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GI physiology > Motility > Flashcards

Motility Flashcards

1
Q

Peristalsis VS segmental contraction:

A

peristalsis = forward propulsions
segmental contractions: mixing

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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)
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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
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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.

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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)
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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

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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
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8
Q

Oesophagus roles:

A
  • Relaxed at rest; closed at both ends
  • Allows retrograde movement
    (belching/vomiting)-passive conduit
  • Movement peristalsis (aided by gravity)
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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).

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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
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11
Q

longitudinal VS circular muscles during peristalsis:

A

The circular muscles contract and longitudinal muscles relax within the propulsive segments during
peristalsis

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12
Q

acetylcholine VS NO, VIP during peristalsis:

A
  • AcH release = contraction, (Acetylcholine acts at
    muscarinic receptors
    on smooth muscle)
  • NO, VIP = relaxation
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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
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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

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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

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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
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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

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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.

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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)
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20
Q

dysphagia:

A

difficulty in swallowing, obstructions
o Causes: neurological control of swallowing, peristalsis, LES
relaxation, muscle defects

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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.

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22
Q

Hypercontractile esophagus

A

(nutcracker esophagus)

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23
Q

Hypocontractile esophagus

A

(scleroderma esophagus)

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24
Q

Hypopharingeal

A

(Zenker’s) diverticula

25
Q

GERD

A

(decreased LES tone). Aggravated by coffee,
chocolate, alcohol, French fries.

26
Q

Functions of the stomach:

A

*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
Q

Origin and GI of motor functions:

A
  • 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
Q

muscle anatomy and functions:

A
  • 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
Q

receptive relaxation:

A

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
Q

factors of receptive relaxation:

A

Intrinsic and vago-vagal
reflexes
Duodenal distension
Nutrients in duodenum
Filling (gastric distension)

31
Q

segmental contraction VS peristalsis:

A

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
Q

receptive relaxation explained:

A

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
Q

mixing and grinding:

A
  • 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
Q

Gastric emptying:

A

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
Q

pyloric valve:

A
  • 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
Q

Driving forces of gastric emptying:

A
  • 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
Q

DUODENAL CONTROL
OF GASTRIC EMPTYING
BY FAT

A

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
Q

DUODENAL CONTROL
OF GASTRIC EMPTYING
BY OSMOTIC
STIMULATION

A
  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
Q

duodenal control of gastric emptying by acid

A
  1. Acid entering
    duodenum stimulates
    secretin release
  2. Circulating secretin reduces IG
    pressure and increases pyloric resistance.
40
Q

THE MIGRATING MYOELECTRIC COMPLEX

A
  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
Q

digestive VS inter-digestive period:

A
  • Digestive period
    o Relaxation→ Storage
    o Peristaltic contractions→ Mixing, size reduction & emptying
  • Interdigestive Period
    o Strong peristaltic waves (MMCs)→ “housekeeping”
42
Q

vomiting VS regurgitation:

A

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
Q

going through the motions:

A
  • 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
Q

Gastric pathophysiology:

A

*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
Q

feed vs fast motility:

A
  • 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
Q

MMC VS digestive motilities:

A
  • 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
Q

peristalsis VS segmentation (SI):

A
  • 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
Q

Emptying of the ileum:

A

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
Q

Colonic motility:

A
  • 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
Q

LI motility:

A
  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
Q

ileo-cecal sphincter

A
  • 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
Q

defecation problems causes:

A
  • 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
Q
  • Food entering stomach and
    duodenum releases gastrin
    and CCK = (ileum wise):
  • Stomach filling increases intestinal
    motility:
A
  • Increased colonic propulsive
    activity
  • Stomach filling induces
    relaxation of ileocolic
    sphincter
54
Q

summary of GI motility:

A
  • 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
Q

haustral shuttling explained easier:

A

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
Q

reflexive relaxation explained easier:

A

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
Q

Intestinal pathophysiology:

A
  • 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
Q

enteric VS para VS sympathetic

A

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 !!

GI physiology (12 decks)

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