How are do excitatory motoneurons work to increase peristalsis?
they use ACh and Substance P to increase the frequency, amplitude, and duration of the plateau phase of slow-waves
What are the two types of thresholds for SM in the GI?
Electrical threshold for firing of APs and then there's a mechanical threshold for contraction. The mechanical one is a more negative potential
How are contractions coupled w/ electrical activity?
depolarization leads to opening Ca channels=>incr. [Ca]=>calmodulin=>activation of MLCK=>phosphorylation of myosin=>crossbridge formation and cycling=>formation of force and contraction
2 types of SM contraction (tonic and phasic)
Tonic: contractile tension is maintained for prolonged periods of time
Phasic: twitch-like contraction due to APs. AP triggering incr. force of contraction. Also freq and number of APs grade the degree and duration of contraction
Tonic contractions (type of SM contraction and where it occurs)
is characteristic of the pharyngoesophageal and gastroesophageal sphincters, pyloric valve, sphincter of Oddi, ileocecal valve, and the internal anal sphincter
Propulsive peristalsis (type of SM contraction and where it occurs)
esophagus, lower 2/3 of the stomach, SI and LI, and the rectum
Reverse peristalsis (type of SM contraction and where it occurs)
antipropulsion that occurs in the proximal colon
Migrating myo-electric complex or migrating motor complex (type of SM contraction and where it occurs)
occurs during fasting or an empty SI
Mass movements (type of SM contraction and where it occurs)
ascending, transverse, and descending colon
Segmentation (type of SM contraction and where it occurs)
Haustration (type of SM contraction and where it occurs)
ascending, transverse, and descending colon
Upper 1/3 of the esophagus (muscle content and innervation)
has circular and longitudinal SKM innervated by cranial nerves
Middle 1/3 of the esophagus (muscle content and innervation)
has both SKM and SM and primary innervation is by the vagus nerve. There's input from the myenteric plexus that is cholinergic muscarinic and therefore atropine sensitive
Lower 1/3 of the esophagus (muscle content and innervation)
Is all SM innervated by ENS with PSNS input from the vagus nerve.
Pharyngoesophageal (upper esophageal sphincter or UES) (function)
prevents air from entering the esophagus
Gastroesphageal sphincter (lower esophageal sphincter or LES) (function)
zone of elevated pressure that prevents reflux of acid.
It is innervated by vagal excitatory fibers and vagal inhibitory fibers that work reciprocally (in-terms of their frequency)
is initiated voluntarily but then it comes under the control of the deglutition reflex
Oral/voluntary phase (Deglutition)
tongue moves bolus to the pharynx this stimulates tactile receptors (beginning of the afferent limb of the reflex) which stimulate swallowing centers in the medulla and pons which sendout efferents to musculature of the pharynx and upper esophagus.
Pharyngeal phase (Deglutition)
upwards movement of soft palate, pulling together of vocal chords and epiglottis covers the larynx. Relaxation of the UES and initiation of the peristaltic wave. Respiration is reflexively inhibited.
Esphophageal phase (Deglutition)
under control of the swallowing ceneter. There's a primary peristaltic wave that pushes the bolus towards the stomach. There can be secondary waves due to distension of the esphageal wall (in case a bolus gets stuck); these are mediated by the ENS
Intraluminal Esophageal Pressure Profile
Pressure in the body of the esophagus is negative: reflecting intrathoracic pressure. However, pressure in the UES and LES is positive during swallowing.
Secondary peristaltic wave
is a local reflex response to stuck bolus (poorly lubricated or too big). Sensory inputs in the myenteric ganglia respond to mechanical and chemical changes (like pH). Efferent then go out to muscles, glands, and epithelial cells. Remember that exitatory interneurons send their signal proximal to the stretch, while inhibitory interneurons send theirs distal. This keeps bolus moving in an aboral direction.
What are the two types of neurons that cause seconday peristaltic waves?
Stretch-sensitive neurons in the myenteric plexus and chemosensitive/mechanosensitive neurons whose soma is in the submucosal plexus. Stimulation of these any of these two neurons leads to ascending excitation and descending relaxation
How are the sensory neurons stimulated in the esophagus?
stimuli to the mucosa causes enterochromaffin-like cells to secrete serotonin in the mucosa. Serotonin stimulates the sensory neurons of the submucosal plexus.
Excitatory and inhibitory compounds to peristalsis
excitatory: ACh and Substance P
Inhibitory: VIP, NO, and ATP
Anatomical subdivisions of the stomach
cardiac, fundus, body (oxyntic glandular mucosa and the pacemaker zone), antrum (pyloric glandular mucosa), pylorus (pyloric sphincter, gastroduodenal juction)
Function of gastric motility
reservoir for large volumes of food. fragmentation of food and mixing w/ gastric secretion. controlled emptying into duodenum.
Where's the pacemaker zone of the stomach?
in the superior part of the body in the wall of the greater curvature.
What occurs in the antrum and pylorus regions in-terms of the slow-wave traveling thru the stomach?
APs are superimposed on the slow-waves in these regions, enhancing the force of contraction.
What modulates the gastric slow-waves?
ACh and gastrin cause increase in amplitude and duration
NE decreases the extent of depolarization and duration of the plateau
Which areas of the stomach have strong and weak slow-waves when gastric muscle is divided into strips?
the fundus region doesn't get slow waves but as you move towards the pylorus region the slow-wave strength increases. You don't start seeing APs till the antrum though. However, if the stomach was to together all the different parts would have the same frequency of slow-waves.
Why can the stomach be stretched from 50ml to a liter w/o significant increases in tension?
Gastric plasticity: gastric SM can be stretched w/o a change in tension
Receptive relaxation: when the stomach is filling and distension occurs, there's a reflexive relaxation of the fundus and body of the stomach caused via the vagus nerve via NO and VIP.
What is the reason behind why the stomach can store food?
The stomach has weak, thin layers of muscle in the fundus and body. Therefore, peristalsis is weak=> weak motility=> storage of unmixed food.
is caused by the peristaltic propagation. When the slow waves reach the antrum and pylorus regions, they cause that region to contract. During this systole the pyloric sphincter closes forcing contractile waves back towards the proximal portion of the antrum (this is called retropulsion). These results in even more effective mixing as bolus/chyme is pushed back into the body. During the systolic contraction, some of the content of the antrum is squirted into the duodenum.
During the systolic contraction, some of the content of the antrum is squirted into the duodenum.
Is regulated at the pylorus region by hormonal and neuronal factors.
Relaxation: inhibitory vagal fibers that use NO and VIP (vasoactive intestinal peptide)
Constriction: excitatory cholinergic vagal fibers, SNS fibers, hormones CCK, gastrin, GIP, secretin
Gastric (Factors influencing rate of gastric emptying)
volume/amount of chyme: distention=>increased motility
fluidity: increase fluidity allows for more rapid emptying
Duodenal/jejunal factors (Factors influencing rate of gastric emptying)
FAT (FAs stimulate I-cells to release CCK and K-cells to release GIP), Hypertonicity (stimulates osmoreceptors), peptides/AAs (stimulates G-cell of antrum & duodenum to release gastrin), and pH triggers S-Cells to release secretin), distension of the duodenum. All of these decrease gastric emptying.
Effects of secretin
Secretin inhibits antral contraction, stimulates pyloric contraction and stimulates bicarbonate-rich secretion from liver and pancreas
Outside factors influencing rate of gastric emptying
Emotions: influence the ANS balance and can stimulate or inhibit gastric motility.
Intense pain: leads to SNS stimulation and inhibition of gastric motility
forceful expulsion of gastric/intestinal content through the mouth
Protective function (emesis)
it prevents overdistention and/or irritation of the stomach and intestines, especially the duodenum.
Reflex center for emesis
is located in the medulla oblongata and it integrates sensory inputs and coordinates emesis
Emesis (what happens)
reverse peristalsis of SI, relaxation of pyloric sphincter. Forced inspiration against a closed epiglottis decreases intrathoracic pressure and increases intrabdominal pressure. Forceful contraction of abdominal muscles sharply increases intrabdominal pressure even more. Relaxation of LES and UES as well as contraction of the pylorus and antrum facilitate movement of intestinal contents. There's an approximation of the vocal chords, closure of the glottis, and inhibition of respiration prevents aspiration into the respiratory tract
precedes emesis and involves the forcing of gastric content into the esophagus but due to closure of the UES the gastric contents do not make it into the esophagus
ANS discharge effects during emesis
salivation, dilation of pupils, sweating, pallor, tachypnea, rapid and irregular heart beats.
Causes of emesis
tactile (stimulation of the back of throat), Irritation/distension of the stomach/duodenum, elevated intracranial pressure (from cerebral hemorrhage), rotation/acceleration of the head (motion sickness), Intense pain, Chemical agents (emetics), emotional factors
Types of motility of the SI
digestive motility pattern that includes segmentation and peristalsis
interdigestive motility pattern involving migrating myoelectric complex
Segmentation in the SI
main purpose is mixing and is most common type of motility in the SI. It is the closely spaced, alternating, contractions of the circular muscle layer that divides the small intestine into small neighboring segments. Alternation of contraction b/w segments results in mixing. As you move towards the gut, the frequency of segmentation contractions decrease. This means slow forward transport of food content and more time for absorption.
Peristalsis in the SI
main function is propulsion. It is the progressive contaction of adjacent, successive, segments of SM in the aboral (orthograde direction)
Regulation of SI motility
APs enhance the contractions. Intramural nerve plexuses regulate segmentation and short peristaltic waves. Extrinsic innervation is involved in long-range reflexes and modulate along w/ humoral factors, the exitability of the SI SM. Remember PSNS enhance, SNS inhibit.
The migrating myoelectric complex
is the interdigestive motility pattern and occurs in fasted organusms. They are bursts of intense electrical and contractile activity for 5-10min that originate from the stomach to the terminal ileum and repeats every 75-90min.
The migrating myoelectric complex (function)
to sweep the contents of the SI into the cecum. This along w/ the ileocecal sphincter helps to prevent migration of bacteria from the colon to the sterile intestine. (its a house keeper function)
Contractions of the muscularis mucosae of the SI
irregular contractions (about 3/min) that enhance the contact b/w the mucosa and content and facilitates absorption. May cause incr. emptying of lacteals and increased intestinal lymph flow.
Short range (Intestinal reflexes)
food bolus causes aboral relaxation and proximal contraction so we get transport in the aboral direction. This is regulated by intrinsic nerves.
Long range (Intestinal reflexes)
Is regulated by intrinsic and extrinsic nerves.
Intestino-Intestinal reflex (Long Range Intestinal Reflexes)
Requires extrinsic nerve innervation, however, it involves the over distension of one segment of the intestine which causes the rest of the SM cells of the intestine to relax.
Ileo-gastric reflex (Long Range Intestinal Reflexes)
distention of the ileum leads to decreases gastric motility
Gastro-ileal reflex (Long Range Intestinal Reflexes)
increased secretory and motor activity of the stomach leads to increased ileal motility and movement of content thru the ileocecal sphincter
Emptying of the ileum
short range peristalsis and distention in the terminal ileum causes the ileocecal sphincter to relax allow squirts of chyme into the cecum. However, distension of the cecum leads to contraction. This is enhanced by the gastro-ileal reflex and Gastrin (form the stomach).
the longitudinal layer of muscularis externa is divided into 3 bands called the teniae coli
Anal sphincter layers
internal layer is circular SM and external layer is SKM
Segmentation (Motility of the colon)
Segmentation via haustra mixes and kneads the chyme. It helps in absorption of salts and H2O
Propulsive Peristalsis (Motility of the colon)
concerted contraction of SM elements. function is to empty neighboring haustra in the aboral direction.
Anti-propulsion (reverse peristalsis)
occurs in the proximal colon and is segmental propulsion towards the cecum. Function is to retain chyme in the proximal colon and facilitate H2O and salt absorption
Mass Movement peristalsis (Motility of the colon)
this a larger and longer peristaltic wave you get about 3X per day. function is to empty the proximal colon into the the distal colon and rectum.
Innervation of the colon
Vagus does the cecum, descending and transverse colon and causes segmental contractions. Pelvic nerves from the sacral SC do the descending colon, sigmoid colon, rectum and anal canal. They cause sustained contractions and expulsive movements.
SNS innervation of the colon
inhibition of colonic movements
Somatic innervation of the colon
motor fibers via the pudendal nerves go to the external anal sphincter.
Colono-Colonic reflex (Colonic Reflexes)
distension of one segment of the colon elicits reflex relaxation of the other parts of the colon
Gastro-Colic reflex (Colonic Reflexes)
filling of the stomach increases motility and frequency of mass movements of the colon
is usually empty b/c of segmental contractions moving its contents retrogradely into the sigmoid colon.
Filling of the rectum though occurs due to mass movements in the sigmoid colon.
The anal canal
is normally closed due to internal and external sphincter closures. Filling of the anal canal causes reflex relaxation of the internal sphincter and constriction of the external sphincter leads to the urge to defecate
is a complex behavior involving voluntary actions and reflexes.
the sacral SC and efferent cholinergix PSNS fibers in pelvic nerves trigger this reflex. Distension of the rectum and relaxation of the internal sphincter are the results of the reflex.
Voluntary actions in defecation
relaxation of the external anal sphincter (innervated by the pudendal nerves) and increase of intraabdominal pressure.