Stages of swallowing :-

1 ) oral ( voluntary )
2 ) Pharyngeal stage ( involuntary) :-
Swallowing centre in lower pons &medulla.
* Soft palat pulled upward to close posterior nares.
* Vocal cords approximated, larynx pulled up, swallowing apnea.
* Upper esophageal sphincter relaxes.
* Pharynx contracts.
3 ) Esophageal stage(involuntary) :-
Upper esophageal sphincter relaxes.
Primary peristalsis: continuation of pharyngeal peristalsis.
Secondary peristalsis: if primary fails to move food. (ENS, vagovagal)
Lower esophageal sphincter relaxes .
.

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 LES lower esophageal sphincter :

** It is a physiological sphincter.
** Prevents HCL regurge from stomach to the esophagus.
** Tone ++ by :-
- Hormones: Gastrin,Motilin.
- A.CH released from vagal nerve endings.

** Tone--- by :-
- Hormones: secretin, GIP, VIP, CCK, glucagon.

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- NO & VIP from interneurones innervated by vagal fibers.

Dysfunction of deglutition

(A) Dysphagia :-
- This is a condition of difficult swallowing. Dysphagia arises when transport
of liquid or a bolus of food along the pharyngoesophageal channel is
impaired.
- Causes:
• Lesions of the 9th or 10th cranial nerve (e.g. due to diphtheria).
• Damage of the deglutition centre (e.g. in poliomyelitis).
• Malfunction of the swallowing muscles (e.g. in myasthenia gravis).
• Esophageal strictures (= narrowing) e.g. cancer or ulceration.
Oropharyngeal dysphagia :-
* Tumor – Stenosis – Postsurgical – Radiation – Idiopathic
*Stroke - Head trauma – Parkinsonism - Myasthenia gravis

Esophageal dysphagia:-
Inflammatory and/or fibrotic strictures – Peptic ulcer – drug induced – Radiation induced –
Carcinoma.

(B)Achalisa :-
● Defintion :- lower esophageal sphincter fails to relax during swallowing. As a result,
food swallowed into the esophagus fails to pass from the esophagus into the stomach.
● Cause :-
Damage in the neural network of the myenteric plexus in the lower two thirds of the
esophagus.
As a result, the musculature of the lower esophagus remains spastically contracted.
● Clinical picture :-
Dysphaiga to liquids then solids .Over months and years, the esophagus becomes
tremendously enlarged until it often can hold as much as 1 liter of food.
● Complications :-
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Ulceration of esophagus
Substernal pain even rupture and death.
● Investigations of achalasia :-
Barium swallow show parrot peak
Endoscopy.

● Treatment :-
1- Stretching the lower end of the esophagus by means of a balloon inflated on the end
of a swallowed esophageal tube.
2- Antispasmodic drugs (i.e., drugs that relax smooth muscle) can also be helpful.

C) Aerophagia:
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It is swallowing of excess air e.g. in nervous people who hyperventilates.

Disorders of Esophagus

GERD “ gastroesphageal reflux disease “

 Defintion :- reflux of acidic gastric content Into esophagus .

 Pathophysiology:-
Decreased tone of LES .

● Risk factors :-
Smoking _ Coffee _ Pregnancy _ Obesity .

● Clinical picture :-
Heart burn _ Chest pain _ Dysphagia _ Cough .

● Complications:-
Ulceration and stricture of Esophagus .
Barret’s esophagus .

● Investigations >> Manometery .

●Treatment :-
life style modification
Medications such as Dompridione

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 Disorders of the Stomach

Gastritis :-
● Defintion :- Inflammation of the Gastric Mucosa.

● Pathophysiology :-
The inflammation of gastritis may be only superficial and therefore not very harmful, or it
can penetrate deeply into the gastric mucosa, in many long¬standing cases causing almost
complete atrophy of the gastric mucosa.

● Gastric Barrier and Its Penetration in Gastritis:

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 1- Stomach is lined with highly resistant mucous cells that secrete viscid and adherent
mucus.
2- It has tight junctions between the adjacent epithelial cells.
The gastric barrier normally is resistant enough to diffusion of hydrogen ions in gastric
juice .
But In case of gastritis, the permeability of the barrier is greatly increased. The hydrogen
ions do then diffuse into the stomach epithelium, leading to a vicious circle of progressive
stomach mucosal damage and atrophy. It also makes the mucosa susceptible to digestion
by the peptic digestive enzymes, thus frequently resulting in a gastric ulcer.

● Causes :-
- Chronic bacterial infection of gastric mucosa.
- Ingested irritant substances can be especially damaging to the protective gastric mucosal
barrier.
- Two of the most common of these substances are excesses of alcohol or aspirin.
- Stress.

Complications :-

Chronic Gastritis Can Lead to Gastric Atrophy and Loss of Stomach Secretions .

Achlorhydria and Hypochlorhydria:

Achlorhydria means simply that the stomach fails to secrete hydrochloric acid .
it isdiagnosed when the pH of the gastric secretions fails to decrease below 6.5 after
maximal stimulation .

Gastric Atrophy May Cause Pernicious Anemia:

Gastric Atrophy means failure of secretion of intrinsic factors
That means failure of absorption of vitamin b 12 , As a result pernicious anemia is
developed .

Peptic ulcer :-
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It is known as a defect in mucosa of git ( Stomach or dudoneum ).

Pathophysiology :-
Damage of gastric mucosal barrier by following mechanisms :-
1 ) H . Pylori which is gram -ve bacili
Increased gastric >> increased HCL
Decreased somatostatin >> increased histamine & gastrin
Urea secretion > increased PH and helps bacteria to peneterate mucosa .
2 ) NSAID >> decreased COX that decrease prostaglandin that decrease mucus secretion ,
HCO 3 and blood supply .
3 ) Smoking >> decreases ulcer healing and increases rate of reccurrence .
4 )Alcohol

Clinical picture :-
1 ) Epigastric Pain , nausea , and vomiting .
2) Bleeding > chronic blood loss > Iron deficiency anemia .

Investigations :-
1) Barium meal
2) Endoscopy
3) Detection of H.pylori by
a- + Ve urease test
b- Stool analysis

Complications :-
Hemorrhage * Fibrosis * Malignancy * Perforation .

Treatment :-
1) Trials to decrease gastric acid secretion
( ex :- use of proton pump inhibtors and H2 receptor blockers )
2)Eradication of H.pylori by antibiotics
3) Milk >> ceratin protein >> buffers acidity .
4) Avoiding Aspirin , Alcohol and Coffee.

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5) Parasympatholytics .
6 ) Anti acids ( Alumium Hydroxide ) .
7 ) Surgical.

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[ Intestinal malabsorption syndrome ]

 Occasionally, nutrients are not adequately absorbed from the small intestine even
though the food has been well digested ..
 Several diseases can cause decreased absorption by the mucosa; they are often
classified together under the general term “sprue.”
 Malabsorption also can occur when large portions of the small intestine have been
removed ..

 Early stages of sprue :-

Intestinal absorption of fat is more impaired than is absorption of other digestive products.
The fat that appears in the stools is almost entirely in the form of salts of fatty acids rather
than undigested fat, demonstrating that the problem is one of absorption, not of digestion.
In fact, the condition is frequently called steatorrhea, which means simply excess fats in the
stools.

 In severe cases of sprue :-

In addition to malabsorption of fats, impaired absorption of proteins, carbohydrates,
calcium, vitamin K, folic acid, and vitamin B12 also occurs.
As a result, the person experiences the following:
A - Severe nutritional deficiency, which often results in wasting of the body.
B - Inadequate blood coagulation caused by lack of vitamin K.
C - Macrocytic anemia of the pernicious anemia type, resulting from diminished vitamin
B12 and folic acid absorption.

Types of sprue :-

1 ) Tropical sprue :-
Occurs in the tropics and can often be treated with antibacterial agents.
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Even though no specific bacterium has been implicated as the cause, it is believed that this
variety of sprue is usually caused by inflammation of the intestinal mucosa resulting from
unidentified infectious agents .

2) Non Tropical Sprue :-

It is called variously celiac disease, idiopathic sprue, or gluten enteropathy.
Results from the toxic effects of gluten present in certain types of grains, especially wheat
and rye.
Only some people are susceptible to this effect, but in those who are susceptible, gluten has
a direct destructive effect on intestinal enterocytes.

Megacolon ( Hirschsprung’s disease )

• Cause:
Lack of or deficiency of ganglion cells in the myenteric plexus in a segment of the sigmoid
colon.
As a consequence, neither defecation reflexes nor strong peristaltic motility can occur in
this area of the large intestine.
The sigmoid becomes small and almost spastic while feces accumulate proximal to this
area, causing megacolon in the ascending, transverse, and descending colons.

 Symptoms :
Severe constipation that bowel movements occur only once every several days or
sometimes only once a week.

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•This phenomenon allows tremendous quantities of fecal matter to accumulate in the colon,
causing the colon sometimes to distend to a diameter of 3 to 4 inches.

• Therapeutic highlights :-
The symptoms of Hirschsprung disease can be relieved completely if the aganglionic
portion of the colon is resected and the portion of the colon above it anastomosed to the
rectum. However, this is not possible if an extensive segment is involved. In this case,
patients may require a colectomy.

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