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GI I Exam I Motility
Based on objectives for her lecture - 18 points on test

Additional Physiology Flashcards




Contractile ring that's proceeded by receptive relaxation, moves material slowly down the GI tract
- involves coordinated contraction and relaxation of the muscle layers and serves to propel contents along the tract. Such contractions are evoked by localized distension of the intestinal wall.
- Constriction: contraction of circular smooth m + relaxation of longitudinal smooth m
- Relaxation: occurs in front of bolus/causes distension: relaxation of circular smooth m + contraction of longitudinal smooth m
- Is a reflex consisting of a contractile ring around the gut and moves forward. Any material in front of the contractile ring is moved forward.
- Requires control of the myenteric plexus
- Stimulation (usually distension or chyme, also irritation or PNS stim) causes reflex to spread along gut tube, *requires active myenteric plexus*
weak reflex reinforced by PNS
Local intermittent constrictive contractions of circular smooth muscle layer. Occur every few cms in gut wall; last 5-30 se. Then new constrictions occur at other points in the gut leading to chopping and shearing of the contents and mixing them with the secretions.
*non-propagating* segmental contractions of the circular muscle coat only. They produce local narrowings that divide the tract into discrete segments at regular intervals. The muscle then relaxes, and a new pattern of segmentation appears such that areas that were previously contracted are now relaxed and areas that were previously relaxed are now contracted.

The effect is to move intestinal contents forward and backward so as to mix them with digestive enzymes and also to maximize contact with the absorbing endothelium.
Called segmentation in SI
Haustrations in the colon
MYOGENIC response - intrinsic to smooth m, only involves circular smooth m layer
Don't require myenteric nerves, not a reflex
Sphincter tone
Tonic contraction: constant entry of Ca++ into cell, cell stays contracted
-UES (skeletal m)
-LES (smooth m) - prevents reflux of gastric contents (high in acid and pepsin)
-Pyloric - b/t stomach and SI - control s slow emptying of stomach
-Ileocecal - ileum and colon, prevents reflux of fecal matter back into SI
-Internal anal - smooth - relaxing as part of peristaltic reflex
-External anal - skeletal - somatic nerve innervation
Oddi - where bile enters SI - tonically contracted - relaxes when you have fats that need to be digested
Swallowing (motor behavior of the LES)
At suitable intervals during the process of chewing and in response to voluntary commands, the tongue presses against the hard palate and separates a bolus and propels it into the oropharynx. Once there, it initiates the swallowing reflex due to stimulation of pharyngeal receptors.
Initial phase: requires central nervous system coordination of respiration, speech, and UES relaxation.
Subsequent transport of food toward the lower esophageal sphincter is due to the sweeping waves of peristalsis.
Pharyngeal stage: involuntary, brainstem swallowing center, initiated by swallowing receptors in pharynx, trachea & nasopharynx closed by glottis
Esophageal stage: involuntary, primary & secondary peristalsis
-Primary peristaltic wave: progressive, circular contraction that begins in the upper esophagus and moves distally, is induced as part of the swallowing reflex. It is initiated and coordinated in the brainstem and results from the sequential excitation of the intramural excitatory cholinergic neurons. *vagal nerves and myenteric plexus*
-Secondary peristaltic wave: initiated when stretch sensors in the body of the esophagus are activated by the passing bolus. The LES relaxes during swallowing so that the bolus can enter the stomach. The mechanism of relaxation depends on nonadrenergic/noncholinergic (NANC) neurons that inhibit tonic sphincter contraction. Swallowing conveys food into the stomach within a few seconds. *intrinsic neural circuits in myenteric plexus, mediated by myenteric and vagal nerve fibers*
-Receptive relaxation of the stomach
Voluntary: somatic nerves -> skeletal m of mouth/jaw
Reflex: contraction of jaw m -> pressure of food against gums, hard palate, tongue -> mechanoreceptors -> inhibition of jaw m -> reduced pressure -> contraction
Chewing is normally a voluntary act. Once you stimulate the mm, the brainstem causes us to contract/relax
Gastric emptying - control
Neural signals (vagal, ACh) caused by distension of the stomach, increases rate of emptying
Gastrin: released from antrum mucosa
Duodenal signals: depress emptying by initiating negative feedback signals to inhibit gastric motility: nervous and hormonal (secretin, CCK, GIP)
Small intestine - motility
Segmentation - ICC (interstitial cells of Cajal)
- duodenum 12-14/min
- ileum 8-9/min
- moves contents toward iliocecal valve
Stim: distention (mediated by a myogenic response, you still see segmentation in a deenervated SI)
Myenteric plexus

After absorption: propulsive contractions
- distention; usually weak
- PNS and myenteric nerves, nervous signals, hormones
Interdigestive migrating motor complex
Between meals. During the interdigestive period, motor activity in the small intestine is characterized by the interdigestive migrating motor complex (IMMC).
- It occurs cyclically at 1- to 2-hour intervals at any single location in the fasting bowel, and the entire cycle migrates toward the colon.
- In addition to the IMMC, the early portions of the fasting small intestine can show regular clusters of migrating contractions.
Small bowel interdigestive motor patterns show clear circadian rhythm.

Related to motilin

Keeps lumen cleared out during interdigestive period, stops immediately with feeding
Defecation reflex
Initiated by propulsive "mass" mvmt of LI
-mass mvmt peristaltic reflex is initiated by: gastrocolic, duodenocolic, orthocolic reflexes; intense PNS stim; overdistension of colon; irritation

Initiation: when a mass movement (initiated by gastro-colic, entero-colic reflexes) forces feces into the rectum the desire to defecate is initiated; constant dribble of fecal matter into the rectum is prevented by tonic constriction the internal and external anal sphincters external anal sphincter under voluntary control by the somatic nervous system

Intrinsic Defecation Reflex: when feces enter the rectum by propulsive, movements, distension of the rectum initiates afferent signals that spread through the myenteric plexus to initiate peristaltic waves in the descending colon, sigmoid, and rectum, forcing feces toward the anus as the peristaltic wave approaches the internal anal sphincter; is inhibited by receptive relaxation mechanism, and if the external anal sphincter is relaxed, defecation will occur

Intrinsic myenteric reflex: weak, and to be effective must be fortified by autonomic (parasympathetic) reflex

Parasympathetic Defecation Reflex: strong; greatly intensifies the peristaltic waves and converts the intrinsic defecation reflex from an ineffectual weak movement into a powerful process of defecation. Forces fecal contents of colon toward anus

If contraction is maintained, the defecation reflex dies out after a few minutes and usually will not return until an additional amount of feces enters the rectum

Defecation reflexes initiate other effects such as: valsalva maneuver to increase abdominal P and force colonic contents down and help inhibit the external anal sphincter.
If you inhibit natural reflex too often, constipation can result

Relaxation of external anal sphincter -> defecation ->
failure of an ingested bolus to clear the esophagus, resulting in intraluminal accumulation, distention, and discomfort. May result from functional motility disorder or mechanical obstructing lesions. Major complaint: food sticking or caught in the chest and will not go down.
Symptoms: chest pain, coughing, regurgitation, and heartburn

Can be caused by skeletal m disease (myasthenia gravis, dystrophies, poliomyelitis, amyotrophic lateral sclerosis, brain stem lesions), also deep anesthesia, affect upper regions of esophagus

Different from odynophagia (painful swallowing, inflammatory conditions of esophagus)
LES failure to relax (high normal or elevated pressure, normal ~20)
Degeneration of ganglion cells of myenteric plexus around LES, LES never relaxes/no peristaltic contractions


Abnormal function of lower 2/3 of esophagus -> aperistalsis

*When you see high LES pressure (above 20 mmHg) think achalasia*
Esophageal spasm
Nutcracker - high amplitude peristaltic waves, causes extreme pain

DES - high amplitude non-peristaltic, uncoordinated contractions, "corkscrew," chest pain can mimic angina, tx CA++ channel blockers, nitrates
heartburn indigestion or pyrosis - is the most common symptom related to the esophagus and typically refers to a retrosternal burning sensation, usually due to esophageal reflux of gastric acid.
It is almost never associated with the act of swallowing.
Common causes: pregnancy (progesterone), advanced pregnancy (increased intra-abdominal pressure), after large meals, hiatal hernia (weakening in diaphragm wall so LES can slide up into thorax/thorax is neg pressure and pulls esophagus open), ascites, bending, squatting, heavy lifting, constrictive clothing, obesity, reduced LES pressure or inappropriate relaxation, esophagitis, defective esophageal clearance mechanisms (peristalsis, saliva), increased gastric secretion (acid, pepsin) and delayed gastric emptying, impaired esophageal epithelial resistance (mucus, unstirred water layer, bicarbonate ions, salivary hyposecretion), smooth muscle atrophy (scleroderma), deep anesthesia
Sx: dysphagia, heartburn, regurg
Refluxed material can damage the esophageal epithelium, causing irritation, inflammation, erosion, ulceration.
Treatment: lifestyle changes, lose weight, quit smoking, do not eat before going to bed, antacids, H2-blockers, promotility agents (bethanechol, etc.). Avoid foods and stimulants that lower LES pressure (anticholinergic agents, ß-agonists, theophylline, benzodiazepines, calcium blockers, opiates
Barrett's esophagus - stricture formation, intestinal/gastric metaplasia, may result in adenocarcinoma
Flatus ‑ gas in the stomach and intestine
Flatulence ‑ distension of the stomach or intestines by an abnormally large amount of gas
Borborygmus ‑ the noise produced by the movement of gas within the GI tract
CO2, N, H, CH3
Sources of gas - or bloat
1. swallowing air
2. foods
3. diffusion of O2, CO2, N2 from the blood
4. emotions which upset normal motility of intestine & allow gas to accumulate (fatigue, depression, pain ® decreased motility)
5. bowel obstruction (torsion of a loop, tumors, hernias)
6. post-op ® decreased motility, so gases accumulate in bowel
7. inflammatory diseases (peptic ulcer, colitis)
Composition of gases in GI tract
The 50 cc of gas normally found in fundus of stomach due to swallowed air contained in frothy saliva or fluffy foods, and from large bubbles or air swallowed along with food or with just saliva
1. also originates from CO2 liberated from ingested bicarbonate upon reaction with gastric acid

2. some of the swallowed air is belched, some is passed into the small intestine, and some remains in the stomach, leading to borborygmi

Not much gas usually present in the small intestine because it passes through very rapidly. As gas passes through small intestine, it produces borborygmi at a rate of 8‑12 per min.

Gas in the colon differs in volume and source from gas in the small intestine. Colonic gas or flatus produced in large volumes - 7-10 l/day.
1. most of this gas is formed in colon by bacterial action on undigested nutrients that reach the colon, and includes nitrogen, methane, carbon dioxide, hydrogen, oxygen and hydrogen sulphide. Colonic gas is therefore combustible. If the methane gas is entrapped in feces that causes it to float. The ability to produce appreciable quantities of methane is familial ‑ if both parents produce CH3, then there is a 95% chance the children will.
1. All of these gases except N2 diffuse readily through the intestinal mucosa, thus reducing the volume of gas to be expelled to about 600 ml/day (N2 is the predominant gas expelled).
2. Intermittently 14 X per day colonic flatus is expelled through the anus. Passage is accompanied by increased motor activity and is associated with food ingestion. Flatulence begins 1 hr after start of a meal & lasts for 20 min or more.
Phases of Digestion
Interdigestive: fasting state - period of time between end of eating a meal and start of the next meal. Spend most of our time in this phase (12-15 hours). Stomach and small intestine are empty.
Cephalic: begins when we start smelling, seeing, thinking about food, chewing food, swallowing food. Controlled entirely by parasympathetic nervous system. Note – parasympathetic stimulation will cause release of gastrin from gastric antrum G-cells.
Gastric phase: begins when food enters stomach. Controlled by parasympathetic, myenteric, submucosal nerves, hormones.
Early intestinal: food empties from stomach into small intestine. Controlled by parasympathetic, myenteric, submucosal nerves, hormones (most important regulator).
Late intestinal: food in small and large intestine (upper duodenum empty). Controlled by parasympathetic, myenteric, submucosal nerves, hormones.
Deglutitation (what happens when food first passes from LES to stomach)
Reception and temporary storage of food: When food first enters the stomach, it is accommodated in the fundus portion. This region acts as a reservoir because it responds to local stretch with active smooth muscle relaxation. This reflex is also called receptive relaxation.
Receptive relaxation: a vagovagal reflex in that both its afferents and efferents are vagal fibers. The efferents are NANC inhibitory fibers. Receptive relaxation of the fundus is followed by gastric accommodation or adaptive relaxation, which is a further relaxation that allows temporary storage of increasing volumes without increasing the pressure above a level that is just enough to move the stomach contents toward the antrum.
The third phase of food reception is a period of continuous tonic contractions that maintain a propulsive pressure gradient from the fundus to the pylorus.
Peristalsis and mixing: fundus portion of the stomach is relatively quiescent and shows no mixing waves. In contrast, the distal half of the stomach shows regular waves of ring contractions. They are peristaltic and serve both mixing and propulsive functions.
Factors increasing LES tone
Muscarinic agonists (ACl, bethanecol) - i/c LES tone means stronger contraction which prevents reflux into esophagus

Alpha agonists (phenylephrine, pseudoephedrine, phenylpropanolamine, amphetamines, etc.) - causes Ca++ to be released from SR, smooth m contracts

Hormones (gastrin, motilin, NPY)

Food (digested protein, Ca++ (via gastrin release)

Antacids, alkali
Factors decreasing LES tone
All promote reflux

Purinergic agonists (ATP, VIP)


Beta agonists (epi, isoproterenol, asthma meds)

Hormones (CCK, secretin, VIP, glucagon, histamine, NO, progesterone)

Foods (fats, carbs, chocolate, cola, mint)

Drugs (anticholinergics, nitrates, nicotine, alcohol, caffeine, Ca++ channel blockers)

Increased abdominal pressure

Hiatal hernia
Gastric emptying rates
1) liquids (2-3 min) faster than solids (15-20 min)
2) small particles > larger
3) easily fragmented food such as noodles faster than meat
4) large, heavy persons empty faster than obese non‑obese
5) inverse with caloric content, not meal weight (noncaloric liquids [water] empty first)
6) after gastrectomy or resection, solids empty faster than before (8O% of contents in 10 min)
7) CHO > protein > fat
8) neutral acids first
9) isotonic > hypo‑ or hypertonic
Inhibition of gastric emptying
CNS - sympathetic acitivity
Acid, hypertonicity -> duodenum secretes secretin
Fats -> gall bladder releases bile into SI)
CHO -> GIP, relaxes smooth m, pancreas secretes insulin
Amino acids, peptides -> gastrin release
Dumping Syndrome
After gastric bypass...

Bloating, nausea, diarrhea, dizziness, rapid heartbeat; 30-60 min post-meal and again 2-3 hours after eating

Concentrated sugar passes too rapidly from stomach to intestine -> body dilutes sugar mixture by bringing fluid from body tissues into intestine -> sense of fullness, cramping, diarrhea
-water loss from tissues -> hypotension -> sympathetic baroreflex -> increased HR, CO, vasoconstriction

Rapid absorption of sugar into bloodstream -> i/c blood sugar -> insulin -> d/c blood sugar -> weakness, hunger, rapid HR 2-3 hours post-meal

Post-gastrectomy diet, possibly B12 injections
Causes of delayed gastric emptying
diabetic autonomic neuropathy
damage to gastric pacemaker cells
smooth m dysfunction
opiates, antidepressants
SI Motility control
Local enteric neurons coordinate motility

PNS: circular smooth m (contractions/shortening), longitudinal m shortening, distention of intestine

Other impulses regulate circular m

Gastroileal reflex and gastrin: relax the iliocecal sphincter, allow chyme to pass into large intestine
Factors increasing SI motility
ACh (vagal, myenteric)
*CCK* (different effects in stomach and SI)
Distention (pressure)
Intense irritation
Castor oil
Factors decreasing SI motility
Malabsorption syndrome
Peristaltic rush
Stim: intense irritation of intestinal mucosa
Initiated by intrinsic nerve reflexes (PNS-mediated)
Enhanced by myenteric plexus reflexes
Strong, intense, long-lasting (20 sec), giant migrating contractions which travel long distances in SI
Sweeps contents into colon -> diarrhea
Gastroenteric reflex
Stimulates motility and secretion along entire SI
- Gastroileal reflex: triggers relaxation of iliocecal valve, allows material to pass from SI into LI
Iliocecal valve
Prevents back-flow of fecal matter into SI
Normally remains mildly constricted
- distention of colon -> contraction, delays emptying
Slows emptying of ileal contents into cecum
- prolongs stay of chyme in ileum, facilitates absorption
Relaxes by gastroileal reflex, *gastrin*
Periodic relaxation is dependent on NANC nerves
Mixing movements of the colon - bag-like sacs
Move slowly analward
Myogenic; myenteric plexus
Sluggish (4-9/min), last 60 sec
8-15 hrs to move chyme from iliocecal valve to transverse colon
Regulated by myenteric plexus in proximal colon, PNS nerves in distal colon
-metabolic alkalosis and hypokalemia (loss of H+, K+)
-acid damage to teeth, mouth
Antiemetic drugs:
-Antihistamines (act on H1 vomiting center and cortex and in vestibular system)
-Anticholinergics (scopolamine)
-Dopamine antagonists
-5-HT3 receptor antagonist
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