• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

Card Range To Study



Play button


Play button




Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

48 Cards in this Set

  • Front
  • Back
What is the major muscle coat in the gut?

Muscularis propria:
Longitudinal muscle layer
Circular muscle layer
Longitudinal muscle layer:
Mediated by?
Shortens the intestine, expands the radius

Medicated by influx of extracell Ca2+
Circular muscle layer:
Mediated by?
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
Triggering Contraction:
Pharmaco-mechanical coupling vs Electro-mechanical coupling
Bind ligand (neurocrine, paracrine, endocrine secretion) to receptor activates signaling PW, resulting in release of Ca2+ (extra and intracell)

Membrane depol opens voltage gates Ca2+ channels
Discuss the steps in cross-bridge cycling.
Begin with intestines at rest.
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
When is maximal force developed in GI smooth muscle?
When there is optimal overlap of thick and thin filaments
Passive tension is due to ______, whereas active tension is due to _______.
Passive tension due to stretch

Active tension due to cross-bridge formation and sliding filaments
What is basic electrical rhythm?

Propagated by?

Cyclic depolarization of muscle cell membranes

Propagated by nexuses of adjacent cells

Sets up timing/frequency of contraction
Basal electrical rhythm by segment of GI tract.
Stomach: 3/min
Duodenum: 11/min
Ileum: 8/min
Colon: 3-6/min
______ are contracted at rest.
This sphincter separates the oral cavity and esophagus.
Upper esophageal sphincter
This sphincter separates the esophagus and stomach.
Lower esophageal sphincter
This sphincter separates the stomach and small intestine.
This sphincter separates the small intestine and large intestine.
Ileo-cecal sphincter
Describe pressure states in sphincters at:
Resting State
Resting state: Pressure > adjacent segments

Relaxation: Pressure = adjacent segments

Contraction: Pressure >> adjacent segment (prevents retrograde flow)
Swallowing Phases (3):
Muscle Group (striated/smooth)
Neural Control
Voluntary Control
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
Describe the events that occur in bolis transfer from the mouth to the esophagus.

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

Pharynx contracts
UES opens
Airway closed
Larynx elevated

Bolus enters esophagus
Primary vs Secondary Peristalsis
Primary: Swallowing
Secondary: Distention (pill stuck in throat)
Describe the mechanisms by which upper esophageal peristalsis is propagated.

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.
Describe the mechanisms by which lower esophageal peristalsis is propagated.

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
When and how is the lower esophageal sphincter relaxed?
Swallowing-->involuntary reflex via medulla-->relaxation of LES
What is transient lower esophageal sphincter relaxation?
Transient lower esophageal sphincter relaxation:
gastric distention-->
vagal afferents-->
inhibitory efferents-->
Relax LES

This is a normal process, and tends to be overactive in those with GERD.
Which regions of the stomach comprise the reservoir?

Type of contraction?
Reservoir = fundis, body

Tonic contractions
Which regions of the stomach comprise the antrum?

Type of contraction?
Antrum, pylorus

Phasic contractions
Antral pump:
What is it?
Where is pace generated?
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
Gastric reservoir:
Accomodate arrival of meal

Maintain constant force (tonic force) on contents to push into antral pump
3 Types of Gastric Relaxation:
Relaxation Type
Origin of Stimulus
Nerve that mediates relaxation
Receptive - Swallowing, originates in pharynx

Adaptive - gastric distention, originates in stomach

Feedback - nutrients, originates in small intestine

Gastric emptying:
Factors affecting rate of emptying
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)
What stimuli inhibit gastric emptying?
Duodenal distention

Release of CCK due to presence of proteins/fats in duodenum
Describe circular muscle activity, longitudinal muscle activity, and luminal radius for:
Physiologic ileus
Propulsive segment of ileus
Receiving segment of ileus
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)
Segmental Contraction:
Region of GI tract that exhibits this
Under control of what branch of nervous system?
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

Why is segmental contraction segmental? What allows for this?
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)
Migrating Motor Complex:
Which region of the GI tract exhibits this?
How often do waves repeat?
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.
How is bile returned to enterohepatic circulation between meals?
Migrating Motor Complex propels bile acids to ileum where they're absorbed into portal circulation
When a fast is broken, how do motility patterns shift to segmental contraction in the stomach and duodenum?
Activation of extrinsic nerves (vagal innervation)

Release of CCK and gastrin which are released during a meal
Large intestine:
What separates it from the small intestine?
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)
How is muscle distribution in the large intestine unique?
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.
How does motility in the right and left colon differ?
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
What are haustral migrations? What region of the GI tract exhibits them?
Haustral migrations = short (few cm) propulsive movements

Exhibited by large intestine
What are the three types of spike activity in the colon?

What is each responsible for?
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
How does muscle activity in the large intestine differ from the stomach and small intestine?
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.
Large intestine:
Parasympathetic Effects
Sympathetic Effects
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
Events if OK to poop
Events if not OK to poop
Distention of rectosigmoid-->
Relaxation of internal anal sphincter (smooth muscle)-->
Contraction of external anal sphincter
-->if brain gives go-ahead
-->rectosigmoid parastalsis

-->internal anal sphincter contracts
-->reverse peristalsis
What 3 things are required for anorectal continence?
1) internal anal sphincter contiguous with circular muscle of adjacent colon

2) striated muscle of external sphincter

3) puborectalis muscle (forms sling)
Why does squatting assist in defecation?
Hip flexion straightens acute angle of anal canal made by puborectalis sling.

Puborectalis and external sphincter relaxes.
How does the pressure of the rectum differ from the rest of the anal canal?
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.
How does GI motility differ with age?

Explain pathophys.
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