Large Intestine Physiology

Dr. Asad Zeidan

a.zeidan@qu.edu.qa
 Learning outcomes

1. Identify the functions of large intestine.

2. Identify how the mucosa of the large intestine differs from

that of small intestine.

3. Discuss the types of contractions that occur in the colon.

4. Explain the gastrocolic reflex.

5. Discuss the neurological control of defecation.

General
Large Intestine vs Small Intestine
 Functions of large intestine
1. Absorption of Water and Electrolytes: The primary function of the LI is to absorb water
from the undigested food material. It also absorbs some electrolytes like Na+ and K.

2. Formation and Elimination of Feces: After the absorption of water, the remaining waste
material becomes more solid and is formed into feces.

3. Bacterial Fermentation: It houses a diverse microbiota (a community of beneficial

bacteria). These bacteria ferment un-absorbed carbohydrates, producing short-chain fatty
acids (like acetate, propionate, and butyrate) which can be used as an energy source by
the body.

4. Synthesis of Vitamins: The bacteria can synthesize certain vitamins that are beneficial
to the host, particularly Vitamin K and some B vitamins (like biotin and folate).

5. Immune Function: The intestinal walls contain lymph nodes that produce and house
immune cells, which defend against pathogenic bacteria.

6. Storage: The rectum serves as a temporary storage site for feces until it can be
eliminated.
Absorption of Water
 Functions of the large intestine
Na⁺ absorption in the Large Intestine

- The mechanisms of Na+ transport vary between the proximal and distal
colon, ensuring efficient absorption and maintenance of the body’s sodium
balance.
- These transport mechanisms also affect water movement and help form
solid feces.

- Proximal colon: Na+- transport mostly

occurs through Na+-uni-transport
(electrogenic).

- Distal colon: Mostly through coupled Na+-

H+ anti-port
Chloride
- Absorbed by exchange with
bicarbonate.
- The movement of sodium into
the plasma produces an
basolateral
electrochemical gradient to
allow absorption of chloride

Water
– The absorption of these electrolytes creates an osmotic gradient to allow
further absorption of water.
 Regulation of Absorption
Absorption in the GI tract is regulated by neuro-endocrine mechanisms.

Endocrine mechanisms:

Aldosterone, Glucocorticoids and Somatostatin

- Increases the net absorption of water and electrolytes by stimulating the
basolateral Na+-K+ ATPase. This increases the electrochemical gradient and
driving force for sodium absorption.
- It also increases transcription of epithelial sodium channels.

Enteric nervous system:

Parasympathetic innervation promotes net secretion from the intestines

Sympathetic innervation promotes net absorption from the intestines.
 Functions of the large intestine
Bacterial digestion
A. Fermentation of Carbohydrates:
Undigested carbohydrates that reach the large intestine are fermented by
the colonic bacteria. This fermentation process produces:

- Several gases like CO2, methane, and hydrogen.

- Short-chain fatty acids like acetate, propionate, and butyrate

B. Digestion of Proteins:
Bacteria can also digest proteins that weren't completely digested in the
small intestine.
- This bacterial protein digestion results in the formation of simpler
compounds, including amines and ammonia.

C. Synthesis of Vitamins: vitamin K, biotin, and some B vitamins.

 Motility in the Large Intestine
The proximal half of the colon is concerned with absorption
and the distal half with storage
1. Segmentation Movements (Haustrations):
- These are the most common type of movement in the colon.
- Haustral contractions occur roughly every 30 minutes.
- Mixing movements that help expose fecal material to the colon's surface,
aiding absorption.
- The contractions segment the colon into pouches, called haustra.

2. Propulsive Movements (Mass Movements):

- These are long, slow-moving (3 times/day), propulsive contractions.
- Help move the fecal matter towards the rectum.
- Important in the transverse and descending colon.
- Can occur after meal - Gastro-colic reflex - Duodeno colic reflex

Irritants, e.g., castor oil, threatening agents such as parasites and

enterotoxins can initiate mass movement
 Mass Movement
Gastrocolic and Duodenocolic Reflexes: These reflexes enhance colonic motility
in response to stomach and duodenal stretching respectively. They might be
responsible for the urge to defecate following a meal.
 Physiological Role of the Ileocecal Sphincter
Acts as a valve and a sphincter

1. Regulation of Transit: The sphincter helps modulate the rate at which digested
food enters the large intestine, ensuring optimal absorption of nutrients and water.
2. Prevention of Cecal Backflow: Prevents bacteria-laden
contents of the colon from returning into the SI.
Influence of Pressure and Chyme
• Ileal Distension: Increases sphincter relaxation, allowing
chyme to pass into the large intestine.

• Cecal Distension: Tightens the sphincter, inhibiting

backward flow.

Protective Functions
- Bacterial Control: Prevents the migration of bacteria
from the large intestine to the semi-sterile environment of
ileum
 Mechanism of Control of the Ileocecal Sphincter
•Neural Control:
The sphincter is controlled by the enteric nervous system, primarily influenced by reflexes
that respond to distension in the ileum or cecum.

•Hormonal Control:
Gastrin: Secreted by the stomach in response to food intake, gastrin promotes gastro-
intestinal motility and indirectly influences the ileocecal sphincter by relaxing it, allowing
chyme to move into the cecum.

Motilin: Secreted during fasting, this hormone stimulates migrating motor complexes
(MMCs), which also help regulate the sphincter, ensuring periodic relaxation.

CCK: Though its primary role is in stimulating gallbladder contraction and pancreatic
secretion, CCK can also influence the motility of the gastrointestinal tract, including the
sphincter.
Clinical Relevance
•Dysfunction: Issues with the ileocecal sphincter can result in conditions such as ileocecal valve
syndrome or contribute to small intestine bacterial overgrowth (SIBO).
 The physiology of different LI regions
1- The Ascending Colon
- Function: Primarily processes chyme by absorbing water and
salts from the indigestible food matter.

- Duration: Chyme remains in the ascending colon for

- approximately 87 minutes.

- Role: Major site of water absorption, turning chyme into semi-solid feces.

- Motility:
- Slow haustral contractions aid in mixing and absorption.
- Limited peristalsis compared to the small intestine.
 The physiology of different large intestine regions

2. The Transverse Colon is specialized for the storage and

dehydration of feces (24 hrs).
The transverse colon is the primary site for
1. The removal of water and electrolytes
2. The storage of feces

3. The Descending Colon is a conduit

between the transverse and sigmoid
colon
This region has the neural program for
power propulsion
 The physiology of different large intestine regions

4. The Recto-Sigmoid Region

• Anatomy:
• The junction between the sigmoid colon and rectum.
• Fecal material is stored in this region until defecation.

•Function:
• Storage: The rectum acts as a temporary holding chamber for fecal matter
(500 ml).
• Sensory Function: Stretch receptors in the rectum detect fullness, signaling
the need for defecation.
• Muscular Contraction: The smooth muscles in this region help retain fecal
material by contracting and relaxing as needed.
•Definition: Fecal Continence
• The ability to control the passage of stool and gas.

• Maintained by the coordination of the

1. Recto-sigmoid region,
2. Anal canal
3. Pelvic floor muscles (including the puborectalis,
external anal sphincter)

The puborectalis muscle maintains

the angle between the rectum and
anus, which helps keep feces in the
rectum.

Mechanism of Fecal Continence

• At rest, the internal anal sphincter remains contracted, and the puborectalis muscle
maintains the anorectal angle.
• The external anal sphincter stays contracted, providing extra control.
 Factors Affecting Continence

• Age-related Weakness: Weakening of the pelvic floor muscles with age can
lead to fecal incontinence.

• Neurological Disorders: Conditions like spinal cord injuries can impair the
control of sphincters and pelvic muscles.

• Diet and Fiber: A diet high in fiber helps in forming bulkier stools, aiding in
continence.
Defecation Reflex
Defecation Reflex 1.Gastro-colic reflex moves feces into
rectum

1. Defecation Reflex:

- Spinal reflex initiated by the distension of rectum.

- Aided by voluntary contractions of the diaphragm and
abdominal muscles.
- The external anal sphincter can be voluntarily
controlled (except in infants) to allow or postpone
defecation.

Two reflexes are involved:

1. Intrinsic Defecation Reflex: This is mediated by the local enteric nervous
system. When the rectum is stretched, it initiates a peristaltic wave pushing the
feces toward the anus.

1. Parasympathetic Defecation Reflex: This reflex intensifies the intrinsic

reflex. It's initiated by stretch receptors in the rectum sending signals to the spinal
cord, which then amplify the peristaltic waves and relax the internal anal sphincter.
 Neural Control of Defecation
1. Involuntary Control (Autonomic Nervous System)
a. Parasympathetic Stimulation:
1. When feces enter the rectum, the walls stretch. This stretching activates stretch
receptors in the rectal walls.
2. These receptors send signals via afferent nerves to the sacral regions of the spinal
cord.
3. From the spinal cord, parasympathetic efferent fibers travel to the smooth muscles
in the colon and rectum.
4. The result is the contraction of the rectal muscles and relaxation of the internal anal
sphincter, which is an involuntary smooth muscle.

b. Sympathetic Inhibition:
1. The sympathetic nervous system usually maintains tone in the internal anal
sphincter, keeping it contracted.
2. During defecation, there's an inhibition of this tone, aiding in the relaxation of the
internal anal sphincter.
 Neural Control of Defecation
2. Voluntary Control (Somatic Nervous System)
1.a. External Anal Sphincter:
1. The external anal sphincter is a skeletal muscle under voluntary control.
2. Once the internal sphincter relaxes due to the presence of feces in the rectum and
the resulting urge to defecate, a person can choose to voluntarily contract the
external anal sphincter, thereby postponing defecation if it's not a suitable time.
3. Conversely, one can relax the external sphincter, allowing for defecation.

Spinal cord injury patient are typically constipated, why?

Large intestine Secretion
(Protective)
 Large intestine Secretion (Protective)
- Does not secrete enzyme, Why?
Digestion : complete before chime gets to colon

Colonic secretion = Alkaline (HCO3) mucus solution

- Increase secretion via

- Mechanical/ chemical stimulation of colonic mucosa
- Mediated by short reflexes and PSN
Role:
- Protect the LI mucosa from mechanical and chemical injury
- Mucus …….. lubrication …….. facilitate passage of feces
- Alkaline secretion …….. Neutralizes acids
Where might this acid come from?
Local bacterial fermentation
 Summary
Key Points:
• The large intestine is primarily responsible for water
absorption and feces formation.

• Defecation involves both reflexive and voluntary

mechanisms.

• Coordination between intrinsic, parasympathetic,

and voluntary control is crucial for proper
defecation.
Thank you
 Recommended learning resources

- Guyton and Hall, Textbook of Medical Physiology, 13th Edition

(Pages 814-816; 831-832, 841-842)
- Berne and Levy Physiology 7th Edition
Chapter 31. The Colonic Phase of the Integrated Response to a Meal
Bacteria are present in the small intestine, but their concentration is much lower compared
to the large intestine due to several protective mechanisms in the small intestine. According
to Guyton and Hall's Textbook of Medical Physiology, the small intestine contains bacteria,
particularly in the ileum, which is the part closest to the large intestine, where bacterial
numbers start to increase.

However, there are several mechanisms that keep bacterial growth in the small intestine
relatively low:
1.Gastric acid: The acidic environment from the stomach helps to kill many bacteria before
they can enter the small intestine.
2.Peristalsis: The movement of contents through the small intestine prevents the overgrowth
of bacteria by constantly propelling the chyme (digested food) forward.
3.Bile salts: Bile secreted from the liver helps to limit bacterial growth in the upper parts of
the small intestine.
4.Immune defenses: There is a presence of gut-associated lymphoid tissue (GALT) in the
small intestine, which contributes to immune protection against excessive bacterial
colonization.
In comparison, the large intestine hosts a dense population of bacteria (up to trillions),
where these microbes play a key role in processes like fermentation, vitamin synthesis (e.g.,
Vitamin K), and digestion of fibers.
 Questions
2- Spinal cord injury (SCI) patient are typically constipated, why?
The reasons for this are multifaceted:

1.Loss of Voluntary Control: Depending on the level and severity of the spinal cord injury, there might be a loss of
voluntary control over the external anal sphincter. This can make it difficult to intentionally initiate defecation.
2.Altered Reflexes: The defecation reflex, which is mediated by the sacral regions of the spinal cord, can be
impaired or absent following an SCI. This can hinder the natural reflex that promotes defecation.
3.Reduced Motility: Spinal cord injuries can lead to a general decrease in gastrointestinal motility, slowing the
transit time of feces through the colon. This slower transit time allows for more water to be reabsorbed from the
feces, making it harder and more difficult to pass.
4.Medication Side Effects: Many individuals with SCI are on medications for pain, muscle spasms, and other
complications. Some of these medications, notably opioids, have constipation as a common side effect.
5.Decreased Physical Activity: Reduced mobility and physical activity can contribute to constipation. Physical
movement and exercise can stimulate bowel motility, so a lack of movement can exacerbate constipation.
6.Dietary Changes: After an SCI, dietary habits might change due to factors like decreased appetite, changes in
metabolic needs, or difficulties in meal preparation. Insufficient intake of dietary fiber or fluids can contribute to
constipation.
7.Impaired Abdominal Muscle Function: Injuries to the upper spinal regions can impair abdominal muscle function.
Abdominal muscles play a role in defecation by increasing intra-abdominal pressure, assisting in stool expulsion.
8.Psychological Factors: The stress, depression, and anxiety that can accompany an SCI may further impact bowel
function.