Motility Flashcards
1
Q
Peristalsis VS segmental contraction:
A
peristalsis = forward propulsions
segmental contractions: mixing
2
Q
Peristalsis:
A
- Reflex response to stretch
- Affects all GI tract segments
- Contraction followed by relaxation (2-25cm/s)
- Independent of extrinsic innervation
- Involves 5HT (activates myenteric)
- Substance P and Ach contract muscle
- NO, VIP, ATP cause relaxation ahead stimulus
(Peristalsis: Contraction
behind and relaxation in
front of stimulus
Moves content from oral to
caudal direction)
3
Q
segmentation & mixing:
A
- Similar to peristalsis
- Retard movement for optimal digestion
- Contractions at both ends and in the center
- Antero and retrograde movement (unlike
peristalsis)-for efficient mixing - Programmed by ENS
- Independent of central input
4
Q
BER explanation:
A
This electrical activity originates from specialized pacemaker cells called interstitial cells of Cajal (ICCs), which are located in the walls of the GI tract. The BER does not directly cause muscle contractions but serves as the underlying electrical rhythm that coordinates and regulates the timing of contractions in the gut.
5
Q
BER: (basic electrical rythm):
A
- Spontaneous rhythmic fluctuations in
smooth muscle membrane potential - Present in ALL segments, except for
esophagus and proximal stomach (pcq interstitial cajal cells = only in the gut = pacemaker of the gut) - Initiated by interstitial cells of Cajal
(pacemaker, ICC) - Coordinates peristalsis&other motor
activities - Contractions occur only during
depolarization - BER rarely causes muscle contraction
- Spike potentials on BER waves increase
muscle tension - BER rate: 4/min (stom); 12/min (duod);
8/min distal ileum; 2/min (cecum); 6/min
(sigmoid)
6
Q
migrating motor complexes:
A
= essential role in the housekeeping functions of the digestive system, clearing out undigested food, bacteria, and waste from the stomach and intestines.
during fasting = 3 phases = quiescence, irregular then electrical BER
7
Q
migrating motor complexes process:
A
- Cycles of motor activity migrate from
stomach to ileum - Occur during fasting between periods
of digestion (3 phases) - Initiated by motilin
- Migrate aborally (5cm/min), occur
every 90min - Gastric, pancreatic, bile secretion
increases during MMC - Clear the stomach and intestine of
luminal contents for next meal - Eating stops MMC, inhibits motilin,
resumes peristalsis and BER
GENERAL PATTERNS OF MOTILITY
8
Q
Oesophagus roles:
A
- Relaxed at rest; closed at both ends
- Allows retrograde movement
(belching/vomiting)-passive conduit - Movement peristalsis (aided by gravity)
9
Q
oesophagus structural and regulatory aspects:
A
◦ Upper third : circular and longitudinal
muscle layers are striated;
innervation via cranial nerve
(glossopharyngeal & vagus
◦ Middle third: coexistence of skeletal
and smooth muscle.
Primary innervation from vagus
nerve input from neurons of
myenteric plexus to brainstem (NTS)
◦ Lower third: smooth muscle, enteric
nervous system (input from vagus nerve
to enteric nervous system).
10
Q
longitudinal VS circular muscle:
A
- Longitudinal:
- Thin Muscle Coat
- Contraction shortens intestine
length & expands radius - Innervated by excitatory motor
neurons - Activated by excitatory motor
neurons - Few gap junctions to adjacent
fibers - Extracellular Ca2+ influx
important in excitation-
contraction coupling - Circular:
- Thick Muscle Coat
- Contraction increases intestine
length & decreases radius - Innervated by excitatory &
inhibitory motor neurons - Activated by myogenic
pacemakers & excitatory motor
neurons - Many gap junctions to adjacent
fibers - Intracellular Ca2+ release
important in excitation-
contraction coupling
11
Q
longitudinal VS circular muscles during peristalsis:
A
The circular muscles contract and longitudinal muscles relax within the propulsive segments during
peristalsis
12
Q
acetylcholine VS NO, VIP during peristalsis:
A
- AcH release = contraction, (Acetylcholine acts at
muscarinic receptors
on smooth muscle) - NO, VIP = relaxation
13
Q
lower + upper oesophageal sphincter:
A
- UES = prevents entry of air
- LES = zone of elevated resting
pressure (~ 30 mm Hg) - Prevents reflux of corrosive acidic stomach content.
- Is tonically active (contracted) but relaxes on swallowing
LES tone is regulated by extrinsic and intrinsic nerves, hormones
and neuromodulators - Contraction:
- Vagal cholinergic nerves (nicotinic, i.e. atropine insensitive)
- Sympathetic nerves ( -adrenergic).
- Relaxation: (allows bolus to move into the stomach)
- primary peristalsis –> inhibitory vagal nerve input to circular
muscle LES (neurotransmitters (VIP and NO) and reduced
activity of vagal excitatory fibers (cholinergic, nicotinic). - Pressure gradient: peristaltic waves move bolus distally +
negative pressure from the stomach = fast movement through
sphincter
14
Q
peristalsis process:
A
Ring like-waves circular smooth muscle contractions (~4 cm/sec)
Pharyngeal and Esophageal Phases
Stimulated by distention
Mechanoreceptors on sensory afferents stimulate DVC
>vagal efferents>striated muscle/ENS
ENS releases Ach to induce contraction above bolus OR
NO (to relax) below bolus
EFFECT: moves bolus aborally
15
Q
peristalsis, pressure and LES:
A
Primary peristalsis triggered
by swallowing in the
esophagus. Note that the
pressure wave that moves
down the esophagus is
coordinated with LES
opening
The resting pressure of LES
exceeds intragastric pressure
and prevents reflux of gastric
contents into the distal
esophagus
16
Q
primary VS secondary oesophageal peristalsis:
A
- PRIMARY ESOPHAGEAL PERISTALSIS IS
INITIATED BY SWALLOWING REFLEX.
SECONDARY PERISTALSIS IS
TRIGGERED BY DISTENSION TO
CLEAR ESOPHAGUS - SECONDARY PERISTALTIC WAVES
ARE TRIGGERED BY MATERIAL
LODGED IN ESPOPHAGUS, OR
WHICH REFLUXES FROM
STOMACH
17
Q
LES overshooting (peristalsis):
A
On pharyngeal contraction, LES relaxes until bolus passes in the
stomach.
Then contracts overshooting resting pressure 2-3x before returning
to resting. Transient relaxation of LES after meals lasts 5-30s and may
play a role in belching
18
Q
LES relaxation:
A
The final component of
esophageal motility.
Under resting conditions the
LES is tonically contracted
◦ Myogenic: contractile state of
the muscle is independent of
neural input
◦ Increases intrinsically as
stretched.
The tone of sphincter can be
increased by neurohumoral
agents (Ach contracts; NO, VIP,
relaxes) during ingestion of a
meal.
Increase in LES pressure during
inspiration and coughing.
19
Q
anti-reflux mechanisms:
A
- High tone of LES
- Secondary esophageal peristalsis
o Particularly important for pregnant
women - Pinching of LES by the diaphragm
o Only functional anti-reflux mechanism in
infants - Reflexes (gastric and abdominal pressure)
20
Q
dysphagia:
A
difficulty in swallowing, obstructions
o Causes: neurological control of swallowing, peristalsis, LES
relaxation, muscle defects
21
Q
achalasia:
A
LES often fails to relax completely, coupled
with loss of peristalsis = impaired transmit of food)
difficult swallowing, aspirate esophageal contents,
become malnourished. Degeneration of myenteric
plexus ganglia.
22
Q
Hypercontractile esophagus
A
(nutcracker esophagus)
23
Q
Hypocontractile esophagus
A
(scleroderma esophagus)
24
Q
Hypopharingeal
A
(Zenker’s) diverticula
25
GERD
(decreased LES tone). Aggravated by coffee,
chocolate, alcohol, French fries.
26
Functions of the stomach:
*Reservoir for large volumes of
food
*Homogenizer Fragmentation
of food and mixing with gastric
secretion --> digestion
*Controls emptying of gastric
content into duodenum
*Satiation via distention
*House keeping (non-digestible
material via MMC)
27
Origin and GI of motor functions:
- myogenic: o Smooth Muscle
o Interstitial Cells of Cajal (Origin of
Phasic and
Tonic
Contractions)
- * Neurogenic
o Intrinsic (Enteric NS)
o Extrinsic (SNS and PNS)
* Endocrine
* Paracrine
(Modulate
Contractions)
28
muscle anatomy and functions:
- The abundant smooth muscle in the stomach is responsible for gastric motility
The proximal stomach: (cardia,
fundus, proximal body). Serves as
reservoir and moving the gastric
contents. Tonic contractions in
gastric emptying.
The distal stomach: (distal body,
antrum). Serves as grinding and
triturating the meal.
◦ Pylorus controls food exit
◦ Pylorus relaxes during MMCs
29
receptive relaxation:
The ability of the stomach to relax as its volume increases
* Swallowing causes relaxation of gastric smooth muscle
* Mediated by vagus nerve. (Vagotomy affects accommodation)!!!
* Receptive relaxation increases compliance, so that luminal pressure
changes very little between the empty state (50 mL volume) and
filled state (1500 mL volume)
30
factors of receptive relaxation:
Intrinsic and vago-vagal
reflexes
Duodenal distension
Nutrients in duodenum
Filling (gastric distension)
31
segmental contraction VS peristalsis:
Segmental contractions are important because they allow for more thorough mixing without moving the contents rapidly along the digestive tract, unlike peristaltic contractions, which push the contents forward.
32
receptive relaxation explained:
When food enters the stomach from the esophagus, the stomach walls undergo receptive relaxation. This allows the stomach to stretch and accommodate larger volumes of food without significantly increasing internal pressure. This process is part of normal digestion, helping to prevent discomfort and maintain efficient processing of food.
receptive relaxation = dependant on the vagus nerve
33
mixing and grinding:
* Pacemaker Region induces peristaltic contraction
from the body to the antrum, which closes the
pyloric sphincter.
* Pacemaker Cells (ICC) induce slow waves (BER) ~
3 times per minute.
* Force of Contraction, Regulation:
o Increased by gastric distension, via short reflexes
and gastrin.
o Inhibited by 1) duodenal distension, 2) appearance
of fat, protein, acid or hypertonic chyme in the duodenum, 3) increased sympathetic tone
!! grinding = contractions after the stomach traverses the pyloric sphincter and it closes!!
34
Gastric emptying:
Emptying of the stomach involves both tonic contractions of the
proximal region and phasic distal contraction (like a pump)
Pylorus regulates emptying
Neural and humoral regulation (5-HT, CCK)
◦ Gastric distension and increased intragastric volume increases
emptying (rate is proportional to size of meal).
◦ Gastric emptying inhibited by:
Entry of chyme into duodenum
Fat, protein digests in duodenum
Acidity (pH < 3.5) in duodenum
Hypo/hyper-osmotic chyme in duodenum
Distention of duodenum
Solids more inhibitory than liquids.
35
pyloric valve:
* Regulates emptying of gastric content
* Prevents regurgitation of duodenal content
* Pyloric relaxation: inhibitory vagal fibers (mediated by VIP and
NO)
* Pyloric constriction: excitatory cholinergic vagal fibers,
sympathetic fibers and hormones, CCK, gastrin, gastric inhibitory
peptide secretin.
36
Driving forces of gastric emptying:
- stimulate: volume, liquid vs solid, type of food, hormones, neural, drugs
- inhibit: duodenal distention, osmolarity of chyme, type of food, acid, temperature, hormones, neural, patient factors
37
DUODENAL CONTROL
OF GASTRIC EMPTYING
BY FAT
When fat enters the duodenum, it stimulates the release of cholecystokinin (CCK), a hormone produced by the small intestine.
CCK signals the stomach to slow down gastric emptying, giving the small intestine more time to digest the fat.
It also stimulates the release of bile from the gallbladder and pancreatic enzymes to aid in fat digestion.
38
DUODENAL CONTROL
OF GASTRIC EMPTYING
BY OSMOTIC
STIMULATION
1. Hyperosmotic gastric
content enters duodenum.
2. Osmotic stimulus
activates vagal sensory
fibers.
3. Vagal inhibitory fibers
reduce intragastric pressure
and increase pyloric
resistance
39
duodenal control of gastric emptying by acid
1. Acid entering
duodenum stimulates
secretin release
2. Circulating secretin reduces IG
pressure and increases pyloric resistance.
40
THE MIGRATING MYOELECTRIC COMPLEX
1. MMC starts at LES and sweeps through GI
tract to distal ileum.
2. MMC occurs at regular interval during the non-
fed state.
Absence of MMC results in increase in intestinal bacteria
41
digestive VS inter-digestive period:
* Digestive period
o Relaxation→ Storage
o Peristaltic contractions→ Mixing, size reduction & emptying
* Interdigestive Period
o Strong peristaltic waves (MMCs)→ “housekeeping”
42
vomiting VS regurgitation:
VOMITING – Forced expulsion of contents of stomach and proximal
small intestine, accompanied by retching and forceful contraction of
abdominal muscles. Associated with nausea.
* REGURGITATION – Non-forceful emptying of stomach or esophagus
without retching or strong abdominal contraction.
43
going through the motions:
* Reversed intestinal
peristalsis (RGC)
* Retching begins
* Relaxation of the
proximal stomach
* Closure of the glottis,
with inspiratory effort
against closed glottis
* Increased contraction
of antral portion of
stomach
* Relaxation of the LES
* Inhibition of
ventilation
* Contraction of
abdominal muscles
* Expulsion of vomitus
Vomiting
44
Gastric pathophysiology:
*Pyloric Stenosis (congenital, failure to relax after a meal)
*Regurgitation, vomiting
*Absence inhibitory influences to the pylorus (lack NO?)
*Gastroparesis (collection of disorders)
*Delayed gastric emptying
*Satiety, vomiting, nausea, bloating
*Idiopathic common
*Diabetes, scleroderma.
*Dumping syndrome (rapid emptying)
*Functional dyspepsia (impaired fundic relaxation;
hypersensitive antrum)
45
feed vs fast motility:
* Marked distinction in transit time
* Type of interdigestive motility pattern in small intestine is exhibited by MMC (3
phases).
* Feeding increases motility & stops MMCs
* Many contractions do not propel food and are retrograde (duodenum)
* The last phase of MMC, as in stomach, sweeps the intestine clear of any remaining
residues of the meals
MMC in duodenum and jejunum in a fasting human by manometry.
Intense contractions occurring rhythmically during phase III
propagate aborally
46
MMC VS digestive motilities:
- MMC = intermittent, strong, pyloris = open, SI = peristaltic waves, functions = removing undigestible materials, + preventing bacterial growth in SI, mediator = motilin
- Digestive motilities = constant, intermediate, pylorus = closed/ narrowly open, SI = segmentation, function = optimizing digestion + absorption, mediator =
47
peristalsis VS segmentation (SI):
* Two major types of contractions occur in small intestine:
o Peristalsis: weak and slow, occurs mostly because pressure at
pyloric end is greater than at distal end
!! Progressive contraction of successive sections (short distances) of
circular smooth muscle in orthograde direction !!
!! Intestinal distention triggers
peristalsis!!
o Segmentation: major contractile activity of small intestine
Contraction of circular smooth muscle mixes chyme
48
Emptying of the ileum:
Ileocecal sphincter: normally
closed. Short-range peristalsis in
terminal ileum and distension
relaxes IC sphincter --> small
amount of chyme is squirted
into the cecum.
* Distension of cecum contracts
IC sphincter.
* Gastro-ileal reflex enhances ileal
emptying after eating.
* The hormone gastrin relaxes
ileocecal sphincter.
49
Colonic motility:
* Contains circular and longitudinal muscle layers
in different arrangement- taenia coli
* Haustration (circular muscle contractions;
corresponds to segmentation in small intestine).
Not permanent structures-permit propulsion.
* Segmental propulsion or systolic multihaustral
propulsion (short: circular muscle, 8s; long: long
muscle, 20-60s).
* Sigmoid and rectum-enveloped in longitudinal
muscle (reservoir; defecation)
* Rectum: transverse fold-retard feces
* Anal canal: smooth+striated muscles
* Antipropulsion (reverse peristalsis, ascending,
transverse)
* Mass movement
50
LI motility:
1. segmentating non peristaltic contractions (haustral shutting) to slow fecal stream
2. H20 and electrolytes
3. occasional peristaltic activity to push stool aborally
!! Propulsive motility of colon is relatively slow,
until mass peristalsis and defecation !!
51
ileo-cecal sphincter
* Main function: limit reflux of colonic
contents (unlike proximal sphincters)
* An urge of defecation shortly after a
meal is produced by the gastrocolic
reflex
* The reflex produces a generalized
increase in colonic motility with mass
movement of feces.
* 5-HT and Ach appear to be important
mediators of the response.
* The function of this reflex is to clear
the colon to ready it to receive the
residues of the new meal.
52
defecation problems causes:
* Diet low in insoluble fiber (insufficient stimulation of baroreceptor):
o Correctable
* Insufficient fluid intake (insufficient stimulation of baroreceptor):
o Correctable
* Excessive delay in defecation (insufficient stimulation of baroreceptor):
o Correctable
* Drug abuse (morphine inhibits secretion, increases muscle tone and
resistance to movement):
o Correctable
* Old age (reduction in food intake, muscle activities and reflexes):
o Hopefully correctable!
53
- Food entering stomach and
duodenum releases gastrin
and CCK = (ileum wise):
- Stomach filling increases intestinal
motility:
- Increased colonic propulsive
activity
- Stomach filling induces
relaxation of ileocolic
sphincter
54
summary of GI motility:
* Mouth: Chewing (mastication)
* Esophagus: swallowing
* Stomach: receptive relaxation, accommodation, emptying and
MMC
* Small intestine: segmentation and peristalsis
* Ileo-Cecal Sphincter: reflexive relaxation and contraction.
* Large intestine: Haustral shutttling and mass movement
* Rectum: defecation
55
haustral shuttling explained easier:
Segmental Contractions:
Haustral shuttling involves localized contractions of the circular muscle layer of the colon, creating bulges in the haustra. These contractions are often referred to as haustral contractions.
Mixing and Moving Contents:
The primary function of haustral shuttling is to mix the contents of the colon and facilitate the absorption of water and electrolytes. This movement helps to move the fecal matter slowly through the colon, allowing for optimal absorption.
Enhancing Absorption:
By shuttling the contents back and forth, haustral shuttling increases the surface area available for absorption, helping to concentrate the waste material before it is eliminated from the body.
Slow Movement:
Unlike peristalsis, which is a more vigorous and coordinated movement that propels contents along the digestive tract, haustral shuttling is slower and more subtle, allowing for more time for absorption.
Role in Defecation:
Eventually, the contents of the colon will be propelled towards the rectum through more forceful peristaltic contractions, leading to defecation. Haustral shuttling prepares the material for this eventual movement.
56
reflexive relaxation explained easier:
Peristaltic Reflex: When a segment of the intestine stretches, reflexive relaxation can promote coordinated peristaltic contractions in the adjacent segments, facilitating the forward movement of intestinal contents.
57
Intestinal pathophysiology:
* Ileus: temporary or permanent state of inhibited GI motility.
* Hirschsprung’s Disease: congenital megacolon, is a developmental
abnormality that results when the enteric nervous system fails to
develop appropriately
* Functional (or irritable) Bowel Disorder: abdominal pain,
bloating, constipation, and/or diarrhea, but for which no organic
cause can be found
* Fecal incontinence: failure of the external anal sphincter to
maintain appropriate tone of the anal canal, therefore, release of
rectal contents against one’s wish.
58
enteric VS para VS sympathetic
The enteric nervous system can function independently to control digestive activities, which is why it's sometimes called the second brain. So the parasympathetic input basically enhances digestion, and sympathetic input inhibits digestion.
!! para = the mainly used one entre symp dans GI !!
