Gastro Intestinal

Disorders
 Introduction

• The digestive system provides the body with nutrients

and water as well as various vitamins and minerals
• It consists of the alimentary canal (= gastro-intestinal
tract or GIT) and the glands that secrete digestive
juices in it (= salivary glands, liver and pancreas).
• The GIT extends from the mouth to the anus, it
includes: the buccal cavity, pharynx, esophagus,
stomach, small intestine and large intestine (= colon)
which ends by the rectum and anal canal
 SWALLOWING DISORDERS

DYSPHAGIA
This is difficult swallcwing. Its common causes are
the following :
• Lesions of the 9th or 10th cranial nerves (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. due to
cancer or scarring.
 ACHALASIA ( CARDIOSPASM)
• This is a condition characterized by increased resting
tension in the LES. As a result, food transfer from the
esophagus to the stomach is delayed or blocked, so food
accumulates in the esophagus and, accord­ingly, it becomes
severely dilated.
• The condition is due to deficiency of NO and VIP as a result
of defective development of the myenteric plexus in the
lower part of the esophagus. It can be treated by either (a)
Pneumatic dilatation of the LES or (b) Incision of the
esophageal muscle ( myotomy).
 PEPTIC ULCER

This is erosion of an area in the mucosa of the stomach,

duodenum or esophagus due to autodigestion by the
gastric juice.
• It occurs as a result of an imbalance between the rate
of gastric secretion and the degree of mucosal
protection against autodigestion due to one of the
following causes :
• Excessive gastric secretion due to either
(1) Hereditary factors
(2)Prolonged stress, depression or anxiety
(3) Increased gastrin secretion from certain tumours
called gastrinomas (Zollinger-Ellison syndrome).
 Excessive exposure of the mucosa to the gastric juice : This
is the main cause of
(1) Esophageal ulcers (due to frequent gastroesophageal
reflux of the gastric juice)
(2) Duodenal ulcers (due to deficiency of the defensive
mechanisms that decrease duodenal acidity).
Disruption (breakdown) of the mucosal barrier : This is the
main cause of gastric ulcers, and it may occur due to
either :
• Decreased mucus secretion (or secretion of an abnormal
mucus).
• Excessive intake of gastric irritants (e.g. alcohol, vinegar
• Excessive intake of aspirin. This irritates the
gastric mucosa and inhi­bits synthesis of
prostaglandins, which normally decrease HCl
secretion by antagonizing the action of
histamine
• Infection of the gastric mucosa with certain
types of bacteria (helicobacter pylori).
• Excessive smoking (due to increased nervous
stimulation of gastric secretion) and alcohol
(which breaks down the mucosal barrier).
 Physiology of treatment of peptic ulcer
• Sedatives (which help to relieve depression,
anxiety and stress).
• H2 receptor blockers which prevent the action of
histamine (e.g. cimetidine, ranitidine and
famotidine).
• Prostaglandin agonists (e.g. misoprostol).
• H+-K+ ATPase blockers (e.g. omeprazole).
• Drugs that increase the mucosal resistance to acid
by forming adherent protein complexes at the
sites of ulcers (e.g. sucralfate).
• Antacid drugs (commonly aluminium or
 VOMITING
• This is reflex expulsion of the gastric contents
outwards through the mouth and it often starts
with the sensation of nausea.
• The act of vomiting is controlled by a vomiting
centre located in the medulla oblongata.
Excitation of this centre leads to the following
effects that result in vomiting (through
discharging impulses in the 5th, 7th, 9th, 10th
and 12th cranial nerves and the spinal nerves that
supply the diaphragm and abdominal muscles)
• Forced inspiration (which moves the diaphragm
downwards)
• Closure of the glottis and elevation of the soft palate to
prevent the vomitus to enter the trachea and nasal
cavities (as occurs in deglutition).
• The body of the stomach and cardiac sphincter relax
while the pyloric antrum contracts at the incisura
angularis .
• The abdominal wall muscles contract. This together with
the down­ward movement of the diaphragm markedly
increase the intraabdominal pressure.
• The raised intra-abdominal pressure squeezes the relaxed
stomach leading to ejection of its contents into the
esophagus then outwards.
 There are 2 main causes of vomiting :
1.Reflex vomiting : This may occur as a result of either :
• Conditioned reflexes (psychic vomiting) e.g. certain scenes
or nauseating smells may induce vomiting.
• Unconditioned reflexes : A wide variety of conditions initiate
signals that are discharged via afferent nerves to the medulla
oblongata where they stimulate the vomiting centre,
resulting in vomiting e.g. :
• Gastric irritation, peritonitis and intestinal obstruction (by
impulses discharged in afferent sympathetic and
parasympathetic nerve fibres).
• Irritation of the posterior part of tongue and oropharynx.
• Myocardial infarction.
• Motion sickness (by impulses from the semicircular canals).
2.Central vomiting : Certain nervous diseases (e.g.
meningitis, migraine and increased intracranial
tension) and drugs (eg. apomorphine and digitalis)
induce vomiting by exciting the vomiting centre. These
drugs are called emetic drugs and they do not
stimulate the vomiting centre directly. They first
stimulate a nearby area in the medulla called the
chemoreceptor trigger zone (CTZ) which, in turn,
stimulates the vomiting centre.
Stimulation of the semicircular canals induces vomiting
also by stimulating the CTZ. Stimulation of this zone is
also the cause of vomiting in pregnancy, uremia and
diabetic ketoacidosis.
 FUNCTION OF VOMITING

• In cases of irritation of the upper part of the GIT

(which is the commonest cause of vomiting),
vomiting provides rest and helps to drive out
the irritant However, in many conditions,
vomiting performs no function e.g. in pregnancy,
myocardial infarction and motion sickness.
 Effects of excessive (or prolonged) vomiting

1.Dehydration. (2) Loss of electrolytes (specially

Na+and K+).
3.Alkalosis, due to loss of H+ (HCI).
Treatment of vomiting
1.Treatment of the cause. 2. Vomiting can be
stopped by certain drugs that inhibit the vomiting
centre ( anti-emetic drugs) e.g. chlorpromazine.
• The effects of vomiting can be corrected by
supplying fluids, electro­lytes (specially K+) and
acidifying salts (to prevent alkalosis).
 Effects of extirpation (damage) of the pancreas

• Diabetes mellitus due to lack of insulin

• Digestive and nutritional disturbances : The
various food constituents are not properly
digested leading to deficient absorption and loss
of considerable amounts of the ingested protein
and fat in the feces.
• Fat loss causes steatorrhea (fatty diarrhea) in
which the feces becomes bulky, pale, loose and
greasy, and the result is marked undernutrition.
 Effects of loss of the pancreatic juice

• This often occurs secondary to severe diarrhea,

and it leads to :
• Marked digestive and nutritional disturbances
(see above)
• Dehydration due to the large volume of the juice
• Acidosis due to loss of NaHCO3.
 Examination of the pancreas
Examination of the pancreas can be achieved by :
• Ultrasonography : This is specially helpful in detection of
pancreatic masses.
• Stool analysis : In cases of pancreatic insufficiency, the stool
contains excessive amounts of undigested protein and fat
( steatorrhea) and becomes bulky, pale, loose and greasy.
• Estimation of the amylase and lipase blood levels : These
enzymes are normally present in the blood but in very small
amounts. They are markedly increased in conditions of
pancreatic duct obstruction and in cases of acute pancreatitis
particularly amylase.
• Studying pancreatic functions by tests like the secretin test
and analysis of the duodenal contents is no longer used now.
 Examination of the gallbladder

This can be achieved by the following methods

1.Ultrasonography
2.Tomography (CT) .
3.Nuclear cholescintigraphy (gallbladder
visualization by isotopes).
 JAUNDICE (ICTERUS)
• This is a disease characterized by a yellowish
colouration of the skin, mucous membranes and
sclera of the eye due to presence of excessive
amounts of bilirubin in the blood.
• Normally, the total bilirubin serum level is normally
0.5 (up to 1) mg %. Jaundice appears when this
concentration rises to 1.5 - 2 mg
• Depending on the cause, jaundice can be classified
into 3 types:
1.Hemolytic (prehepatic) jaundice.
2. Hepatocellular (hepatic) jaundice.
3. Obstructive (posthepatic) jaundice
 Effects of obstruction of the common bile duct

1.Obstructive jaundice .
2.Impaired liver functions (due to back pressure on the liver cells).
3.Decreased flow of bile salts into the intestine, which causes :
a.Deficient fat digestion and absorption: As much as 50 % of the
ingested fat is lost in feces leading to steatorrhea (fatty
diarrhea).
b.Deficient absorption of fat-soluble vitamins (vitamins A, D, E, K)
leading to signs of their deficiency.
c.Protein putrefaction (page 39).
d.Constipation (due to absence of the laxative effect of bile salts).
• Pruritis ( itching) and bradycardia : These are produced by the
excessive amounts of bile salts in the bloodstream (as a result
of their regurgitation from the bile canaliculi).
 Differences between the 3 types of jaundice

Hemolytic j. Obstructive j. Hepatic j.

Cause Excessive RM3.C.S breakdown Obstruction of the common bile Liver disease

duct

Cause of yellow colour Increased serum hemobilirubin Increased serum cholebilirubin Increased serum cholebilirubin

and hemobilirubin

Depth of colour Mild Severe Moderate

Van Den Berg test Indirect Direct Biphasic

Fat digestion Normal Markedly impaired Moderately impaired

Liver functions Normal Moderately impaired Markedly impaired

Urine colour Normal (acholuric) Dark brown brownish

Urine foam White Intense yellow Yellowish

Stool colour Dark Very pale Pale

Blood Anemia, reticulo- cytosis and Marked Increase in cholesterol, Moderate increase in cholesterol,

may be the cause of hemo­lysis alkaline phosphatase and bile alkaline phosphatase and bile

salts salts
 THE LIVER FUNCTION TESTS

Tests depending on estimation of enzymes

• The serum levels of the following enzymes increase in
liver disease :
1.The transaminases : These include 2 enzymes :
a- Alanine aminotransferase (ALT) : This is also called
GPT (glutamic pyruvic transaminase) and its normal
serum level is 3 - 48 units / litre
b- Aspartate aminotransferase (AST) : This is also
called GOT (glutamic oxalacetic transaminase and its
normal serum level is 0-55 units / litre.
2. The alkaline phosphatase (normal level 13-39 units /
litre).
Tests depending on determination of the plasma proteins
1.Determination of serum albumin level : This is decreased
in liver disease (normal amount 3.1 - 4.3 gm %).

2.Determination of albumin/globulin (A/G) ratio : This ratio

(which is normally 1:2-1.6) is lowered in liver disease
because albumin synthesis is decreased (refer to blood).

3.Determination of prothrombin level and prothrombin

time : In liver disease, the plasma prothrombin level
(which is normally 10-15.mg %) is lowered and the
prothrombin time (which is normally 12 seconds) is pro­
longed (see in blood) and such disorders are not corrected
by vitamin K.
 Tests depending on metabolic functions
• The galactose tolerance test :
The fasting subject ingests 40 gm galactose in 400
ml water and its blood level is determined every
1/2 hour for 2 hours. Normally, it rises slightly
within one hour then falls within 2 hours, and
the sum of the 4 values (galactose index) should
not exceed 160 mg %. Such index rises in cases
of liver disease due to inability of the liver to
convert galactose to glucose.
 Tests depending on detoxification functions
• The hippuric acid excretion test:
A test dose of Na benzoate is given to the subject (orally or i.v.) and the
hippuric acid is estimated in the urine after one hour. Normally, its excretion
should markedly increase, but in liver disease no or insignificant increase
occurs because of inability of the liver to conjugate benzoate to glycine.
Tests depending on hepatic excretory functions
a. Determination of the serum bilirubin level : The total serum bilirubin level
(conjugated and unconjugated) is normally up to 1 mg % while the level of
conjugated bilirubin only is up to 0.4 mg %. Total bilirubin increases in liver
disease mainly due to increased amount of the unconjugated part
(hemobilirubin) as a result of failure of the liver cells to extract it from the
blood. The conjugated part (cholebilirubin) level specially increases if there is
intrahepatic biliary obstruction .
b.Bromsulphalein retention test : Bromsulphalein is a dye that is excreted by
the liver in bile. A test dose of this dye is i.v. injected and its concentration in
the blood is estimated after one hour. Normally, only 0 % of the injected
dose is retained in the blood, but in liver disease a greater amount is
retained.
 Adynamic ileus ( paralytic ileus)
This is a condition of marked decrease of intestinal
motility that may occur after abdominal
operations. It occurs as a result of either
(1) Intestinal trauma which inhibits the smooth
muscle directly or through activation of the opiod
receptors
(2) Peritoneal irritation which causes re­flex
inhibition of the intestinal muscle through
increased discharge of nor­adrenergic impulses
along the sympathetic fibres in the splanchnic
nerves.
 DIARRHEA
• Result from rapid movement of fecal matter through the
large intestine. Several causes of diarrhea with important
physiologic sequelae are the fallowing;
1.Enteritis – inflammation of the intestinal tract usually
cause either by a Virus or by Bacteria in the intestinal
tract.
2.Psychogenic diarrhea – is caused by excessive
stimulation of the parasympathetic nervous system,which
greatly excites both (1)motility and excess secretion of
mucus in the distal colon causing marked diarrhea.
3.Ulcerative colitis – extensive areas of the walls of the
large intestine became inflammed and ulcerated with
unknown cause
 CONSTIPATION

In normal persons, the frequency of defecation

ranges from several times/day to once every 2-3
days. Constipation means slow movement of the
feces through the large intestine. It
ischaracterized by prolongation of the intervals
between defecations and excretion of dry hard
stool.
 Causes of constipation

• Frequent voluntary inhibition of the defecation reflexes (the commonest cause).

This leads to overstay of feces in the colon resulting in excessive water
absorption (which renders it more dry and hard).
• Pathological obstruction of the large intestine e.g. by tumours and adhesions.
• Decreased motility of the colon as a result of either :

a.Prolonged ingestion of diets that leave little residue (i.e. contain little dietary
fiber specially cellulose), thus the bulk of feces becomes small and ineffective to
initiate the defecation reflex.

b.Old age, general weakness, lack of activity and debilitating dis­eases. These cases
are associated with decreased colonic tone (= atonic colon) and weak defecation
reflex.

c.Emotional stress : These cases are associated with spasm of a colonic segment
(spastic colon) which results in decreased motility .

d.Hirschsprung's diseas ;