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Phys4 GI Lect4
Phys4 GI Motility I
Question | Answer |
---|---|
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. |