Physiology / 2009-10 Dr. Ahmad .S.

Alarabi

The digestive
system

The digestive system is composed of:

• Alimentary canal [gastro intestinal tract (GIT)]: [mouth, pharynx, esophagus, stomach,
small intestine (duodenum, jejunum, ileum), large intestine, rectum, and anal canal].
Some of these parts are separated by special muscles called sphincters to control the
passage of contents
• Digestive glands: [salivary – gastric & intestinal glands – pancreas – liver – gall
bladder].

Structure of GIT wall: from inside to outside:

1- Mucosa: it contains bl. & lymphatic Vessels, gastric and intestinal glands.
2- Submucosa: it contains meissner’s nerve plexus.
3- Musculosa: it contains outer (longitudinal) and inner (circular) muscle layer. And
contains also myentric (auerbach’s) nerve plexus between the 2 muscle layers.
4- Serosa: it is the peritoneal covering of the GIT.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Function of the GIT

a- Motility: [mastication / propulsive (peristaltic) / mixing (segmenting)] movements.

b- Secretion.
c- Digestion: from large into smaller molecules [e.g. proteins → amino acids].
d- Absorption.
e- Excretion.

Regulation of GIT functions

The GIT motility and secretion are regulated by 2 mechanisms [nervous regulation –
hormonal regulation].

I- Nervous regulation: it is a rapid regulation. It is mediated by:

1- Autonomic nerves:

• Parasympathetic: through [vagus / pelvic] nerves.

• Sympathetic: through [T8 – L2].

2- Local nerve plexuses: they are plexuses that are found inside the GIT wall and they
can control the function of GIT either by their direct effect, or through the AN fibers.
They include:

a- Meissner’s plexus: it is located in the submucosa, so it controls mainly the

secretory function of the GIT.
b- Myentric plexus: it is located between the muscular layers (longitudinal &
circular) in the musculosa. So, it controls the mainly the motor function of the GIT.

Notes:
• Most of the autonomic nerves terminate on both the myentric & meissner’s plexuses
to control the GIT function [except some sympathetic fibers].
• Usually, the agent that causes contraction in the wall of certain area will cause
relaxation of the sphincters at that area.
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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

• The autonomic action of the GIT (motility & secretion) is adjusted by the mean of
reflexes. They are either [local reflexes] or [central reflexes].

To know the effects of both symp & parasymp please review the ANS sheet.

II- Hormonal regulation: it is a slow regulation.

The GIT hormones are released by special mucosal cells by the mean of local reflex.

Gastrin GIP Secretin CCK

Site of • G cells in the • K cells in • S cells in the • I cells in the
release antral mucosa. the duodenal duodenal & duodenal &
& jejuna jejuna mucosa. jejuna mucosa.
mucosa.
Stimulus • Gastric • Presence of • Acidity of Presence of:
for distention. glucose & fat upper small • Protein
release • ↓ acidity. in duodenum intestine. digestive
• Presence of • Presence of products
protein protein digestive • Fatty acids
digestive products [AA&
products [AA & peptides]
peptides].
Actions •↑ gastric • ↓ gastric • ↑ secretion of • ↑ secretion of
secretion [HCl & secretion. aqueous enzymatic
pepsin]. • ↓ gastric pancreatic juice. pancreatic juice.
• ↑ gastric motility. • ↑ HCO3 • contraction of
motility. • ↑ insulin secretion from gall bladder &
• Contraction of secretion. the biliary tract. relaxation of
lower • ↓ gastric sphincter of oddi.
esophageal secretion. • contraction of
Sphincter • Contraction of pyloric sphincter.
• ↑secretion of pyloric • ↑ sm.
insulin & sphincter. Intestinal
glucagon • Augments the motility.
action of CCK. • Augments the
action of
secretin.
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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Motility of the GIT

Each part of the alimentary canal has its own type of movement to achieve its function
starting from the buccal cavity [mouth] to the anus.

Mastication (chewing)

Definition: it is the process by which the sk. muscles in the jaw, lips, cheeks and tongue
are used to permit the teeth to grind the food.

Function of mastication:

1- The grinding of food into smaller particles helps the digestion by:

a- ↑ exposed surface area of food.

b- Facilitate the swallowing of food.
c- Prevent the mechanical damage [excoriation] of the GIT mucosa.

2- Stimulate the secretion of saliva which soften and lubricate the food.

Swallowing (deglutition)

Definition: it is the transport of food bolus from the mouth to the stomach.
It is divided into 3 stages (phases):

1- Buccal phase (voluntary): it is the passage of food from the mouth to the pharynx. It
is done by upward (against hard palate) and backward movement of the tongue. During
this phase, the mouth should be closed.

2- Pharyngeal phase (involuntary): it starts after the touching of food bolus to the
swallowing receptors in the pharyngeal opening. This will leads to the following:
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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

• Elevation of soft palate to close the posterior nasal opening.

• Continuation of elevation of the tongue against hard palate.
• Covering of the larynx by epiglottis and approximation of vocal cords [this will close
the air ways].
• Peristalsis of the pharyngeal muscles.

All of these effects will guide the food bolus to the esophagus without escaping to any
other area [e.g. trachea or nose].

3- Esophageal phase (involuntary): it is occurs as the following:

• On reaching of the bolus by pharyngeal peristalsis to the upper esophageal sphincter

(UES) [which is normally closed to prevent entering of gases into stomach during
inspiration], this sphincter will relax to allow the bolus to pass, then close again [to
prevent reflux of the bolus].
• Then the bolus travels down along the esophagus by esophageal peristalsis [for
semisolid bolus] or by gravity [for liquid bolus] until reach the lower eso. Sphincter (LES).
• Then the LES will relax [which is normally closed to prevent reflux of gastric contents].
• This will allow the passage of food from the esophagus into the stomach.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

The swallowing reflex

Receptors: at the pharyngeal opening [especially on tonsillar pillars].

Afferent: 5, 9, 10 cranial nerves.
Center: swallowing center in the medulla oblongata (MO).
Efferent: 5, 9, 10, 11, 12 cranial nerves.
Effector: muscles of swallowing.

Swallowing disorders
Dysphagia: it is difficulty of swallowing du to lesion in one of components of the
swallowing reflex arc [receptor → effector].

Achalasia (cardiospasm): high tone in the LES which fail to relax.

Gastric motility

The motor functions of the stomach include:

1- store the food until it can be processed in duodenum.
2- Mix the food with gastric secretions until the chyme is formed.
3- Emptying the food in suitable rate for proper digestion and absorption in small
intestine.

The stomach is composed of [cardia – fundus – body – antrum – pylorus].

Both of the cardia and pylorus have their sphincters [cardiac & pyloric sphincters].

Physiologically, the stomach is divided into 2 parts [units]:

• Proximal motor unit: it comprises the fundus and upper 2/3 of the body. It is
mainly for storage of food where it can accommodate up to 1.5 L of food & fluids.

• Distal motor unit: it comprises the lower 1/3 of body and the antrum. It is mainly
for mixing and emptying of the gastric contents by the action of gastric peristalsis

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

[peristaltic movement starts at the midpoint of greater curvature and propagate all over
the wall of the stomach].

Gastric emptying
(evacuation)

On arriving of gastric peristalsis [about 3 waves/min] to the antrum, it becomes stronger

→ strong antral contraction → ↑ antral pressure > duodenal pressure → forcing several
milliliters of chyme into the duodenum; this is called the pyloric pump.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Factors affecting gastric emptying

1- Food factors:

• Liquids are evacuated more easily than solids.

• Food type [carbohydrates rich food evacuated rapidly > proteins > fats]. So the fat
rich food takes much more time in the stomach before it is evacuated.

2- Gastric factors [stimulators]:

• Gastric distension: ↑ distension of gastric wall [by food] → ↑gastric emptying

[within limits].
• Gastrin hormone [secreted from antral mucosa] → ↑ gastric emptying.

3- Intestinal factors [inhibitors]:

• Distension of the intestinal (duodenal) wall → ↓ gastric emptying.

• ↑ acidity in duodenum → ↓ gastric emptying.
• ↑ fat content in duodenum → release of inhibitory hormones [GIP, CCK, motilin, VIP
and secretin] → ↓ gastric emptying.

These mechanisms [i.e. intestinal] called Enterogastric reflex [they are the most
important determinant of Gastric emptying].

4- Other factors:

• Pain → inhibition of gastric emptying.

• Emotion: the fear and depression slow gastric emptying while the anxiety and
anger accelerate it.
• Drugs: stimulators [Ach – coffee] / inhibitors [adrenergic drugs – atropine –
excessive smoking].

Hunger pain (H. contractions)

These are intense rhythmic peristalsis in the body of stomach that occurs after long time
of starvation [starts after 24 hours starvation].

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Vomiting

Definition: expulsion of the gastric contents to the outside through the mouth. It is due
to stimulation of the vomiting center [in the medulla] by:

• Mechanical stimulation of the posterior part of the tongue or back of the throat.
• Irritation of gastric mucosa [e.g. gastroenteritis (GE)].
• Intestinal obstruction.
• Stimulation of chemoreceptor trigger zone (CTZ) [an area in the medulla near
the vomiting center] by:

• Drugs [emetic drugs].

• Psychic stimulus.
• Motion sickness.
• Acidosis.
• Hypoxia.

Mechanism of vomiting

The previous causes stimulate the vomiting center and leads to:

1- Nausea, excessive salivation, sweating, pallor, and tachycardia [before vomiting].

2- Protection of airways by:

• Elevation of soft palate [close the nose].

• Closure of the glottis and approximation of vocal cords [close the larynx].
• Apnea [stopping of breathing].

3- Relaxation of the body of stomach and cardia [gastroesophageal sphincter (LES)].

4- Strong contraction of the diaphragm & abdominal wall muscles → ↑ intra abdominal
pressure → squeezing of gastric contents.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Effects of vomiting on gastric contents

1- Loss of fluid → dehydration → hypotension & tachycardia.

2- Loss of acidic gastric contents → alkalosis.
3- Loss of electrolytes [especially Na+ & K+].

Small intestine motility

Types of intestinal movements:

a- Mixing (segmenting) movement:

It is a several constrictions divide the intestine loop into segments (equal part), which
will disappear and replaced again by another constrictions between the previous
constrictions. It occurs at frequency of 9 – 12 constriction / minute. The control of this
movement is mainly Myogenic (not nervous).

This movement helps in:

• The digestion by mixing food with digestive
enzymes.
• Absorption by contact of food with intestinal
wall.

b- Propulsive (peristaltic) movement:

With control of Myentric plexus, the stretch of
part of intestinal wall by chyme leads to:
• Contraction proximal to this area.
• Relaxation distal to this area.
This will propel the food distally.

* Mass peristalsis (Peristaltic rush): a very rapid peristalsis occurs in abnormal

conditions when the small intestine is irritated by toxins [it is associated with diarrhea].

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Regulation of the small

intestinal motility

Stimulants of Int. motility:

• Distension of the intestinal wall.
• Parasympathetic stimulation.
• CCK and gastrin hormones.
• Serotonin & substance P.

Inhibitors of Int. motility:

• Sympathetic stimulation.
• Secretin and GIP hormones.

Paralytic ileus (adynamic ileus)

Def: it is a condition in which there is a relaxation of In. wall muscles → ↓ or absence of

Intestinal motility. It is a usual complication of major abdominal surgery.
It is treated by giving nothing by the mouth (until peristalsis starts) and giving
intravenous (I.V) fluids during this period.

Movement of large intestine

Functionally, the large intestine is divided into 3 main parts:

1- Proximal colon: includes [cecum – ascending colon – proximal ½ of transverse colon].

Its main function is absorption of water and electrolytes.
2- Distal colon: includes [distal ½ of transverse colon – descending & sigmoid colon].
Its main function is storage of feces.
3- Rectum and anal canal: their function is defecation.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

The large intestine also [like sm.

Intestine] has 2 types of movements:

• Mixing (segmenting) movement.

• Propulsive (peristaltic) movement.

The motility of large intestine is

regulated by:

• Stimulants: [parasympathetic
stimulation – gastrin hormone].
• Inhibitors: [sympathetic
stimulation - adrenaline].

Note: the mass peristalsis (peristaltic rush) in the large intestine occurs physiologically
once or twice per day. It is caused by Gastrocolic & Duodenocolic reflexes.

Defecation

Definition: emptying of the colon contents through the anal canal.

Mechanism of defecation

1- Distension of the rectum with feces → initiation of intrinsic (local) defecation reflex →
↑ peristaltic waves in [(desc. & sigmoid) colon & rectum] and relaxation of the internal
anal sphincter. [This reflex is often too weak to start defecation].

2- In the same time, the spinal defecation reflex [the main reflex] starts. Where, rectal
or anal distension → send signals through the pelvic nerve → defecation center [2,3,4
sacral segment] → pelvic and pudendal nerves → contraction of the rectal wall,
relaxation of the internal and external sphincter, and contraction of levator ani muscles
[which pull the anal canal upward]. All of these effects will lead to expulsion of the
feces.
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Note: both of the 2 mentioned reflexes [local & spinal] are autonomic (involuntary).

3- The defecation has voluntary control. This control is mediated by the cerebral cortex.
If the situation [time & place] was suitable, the cerebral cortex initiates the defecation
voluntarily by:

• Activation of defecation center.

• Relaxation of internal and external anal sphincters.
• Straining (forced expiration against closed glottis) → ↑ intra abdominal pressure.

But if situation was not suitable, the cerebral cortex will sends inhibitory impulses to the
defecation center which will cause contraction of the external anal sphincter.

Defecation abnormalities

1- Constipation: it is ↑ intervals between defecations more than normal for the

person, with hard consistency in the stool.
2- Diarrhea: it is ↑ frequency of defecation with soft or watery stool.

Gastro intestinal secretions

Salivary secretion
The mouth contains 3 pairs of salivary glands [Parotid – Submandibular – Sublingual],
that produce about 1.5 L / day of saliva that has a PH of (6 – 7). The saliva composes of:
• Water (99%).
• Electrolytes [Na+, K+, Cl-, HCO –3, etc].
• Organic compounds:

• Digestive enzymes [e.g. salivary amylase, lingual lipase].

• Mucous [for lubrication].
• Proteolytic enzymes [mainly lysozyme].
• Immunoglobulin A [IgA].
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Functions of saliva

1- Digestion: • salivary (alpha) amylase splits the starch into maltose.

• Lingual lipase digests less than 10% of ingested triglycerides.

2- Facilitate the swallowing and speech.

3- Maintain healthy oral tissue through:

• Antibacterial action [lysozyme & IgA].

• Maintaining the PH of saliva around 7 [the acidic PH → ↑ solubility of
Ca+ in saliva → loss of Ca+ from teeth → dental caries].

4- Excretion of some metals [e.g. iodide, mercury, lead].

Regulation of salivary secretion

The secretion of saliva is only under nervous control.

1- Parasympathetic: it stimulates the secretion of true salivary secretion [watery

(large in volume), rich in electrolytes, poor in enzymes], and cause vasodilatation in the
glands.

2- Sympathetic: it stimulates the secretion of trophic saliva [viscid (small in amount),

poor in electrolytes, and rich in enzymes], and causes vasoconstriction of the gland.

The secretion of saliva is through the ANS is controlled by:

• Unconditioned (inherent) reflex: [presence of food in the mouth].

• Conditioned (learned) reflex: [seeing, smelling, or hearing the food].

The acidic food [e.g. lemon] is the most powerful stimulus for saliva.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Gastric secretion

The gastric mucosa contains many deep glands that open on a common duct that in turn
open on the surface of mucosa.

The gastric glands contain 3 types of cells; each one has its own secretions:

1- Mucous (neck) cells: secrete Mucous.

2- Parietal (oxyntic) cells: secretes HCl & IF (intrinsic factor).
3- Peptic (chief) cells: secrete Pepsinogen.

The gastric glands secretes about 2 L / day of the highly acidic gastric juice.
It is composed of [enzymes, mucous, IF, water, electrolytes, & HCl].

A- Enzymes:

1- Pepsinogen: it is the main enzyme (proteolytic). It is secreted from peptic cells.

It is in inactive form. It is activated by the HCl [acidity (PH=2)] which convert it to
pepsin (active form).
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Its function is the digestion of proteins into polypeptides and peptones.

After finishing its function, the pepsin is inactivated by alkalinity of the intestine.

2- Other enzymes: they are secreted from peptic cells in very small amounts:

a- Gastric amylase: have major role in digestion of starch.

b- Gastric lipase.
c- Gilatinase.

B- Mucous (mucin): it is of 2 types:

1- Soluble (thin) mucous: it lubricates the gastric chyme.

2- Insoluble (thick) mucous: it lubricates the mucous membrane, and neutralizes the
gastric acid [because it contains HCO –3 with it] before reaching the epithelium.

C- Intrinsic factor (IF): it is secreted by parietal cells. It is essential fro vitamin B12
absorption at terminal ileum.

D- Water & electrolytes [e.g. Na+, K+, Cl–, and HPO – 4].

E- Gastric acid (HCl).

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Gastric HCl

It is secreted from parietal [oxyntic] cells by the following mechanism:

Factors affecting HCl secretion

Stimulate it:
• Acetylcholine: via its action on muscarinic (M1) receptors [blocked by atropin].
• Gastrin: acts via gastrin receptors.
• Histamine: acts via H2 histamine receptors [blocked by H2 receptors Antagonists
(e.g. cimetidine “Zantac”)].

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Inhibit it:
• Some GIT hormones [e.g. GIP, Secretin, CCK, and VIP].
• Prostaglandins [especially pg E]. any drug ↓ pg will lead to ↑ HCl secretion and
development of peptic ulcer [e.g. anti inflammatory drugs].

Functions of HCl
1- Convert the pepsinogen (inactive) into pepsin (active).
2- Gives the optimum PH for pepsin action.
3- Help the pepsin in the digestion of proteins.
4- Stimulate the secretion of bile and pancreatic juice.
5- Delays gastric emptying.
6- Important for Ca+ absorption, and in the reduction of ferric into ferrous iron.

Mechanism of gastric secretion

The ↑ in secretion of gastric juice in response to meal passes in 3 phases:

1- Cephalic phase: it occurs before reaching of the food into the stomach [accounts
for 20% of secretion (during eating)]. It is achieved by mean of:

a- Conditioned reflexes: [seeing, smelling, or thinking food].

b- Unconditioned reflexes: [presence of food in the mouth].

2- Gastric phase: it occurs when the food enters the stomach. It is the main phase
[constitutes about 70% of the secretion]. It continues for about 3 hrs.

3- Intestinal phase: it occurs when the chyme enters the duodenum [sometimes]

Gastro duodenal mucosal barrier

The gastric and duodenal mucosa is protected from the irritation by HCl and auto
digestion [caused by pepsin (proteolytic)] by the following protective factors:

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

1- Thick, viscid alkaline mucous that covers the gastric & duodenal mucosa.
2- Prostaglandin: →↑ mucous secretion & ↓ HCl secretion.
3- Neutralization of gastric acid by alkaline duodenal juice [in the duodenum].
4- Continuous regeneration of gastric mucosa.

Peptic ulcer

Definition: an eroded area in the GIT mucosa due to auto digestion by gastric juice.
It could be:

• 1st part of Duodenum. [The most common site].

• Stomach.
• Lower end of esophagus [less common].

It is caused by one of the following factors:

1- ↑ gastric secretion by: [stress, anxiety, coffee, etc].

2- ↓ activity of mucosal barrier due to: [↓ mucous, excessive irritation by alcohol or
spices, excessive intake of anti inflammatory drugs, excessive smoking, and infection of
mucosa by bacteria (helicobacter pylori)].

Treatment: it started in the following sequence [according to the severity]:

1- Reduction of stressful conditions.
2- Neutralization of acid by antacid drugs.
3- Reduction of secretion of acid by:

a- H2 receptor blockers [e.g. cimetidine (Zantac)].

b- H+ – K+ pump blockers [e.g. omeprazole].

4- Excessive intake of milk.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Pancreatic secretion

The pancreas is mixed endocrine & exocrine gland. We are here concerned with the
exocrine part.

The exocrine pancreas secretes about 1.5 L / day of the pancreatic juice. It is alkaline
[PH=8] because it has a high HCO –3 content. The pancreatic juice composes of:

1- Digestive enzymes: 3 groups of enzymes are secreted by acinar cells:

a- Pancreatic amylase: it is (α) amylase that hydrolyzes the polysaccharides

[e.g. starch & glycogen] into disaccharides.
b- Pancreatic lipases: they include [lipase (active)] & [phospholipase
(inactive, and activated by trypsin)]. They hydrolyze the TG → MG
(monoglycerides) + FFA + glycerol.
c- Pancreatic peptidases: they include [Trypsin / Chemotrypsin /
Carboxy peptidase].
They are secreted in inactive form [Trypsinogen / Chemotrypsinogen /
Procarboxy peptidase].

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

The Trybsinogen is activated into Trypsin by the action of enterokinase enzyme

secreted by duodenal mucosa.
Then, the Trypsin activates the Trypsinogen [autoactivation] and the other inactive
enzymes.

Action: these enzymes hydrolyze the polypeptides → di & tri peptides + AA.
Note:

• The pancreatic amylase is more potent than salivary amylase.

• All proteolytic enzymes are secreted inactive and it is activated only in the
intestine [to prevent the autodigestion of the pancreas].

2- Sodium bicarbonate:
it is mainly secreted by
epithelia cells of the
pancreatic ducts.

♦ Mechanism of
[Na+ HCO – 3] secretion

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Function of bicarbonate

• Neutralize the acidic chyme to protect the intestinal mucosa.

• Provide optimum PH for action of pancreatic enzymes that needs alkaline
or neutral PH.

3- Water & electrolytes:

According to the content of water, the pancreatic juice is divided into 2 types:

Aqueous juice Enzymatic juice

Characters • Large in volume. • Small in volume.

• Rich in bicarbonate. • Poor in bicarbonate.
• Poor in enzymes. • Rich in enzymes.
Site of secretion • Duct cells. • Acinar cells.

control • Stimulated by secretin. • Stimulated by CCK.

Control of secretion of P. J

Like gastric juice secretion, the P.J secretion occurs in 3 phases:

1- Cephalic phase: before reaching of food into the stomach [cond. & uncond Reflex].
2- Gastric phase: occurs when the food enters the stomach.
3- Intestinal phase: occurs when the food reaches the intestine through the release of:

• Secretin hormone [stimulate the secretion of aqueous juice].

• CCK hormone [stimulate the secretion of enzymatic juice].

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Liver & gall bladder

The liver is the largest organ in the body. Its functions include:

1- Excretory function: excretes [bile pigments, cholesterol, & other substances] in the
form of bile.
2- Metabolic function: it aids in the metabolism of

a- Carbohydrates [the site of glycogenesis, glycogenolysis, gluconeogenesis].

b- Fats [oxidation of FA & formation of lipoproteins, cholesterol, and phospholipids].
c- Proteins [synthesis of nonessential AA, Pl.Pr, most cl. Factors, urea, etc].

3- Storage function: stores [glycogen, vitamins, metals, (e.g. Fe, Cu), etc].
4- Detoxification & inactivation: it detoxifies & inactivates many drugs & hormones.
5- Defective function: it is part of the RES [contains tissue macrophages and lymphoid
tissue (clones of B & T lymphocytes)].

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

The bile

Physiological anatomy of the biliary system [see the figure in the previous page].

Bile secretion
The liver secretes continuously about 1 L / day of alkaline bile [PH≈8].
When this bile goes and becomes stored in the gall bladder, its PH becomes neutralized
or slightly acidic [PH around 7].
The bile composes of [water, electrolytes, bile salts, bile pigment (bilirubin), and small
amounts of (cholesterol, FAs, and alkaline phosphatase enz.)].
The bile is secreted during meals by the relaxation of sphincter of oddi and contraction
of gall bladder wall [→ evacuation of the bile from the G.B into the duodenum].

The secretion of bile is affected by many factors including:

A- Factors ↑ bile formation by the liver [e.g. bile salts, Ach, secretin hormone].
B- Factors → contraction of G.B wall [mainly the CCK hormone].

Note: after secretion of bile salts (B.S) in the bile, 10% of this bile is lost in stool, while
90% is reabsorbed actively at terminal ileum to the liver to be resecreted through the
bile; this is called Enterohepatic circulation of bile salts.
If the EHC is interrupted [e.g. diseased or excised terminal ileum] → loss of most of B.S
in the stool → B.S deficiency.

Formation of bile salts

1- The primary bile acids [cholic acid & chenodeoxy cholic acid] are formed in the liver.
2- Then, these acids conjugate in the liver with amino acids [glycin (mainly) & taurine] to
form conjugated bile acids [e.g. glycocholic & taurocholic acids].
3- In bile canaliculi, Na+ and K+ will be actively transported and added to the conjugated
bile acids → formation of bile salts [e.g. Na+ glycocholate & Na+ taurocholate].

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Functions of bile salts

1- Helps in the digestion of fats by:

a- Emulsification of the fat particles → ↑ the surface

area on which the lipases act.
b- Activate the lipases.

2- Help in fat absorption: by forming water soluble complexes with the lipids called
micelles. These complexes make the fat absorbed more easily.
3- Essential for absorption of fat soluble vitamins [A, D, E, K].
4- Stimulates the intestinal peristalsis [prevent constipation (laxative action)].
5- Keep the cholesterol dissolved in bile and prevent its precipitation [stone formation].
6- The bile salts are the most powerful choleretic [stimulate the liver to secrete bile].
7- Antiputrefactive action: they prevent protein putrefaction by helping the digestion of
fat [because undigested fat impairs the action of proteolytic enzymes on proteins].

If the bile salts failed to reach the intestine, this will lead to:

• ↓ Fat absorption → fat lost in stool → steatorrhea.

• ↓ Fat soluble vitamins.
• Protein putrefaction.
• Constipation.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Bile pigment

The bile pigment [bilirubin] is the metabolic end product of hemoglobin. It is excreted
mainly in the stool through the bile.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Jaundice [icterus]

Definition: it is a disease characterized by yellowish discoloration of [skin, sclera, and

mucous membrane] due to the ↑ of total bilirubin in the blood.

The normal concentration of total bilirubin in the plasma is up to 1 mg% [most of it is

unconjugated bilirubin]. The jaundice occurs when the total bilirubin conc. in the
plasma exceeds the level of 2 mg%.

Types of jaundice

The jaundice is classified according to the cause into 3 types:

I- Hemolytic [Prehepatic] jaundice:

It is caused by ↑ destruction (Hemolysis) of RBCs due to [drugs / toxins / cell membrane
defect / Hb defect / incompatible Bl. Transfusion/ etc].
In these cases, the rate of formation of bilirubin [due to ↑ Hemolysis] exceeds the rate
of uptake and excretion by the liver. This will lead to the following:

1- ↑ the unconjugated bilirubin only (Hemobilirubin) while the [conjugated

bilirubin & bile acids are normal].
2- Normal content of biliribin in urine [normal colour], because Hemobilirubin
can’t filtrate through glomeruli.
3- ↑ Stercobilinogen → very dark stool.

II- Obstructive [Posthepatic] jaundice:

It is caused by obstruction of the common bile duct by [gall stone / tight stricture /
cancer head of pancrease].
In these cases, the formation and uptake of bilirubin is normal, but its excretion into
intestine is markedly ↓ → its stagnation in biliary passages → its regurgitation into the
blood stream. This will leads to:

a- ↑ Cholebilirubin and bile salts in the blood [while hemobilirubin is normal].

b- ↑ in the blood of substance that are normally secreted in the bile.
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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

c- ↑ Cholebilirubin in the urine [can filtrate through glomeruli] → very dark urine.
d- ↓ in Stercobilinogen in stool [due to obstruction] → very pale stool.

III- Hepatic jaundice:

It is caused by damage of liver cells [commonly due to hepatitis or toxic drugs].
In this case, the bilirubin formation is normal, but the uptake from the plasma by the
liver is decreased [due to liver cells damage] → ↑ Hemobilirubin.

At the same time, there is intrahepatic biliary ducts obstruction → regurgitation of

Cholebilirubin. All of these changes will lead to:
a- ↑ of both Hemobilirubin & Cholebilirubin & alk. Phosphatase in the blood.
b- ↑ Cholebilirubin in the urin.
c- ↓ Stercobilinogen in the intestine → Pale stool.

Hemolytic Obstructive Hepatic

jaundice jaundice jaundice

Blood
1- Hemobilirubin Markedly ↑ Normal nearly Moderate ↑
2- Cholebilirubin Normal Marked ↑ Moderate ↑
3- Bile salts Normal Marked ↑ Moderate ↑
4- Alkaline Normal Marked ↑ Moderate ↑
phosphatase
Urine
1- Cholebelirubin Normal trace Marked ↑ Moderate ↑
2- Colour Normal Very dark brown Dark brown

Stool
1- Stercobilinogen Increased Nearly absent Decreased
2- Colour Dark Very pale Pale

Hemolytic anemia Present Absent Absent

Liver function Normal May be impaired Highly impaired

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Functions of the gall bladder

1- Storage of bile [between meals] that will be evacuated when needed [during meals].
2- Concentration of bile [5 – 10 times more than that in the liver].
3- Acidification of bile [from 8 to be about 7] to prevent precipitation of Ca+ [this
prevent the gall stones].

Small intestinal secretion

The small Intestine secretes about 1.5 L / day of alkaline secretion [PH≈7.5] which is
composed of:

1- Mucous: secreted by goblet cells. It protects the duodenal mucosa from the acidic
chyme, and lubricates it to facilitate the passage of food and prevent its damage.
2- Alkaline fluid: it contains mainly NaHCO3 .
3- Digestive enzymes: present in sloughed cells at microvilli surface. They include:

a- Disaccharidases: split disaccharide into monosaccharide

[e.g. Surase, Maltase, Lactase, etc].
b- Peptidases: splits the small peptides into amino acids [AA].
c- Lipase: in small amount [splits neutral fats into Glycerol & FA].
c- Enterokinase: activates the trypsinogen into trypsin.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Metabolism

Absorption in GIT

Definition: it is the passage of digestive products through the wall of the alimentary
canal to the blood stream.

Sites of absorption

A- Stomach: because of the lack of villi, the stomach has a poor absorptive surface,
and only small amount of water, alcohol, glucose & drugs [e.g. aspirin] can be absorbed.

B- Small intestine: it is the main absorption site for water, electrolytes & nutrients.
٠ About 9 liters of fluid must be absorbed daily [1.5 L ingested + 7.5 L GIT secretions]
mainly by small intestine [they absorb about 8 L] and this is as result of its large surface
due to the presence of villi & microvilli.

C- Large intestine: they absorb water & electrolytes [but not nutrients].
This absorption occurs in the proximal colon.

Mechanism of absorption

I- Absorption of ions & water:

As in renal tubules, the Na+ is reabsorbed passively [by facilitated diffusion] at luminal
border and actively at basal border. This transport is followed by:

a- Absorption of Cl- HCO3- passively [by electrical gradient].

b- Absorption of H2O [by osmosis].
c- Absorption of glucose and amino acids actively [by co-transport with Na+].
d- Secretion of K+ and H+ actively [by counter transport with Na+].

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

II- Absorption of nutrients:

• Carbohydrates:
The carbohydrates are absorbed mainly as monosaccharides [80% in the form of
glucose] actively at luminal border [co-transport with Na+] and passively at basal border
[by facilitated diffusion].

• Proteins:
They are absorbed mainly in the form of amino acids [in the same way as glucose].

• Lipids:
They are absorbed mainly in the form of monoglycerides and free fatty acids by the
formation of micelles and chylomicrons.

Metabolic rate

Definition: it is the amount of energy produced per unit of time [per hour].

Factors affecting metabolic rate

A- Physiological factors:

1- Exercise: it is the factor that produces the most marked increase in M.R; so, it is
more in athletics.

2- Recent ingestion of food [specific dynamic action (SDA)]:

SDA is the increase in M.R after food ingestion. It starts after 1hr of food ingestion
to reach its maximum in 4 – 5 hrs and decline to its original level in 10 – 12 hrs.
It is mainly due to stimulatory action of the ingested amino acids and fatty acids on
the cellular chemical reaction [Proteins = ↑30% – CHO & Fat = ↑4%].

3- Environmental factors (climate): exposure to cold → ↑ heat production (M.R).

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

4- Age: the maximum M.R is at the period of [2y – till puberty] which will decline
then after age of 20y.
5- Sex: M.R is 10% less in females than males.
6- Pregnancy: it ↑ M.R especially in late months.
7- Emotions: they ↑ M.R due to sympathetic stimulation.
8- Sleep: it ↓ M.R 10 – 15 %.
9- Hormones: [thyroxin – epinephrine – norepinephrine – growth hormone – male
sex hormone] all of them ↑ the M.R.

B- Pathological factors:

1- Fever: it ↑ the body temperature (M.R) about 13%.

2- Blood diseases (e.g. polycythemia & leukemia) → ↑ M.R.
3- Diabetes insipidus, undernutrition ,and hypothermia, all of them ↓ M.R.

Basal Metabolic rate

(BMR)

Definition: it is the rate of energy production per unit of time (per hour) per square
meter surface area under the following 3 basal conditions:

1- Complete physical and mental rest for at least 1 hr [but without sleep].
2- Post absorptive state: 12hrs after the last meal [to avoid SDA].
3- Comfortable external temperature [20 – 28 c° for dressed person].

• The BMR in normal adult man is [40 K cal / hour / m2].

• The factors that affect the BMR are the same factors that affect the M.R.

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Physiology / 2009-10 Dr. Ahmad .S. Alarabi

Obesity

Definition: it is excessive storage of body fat. It is caused by either increase in energy

input [excessive feeding (hyperphagia)] or decreased energy output [e.g. sedentary
life].

Complications

1- Flat foot & osteoarthritis of lumbar vertebrae, hip, and knee joints.
2- Predispose to diabetes mellitus.
3- Heart failure, atherosclerosis, hypertension [ischemic heart diseases].
4- Fatty liver and stones of gall bladder.

Treatment

1- Decreases the energy input by: restriction of fat & carbohydrates with allowing to
proteins and vegetables intake, or by taking anorexic drugs.
2- Increase the energy output [by regular exercise].

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