Motility In The GI System Flashcards
Muscularis Mucosae
SM that contract to change the shape and SA of the epithelium
Slow waves are found where
What is it
when do APs occur
In the SM of GI tract
Depolarization and repolarization make no AP
AP happens when depolarization moves above threshold and = mechanical response (due to H. Or Nerve)
* slow waves sets the f of APs
Phasing contractions and where are they found
Periodic contractions followed by relaxation
Upper esophagus, Antrum stomach, SI, anything for mixing and propulsion
Tonic Contractions and where are they found
Constant level of contraction without regular relaxation periods
Lower esophagus, Orad stomach, Ileocecal sphincter, internal anal sphincter
How to increase the contraction strength
Higher number of AP on top of the slow wave
What increases AP on slow waves
ACH, Stretch, and Parasympathetics increase Amplitude and number of APs(strength of contraction)
what decreases APs of slow waves
NE and Sympathetics decrease number of APs(strength of contractions)
Submucosal plexus (meissner’s)
In the submucosa externally to it
GI secretions and local BF
Myenteric Plexus (Auerbach’s)
GI movements
The submucosa and myenteric plexus are part of the
ENT which does not need the CNS to operate
However it can in some instances relay information to the CNS
Interstitial cells of Cajal (ICC)
Pacemaker cells in the GI SM
They initiate and generate SLOW WAVES (spontaneous slow waves in ICC spreads to nearby SM cells by gap junctions)
The control strength of contraction
Spontaneous SLOW WAVES in the ICC due to
Opening of voltage gated CA+2 channels, pass along through gap unctions to open Ca+2 channels of SM cells
Mastication
Voluntary and in voluntary controlled by CN5 with nuclei in brain stem (Mastication Reflex)
4 phases of swallowing
1 . Oral phase : Voluntary - initiate swallowing
- Pharyngeal phase : Involuntary - soft plate pulled UP = epiglottis moves = UES relaxes = peristaltic wave of contractions initiated by pharynx ——> food moves to UES
- Esophageal Phase : Involuntary- ENS and swallowing reflex controls this, = Primary and secondary peristaltic waves to move food past LES (continuous from pharynx wave)
How the pharynx starts the peristaltic wave of contraction
- Food is sensed in pharynx by CN X + CN 9
- CN X + CN 9 go to the swallowing center (medulla)
- Sends info to brain stem nuclei
- Send signal through the nucleus ambiguous to pharynx to contract
Primary Peristaltic wave in the epiglottis
Continuous with pharyngeal wave contraction
Controlled by medulla also
Uses CN 10 to send signal from here
NONE after VAGOTOMY
Secondary Peristaltic wave
Occurs if primary doesn’t get rid of all food or during gastric reflex
Controlled by Medulla (CN X ) and ENS
Not continuous or so trolled by any previous peristaltic wave contraction = UES does not need to open
CAN HAPPEN STILL AFTER VAGOTOMY
How is the pressure at rest through the esophagus
Upper part (UES) : high pressure due to no acid reflux, above 0mmHg
A little lower (level of Thorax) : below 0mmHg - flaccid
Right below or at diaphragm: a little above 0mmHg,
LES : HIGH pressure above 0mmHg
Fundus of stomach : HIGH above 0mmHg
How is the pressure during swallowing through the esophagus
Upper (UES) : decreases quick to open
(Level of thorax) : increase after the initial UES opening
At or below diaphragm: slight increase spike
LES : broad decrease spike (starts even before food is right there)
Fundus : very slow broad decrease (starts before food comes there)
Reason UES and LES are closed at all times unless food is passing
To keep air out of esophagus at upper end
To prevent gastric acid contents out from lower end
What happens in achalasia
- The peristaltic waves impaired
- LES doesn’t relax all the way (when swallowing)
- LES resting pressure is very elevated
Reasons for achalasia to occur
Ganglionic cells in the myenteric plexus (in Muscularis Externa) decreased
= inhibitor neurons make NO + VIP —> damaged specifically
= no contraction or relaxation when needed
Achalasia Sx:
Regurgitation of food liquid and solid
Hard swallow (DYSPHAGIA)
Heartburn
Chest pain
What happens in GERD
Barrier between esophagus and stomach changes due to weakened LES (abnormally relaxed)
= gastric reflux is common (during pregnancy, lifting, large meal)—> they tend to relax LES
= gastric acid + bile + pepsin into esophagus—> heartburn and regurgitation of acid
What can make GERD happen and complications
Persistent reflux and inflammation damages the ENT neurons in the myenteric plexus that signal contraction
GI bleeding, (irritation) Esophagitis, Barrett’s esophagus, scarring in esophagus
CASE 1: 5 years Dysphagia. HTN. Foods stick to upper sternum area after meal. Can get it down with repeated swallows or drinkin water. Spontaneous regurgitation and cough at night. Weight loss
Chest pain, no heartburn, traveled to mexico one month before.
DX: Achalasia
Chagas Disease
Innervation of the stomach
Extrinsic innervation - para and sympa
Intrinsic innervation - myenteric and submucosa plexus
to pass food rom orad to the caudal is
Receptive relaxation
Decrease P and Increase V in orad region
VAGOVAGAL REFLEX
Orad function
Little contraction and mixing, more for receiving food
CCK in the duodenum causes
Decrease contraction
Increase Gastric Distensibility
* in stomach
Contraction strength and velocity in stomach
Increases as you move closer to the Pyloris (from mid stomach)
REPULSION
When increased P on Pyloris closes it and food is pushed back up to the Orad to mix food more
How long food goes to duodenum completely
3-4hrs
What increases AP and contraction force in stomach
PARASYMPATHETIC (*CN10), GASTRIN, MOTILIN
What decreases AP and contraction force in stomach
SYMPATHETIC, SECRETIN, GIP
4 factors promoting gastric emptying to the duodenum
- Decrease DISTENTION of orad(contract more)
- Decrease TONE of Pyloris (Relax more)
- Increase FORCE of Perictaltic contractions of Caudal stomach
- Increase DIAMETER and INHIBIT contraction of proximal duodenum
3 factors that inhibit gastric emptying
- Relax orad
- Decrease force of peristaltic contraction of caudal stomach
- Increase pyloric tone and proximal duodenum contractions
Entero-Gastric Reflex
in duodenum is ACID
FATS
HYPERTONIC
When contractions are high in duodenum = - feedback to stomach to not empty, using secretin, GIP, CCK
(To keep pH right and not overwhelm duodenum)
1. Acid = secretin ——I stomach (by —I Gastrin)
2. Fats + AA = CCK + GIP —— I stomach
3. Hypertonicity = unknown H. ——I Gastric emptying
Gastric emptying disorder
Sx:
Causes
Tx:
Sx: fullness, Loss of appetite, N, V
Causes: Gastric ulcer, cancer, eating disorder, vagotomy (used in past to reduce acid secretion)
Tx: pyloroplasty, balloon dilation
Gastroparesis
Slow emptying of stomach or paralysis of stomach
Common cause = diabetes (20% T1D)
Vagus N injury (no mechanical obstruction)
Sx: N, V, fullness, weight loss, boating ,ABD discomfort
How are large particles of undigested and bacteria that remain in the stomach
MMC (Migrating Myoelectric Complex, Migrating Motor Comlex)
ONLY DURING FASTING
Periodic bursting peristaltic contractions moving from the fundus of stomach to the rectum (90min) to clean the GI
MOTILIN = important role
Disfunctioning MMC
Bacterial overgrowth (SIBO) - if in SI = can cause motility dysfunction in SI —> N, anorexia, bloating
How is SI digestion happening
2 types of contraction
- Segmentation contractions =
Compress in middle of food boules and makes it split, relaxes and 2 halves come back together
No forward movement, allows enzymes to mix and absorb - Peristaltic Contraction = circular and longitudinal muscles move food forward Orad——> Caudal
How do circular and longitudinal muscles work together
When one contracts the other relaxes (always opposite) to move the food
What electrical impulses are present in the SI
SLOW WAVES ; always present even with no contractions
——> they DONT initiate contractions (the AP is what initiate any contraction)
——> they do set the number of contractions/min by increasing frequency
SLOW WAVE f in the SI
Highest at proximal SI
Decreases down the SI
How signals in lumen are collected and make a GI response
Wall of SI : cells sense mechanical/contents in lumen (enterochromaffin cells) ——> SEROTONIN ——> IPAN receptor ——> interneurons (excitatory + inhibitor)——> muscle for peristaltic reflex
*there are interneurons (ACH + Substance P - excitatory) and (VIP + NO- inhibitory) that get info from enterochromaffin
Para and sympa Serotonin Prostaglandin Epinephrine Gastrin CCK Motilin Insulin Secretin Glucagon
Para = stimulates contraction Sympa = inhibits contraction
Serotonin = stimulates contraction Prostaglandin = stimulates contraction Epinephrine = inhibits contractions Gastrin = increase contractions CCK = increase contractions Motilin = increase contractions Insulin = increase contractions Secretin = inhibit contractions Glucagon = inhibit contractions
What coordinates vomiting reflex
Uses Medulla which uses VAGUS + SYMPATHETIC AFFERENTS to many places in the Brianstem ——> chemoreceptor zone by area postrema——> Medulla——> vomit reflex
- Revers peristaltic contractions
- Stomach relaxed
- Inspire forcibly to increase ABD P
- LES relaxations + Close glottis
- Movement of larynx
Ileocecal Junction
When is sphincter relaxed/ contracted
Relaxed = when ileum is distended Contracted = when colon is dilated
What do the Longitudinal Muscles of the LI have
Taeniae Coli = 3 bands from cecum to rectum
Circular muscles of LI
Cecum to Anal canal
HAUSTRA are formed , disappear and reappear
Pelvic Splanchnic N innervates
Inner Anal Sphincter (parasympathetic)
Peudendal N innervates
External Anal Sphincter (somatic)
ENT (myenteric) innervates
under teneae coli, and muscles layer of external Muscularis
Parasympathetic NS innervates in LI
Vagus ——> Cecum, A.C, T.C.
Pelvic NS S1-S4 ——> D.C, S.C, Rectum
Sympathetic innervates in LI
Superior mesenteric——> Proximal regions
Inferior Mesenteric ——-> Distal Regions
Hypogastric——> Distal Rectum and Anal Canal
Unique feature of LI to make poop
MASS MOVEMENT
1-3 times a day
Defacation reflex
In colon (T.C is most common) over large distance
LI absorption
VIT and H2O
Rectum movement
Mass movement
Segmented contractions
1. SM contract + Internal anal sphincter relaxes
*RETROSPHINTERIC REFLEX)
2. External Anal sphincter closes when you want to and don’t want to poop at the moment
What controls the RECTOSPHINCTERIC REFLEX
Neural ENS and spinal cord nerves(senses rectal distension) ——> muscles
External sphincter nerves travel to cerebral cortex ——> muscle
* if damaged = problems of voluntary control of poop
Normal tone means
Muscle or sphincter in not defected
If there is a problem it is the nerve in this case
Hirschsprung Disease
Ganglion cells absent from colon (VIP levels are low)
= SM contractions + no controlled movement
= feces accumulate
= if at birth : congenital megacolon (no meconium), jaundice, X feeding
=older patients : constipation, malnutrition
=Tx: surgery to put ganglia from other locations to the part of colon without
