13-1: 1/24 - Gi Motility

Front 1

What is the major muscle coat in the gut?

Layers?

Back 1

Muscularis propria:
Longitudinal muscle layer
Circular muscle layer

Front 2

Longitudinal muscle layer:
Function
Mediated by?

Back 2

Shortens the intestine, expands the radius

Medicated by influx of extracell Ca2+

Front 3

Circular muscle layer:
Function
Mediated by?

Back 3

Shortens intestinal radius, increases length of intestine

Contraction mediated by release of INTRAcellular Ca2+ from stores

Note: Circular muscle layer is thicker and more luminal than longitudinal layer

Front 4

Triggering Contraction:
Pharmaco-mechanical coupling vs Electro-mechanical coupling

Back 4

Pharmaco-mechanical:
Bind ligand (neurocrine, paracrine, endocrine secretion) to receptor activates signaling PW, resulting in release of Ca2+ (extra and intracell)

Electro:
Membrane depol opens voltage gates Ca2+ channels

Front 5

Discuss the steps in cross-bridge cycling.
Begin with intestines at rest.

Back 5

At rest, low cytosolic Ca2+ levels, myosin and actin not attached

When cytosolic Ca2+ levels increase (due to electro/pharamco-mechanical coupling); Ca2+ binds and activates calmodulin

Calmodulin activates myosin light chain kinase

Phosphorylates light chain of myosin using ATP, allowing for attachment to actin

When Ca2+ returns to unstiml'd levels, myosin is dephosphorylated by myodin phosphatase, and thick/thin fils no longer attached

Front 6

When is maximal force developed in GI smooth muscle?

Back 6

When there is optimal overlap of thick and thin filaments

Front 7

Passive tension is due to ______, whereas active tension is due to _______.

Back 7

Passive tension due to stretch

Active tension due to cross-bridge formation and sliding filaments

Front 8

What is basic electrical rhythm?

Propagated by?

Importance?

Back 8

Cyclic depolarization of muscle cell membranes

Propagated by nexuses of adjacent cells

Sets up timing/frequency of contraction

Front 9

Basal electrical rhythm by segment of GI tract.

Back 9

Stomach: 3/min
Duodenum: 11/min
Ileum: 8/min
Colon: 3-6/min

Front 10

______ are contracted at rest.

Back 10

Sphincters

Front 11

This sphincter separates the oral cavity and esophagus.

Back 11

Upper esophageal sphincter

Front 12

This sphincter separates the esophagus and stomach.

Back 12

Lower esophageal sphincter

Front 13

This sphincter separates the stomach and small intestine.

Back 13

Pylorus

Front 14

This sphincter separates the small intestine and large intestine.

Back 14

Ileo-cecal sphincter

Front 15

Describe pressure states in sphincters at:
Resting State
Relaxation
Contraction

Back 15

Resting state: Pressure > adjacent segments

Relaxation: Pressure = adjacent segments

Contraction: Pressure >> adjacent segment (prevents retrograde flow)

Front 16

Swallowing Phases (3):
Phase
Muscle Group (striated/smooth)
Neural Control
Voluntary Control

Back 16

Oral phase: striated muscle, cortical/medulla control, fully voluntary

Pharyngeal phase: striated muscle, medulla control, some voluntary control

Esophageal phase: striated/smooth muscle, medulla/ENS control, no voluntary control

Front 17

Describe the events that occur in bolis transfer from the mouth to the esophagus.

Begin with bolus in mouth.

Back 17

Bolus in mouth, nasopharynx closed. Tongue thrust up and back.

Pharynx contracts
UES opens
Airway closed
Larynx elevated

Bolus enters esophagus

Front 18

Primary vs Secondary Peristalsis

Back 18

Primary: Swallowing
Secondary: Distention (pill stuck in throat)

Front 19

Describe the mechanisms by which upper esophageal peristalsis is propagated.

Back 19

MEDIATED VIA NEUROGENIC MECHANISM

ACh release from cholinergic neurons propagates wave of contraction.

Nitrous oxide from NANC (non-adrenergic, non-cholinergic) nerves cause wave of relaxation that precedes contraction.

Relaxation of muscle provides room for bolis in lumen of esophagus.

Front 20

Describe the mechanisms by which lower esophageal peristalsis is propagated.

Back 20

LOWER ESOPHAGUS MEDIATED BY MYOGENIC AND NEUROGENIC MECHANISM

muscle spontaneously produces 2nd messengers to keep muscle in tonic (contracted) state.

provides barrier to prevent reflux of stomach contents.

Relaxes by NEURAL mechanism to allow passage of bolus into stomach from vagal stimuln, and NO from NANC

Front 21

When and how is the lower esophageal sphincter relaxed?

Back 21

Swallowing-->involuntary reflex via medulla-->relaxation of LES

Front 22

What is transient lower esophageal sphincter relaxation?

Back 22

Transient lower esophageal sphincter relaxation:
gastric distention-->
vagal afferents-->
BS-->
inhibitory efferents-->
Relax LES

This is a normal process, and tends to be overactive in those with GERD.

Front 23

Which regions of the stomach comprise the reservoir?

Type of contraction?

Back 23

Reservoir = fundis, body

Tonic contractions

Front 24

Which regions of the stomach comprise the antrum?

Type of contraction?

Back 24

Antrum, pylorus

Phasic contractions

Front 25

Antral pump:
What is it?
Where is pace generated?
Role?

Back 25

Pacemaker located in mid-corpus

Produces phasic contractions to push material into terminalantrum

Terminal antrum grinds material and sends back toward corpus, breaking material into smaller pieces

Front 26

Gastric reservoir:
Functions

Back 26

Accomodate arrival of meal

Maintain constant force (tonic force) on contents to push into antral pump

Front 27

3 Types of Gastric Relaxation:
Relaxation Type
Stimulus
Origin of Stimulus
Nerve that mediates relaxation

Back 27

Receptive - Swallowing, originates in pharynx

Adaptive - gastric distention, originates in stomach

Feedback - nutrients, originates in small intestine

ALL MEDIATED BY VAGUS

Front 28

Gastric emptying:
Stimulus
Effects
Factors affecting rate of emptying

Back 28

Chyme enters antrum

Antral distention causes pyloric sphincter to relax

Chyme enters duodenum

Rate of emptying depends on content of chyme (lipid content, pH, calories, particle size)

Front 29

What stimuli inhibit gastric emptying?

Back 29

Duodenal distention

Release of CCK due to presence of proteins/fats in duodenum

Front 30

Describe circular muscle activity, longitudinal muscle activity, and luminal radius for:
Physiologic ileus
Propulsive segment of ileus
Receiving segment of ileus

Back 30

Ileus = small bowel

Physiologic (empty) state:
Circ and longitudinal relaxed, luminal radius = baseline

Propulsive segment of peristaltic wave:
Circ muscle is contracted, long muscle is relaxed, luminal radius is small

Receiving segment of peristaltic wave: circ muscle is relaxed, long muscle is contracted, luminal radius is increased (and secreting digestive enzymes)

Front 31

Segmental Contraction:
Region of GI tract that exhibits this
Stimulus
Effects
Under control of what branch of nervous system?

Back 31

Segmental contraction seen in small intestine

Entry of nutrients stimulates it (FED STATE)

Moves chyme back and forth over mucosa, maximizing exposure to digestive enzymes

UNDER ENTERIC NS CONTROL

Front 32

Why is segmental contraction segmental? What allows for this?

Back 32

There are segments of small intestins undergo mixing, with propulsive segments in between.

This is accomplished through inhibitory neuronal activity--receiving segments are inhibited (since they're not contracted, there's more room for mixing)

Front 33

Migrating Motor Complex:
Which region of the GI tract exhibits this?
Stimulus
Effects
How often do waves repeat?

Back 33

Small intestine

1.5-2.0 hours after a meal (FASTING STATE), motilin released into blood, initiates migrating motor complex (MMC)

MMC = large wave of forceful contractions from stomach to small intestine

Empties stomach of large particles, empties small intestines

Waves repeat every 90 mins.

Important for eliminating large, indigestible particles.

Front 34

How is bile returned to enterohepatic circulation between meals?

Back 34

Migrating Motor Complex propels bile acids to ileum where they're absorbed into portal circulation

Front 35

When a fast is broken, how do motility patterns shift to segmental contraction in the stomach and duodenum?

Back 35

Activation of extrinsic nerves (vagal innervation)

Release of CCK and gastrin which are released during a meal

Front 36

Large intestine:
What separates it from the small intestine?
Function?

Back 36

Separated from small intestine by ileocecal sphincter (works just like other sphincters--proximal distension relaxes sphincter and distal distention contracts sphincter)

Large intestine absorbs water and electrolytes (RIGHT colon), eliminates waste (LEFT colon)

Front 37

How is muscle distribution in the large intestine unique?

Back 37

Like the rest of the bowel, the large intestine has a continuous layer of circular smooth muscle.

However, longitudinal muscle exists as 3 bands called tenae coli. Where there is no longitudinal layer, the intestine is contracted and narrow.

Front 38

How does motility in the right and left colon differ?

Back 38

In right colon, there are segmental contractions to move luminal contents back and forth for absorption

In left colon, there is mass movement--large contractions for eliminaiton of waste

Front 39

What are haustral migrations? What region of the GI tract exhibits them?

Back 39

Haustral migrations = short (few cm) propulsive movements

Exhibited by large intestine

Front 40

What are the three types of spike activity in the colon?

What is each responsible for?

Back 40

Short spike bursts on a single slow wave--haustral contractions

Long spike bursts that extend through several slow waves--haustral propagations

Migrating spike bursts--rapid oscillations not related to slow waves; MASS MOVEMENTS

Front 41

How does muscle activity in the large intestine differ from the stomach and small intestine?

Back 41

FNote: colon includes meals from 2-3 days

unlike stomach and small bowel, colon is always active (no fast/fed states).

Motor activity increases after a meal w/inc'd probability of mass peristalsis.

Front 42

Large intestine:
Parasympathetic Effects
Sympathetic Effects

Back 42

PSymp:
Vagus-->ACh and Non-ACh stimulation of colonic smooth muscle (SEGMENTAL CONTRACTION)

Symp-->dec'd colonic activity by reducing freq. of slow waves and spikes

Front 43

Defecation:
Stimulus
Events if OK to poop
Events if not OK to poop

Back 43

Distention of rectosigmoid-->
Relaxation of internal anal sphincter (smooth muscle)-->
Contraction of external anal sphincter
-->if brain gives go-ahead
-->rectosigmoid parastalsis

IF NOT OKAY
-->internal anal sphincter contracts
-->reverse peristalsis

Front 44

What 3 things are required for anorectal continence?

Back 44

1) internal anal sphincter contiguous with circular muscle of adjacent colon

2) striated muscle of external sphincter

3) puborectalis muscle (forms sling)

Front 45

Why does squatting assist in defecation?

Back 45

Hip flexion straightens acute angle of anal canal made by puborectalis sling.

Puborectalis and external sphincter relaxes.

Front 46

How does the pressure of the rectum differ from the rest of the anal canal?

Back 46

Rectum is highly compliant and expands to accomodate added stool. Maintains a relatively low pressure.

Note: as rectum distends, sensory message conveyed centrally, alerting individual of presence of stool and prompting urge to defecate.

Front 47

How does GI motility differ with age?

Explain pathophys.

Back 47

No gross changes in GI motility until 70s.

Fecal incontinence due to reduced rectal compliance, impaired rectal sensation, dec'd sphincter pressures

Dysphagia often result of co-morbid conditions (after a stroke)

Constipation may be due to lack of physical activity than loss of motor fn to colon

Front 48

Back 48