Motility of the GI System

Question 1

Tonic vs phasic contractions

Answer 1

Tonic- maintain constant level of contraction without regular periods of relaxation - Stomach, lower esophagus, ileocecal and internal anal sphinctors
Phasic- periodic contractions followed by relaxation- esophagus, stomach, small intestine and tissues involved in mixing and propulsion

Question 2

Slow waves

Answer 2

They are not APs
Bring membrane potential closer to threshold, number of APs on top of slow wave determine strength of contraction
Increases probability Ca channels will open in smooth muscle

Question 3

Factors increasing amplitude of slow waves and number of APs

Answer 3

Stretch
Ach
Parasympathetics

Question 4

Factors decreasing amplitude of slow waves and number of APs

Answer 4

NE

Sympathetics

Question 5

Submucosal plexus

Answer 5

Controls GI secretions and local blood flow

Generate spontaneous slow wave activity

Question 6

Myenteric plexus

Answer 6

B/w longitudinal and circular layers
Controls GI movements
Generate spontaneous slow wave activity

Question 7

Interstitial cells of cajal

Answer 7

Pacemaker cells for GI smooth muscle
Generate and propagate slow waves
Slow waves spread rapidly to smooth muscle via gap junctions
Located in myenteric plexus (and submucosal plexus?)

Question 8

3 phases of swallowing

Answer 8

Oral phase- voluntary
Pharyngeal phase- involuntary
Esophageal phase- involuntary- control by the swallowing reflex and enteric nervous system

Question 9

Pharyngeal phase of swallowing

Answer 9

Soft palate is pulled upward–>epiglottis moves–>UES relaxes–>peristaltic wave of Cxs initiated in pharynx–>food propelled through open UES

Question 10

Esophageal phase of swallowing

Answer 10

Primary/Secondary peristaltic wave
Food in pharynx–>afferent sensory input via vagus/glossopharyngeal nerve–>swallowing center in medulla–>brainstem nuclei–> efferent input to pharynx

Question 11

Primary peristaltic wave

Answer 11

Continuation of pharyngeal peristalsis
Controlled by the medulla
Cannot occur after vagotomy

Question 12

Secondary peristaltic phase

Answer 12

Occurs if primary wave fails to empty the esophagus or if gastric contents reflux into the esophagus
Medulla and ENS are involved
Can occur in absence of oral and pharyngeal phases
Occurs even after vagotomy

Question 13

Achalasia- what happens

Answer 13

Difficulty getting food into stomach from esophagus
Impaired peristalsis
Incomplete relaxation of LES during swallowing, food backs up
Elevation of LES resting pressure

Question 14

What causes those problems to happen in achalasia

Answer 14

Decreased numbers of ganglion cells in myenteric plexus
Degeneration preferentially involves inhibitory neurons involving NO/VIP
Damage to nerve sin the esophagus, preventing it from squeezing food into stomach

Question 15

GERD - what causes

Answer 15

Changes in the barrier b/w the esophagus and stomach (e.g. LES relaxes abnormally or weakens)
Motor abnormalities that result in abnormally low pressures in LES; if intragastric pressure increases such as following a large meal, during heavy lifting or pregnancy

Question 16

Receptive relaxation

Answer 16

Decrease pressure and increased volume of the orad region of stomach
Vagovagal reflex
CCK decrease contractions and increased gastric distensibility

Question 17

Retropulsion

Answer 17

Peristaltic waves move food from mid stomach to antrum (caudad portion of stomach)
Wave of contraction closes the pylorus
Retropulsion is contraction in reverse direction sending gastric contents back up into stomach for further mixing and reduction of size

Question 18

Secretin and GIP effect on gastric contractions

Answer 18

Decrease AP and force of contractions

Question 19

Factors increasing rate of gastric empty time

Answer 19

Decreased distensibility of the orad stomach
Increased force of peristaltic contractions of caudad stomach
Decreased tone of pylorus
Increased diameter and inhibition of the segmenting contractions of the proximal duodenum

Question 20

Factors inhibiting gastric emptying

Answer 20

Relaxation of orad (increase in distensibility)
Decreased force of peristaltic contractions
Increased tone of pyloric sphincter
Segmentation contractions in intesine

Question 21

Entero-gastric reflex- fats vs acids vs hypertonicity in duodenum

Answer 21

Negative feedback from duodenum will slow down the rate of gastric emptying
Acid in duodenum–>stimulate secretin release–>inhibit stomach motility via gastrin inhibition
Fats in duodenum–>stimulate CCK and GIP–> inhibit stomach motility
Hypertonicity in duodenum–> unknown hormone–>inhibit gastric emptying

Question 22

Gastroparesis description and cause

Answer 22

Slow emptying of stomach/paralysis of stomach in absence of mechanical obstruction
Diabetes mellitus is common cause
Injury to vagus nerve can cause

Question 23

Migrating myoelectric complex MMC

Answer 23

Large particles of undigested residue remaining in the stomach are emptied by this complex
Periodic, bursting peristaltic contractions occurring at 90min intervals during fasting
Motilin plays significant role in mediating the complex
Inhibited during feeding

Question 24

MMC and bacterial overgrowth

Answer 24

Small intestinal bacterial overgrowth SIBO is condition of colonic bacteria overabundance in small intestine
MMC is importing for cleansing mechanisms in the small intestine and preventing SIBO

Question 25

Segmentation contractions

Answer 25

Generates back and forth movements Produces no forward, propulsive movement along the small intestine My guess is helps with mixing/absorption

Question 26

Slow waves in the intestine

Answer 26

Always present whether contractions are occurring or not Unlike in stomach, slow waves do not initiate contractions in small intestine Spike potentials (APs) are necessary for muscle contraction to occur Slow wave frequency sets the maximum frequency of contractions

Question 27

Myenteric plexus vs submucosal (Meissner) plexus regulation

Answer 27

Myenteric plexus mainly regulates the relaxation and contraction of the intestinal wall Submucosal plexus senses the lumen environment

Question 28

Serotonin role in regulation of peristaltic contractions

Answer 28

Serotonin is released by enterochromaffin cells and binds to receptors in the IPANs, initiating the peristaltic reflex

Question 29

Gastrin, CCK and motilin effect on contractions

Answer 29

Stimulate (as well as insulin)

Question 30

Secretin effect on contractions

Answer 30

Inhibit (as well as glucagon)

Question 31

Vomiting reflex

Answer 31

Coordinated by medulla Nerve impulses transmitted by vagus and sympathetic afferents to brain stem nuclei Reverse peristalsis in small intestine-->stomach and pylorus relaxation-->forced inspiration to increase abdominal pressure-->movement of the larynx-->LES relaxation-->glottis closes-->forceful expulsion of gastric contents

Question 32

Regulation of flow of contents into large intestine at ileocecal junction

Answer 32

Distention of ileum causes relaxation of the sphincter -allows flow of contents from ileum into colon Distention of colon causes contraction of sphincter -prevents passage of contents from colon to ileum

Question 33

ENS innervation of large intestine

Answer 33

Concentrated beneath teneae | Innervate muscle layers

Question 34

Parasympathetic innervation of large intestine

Answer 34

Vagus- Cecum, ascending and transverse colon | Pelvic nerves: sacral portion of spinal cord S2-4: descending and sigmoid colon, rectum

Question 35

Sympathetic innervation of large intestine

Answer 35

Superior mesenteric ganglion- proximal regions Inferior mesenteric ganglion- distal regions Hypogastric plexus- distal rectum and anal canal

Question 36

Innervation of external anal sphincter

Answer 36

Somatic pudendal nerves

Question 37

Motility of rectum and anal canal and rectosphincteric reflex

Answer 37

If passive distention of rectum is sufficiently large, it triggers active contraction of rectal smooth muscles Passive rectal distention also triggers relaxation of the smooth muscle of the internal anal sphincter (rectosphincteric reflex) If defecation is not desired, the skeletal muscle of the external anal sphincter contracts by an involuntary reflex

Question 38

Rectosphincteric reflex neural control

Answer 38

Controlled partially by ENS Reflex is reinforced by activity of neurons within the spinal cord Sensation of rectal distention and voluntary control of the external anal sphincter are mediated by pathways within the spinal cord that lead to cerebral cortex -Destruction of these pathways causes a loss of voluntary control of defecation

Question 39

Hirschsprung disease

Answer 39

Caused by absence of ganglion cells from segment of colon Results in low VIP levels-->smooth muscle constriction/loss of coordinated movement-->colon contents accumulate Present at birth, causes constipation Newborn may present with poor feeding, jaundice, vomiting

Question 40

Vicro-vagal reflex

Answer 40

Generally stimulatory- increase motility, secretomotor, vasodilatory activities Vagus carries both afferents and efferents

Question 41

Intestino-intestinal reflex

Answer 41

Depends on extrinsic neural connections; inhibitory | If an area of the bowel is grossly distended, contractile activity in the rest of the bowel is inhibited