Dr. M. H.

GIT

General GIT functions: -

❖ Mouth – pharynx – oesophagus:
▪ Chewing.
▪ Saliva formation (starts digestion of CHO).
▪ Swallowing (deglutition).
❖ Stomach:
▪ HCL production.
▪ Gastric juice which breaks down proteins.
❖ Small intestine:
▪ In which the process of digestion is completed (CHO →
glucose & proteins → a.as and Fats → FFa and glycerol).
▪ Contain villi and microvilli that undergoes the function of
ABSORPTION.
▪ Secretion of intestinal juice.
❖ Large intestine: Storage of undigested food and defecation
❖ Pancreas:
▪ Release digestive alkaline juice that helps in digestion of
(CHO, Fat & proteins).
▪ It’s the most alkaline fluid in the body PH=8.3
▪ It’s the most important digestive organ.
❖ General functions of GIT:
1- motility 2- digestion. 3- secretion 4- absorption.
❖ Liver:
▪ Largest gland in the body.
▪ Functions:
✓ Formation of lipoproteins, plasma proteins, Urea (to be
excreted in urine).
✓ Storage of glucose in the form of glycogen (important for
glucose homeostasis)
✓ Detoxification of toxic substances.
✓ Destruction of multiple hormones and drugs.
✓ Bile formation and release.

1
 Dr. M. H. GIT

✓ Conjugation of bilirubin.
✓ Synthesis of bile
✓ Share in activation of vit D
✓ Storage of iron & vit B12
✓ Synthesis of 15,4 erythropoietin hormone

1) Salivary secretions
➢ Function:
1. Lubrication helps (swallowing - speech)
2. Protection:
a. Against microorganisms as bacteria by the presence of
IgA and lysozymes.
b. against dental caries.
3. Excretion: of some toxic substances e.g., mercury and lead.
4. Water balance and temperature control specially in
panting animals as dogs
5. starts digestion of starch by salivary amylase.

➢ Formation and compassion

• Saliva is 99.5 % water and 0.5 %electrolytes and proteins.
• Saliva contains
- Serous secretion: alpha amylase (ptyalin) for digestion of
carbohydrates.
- Mucous secretion: mucin for lubricant function of saliva.
NB: - Parotid secrets only serous secretion, while
submandibular and sublingual glands secrete
both serous and mucous scallion.
• Saliva is formed by acini (1ry salivary secretion) which is
similar to plasma in electrolyte composition (isotonic) and in
PH.

2
 Dr. M. H. GIT

• The composition of saliva is modified during its passage in

the ducts of the glands and is called (2ry. salivary
secretion) which is characterized by: -
↓ Na+ & ↓ Cl- → (hypotonic)
↑ K+
↑ HCO3- → (more alkaline)
• Volume = 1 – 1.5 L/day
•PH = 8 (alkaline)
• After discharge of 1ry saliva form the acini, it becomes
modified within the duct cells as follows:
1. Active reabsorption of (Na+) by using Na+ - K+ pump.
2. Secretion of (K+) against (H+) by H+/K+ exchange
3. Secretion of (HCO3-) against Cl- reabsorption.
• So the 2ry saliva becomes:
poor in Na+&CI- (NaCl) & rich in K+ & HCO3- (KHCO3).

➢ Regulation: Regulation of saliva is only nervous

❖ Nervous regulation: -
1- Autonomic:
✓ Sympathetic: low vol. ↑ mucous and increase viscosity
and enzymes.
✓ Parasympathetic:
3
 Dr. M. H. GIT

▪ Major role (responsible for basal continuous salivary

secretion).
▪ Large volume (increased flow) + ↑ (electrolytes & water)
Sympathetic and parasympathetic nerves are
complimentary on salivary secretion.
2- Conditioned and unconditioned reflexes (discuss....)

❖ Conditioned reflex: (need cortical experience)

• Stimulus: smelling or hearing or vision of food.
• Receptors: olfactory or hearing or photoreceptors.
• Afferent: olfactory nerve - cochlear nerve – optic nerve.
• Center: cerebral cortex which has the memory of food
and stimulates brain stem centers.
• Efferent: 7th -9th cranial nerves for salivary glands and 10th
(vagus nerve) for GIT.
• Response: increased salivary secretions and GIT functions
(motilities and secretions).

❖ Unconditioned reflex: (doesn’t need cortical experience)

• Stimulus: food in mouth.
• Receptors: taste and receptors and touch receptors.
• Afferent:
7th, 9th and 10th cranial nerves for taste
5th cranial nerve for touch of food
• Center: medulla oblongata (brain stem).
• Efferent: 7th -9th cranial nerves for salivary glands and the
10th cranial nerve (vagus nerve) for GIT.
• Response: increased secretions and GIT functions.

4
 Dr. M. H. GIT

➢ xerostomia
Decreased salivary secretion (dry mouth) which leads to bad odor
of mouth, dental caries, difficult chewing, swallowing and speech.

Chewing:
➢ Function: -
1- Grinding of food
2- Mixing food with saliva
3. Stimulate taste buds
➢ mechanism: -
▪ It may be voluntary but mostly it is rhythmic contraction
of muscles of mastication (reflex) through pressure of
food on oral tissues.
➢ Chewing reflex: -
Bolus of food causes reflex inhibition of jaw muscles --->
drop the mandible --> stretch of muscles of mastication
--> contraction of muscles of mastication --> compression
of bolus of food in mouth --> reflex inhibition of jaw
muscles again and the cycle will be repeated.

Deglutition = Swallowing
➢ Process of moving bolus of food from mouth to stomach.
➢ Center: - it is controlled by deglutition center in brain stem
(medulla oblangata).
➢ Phases: -
o Buccal
o Pharyngeal
o Esophageal
1) Buccal phase
o It is voluntary phase
bolus
5
 Dr. M. H. GIT

o Mouth pharynx
o Mechanism: Tongue pushes the bolus into pharynx by
moving upward and backward.
o Duration: less than one second.

2) Pharyngeal phase
o It is involuntary phase induced by contact of the bolus of
food with the pharyngeal mucosa.
o It leads to passage of food from pharynx to upper esophagus.
o The passage of bolus into esophagus and inhibited to
direct in false passages as follows
o Nose (posterior nasal opening) closed by elevation of soft palate.
o Mouth: closed by continuous elevation of tongue
against the hard palate
o Larynx (glottis): closed by:
1. Upward elevation of the glottis and downward
movement of the epiglottis
2. Approximation of the vocal cords.
3. Temporary inhibition of respiration (apnea) by
inhibition of respiratory center
o Bolus is then pushed into the esophagus by peristaltic
movement of pharyngeal muscles with relaxation of
upper esophageal sphincter.
o This action is mediated by pharyngeal reflex
- Stimulus --> contact of food with pharyngeal mucosa
- Receptor --> touch and pressure receptors
- Afferent --> 9th and 10th crania nerves.
- Center --> deglutition center in medulla oblongata |
- Efferent --> 9th and 10th nerves.

6
 Dr. M. H. GIT

- Response --> pharyngeal peristalsis and relaxation of

upper esophageal sphincter.

3) Esophageal phase
o It is involuntary phase induced by contact of bolus of
food with esophageal mucosa.
Bolus
o Aim: bolus from esophagus stomach
Peristaltic movement
o travelling of bolus along esophagus is mediated by
peristaltic movement (2-4 cm/sec) and helped by
gravity. This is accompanied by relaxation of lower
esophageal sphincter (LES).

Types of esophageal peristalsis

1ry peristalsis 2ry peristalsis
Contact of food with Distention of esophagus
Stimulated by pharyngeal mucosa or a with bolus
new reflex
It Is continuity of It occurs following the 1ry
peristaltic movement of peristalsis
Nature:
pharyngeal ms or new
reflex
Depends on vagal supply Depends on both:
to esophageal ms 1. Myenteric plexus i.e.
Mech:
local reflex
2. Vagus nerve

7
 Dr. M. H. GIT

N.B.:
lower esophageal sphincter (LES): -
✓ Relaxation of lower esophageal sphincter is controlled by
vagus nerve (which is chemically mediates) by the release
of VIP and nitric oxide (NO) as neurotransmitter.
✓ LES is always closed (except during swallowing) to prevent
reflux of acidic contents of stomach into esophagus.

o Nervous pathway of deglutition:

pharyngeal and esophageal phases occur reflexly and
controlled by deglutition center in MO.
- Stimulus: bolus inside the pharynx and eosophagus.
- Receptors: in the pharyngeal and esophageal mucosa
- Afferent: 9th and 10th cranial nerve
- Center: deglutition center (in medulla oblongata)
- Efferent: 9th and 10th cranial nerve
- Effector: pharyngeal and esophageal ms causing contraction
and peristaltic movement.

N.B.:
In cases of vagotomy, deglution is impossible in upper ½ of
esophagus which depends completely on vagal reflexes.
Therefore, food should be intubated to lower 1/2 of
esophagus which may work by local enteric plexus of nerves
(independent on vagus).

Abnormalities of swallowing: -
1) Achalasia = failure of LES relaxation:
- Due to lack of parasympathetic ganglia or receptors at the LES.
- It may lead to distension of esophagus followed by food
putrefaction —> esophageal rupture —> mediastinitis —>
death.

8
 Dr. M. H. GIT

- Treatment: cardiomyotomy (surgical — or using botox)

2) Reflux esophagitis (Gastroesophageal regurge disease =GERD):
- LES incompetence —> regurge of gastric juice and HCl into lower
part of esophagus —> inflammation and pain.
- It may associate obesity - smoking increased gastric acidity - stress.
- Treatment: treat the cause and antacids.
3) Dysphagia:
- Painful swallowing due to inflammation condition as in
pharyngitis.
Vomiting (emesis)
❖ Definition: expulsion of gastric contents out through mouth.
❖ Centre: vomiting center in MO.
❖ Preceded by: profuse salivation, nausea, tachycardia and sweating.
❖ Such symptoms are due to generalized autonomic stimulation.
❖ Vomiting reflex: -
o Receptors inside and outside GIT.
o Afferent vagal (or) sympathetic nerves.
o Centre vomiting center in MO
o Efferent (motor somatic and vagal nerves) to:
1- Contract abdominal muscles and diaphragm to
increase intra-abdominal pressure.
2- Relax gastric wall, LES and esophagus.
❖ Act of vomiting:
1. Deep inspiration.
2. Closure of glottis with upward and anterior shift of larynx
-To be covered by epiglottis
-To open upper esophageal sphincter.
3. Soft palate -→ elevated to close nasopharynx.
4. Contraction of diaphragm and anterior abdominal wall
muscles → ↑↑↑ intra-abdominal pressure > squeezing
of the flaccid gastric wall (passive).

9
 Dr. M. H. GIT

N.B.: The stomach is lax and flaccid while the surrounding

muscles are contracted
N.B.: Duodenal contraction may force its contents back into
stomach [the color of vomitus becomes yellowish green (bile)]

❖ Causes of vomiting:
1. Irritation of dorsum of tongue and throat.
2. Irritation of gastric wall e.g. (high salt) or gastritis.
3. ↑↑ intracranial tension.
4. Severe pain as in renal colic.
5. Psychic vomiting (e.g., sight of blood —bad odor).
6. Chemoreceptor trigger zone CTZ stimulation. E.g. by drugs,
chemotherapy, accumulation of toxins as in renal failure
(uremia) and increased HCG hormone in pregnancy.
▪ Stimulated CTZ then send impulses to vomiting center
(VC) → vomiting
▪ Such chemicals cannot affect VC directly (because they
can’t pass BBB).
7. Motion sickness: sudden rotation of head —> stimulate
labyrinth -→ +++ VC -→ vomiting.
❖ Complication of vomiting:
1. Dehydration.
2. Loss of weight.
3. Alkalosis due to loss of HCL.
4, Electrolyte disturbance.

Peptic ulcer
❖ Occur due to increase the rate of mucosal cell damage and
death (by HCl) more than the rate of their renewal.
❖ Protective measures against peptic ulcer
1. Thick mucosal barrier (chemical — mechanical protection).

10
 Dr. M. H. GIT

2. Rapid renewal of mucosal epithelium.

3. Tight junction between epithelial cells.
4. Pepsinogen is inhibited to be autoactivated within the cells by
mucus effect.
5. Apical surface of mucosal epithelium is impermeable to H+
ions.

Phases and regulation of gastric secretion

- There is a basal secretion of gastric juice highest at early morning
(5- 11am). Lowest at early night (7-12 pm)
- There are 3 phases for regulation of gastric secretion:
a) Cephalic phase 30%:
- Conditioned and unconditioned reflexes stimulate
gastric secretions through vagus nerve. (Discuss
reflexes......)
b) Gastric phase 60%:
- Presence of food in stomach leads to direct mechanical
stimulation of G cells releasing Gastrin hormone.
c) Intestinal phase: Presence of food in intestine leads to: -
▪ Nervous: (enterogastric reflexes initiated by
hyperosmolarity & acidity in duodenum of fat content).
▪ Hormonal: (enterogastrone hormones GIP - VIP -
secretin & CCK).
Both are inhibitory (Inhibits gastric motility and secretions)

Pancreatic secretion
Pancreas acts as both endocrine and exocrine (mixed) gland.
❖ Regarding the exocrine functions:
❖ The exocrine pancreatic secretions = 1-2 L/day

11
 Dr. M. H. GIT

❖ PH > 8 and may reach 8.3 (alkaline)

❖ The pancreatic juice is rich in:
o Enzymes --> important for digestion of all food stuffs e.g.
(amylase for CHO digestion, Lipase for Fat digestion &
peptidases (proteolytic enzymes) for protein digestion).
Pancreas is the most important digestive organ in the body.
- Pancreatic amylase and lipase are secreted into the
duodenum in the active form, while, trypsinogen and
other proteolytic enzymes are secreted in the inactive
form to inhibit pancreatic autodigestion.
- Activation of trypsinogen occurs within the duodenum into
trypsin. Trypsin then auto activates more trypsinogen into
trypsin and also it activates other proteolytic enzymes.
o Bicarbonates (NaHCO3) --> PH of pancreatic juice >>> 8.3
>>> most alkaline fluid in the body to neutralize gastric
acidity and to provide an optimum PH for the action of
pancreatic enzymes.
o Water and electrolytes.
❖ The most important regulator for pancreatic secretion rich
in enzymes is CCK hormones with acts on acinar cells this
action is mediated by IP3 and Ca++
❖ While the most important regulator for pancreatic rich in
bicarb is secretin which acts on duct cells. This action is
mediated by CAMP.

12
 Dr. M. H. GIT

Pancreatic juice rich in

Pancreatic juice rich in
bicarb and other
enzymes
electrolytes
Secreted by Acinar cells Duct cells
Stimulated by CCK and acetylcholine Secretin hormone
2nd messenger IP3 and Ca++ CAMP

N.B: -
▪ Steatorrhea is failure of fat digestion & absorption and
characterized by:
- Offensive fatty stool.
- Deficiency of fat-soluble vitamins as vit, K (bleeding tendency)
and vit. D (Rickets and osteoporosis)
▪ It may be due to
- Acute pancreatitis or pancreatic failure due to lack of
pancreatic lipase
- Obstruction of common bile duct due to lack of bile salts

Regulation and phases of pancreatic secretion

a) Cephalic 20%:

13
 Dr. M. H. GIT

- Conditioned and unconditioned reflexes .............. discuss.

- Autonomic control: parasympathetic stimulates while
sympathetic inhibits pancreatic exocrine secretions.
b) Gastric 10%:
- (Gastro — pancreatic) reflexes: Presence of food in
stomach stimulates pancreas through such short reflex
mediated by local enteric plexus of nerves.
- Gastrin hormone also potentiates pancreatic secretion.
c) Intestinal 70%:
- Nervous: enteropancreatic reflexes.
Presence of food in intestine stimulates pancreas through
this short reflex mediated by local enteric plexus of nerves.
- Hormonal:
➢ CCK increases pancreatic juice rich in enzymes in
Response to increased duodenal fat content and
products of protein digestion.
➢ Secretin increases pancreatic juice rich in
bicarbonates in response to increased duodenal
acidity by the acid chyme.

Hormonal control of GIT

Gastrin:
▪ Released from: stomach mainly
▪ Actions:
o Stimulation of gastric motility and secretions (HCL - pepsin)
o Stimulation of intestinal motility
o Trophic on the pancreatic (endocrine, ↑ insulin secretin
and exocrine secretion)
CCK
▪ Cholecystokinin is released from upper small intestine in
response to increased fat content of duodenum.

14
 Dr. M. H. GIT

1. As an intestinal hormone, it (↑) intestinal activities (↓)

gastric activities.
2. It stimulates gall bladder (squeezes its wall) and inhibits
the sphincter of Oddi >>> evacuation of gall bladder.
NB: the name of the hormone indicates the function
(cholecyst means gall bladder and kinin means increased
contraction)
3. It increases pancreatic secretion rich in enzymes.
Secretin hormone
Released from upper part of small intestine in response to
presence of acidic PH and/or protein fractions:
1. As an intestinal hormone, it stimulates intestinal
activities and inhibits gastric activities.
2. (secretin >>> ↑ secretions) (+) Bile secretion by liver
cells and (↑) pancreatic secretions rich in HCO3
3. Both secretin and CCK potentiate each other.

15