✅ Functions of the Gastrointestinal (GI) Tract
The GI tract exists to digest food and absorb nutrients. To do this, it performs four
major activities:
1. Motility

Moves food from the mouth → rectum.

Mixes food and breaks it into smaller pieces.

The speed of movement is controlled so digestion/absorption have enough time
to occur.
2. Secretion


Salivary glands, pancreas, and liver add:
o
Fluids
o
Electrolytes
o
Enzymes
o
Mucus
These secretions help digestion and absorption.
3. Digestion

Large food molecules are broken down into absorbable forms.
4. Absorption

Nutrients, water, and electrolytes move from the intestinal lumen → bloodstream.
STRUCTURE OF THE GI TRACT
The GI tract is arranged in order:
Mouth → Esophagus → Stomach → Small intestine (duodenum, jejunum, ileum)
→ Large intestine → Anus
Accessory organs (secrete substances into the GI tract):

Salivary glands

Pancreas

Liver

Gallbladder
The Wall of the GI Tract Has Two Main Surfaces

Mucosal surface → faces the lumen (food).

Serosal surface → faces the blood.
Layers of the GI wall (from lumen → blood):
1. Mucosa
Includes:
a. Epithelial cells

Do absorption and secretion.
b. Lamina propria

Connective tissue containing blood and lymph vessels.
c. Muscularis mucosae

Thin smooth muscle layer.

Its contraction changes the shape/surface area of the epithelium.
2. Submucosa
Contains:

Collagen

Elastin

Glands

Large blood vessels
3. Muscular layers (main motility layers)
Two smooth-muscle layers:
Circular muscle

Thick

Densely innervated

Responsible for mixing and changes in diameter
Longitudinal muscle

Thin

Fewer nerve fibers

Responsible for shortening the tract
Neurons do not form classic synapses on smooth muscle.
They release neurotransmitters from varicosities (swelling-like sites) along their axons.
Nerve Plexuses of the GI Tract
1. Submucosal plexus (Meissner’s)

Between submucosa and circular muscle.
2. Myenteric plexus (Auerbach’s)

Between circular muscle and longitudinal muscle.
Together they make up the enteric nervous system.
INNERVATION OF THE GI TRACT
The GI tract is controlled by:
1. Extrinsic nervous system
(Sympathetic + Parasympathetic)
2. Intrinsic nervous system
(Enteric nervous system)
The enteric nervous system (ENS) is inside the wall of the GI tract and communicates
constantly with sympathetic & parasympathetic nerves.
PARASYMPATHETIC INNERVATION
Carried by:

Vagus nerve (CN X)

Pelvic nerve
Areas supplied:
Vagus nerve supplies:

Upper GI:
o
Upper ⅓ of esophagus (striated muscle)
o
Stomach
o
Small intestine
o
Ascending colon
o
First half of transverse colon
Pelvic nerve supplies:

Lower GI:
o
Distal transverse colon
o
Descending colon
o
Sigmoid colon
Parasympathetic nerve features

Have long preganglionic fibers- VERY IMPORTANT

Synapse in ganglia located within the GI wall (in the plexuses).
Signals from the parasympathetic nerves are:

Coordinated in the myenteric and submucosal plexuses

Then sent to smooth muscle, endocrine cells, and secretory cells
Parasympathetic postganglionic neurons
Two types:
1. Cholinergic neurons → release acetylcholine (ACh)
2. Peptidergic neurons → release peptides:
o
Substance P
o
VIP
o
Others
The vagus nerve is a mixed nerve

75% afferent fibers (sensory)

25% efferent fibers (motor)
Afferent fibers:
Carry information from mechanoreceptors and chemoreceptors in the GI tract → CNS.
Efferent fibers:
Carry motor commands from CNS → GI muscle, secretory cells, endocrine cells.
Vagovagal reflex
Both limbs (afferent + efferent) are in the vagus nerve.
SYMPATHETIC INNERVATION
Preganglionic fibers

Short

Synapse in ganglia outside the GI tract:
Sympathetic ganglia for GI:

Celiac

Superior mesenteric

Inferior mesenteric

Hypogastric
Postganglionic fibers

Release norepinephrine (adrenergic)

Synapse on:
o
Enteric plexuses
o
Or directly on smooth muscle, endocrine cells, secretory cells
Sympathetic fibers are 50% afferent and 50% efferent
Just like parasympathetic nerves.
INTRINSIC INNERVATION (ENTERIC NERVOUS SYSTEM)
The enteric nervous system (ENS) can function completely on its own, even without
CNS input.
Located in:

Myenteric plexus

Submucosal plexus
The ENS controls:

Contraction (motility)

Secretion

Endocrine activity
Inputs to ENS:

Parasympathetic nerves

Sympathetic nerves

Sensory information directly from GI mechanoreceptors & chemoreceptors
Outputs from ENS:

Directly to smooth muscle

Secretory cells

Endocrine cells
The plexuses also communicate using interneurons.
Neurocrines in the Enteric Nervous System (Table 8.1)
Neurocrines = neurotransmitters + neuromodulators.
Most enteric neurons contain multiple neurocrines and may release two or more at
the same time.
FULL LIST (nothing omitted):
Acetylcholine (ACh)

From: Cholinergic neurons

Actions:
o
↑ Smooth muscle contraction
o
Relaxation of sphincters
o
↑ Salivary secretion
o
↑ Gastric secretion
o
↑ Pancreatic secretion
Norepinephrine (NE)

From: Adrenergic neurons

Actions:
o
Relaxation of smooth muscle in walls
o
Contraction of sphincters
o
↑ Salivary secretion
Vasoactive Intestinal Peptide (VIP)

From: Enteric neurons

Actions:
o
Relaxation of smooth muscle
o
↑ Intestinal secretion
o
↑ Pancreatic secretion
Nitric Oxide (NO)- Strong Vasodilator

From: Enteric neurons

Action:
o
Relaxation of smooth muscle
Gastrin-Releasing Peptide (GRP) / Bombesin

From: Vagal neurons of gastric mucosa

Action:
o
↑ Gastrin secretion
Enkephalins (opiates)

From: Enteric neurons

Actions:
o
↑ Contraction of smooth muscle
o
↓ Intestinal secretion
Neuropeptide Y

From: Enteric neurons

Actions:
o
Relaxation of smooth muscle
o
↓ Intestinal secretion
Substance P

From: Cosecreted with ACh by enteric neurons

Actions:
o
↑ Contraction of smooth muscle
o
↑ Salivary secretion
GASTROINTESTINAL REGULATORY SUBSTANCES — FULL, CLEAR, COMPLETE
EXPLANATION
(Nothing is skipped. Everything is rewritten in simple, understandable language.)
The gastrointestinal (GI) tract uses many regulatory substances—hormones,
paracrines, and neurocrines—to control how digestion works. These substances
regulate:

The contraction and relaxation of smooth muscle in the walls and sphincters

The secretion of digestive enzymes

The secretion of fluid and electrolytes

Growth (trophic effects) of GI tissues
Some GI peptides also regulate the secretion of other peptides.
Example: Somatostatin inhibits the secretion of all GI hormones.
CHARACTERISTICS OF GI PEPTIDES
GI peptides fall into three categories:
1. Hormones

Released from endocrine cells of the GI tract

Enter portal circulation → liver → systemic circulation

Travel to target cells that have specific receptors

Targets may be in the GI tract or somewhere else in the body
Example:

Gastrin → acts on stomach parietal cells

GIP → acts on pancreatic β cells to release insulin
Important: GI endocrine cells are not in a gland; instead, they are single cells
scattered throughout the mucosa.
There are four official GI hormones:
1. Gastrin
2. Cholecystokinin (CCK)
3. Secretin
4. Glucose-dependent insulinotropic peptide (GIP), also called gastric inhibitory
peptide
2. Paracrines

Also secreted by endocrine cells of the GI tract

But they act locally, within the same tissue

Travel only short distances by diffusion through interstitial fluid or local
capillaries
Key paracrine: Somatostatin

Inhibits other GI hormones everywhere in the GI tract
Another paracrine: Histamine

Not a peptide

Stimulates gastric acid secretion
3. Neurocrines

Synthesized in neurons of the GI tract

Released after an action potential

Cross synapses and activate receptors on target cells
Major GI neurocrines include:

Acetylcholine (ACh)

Norepinephrine

Vasoactive intestinal peptide (VIP)

Nitric oxide (NO)

Gastrin-releasing peptide (GRP), also called bombesin

Enkephalins

Neuropeptide Y

Substance P
GI HORMONES
Enteroendocrine cells secrete hormones when they sense nutrients.
A substance is considered an “official GI hormone” only if:
1. It is secreted in response to a normal physiologic stimulus
2. It travels through the bloodstream to a distant target and causes a physiologic
effect
3. Its action is independent of nerves
4. It has been isolated, purified, chemically identified, and synthesized
Only four substances pass all tests:
✔ Gastrin
✔ CCK
✔ Secretin
✔ GIP
Several candidate hormones fail ≥1 criterion:

Motilin

Pancreatic polypeptide

Somatostatin

Serotonin (5-HT)

Ghrelin

Leptin

GLP-1, GLP-2

Enteroglucagon

Peptide YY

Neurotensin
TABLE 8.2 — SUMMARY OF THE FOUR OFFICIAL GI HORMONES
I am rewriting the table in clear English while preserving every detail.
1. GASTRIN- Increases acid secretion in stomach
Hormone family: Gastrin-CCK family
Site of secretion: G cells in the antrum of the stomach
Stimuli for secretion:

Small peptides

Amino acids

Distention of the stomach

Vagal stimulation (via GRP, not ACh)
Actions:

↑ Gastric H⁺ secretion

Stimulates growth of gastric mucosa
DETAILS ABOUT GASTRIN
Gastrin promotes hydrogen ion (acid) secretion by parietal cells.
Two major forms:

G17 ("little gastrin") → secreted during meals

G34 ("big gastrin") → secreted between meals
Both forms have separate precursors—not converted into one another.
The C-terminal tetrapeptide is the minimal active fragment, but only 1/6 as powerful as
the full gastrin molecule.
Physiologic stimuli

Protein digestion products (especially phenylalanine, tryptophan)

Gastric distention

Vagal GRP
Inhibitors

Low stomach pH

Somatostatin
Actions
1. ↑ H⁺ secretion
2. ↑ growth of gastric mucosa
Clinical: Zollinger-Ellison syndrome
Caused by a gastrinoma (usually in the pancreas).
Effects:

Massive ↑ H⁺ secretion

Hypertrophy of gastric mucosa

Duodenal ulcers

Steatorrhea (because acid inactivates pancreatic lipase) so less fat digestion
Treatment:

H₂ blockers (cimetidine)

Proton pump inhibitors (omeprazole)

Surgical tumor removal

Gastric resection (last resort)
2. CHOLECYSTOKININ (CCK)
Hormone family: Gastrin-CCK family
Site of secretion: I cells of duodenum and jejunum
Stimuli for secretion:

Fatty acids and monoglycerides (but not triglycerides)

Small peptides

Amino acids
Actions:
1. ↑ Pancreatic enzyme secretion
2. ↑ Pancreatic HCO₃ ⁻ secretion (weak, potentiates secretin)- Neutralizes the acid
3. Contracts gallbladder
4. Relaxes sphincter of Oddi
5. ↑ Growth of pancreas and gallbladder
6. Inhibits gastric emptying
DETAILS ABOUT CCK
CCK = 33 amino acids, closely related to gastrin.
Shares identical C-terminal 5 amino acids with gastrin.
Therefore it has some weak gastrin activity.
Minimal active fragment: C-terminal heptapeptide (CCK-7).
Five major actions of CCK
1. Gallbladder contraction + sphincter of Oddi relaxation → bile enters intestine
2. Pancreatic enzyme secretion → fat, protein, carbohydrate digestion
3. Stimulates HCO₃ ⁻ secretion (by potentiating secretin)
4. Trophic effects on pancreas and gallbladder
5. Slows gastric emptying → gives time to digest fat
3. SECRETIN
Hormone family: Secretin-glucagon family
Site of secretion: S cells in duodenum
Stimuli for secretion:

H⁺ in duodenum (pH < 4.5)

Fatty acids
Actions:

↑ Pancreatic HCO₃ ⁻ secretion

↑ Biliary HCO₃ ⁻ secretion

↓ Gastric H⁺ secretion

Inhibits gastrin’s trophic effects
DETAILS ABOUT SECRETIN
Secretin = 27 amino acids, similar to glucagon.
Unlike gastrin/CCK, all 27 amino acids are required for activity.
Secretin is released when acidic chyme enters the duodenum.
Purpose: Neutralize acid so pancreatic enzymes (especially lipase) work.
Pancreatic lipase requires pH 6–8 and is inactivated below pH 3.
Secretin also inhibits gastrin action on parietal cells.
4. GIP (Glucose-dependent insulinotropic peptide)
Also called gastric inhibitory peptide
Hormone family: Secretin-glucagon family
Site of secretion: K cells of duodenum and jejunum
Stimuli for secretion:
Only GI hormone stimulated by all three nutrients:

Glucose

Amino acids

Fatty acids
Actions:
1. ↑ Insulin secretion from pancreatic β cells (incretin effect)
2. ↓ Gastric H⁺ secretion
3. ↓ Gastric emptying
DETAILS ABOUT GIP
Explains why oral glucose increases insulin more than IV glucose:

Oral glucose → stimulates GIP → stimulates insulin

IV glucose → no GIP stimulation
CANDIDATE HORMONES
Not official because they fail ≥1 hormone criteria.
Motilin

22 amino acids

Secreted during fasting

Initiates interdigestive migrating motor complexes every ~90 min (IMMC)
Pancreatic polypeptide (PP) + PEPTIDE YY (PYY)

36 amino acids

Secreted after meals

Inhibits pancreatic HCO₃ ⁻ and enzyme secretion
Enteroglucagon

Released when blood glucose drops

Increases liver glycogenolysis + gluconeogenesis
GLP-1

Made by L cells from proglucagon

Incretin: ↑ insulin, ↓ glucagon, ↑ satiety, ↓ gastric emptying

Used for type II diabetes therapy
Peptide YY (PYY)

Secreted after meals

↓ Appetite

Inhibits ghrelin

Inhibits pancreatic secretion
PARACRINES
Somatostatin
From D cells og Gastric mucosa, hypothalamus and pancreatic δ cells.

Secreted when lumen pH decreases

Inhibits:
o
All GI hormones
o
Gastric H⁺ secretion
Histamine

Secreted in stomach mucosa

With ACh and gastrin, increases H⁺ secretion
NEUROCRINES
Made in GI neurons → released → act at synapses.
Include:

ACh

Norepinephrine

VIP

NO

GRP/bombesin

Enkephalins

Neuropeptide Y

Substance P
ACh and norepinephrine are from classic ANS; others from peptidergic neurons.
SATIETY AND FEEDING CONTROL
Satiety is feeling (full) feeding means needs food
Located in the hypothalamus:

Satiety center → ventral posterior nucleus (VPN)

Feeding center → lateral hypothalamic area (LHA)

Input from arcuate nucleus
Arcuate nucleus has:

Anorexigenic neurons (decrease appetite-full) → release POMC → ↓ appetite

Orexigenic neurons → release ghrelin→ ↑ appetite
Substances that regulate appetite:
1. Leptin

From fat cells

Proportional to body fat

Crosses BBB

↑ anorexigenic neurons

↓ orexigenic neurons

↓ appetite (long-term effect)

↑ energy expenditure
2. Insulin

Similar to leptin

Short-term appetite reduction
3. GLP-1

From L cells

Decreases appetite
4. Ghrelin

From gastric cells just before meals

Opposite of leptin

↑ Orexigenic neurons

↓ Anorexigenic neurons

↑ Appetite

↑ Food intake

Strongly stimulated during fasting and weight loss
5. Peptide YY (PYY)

From L cells after meals

↓ Appetite directly

Inhibits ghrelin

Inhibits pancreatic secretion
MOTILITY — FULLY EXPLAINED (NOTHING OMITTED)
Motility refers to all the contraction and relaxation movements of the gastrointestinal
(GI) tract walls and sphincters.
Motility has three main purposes:
1. Grinding and breaking down food
2. Mixing food with digestive secretions
3. Propelling food and digested material forward through the GI tract
The muscle type in the GI tract is mostly smooth muscle, except in:

The (pharynx start of pharynx)

The upper one-third of the esophagus

The external anal sphincter
These three areas use striated (skeletal) muscle instead.
Smooth muscle properties
GI smooth muscle is unitary smooth muscle, which means:

The cells are connected to one another by gap junctions (low-resistance
electrical connections).

Because they are electrically linked, action potentials can spread quickly.

This allows coordinated and smooth contractions along the GI tract.
Circular vs longitudinal muscle

Circular muscle contraction → narrows the diameter of a segment.

Longitudinal muscle contraction → shortens the length of that segment.
Types of contraction
Phasic contractions- contraction followed by relaxation done by entire GI

Occur in bursts followed by relaxation.

Found in:

o
Esophagus
o
Gastric antrum
o
Small intestine
These areas are responsible for mixing and propulsion.
Tonic contractions- Constant contraction without intervals of relaxation

Maintain a constant level of tension, without regular relaxation.

Found in:
o
Orad (upper) stomach
o
Lower esophageal sphincter
o
Ileocecal sphincter
o
Internal anal sphincter
Sphincters
Sphincters are specialized circular muscle sections that separate different regions of the
GI tract:

Upper esophageal sphincter (UES) — between pharynx and esophagus

Lower esophageal sphincter (LES) — between esophagus and stomach

Pyloric sphincter — between stomach and duodenum

Ileocecal sphincter — between ileum and cecum

Internal & external anal sphincters — maintain fecal continence
Resting state of sphincters
At rest, sphincters maintain a higher pressure than the organs on either side.

This prevents both forward flow and backflow.

Example:
The LES prevents stomach acid from refluxing into the esophagus.
To move contents past a sphincter, the sphincter must relax and lower its pressure
momentarily.
This relaxation is coordinated with GI muscle activity by reflexes (e.g., swallowing
reflex).
SLOW WAVES- Oscillations of resting potentials
GI smooth muscle contracts only after electrical activity, which begins with slow waves.
What are slow waves?
Slow waves are rhythmic oscillations of the membrane potential:

They are not action potentials.

They alternate between:
o
Depolarization (toward threshold) Ca2+ entering cells
o
Repolarization (away from threshold) K+ leaving the celll
If a slow wave's peak depolarization reaches threshold, action potentials fire on top of
the slow wave.
Action potentials → lead to contraction.
Frequency of slow waves
Different parts of the GI tract have their own slow-wave frequencies:

Stomach: 3 waves/min (lowest)

Duodenum: 12 waves/min (highest)
The slow-wave frequency determines the maximum possible frequency of
contractions because:

Action potentials only occur when slow waves reach threshold.
Slow-wave frequency does NOT change with neural or hormonal input.
But those signals can change the number of action potentials and the strength of
contractions.
Origin of slow waves
Slow waves begin in the interstitial cells of Cajal, found in the myenteric plexus.

These cells depolarize and repolarize spontaneously.

They spread their electrical activity to smooth muscle via gap junctions.
They act as the pacemaker of the GI tract (similar to the SA node in the heart).
Mechanism of slow waves

Depolarization is caused by periodic opening of Ca²⁺ channels → inward Ca²⁺
current.

Plateau is maintained by Ca²⁺ channels staying open.

Repolarization occurs when K⁺ channels open → outward K⁺ current.
Relation between slow waves, action potentials, and contraction
Even if slow waves do NOT reach threshold:

They still produce weak basal contractions (tonic contractions).
If threshold IS reached:

Action potentials appear on top of slow waves.

Stronger phasic contractions occur.
In smooth muscle, individual action potentials do not create separate twitches; they
summate into one long contraction.
CHEWING AND SWALLOWING
Chewing (Mastication)
Functions:
1. Mixes food with saliva → lubrication
2. Reduces food particle size → easier swallowing
3. Mixes carbohydrates with salivary amylase → begins digestion
Chewing is both:

Voluntary (you can choose to chew)

Involuntary (reflex triggered by food in mouth)
Reflex chewing is controlled by mechanoreceptors → brainstem → oscillatory motor
pattern to jaw muscles.
Swallowing
Swallowing starts voluntarily, then becomes automatic and reflex-controlled.
Controlled by the swallowing center in the medulla.
Sensory receptors in the pharynx detect food → send signals via vagus and
glossopharyngeal nerves to the swallowing center.
Three phases
1. Oral phase (voluntary)
Tongue pushes bolus toward pharynx → triggers swallowing reflex.
2. Pharyngeal phase (involuntary)
Purpose: move bolus from mouth → pharynx → esophagus.
Steps:
1. Soft palate lifts → prevents food from entering nasopharynx
2. Epiglottis covers larynx; larynx moves up → prevents food entering trachea
3. Upper esophageal sphincter (UES) relaxes
4. A peristaltic wave begins → pushes bolus through UES
5. Breathing stops momentarily during this phase
3. Esophageal phase
Controlled by both the swallowing reflex AND the enteric nervous system.
Process:
1. Bolus enters esophagus → UES closes
2. Primary peristaltic wave travels down → propels food
o
Gravity helps when sitting/standing
3. As bolus nears LES:
o
LES relaxes due to VIP released by vagus nerve fibers
o
Orad (Beginning of stomach) stomach simultaneously relaxes (receptive
relaxation) so that food can go in stomach
4. LES then contracts again to restore high resting tone
5. If food remains, secondary peristaltic wave by enteric system removes
leftovers (initiated by esophageal distention)
ESOPHAGEAL PHYSIOLOGY
The esophagus is in the thorax, so:

Intraesophageal pressure = intrathoracic pressure

This pressure is lower than atmospheric and lower than abdominal pressure
Problems created:
1. Preventing air from entering at the top → UES solves this
2. Preventing gastric acid reflux → LES solves this
Conditions like pregnancy or obesity ↑ abdominal pressure → risk of reflux.
Achalasia
A disorder where:

LES fails to relax

Peristalsis in lower esophagus is impaired

Results → dilation of esophagus above LES and difficulty swallowing
GASTRIC MOTILITY
Three main functions:
1. Receptive relaxation (relaxation of upper part of stomach) of orad stomach to
receive food
2. Mixing and grinding with gastric secretions
3. Gastric emptying into duodenum
Stomach structure
Three muscle layers:

Outer longitudinal

Middle circular

Inner oblique (unique to stomach)
Innervation:

Parasympathetic → vagus

Sympathetic → celiac ganglion

Enteric → myenteric & submucosal plexuses
Regions:

Fundus + proximal body = orad region (thin-walled)

Distal body + antrum = caudad region (thick-walled, strong contractions)
RECEPTIVE RELAXATION

Orad stomach relaxes to store food (up to 1.5 L)

Triggered when food distends lower esophagus

Mediated by vagovagal reflex

Afferent nerve by vagus causing distention of stomach

Efferent nerve by vagus causes VIP release neurotransmitter that causes
relaxation

Eliminated by vagotomy
MIXING AND DIGESTION

Caudad stomach contracts strongly

Contractions start in the mid-body and become stronger toward pylorus

Propel some chyme through pylorus

Most chyme is pushed back for more mixing (retropulsion)
Slow waves here: 3–5 per minute → sets max contraction rate.
Influences on contraction strength:

↑ contractions → parasympathetics, gastrin, motilin

↓ contractions → sympathetics, secretin, GIP
During fasting: migrating myoelectric complexes (MMC), every 90 min, mediated by
motilin → clear stomach residue.
GASTRIC EMPTYING
Total stomach contents ≈ 1.5 L
Takes ~3 hours to empty.
Faster emptying:

Liquids > solids

Isotonic > hypertonic or hypotonic
Solids must be reduced to 1 mm³ to pass through pylorus.
Two major inhibitors of gastric emptying
1. Fat

Fat in duodenum → CCK release

CCK slows gastric emptying

Allows proper time for fat digestion
2. H⁺ (acid)

Low pH in duodenum → detected by H⁺ receptors

Enteric reflex decreases gastric emptying

Allows time for pancreas to neutralize acid with bicarbonate
✅ SMALL INTESTINAL MOTILITY — FULLY EXPLAINED WITHOUT MISSING
ANYTHING
The small intestine has two main jobs:
1. Digest nutrients
2. Absorb nutrients
To accomplish these, small intestinal motility:

Mixes chyme with digestive enzymes

Mixes chyme with pancreatic secretions

Exposes nutrients to the intestinal mucosa for absorption

Moves unabsorbed chyme forward into the large intestine
Slow Waves and Contraction Rate
Just like in other GI smooth muscle, the frequency of slow waves determines how
often action potentials and contractions occur.
Slow-wave frequency:

Duodenum: 12 waves/minute (highest)

Stomach: lower frequency than small intestine

Ileum: 9 waves/minute (slightly slower than duodenum)
Additionally, every 90 minutes the small intestine performs a special type of contraction
called the:
Migrating Myoelectric Complex (MMC)

Occurs in the fasting state

Clears out leftover chyme and debris

Sweeps material toward the large intestine
Innervation of the Small Intestine
Both parasympathetic and sympathetic nerves control motility.
Parasympathetic

Carried by the vagus nerve

Increases contraction of intestinal smooth muscle

Some parasympathetic nerves release ACh (cholinergic)

Others release peptide neurocrines, such as:
o
VIP (vasoactive intestinal peptide)
o
Enkephalins
o
Motilin
Sympathetic


Nerve fibers originate from:
o
Celiac ganglion
o
Superior mesenteric ganglion
Decreases contraction of intestinal smooth muscle
Patterns of Small Intestinal Contractions
There are two main contraction patterns:
1. Segmentation contractions
2. Peristaltic contractions
Both are coordinated by the enteric nervous system.
⭐ Segmentation Contractions (Mixing)
Segmentation contractions mix chyme; they do not move it forward.
Steps:
STEP 1: A bolus of chyme is in the lumen.
STEP 2: A segment of small intestine contracts, splitting the bolus and pushing it orad
(toward the mouth) and caudad (toward the anus).
STEP 3: That segment relaxes, and the split chyme recombines.
This creates back-and-forth mixing, maximizing digestion and enzyme exposure.
No propulsion occurs.
⭐ Peristaltic Contractions (Propulsion)
Peristalsis moves the chyme forward toward the large intestine.
Steps:
STEP 1: A bolus of chyme is in the lumen.
STEP 2:

Intestine behind (orad to) the bolus contracts

Intestine in front (caudad to) the bolus relaxes
→ This pushes the bolus forward.
STEP 3:
A wave of these coordinated contractions continues down the intestine, moving the
chyme along.
Role of Circular and Longitudinal Muscle
For peristalsis to work:

Circular muscle contraction → narrows diameter

Longitudinal muscle contraction → shortens the segment
These muscles must not contract simultaneously.
So they are reciprocally innervated:

When circular muscle contracts → longitudinal muscle relaxes

When longitudinal muscle contracts → circular muscle relaxes
This prevents conflict and allows efficient propulsion.
How Peristalsis Begins (The Peristaltic Reflex)
The food bolus is detected by enterochromaffin-like (ECL) cells in the mucosa.
These cells release serotonin (5-HT).
5-HT activates intrinsic primary afferent neurons (IPANs).
IPANs trigger the peristaltic reflex:
Behind the bolus (orad): contraction
Excitatory neurotransmitters released in circular muscle:

ACh

Substance P

Neuropeptide Y
Simultaneously, longitudinal muscle is inhibited.
→ Segment narrows and lengthens.
In front of the bolus (caudad): relaxation
Inhibitory neurotransmitters released in circular muscle:

VIP

NO (nitric oxide)
Longitudinal muscle is excited.
→ Segment widens and shortens.
This coordinated pattern propels the chyme caudally.
🚨 VOMITING — FULL MECHANISM (NOTHING OMITTED)
Vomiting is coordinated by a vomiting center in the medulla.
It receives signals from:

The vestibular system (motion sickness)

The back of the throat

The GI tract

The chemoreceptor trigger zone (CTZ) in the 4th ventricle
Sequence of the Vomiting Reflex
1. Normal gastric and small intestinal slow waves stop
→ Halt of normal peristalsis
2. Reverse peristalsis begins
→ Starts in small intestine → moves upward to stomach
3. Stomach and pylorus relax
4. A deep inspiration occurs
→ Increases abdominal pressure
5. Larynx moves upward and forward
6. Lower esophageal sphincter relaxes
7. Glottis closes
8. Forceful expulsion of gastric contents (sometimes duodenal contents are
included)
Retching

Upper esophageal sphincter remains closed

Lower esophageal sphincter is open

Material moves into the esophagus, then falls back into stomach after retch ends
� LARGE INTESTINAL MOTILITY — COMPLETE EXPLANATION
Anything not absorbed in small intestine enters the large intestine as feces.
Feces pass through:

Cecum

Ascending colon

Transverse colon

Descending colon

Sigmoid colon

Rectum

Anal canal
After chyme enters the cecum, the ileocecal sphincter contracts, preventing backflow
into ileum.
⭐ Segmentation Contractions (Mixing) in Large Intestine
Segmentation contractions also occur here (esp. cecum and proximal colon).
They mix contents and help form the characteristic haustra (sac-like segments).
They do not propel feces long distances.
⭐ Mass Movements
Mass movements:

Occur 1–3 times per day

Move feces long distances (e.g., transverse → sigmoid colon)

Are strong, sustained contractions
Water absorption in distal colon makes stool:

Semisolid

Harder to move
A final mass movement pushes feces into the rectum for storage.
🚽 DEFECATION — COMPLETE DESCRIPTION
When rectum fills:
1. Rectum contracts
2. Internal anal sphincter relaxes
→ Rectosphincteric reflex
But defecation does NOT occur yet because:

External anal sphincter (skeletal muscle) is voluntarily kept contracted.
Urge to Defecate
Occurs when rectum is 25% full.
When defecation is appropriate:
1. External anal sphincter relaxes voluntarily
2. Rectal smooth muscle contracts → increases pressure
3. Feces are expelled
Valsalva maneuver (forced expiration against closed glottis) increases abdominal
pressure and assists defecation.
⭐ GASTROCOLIC REFLEX — COMPLETE
Eating food → stomach stretches → signals colon to increase activity.
This increases:

Colon motility

Frequency of mass movements
This reflex:

Afferent limb: stomach → parasympathetic nerves

Efferent limb: colon stimulated by CCK and gastrin