vago-vagal reflex).
How does the swallowing center in the medulla control paristalsis in the esophagus 1.Nucleus Ambiguous: activates the pharynx and striated muscle. 2.Dorsal Motor nucleus: activates smooth muscle. **VAGAL afferents and efferents control this.
A meal high in _____ can cause an opening of the LES leading to reflux? FAT. b/c CCK can activate the inhibitory neurons allowing relaxation.
Innervation of the upper and lower body of the esophagus 1.Upper: Extrensic vagal nerves directly innervating striated muscle. 2.Lower: Extrensic vagal and Enteric nerves innervating smooth muscle (Vagus N synapses onto intrinsic enteric plexus).
Would a disease of myoneruonal junction, striated muscle, or CVA cause UPPER or LOWER esophageal dysfunction? Upper esophagus and pharynx.
Would a disease of entereic nerves and/or smooth muscle cause dysfunction in UPPER or LOWER esophagus? LOWER.
Achalasia Defective Enteric of inhibitory neurons in esophageal smooth muscle, therefore LES is recieve unopposed excitatory neurons. **Dec/uncordinated paristalsis & LES cant open and food can NOT pass through into the stomach.
Bird's Beak Profile with a barium swallow Mega esophagus without anything passing through the LES seen in Achalasia.
Relaxation mechanisms affecting the ORAD stomach 1.Receptive (vago-vagal reflex). 2.Adaptive (Vago-vagal reflex). 3.Feedback (local reflex & hormones). **Relax to accomadate food, then low amplitude tone (tonic contractions)
Adaptive Relaxation in the stomach distention in the stomach (via stretch receptors) activate the vago-vagal reflex with efferents going to in inhibitory Enteric neurons to allow relaxation.
Receptive Relaxation in the stomach VagoVagal Reflex when the food bolus enters, vagal afferents signal the brain then vagal efferents come back to activate enteric inhibitory neurons allowing relaxation.
Feeback Relaxation in the stomach Receptors in small intestine in the presence of nutrients delay stomach emptying. **via local reflex and hormones from gastric endocrine cells.
Contractions in the Caudad stomach during the FED state Triteration: POWERFUL contractions cycling 3-5 minutes that create a propulsion (towards the pyloric sphincter) of the bolus followed by retropulsion (away from pyloric sphincter). **Pulverizes the chyme.
Contractions in the Caudad stomach during the FASTED state Migrating Motor Complex: Periodic bursts of high-amp contractions. **These sweep the stomach clean.
Slow waves (Basic Electrical Rhythm BER) rhythmic oscillations of membrane potential that is ALWAYS ongoing. Start in the stomach and work their way through intestine. **If they get large enough they cause a contraction.
What is responsible for generating slow waves? Interstitial cells of Cajal: Specialized smooth muscle cells that run from mid-stomach to colon. **Pacemaker via opening V-gated Ca channels which the trigger Ca-gated K channels.
Influences on slow waves 1.Temperature & Metabolism Inc the frequency. 2.Nerves & hormones affect height of plateau/occurance of spike potentials. A) Vagal: Inc contractions. B) SNS: Dec contractions. C) ACh, Gastrin, CCK Inc contractions.
Freq of slow waves Permanent per section. 3-5 in stomach. 12 in Duo, decreases on down the GI tract.
Coordination of 3 key areas regulate gastric emptying 1.Stomach. 2.Gastroduodenal junction. 3.Duodenum. **Receptors in the duo are activated by food products, GI hormones & neural refelxes are then used to respond and influence motility.
Created by: WeeG



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