ALIMENTARY SYSTEM

5th February 2018

OUTLINE
Swallowing
Gastric secretion
Digestion
- Control of digestion
Small bowel function
Large bowel function
Bile
Functions of liver
- Carbohydrate, fat and protein metabolism
Vitamins
Postgastrectomy syndrome
Malabsorption syndrome
ALIMENTARY SYSTEM
 Alimentary system
 Alimentary canal
 Mucosa – epithelium
 Submucosa – blood vessels, nerve fibers
and connective tissues
 Muscularis – skeletal (voluntary) or smooth
(involuntary) muscles
 Serosa – visceral peritoneum
ALIMENTARY SYSTEM
SWALLOWING
 3 stages of swallowing
1) Voluntary/oral stage
 The food bolus rolled into the pharynx by pressure of the
tongue.

2) Pharyngeal stage (involuntary)

 Bolus of food enters the pharynx and stimulate swallowing
receptor area.
 Impulse will be send to the swallowing centre in the
medulla to initiates a series of automatic pharyngeal
muscular contraction as follows:
i) The soft palate is pulled upwards
ii) Epiglottis swing backward at the opening of larynx
iii) Larynx move upward
- pharyngoesophageal sphincter relaxed
- muscular muscle wall of pharynx contract to propel the bolus
of food into esophagus.
- the trachea closed, esophagus opened
- fast peristaltic wave originating in pharynx forces the bolus
of food into the esophagus
3) Esophageal stage
 The movement of esophagus conduct food from the pharynx
into the stomach.
 2 types of peristaltic movement
i) 1° peristalsis - continuation of peristaltic wave that begins in
the pharynx, with the aid of gravity pulled food to lower
esophagus.
ii) 2° peristalsis - resulted from distention of esophagus by the
retained food & the peristaltic wave continue until all the food
has emptied into the stomach.
 During swallowing, gastroesophageal sphincter
contract to prevent reflex of gastric acid into
esophagus.
 Flow back of the acidic gastric content due to
high abdominal pressure causing esophageal
discomfort known as heartburn.
 Relaxation of gastroesophageal sphincter allow
the bolus to enter the stomach
 Acalasia, the sphincter fails to relaxed,
instead it contracts more vigorously.
 The food will accumulate in esophagus, which
will cause the esophagus become
enormously distended.
 The detained meal in esophagus may spill
into pharynx and accidentally aspirated into
the lung, causing aspiration pneumonia.
GASTRIC SECRETION
 2 types of secretion:
i) exocrine
- gastric juices (HCl, mucus)
ii) endocrine
- hormone (gastrin)
 Gastric juices are secreted by the gastric mucosa
i) oxyntic area
- lines the fundus & body
* Chief cells -enzyme precursor (pepsinogen)
GASTRIC SECRETION

* Parietal cells -HCI & intrinsic factor (IF)

* Mucus neck cells -thin watery mucus
* Surface epithelial cells - thick, viscous, alkaline mucus
ii) Pyloric gland area (PGA)
Secretes – mucus, pepsinogen, gastrin
HCI SECRETION
 HCI secreted by the parietal cells - reduce the pH of
luminal content to 2 (acidic)
 Fx:
i) Activation of pepsinogen
Pepsinogen HCl pepsin (active enzyme)
ii) Breaking down large food particles (connective
tissues & muscle fibers)
iii) Protection
Act together with salivary lysozyme to kill
microorganism in the mouth
 PEPSINOGEN SECRETION

 Major constituent of gastric secretion

HCl
Pepsinogen Pepsin
(Inactive form/precursor)
Autocatalysis
Ingested protein pepsin
short peptides

* Pr- can be digested by pepsin,  pepsin is only converted into

the active form when it reach the gastric lumen to avoid digestion
of other cells
MUCUS SECRETION

 Mucus cover the surface of gastric mucosa

 Fx:

i) Protect stomach wall from self digestion by pepsin

ii) Lubrication to avoid mechanical injury
iii) Neutralize HCI to prevent acid injury
IF SECRETION

 IF - glycoprotein
 Important in absorption of vitamin B12 in terminal ileum
 Vitamin B12 required for erythropoiesis
 Absence of IF no vit. B12 absorption defective
erythropoiesis pernicious anemia
 Deficiency of vitamin B12 together with folic acid due to
malabsorption syndrome megaloblastic anemia
GASTRIN SECRETION

 Hormone secreted by G cells in PGA

 Fx:

i) stimulate parietal & chief cells to increase secretion

of highly acidic gastric juice
ii) control gastric motility
1. CEPHALIC PHASE
 Factors arising before food reach stomach - think, tasting,
smelling, chewing & swallowing
 Increase in gastric secretion ( secretion of HCl &
pepsinogen)
 Via vagal stimulation :
- via intrinsic nerve stimulate chief & parietal cells to
increase secretion of HCI & pepsinogen
- stimulate PGA to release gastrin, where gastrin will further
increase secretion of HCI & pepsinogen
2. GASTRIC PHASE
• Factors resulted from the presence of food in the stomach
• Stimuli acting in the stomach [Pr-(peptide fragments)], distention,
caffeine, alcohol] increase gastric secretion
• Via vagal stimulation
- via intrinsic nerve stimulate chief & parietal cells to increase
secretion of HCl & pepsinogen
- stimulate PGA to release gastrin, where gastrin will further
increase secretion of HCl & pepsinogen
3. INTESTINAL PHASE

• Factors in duodenum after food left the stomach

- factors originating in the small intestine
• 2 components
I) excitatory II) inhibitory
POST-GASTRECTOMY SYNDROME

 Dumping syndrome
After meal all food will enter & absorb in small intestine
hyperglycemic insulin however 1.5 hours (early), 2-4
hours (late) after meal hypoglycemic
Symptom: weakness, dizziness & sweating after meal
Presence of hypertonic chyme in small intestine fluid will
enter the duodenal lumen plasma volume BV
CO
Symptom: dizziness, faint, cold sweat, pulse rate
Complications:

 Pernicious anemia - IF and vitamin B12

 Iron deficiency anemia (microcytic hypochromic anemia)
Gastric secretion provide suitable environment for
conversion of Fe3+ Fe2+ (absorbable form)
 Osteoporosis – rapid emptying  poor absorption of
calcium at the duodenum and proximal small bowel.
 Weight loss - anorexic, malabsorption
FUNCTION OF THE SMALL INTESTINE
Complete
- digestion
- absorption (most of water & electrolytes together
with all digestion product)
 Involves 2 types of motility
 Segmentation
 Peristalsis
 Factors affecting intestinal motility
 ANS stimulation
- increase/decrease motility
FUNCTION OF THE SMALL INTESTINE
 Factors affecting intestinal motility
 ANS stimulation
- increase/decrease motility
 Hormones
- Gastrin, CCK, insulin, serotonin - motility
- Secretin, glucagon - inhibit motility
 Hypokalemia ( K+ ECF) - paralytic ileus - motility
SECRETIONS OF SMALL INTESTINE
 Mucus
- secreted by the mucous gland (Brunner's gland) into the
lumen for protection of the mucosa

 Intestinal juices
- watery fluid containing Cl- & HCO3- secreted by the epithelial
cells lining the crypt of Lieberkuhn
- no digestive enzyme
 intestinal secretion - slightly alkaline (pH: 7.5-8.0)
 Digestion in small intestine lumen accomplished by the
pancreatic enzyme together with bile secretion that enhance
the fat digestion.
 The brush border contains the digestive enzymes
- enterokinase
Digestion of
- disaccharidases (maltase, lactase & sucrase) peptides & CHO
- aminopeptidases
 These enzymes complete the digestion process while the
food substance are being absorb through the epithelium.
REGULATION OF SMALL INTESTINE
SECRETIONS

 Local nervous reflex - esp. initiated by tactile or

irritative stimuli
 Hormone - secretin, CCK
 Distention
 Digestion & absorption of CHO

Glucose & galactose absorbed by energy dependant secondary

active transport & together with Na+ (co-transport)
Digestion & absorption of protein

Amino acid -absorbed by energy dependent secondary active transport & together with Na+
 Digestion & absorption of fat

Fat not soluble in water,  to be

digested & absorbed – need a
series of transformation:
i) emulsified with bile salt to form
small droplet
ii) digestion by pancreatic lipase
iii) carried in the form of micelles form
by bile salt together with other bile
constituent
iv) inside epithelial cell it is coated
with lipoprotein to form
chylomicrons & enter the central
lacteal via exocitosis
 Absorption of iron
• Proximal duodenum
• Require acidic environment
• Co-transport
 Absorption of water

 Massive quantity of
water
 Occur by osmosis
 Dependent on
absorption of solutes
 Diffusion is in response
to the osmotic gradient
established by sodium

Establishment of osmotic gradient

 Absorption of sodium
 Via passive or active mechanism
 Passive diffusion:
i) Na+ enter epithelial cells
ii) Na+ move from lumen to blood
through tight junction

 Active diffusion:
i) Na+ move through the cells -
energy dependent & carrier
ii) Na+ enter epithelial cells – co-
transported with glucose or a.a
 Absorption of calsium

 Via active & passive

mechanism
 Active:
- duodenum
- need carrier & vit D active
 Passive
- jejunum & ileum
- Ca+ move from high
concentration in lumen into
blood
 Absorption of vitamins

 Water soluble vit: B1, B2, Niacin, C, Folic acid, B6, B12
 Lipid soluble vit: A,D,E,K
 AIl vitamins are absorbed via passive mechanism
except:
- C - passive + active (Na+ dependent)
- B1 - active (Na+ dependent)
- B12 - combined with IF (at terminal ileum)
FUNCTION OF LARGE INTESTINE
 Absorption Na+ & Cl- absorption create
- H2O - osmosis osmotic gradient across
- Na+ mucosa thus causing H2O
absorption
- Cl- - enhance by aldosterone
 Form & store faces
- fecal material - undigested component (cellulose), bilirubin, remaining H2O &
NaCl & .......
 Secretion
- alkaline mucus solution
 Microbial fermentation
- digestion of indigestible component (cellulose) by bacteria
 Vitamin synthesis
- Vitamin K, folic acid, B complex vit.
MOTILITY
 Haustration / haustral movement
 Peristalsis
 Mass movement

SECRETIONS
 HC03-
- neutralize acid produced by bacterial fermentation
 Mucus
- protection against chemical & mechanical injury
* Secretion increase following mechanical & chemical stimulation
& controlled by nerve
Functions of intestinal bacteria

 Vitamin synthesis
- vitamin K, folic acid, B complex vit.
 Color of feces
- pigment formed by bacteria from the bile pigments
 Odor of feces
- peptides breakdown formed indole & skatole
 Gas production
- bacterial fermentation in colon
 PANCREATIC JUICE

 Contains water, bicarbonate & digestive enzymes

 Digestive enzymes include amylase for carbohydrate, trypsin for proteins,
and lipase for fats
 Brush border enzymes are also required for complete digestion
Exocrine pancreatic secretions contain enzymes for the digestion of proteins, carbohydrates,
and fats.
In addition there is also the secretion of modulator peptides that modulate the function of
pancreatic secretory products
Major enzymes
Protein digesting enzymes (proteases), which are stored and secreted in inactive form.
They comprise 80% of proteins secreted by the exocrine pancreas.
These include:

trypsinogen activated by trypsin

chymotrypsinogen activated by trypsin
procarboxypeptidase A and B activated by trypsin
proelastase activated by trypsin
Fat digesting enzymes include:
prolipase activated by bile salts
cholesterol estrase
prophospholipase A2

Carbohydrate digesting enzymes:

amylase
Modulator peptides

Procolipase
(It functions to prevent the inhibitory effect of bile salts on the lipase-
catalyzed intra-duodenal hydrolysis of dietary long-chain triglycerides. It is
required for optimal pancreatic lipase activity).

Trypsin inhibitors

Monitor peptide
(Monitor peptide is a 61 amino acid called trypsin-sensitive
cholecystokinin- releasing peptide that monitors the intake of dietary
protein and has the ability to stimulate the secretion of CCK-PZ and
pancreatic enzyme).

Bicarbonate
Albumin
Globulin
Water and electrolytes (Na+, K+ Cl-)

Volume about 1-2 litres per day.

The liver performs numerous important functions:

1. The liver produces and excretes bile required for emulsifying fats.

Some of the bile drains directly into the duodenum, and some is stored in the
gallbladder.

2. The liver performs several roles in carbohydrate metabolism:

Gluconeogenesis (the synthesis of glucose from certain amino acids, lactate or

glycerol)

Glycogenolysis (the breakdown of glycogen into glucose)

Glycogenesis (the formation of glycogen from glucose)

Storage of glycogen
3. The liver is responsible for protein metabolism:

Deamination and transamination of amino acids, followed by conversion of the non

nitrogenous part of those molecules to glucose or lipids.

Removal of ammonia from the body by synthesis of urea.

Synthesis of non-essential amino acids.

Synthesis of most of the plasma proteins (e.g. albumin).

Synthesis of clotting factors necessary for blood coagulation

(fibrinogen, prothrombin, V, VII, IX, X and XI, as well as protein C, protein S and
antithrombin).

4. The liver also performs several roles in lipid metabolism:

Cholesterol synthesis and production of triglycerides (fats).

 5. The liver breaks down haemoglobin, creating metabolites that are added to bile as
pigment (bilirubin and biliverdin).
6. The liver breaks down toxic substances and most medicinal products in a
process called drug metabolism.

7. The liver stores a multitude of substances, including glucose (in the form of
glycogen), vitamin B12, iron, and copper.

8. In the first trimester fetus, the liver is the main site of red blood cell production. By
the 32nd week of gestation, the bone marrow has almost completely taken over
that task.

9. The liver is responsible for immunological effects

- the reticuloendothelial system of the liver contains many immunologically
active cells, acting as a 'sieve' for antigens carried to it via the portal system.
METABOLISM OF HEME AND BILIRUBIN
BILE
1) Hepatocytes of the liver continuously
synthesize and secrete the constituents of bile
(bile salts, cholesterol, phospholipids, bile
pigments, ions, and water)

2) Bile  bile ducts  gallbladder (concentrates

the bile salts by absorption of water and ions).

3) Chyme reaches the small intestine  CCK 

(i) stimulates contraction of the gallbladder and
relaxation of the sphincter of Oddi, (ii) causing
stored bile to flow from the gallbladder into the
lumen of the duodenum (the bile salts emulsify
and solubilize dietary lipids).
BILE
4) Lipid absorption is complete bile salts
recirculated to the liver via the enterohepatic
circulation.

5) In the enterohepatic circulation (i) absorption of

bile salts from the ileum into the portal circulation
(ii) delivery back to the liver (iii) extraction of bile
salts from the portal blood by the hepatocytes
Regulation of bile secretion

Bile secretion by the liver and its release by the gall bladder.
MALABSORPTION SYNDROME
 Inability to absorb nutrients, vitamins and minerals from the intestinal tract into
the bloodstream.
 Causes:
 Diseases affecting intestines; celiac disease
 Absence or low levels of certain digestive enzymes
 Diseases of the pancreas; chronic pancreatitis
 Diseases caused by parasites; giardiasis
 Changes in bacteria in the intestinal tract
 Surgery; removal of gallbladder
 HIV