DR.

mohammed elagouri

Diseases of Esophagus
- The esophagus is 25 cm long connecting the pharynx to the stomach .
- The mucosa is lined with squamous epithelium .
- The esophagus is protected from acid damage by a number of defenses including
the lower esophageal sphincter pressure , gravity ,salivary bicarbonate & esophageal
bicarbonate secretion .
Hiatus Hernia
- Occurs when part of the upper stomach herniates through the diaphragm into the chest .
– It's extremely common , especially with increasing age & obesity .
– There are 2 types :
1- Sliding 80 % :
- May be asymptomatic .
- May cause acid reflux , aspiration. - Bleeding may occur.
- Investigations : Barium swallow . upper endoscopy .
- Treatment :_ Weight reduction ( Meals should be small )
_ Sleeping in semi-sitting position .
_ H2 blockers & proton pump inhibitors (omeprazole )
_ Prokinetic drug : dompridone ( motilium ).
_ Surgery : indicated in resistant cases (fundoplication )
2- Rolling 20 % : (paraesophageal hernia)
- Here , a small part of the fundus of the stomach rolls up alongside the
esophagus through the hiatus .
-The gastro-esophageal junction is not affected so , there is no reflux
- may obstruct or strangulate .
- A big hernia may lead to mediastinal syndrome .
- Surgery is indicated in severe cases .

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Esophageal Achalasia
Definition : It's a condition of unknown etiology resulting in abnormal peristalsis and
lack of relaxation of the lower esophageal sphincter ( LES ) .
Clinical picture :
oIntermittent dysphagia : to fluid & to solid food .
oRegurgitation , chest pain , infection ,mild weight loss may occur.
Investigation :
Barium swallow:-Esophageal dilatation with a smooth distal (bird's beak).
-Absence of gases in the fundus of the stomach.
Upper endoscopy .
Manometry : - high pressure in lower segment .
- Loss of peristalsis .
Treatment : Endoscopic dilatation or surgical myotomy

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Gastro-Esophageal Reflux Disease

( GERD )
Definition : Reflux of gastric contents into the esophagus.
Etiology & pathogenesis : ( Failure of anti reflux mechanisms )
1- Decrease tone of lower esophageal sphincter ( LES ) .
2- Decrease esophageal clearance of acid due to poor esophageal peristalsis.
3- Delayed gastric emptying .
4- Hiatus hernia may aggravate the condition .
Predisposing factors :
_ obesity . _ smoking . _ alcohol . _ coffee .
_ large meals (especially late at night ) .
_ drugs : Ca antagonist , theophylline , anticholinergic & nitrates .

Clinical picture :

1- Heartburn : the main symptom .

2- Chest pain : - Epigastric & retrosternal ( simulating angina ) _
- Increased on lying down & relieved by antacid .
3- Odynophagia : painful swallowing .
4- Dysphagia : due to disturbed motility .
5- Pulmonary : cough , asthma , aspiration pneumonia may occur .
6- Hematemsis & melena : due to mucosal inflammation or ulceration.
7- Laryngeal irritation .
8- Barrett's esophagus : ( May occur in long standing acid reflux ) .
- The normal squamous epithelium is replaced by the columnar gastric epithelium
- It's a premalignant leading to adenocarcinoma .
Investigations: ( GERD is a clinical diagnosis )
- Esophageal PH monitoring ( gold standard for diagnosis ) . MCQ
- Endoscopy. - Manometry. - Barium swallow : it may show hiatus hernia .

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Treatment :
1- Diet :
_ Limit intake of food & drink that reduce lower esophageal sphincter pressure : fatty
food , acidic foods , onions ,chocolate, coffee , alcohol .
_ Avoid heavy meals especially before sleep ._ Weight reduction . _ Stop smoking .
2- Postural therapy :
_ Raising the head of the bed at night .
_ Avoid lying down after eating .
_ Remain upright at least 2h after eating .
3- Drug therapy :
↓↓gastric acidity :
- Proton pump inhibitors : Omeprazole , most potent single agent.
- Antacid . - H2 blockers : Ranitidine .
↑↑esophageal peristalsis : Domperidone ( motilium )
4- Surgical & Endoscopic therapy : In resistant cases .

DYSPHAGIA
Definition: Difficulty in swallowing ,with a sensation of sticking or obstruction of
the passage of food through the mouth , pharynx or the esophagus .
Causes :
Oropharyngeal dysphagia:
(alteration of neuromotor mechanism of the oropharyngeal phase, neurological causes)
_ Bulbar palsy .
_ Myasthenia gravis .
_ Stroke .
Esophageal dysphagia:
_ Achalasia .
_ Scleroderma .
_ Esophageal spasm .

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_ Esophageal stricture .
_ Cancer esophagus .
_ All causes of mediastinal syndrome : Goitre , bronchogenic carcinoma , LN
Odynophagia : ( painful swallowing )
_ Inflammation of (mouth, tongue, pharynx, tonsils or esophagus)
Hysterical : (Globus hystericus )
Diagnosis of a case of dysphagia :
History_analysis_: Ask about :
_ Onset , Course , Duration.
_ Type of food (solid or liquid )
_ Painless or painful .
_ Associated symptoms .
_ Site of obstruction .

Examples :
Oropharyngeal dysphagia:
_Onset : Acute _ Course : variable .
_Type of food : more to liquid .
_Associated symptoms: Nasal regurgitation , Dysphonia, neurological manifestations.
achalasia
_ Intermittent & may progress –long duration.
_ Liquid=solid.
_ Relieved by repeated swallowing.
_ Associated symptoms : Heartburn precipitated by eating , no marked loss of weight .
. scleroderma
_ Intermittent course .
_ Both solids & liquids .
_ Associated symptoms : Nocturnal cough , regurgitation .

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cancer esophagus
_ Progressive – short duration .
_ Dysphagia to solids that may progress to include liquids.
_ Associated symptoms : weight loss , chest & back pain .
Investigations:_
_ Barium swallow: (initial_diagnostic_step_after_history__&_examination)
_ Endoscopy .

DYSPEPSIA
Definition:
Any abdominal discomfort related to meal e.g. heartburn , epigastric pain , distension ,
nausea,…….
Causes of dyspepsia :
_ GIT causes : - reflux esophagitis – peptic ulcer – cholecystitis
- pancreatic disorders – hepatic diseases.
_ Systemic diseases : Renal failure , hypercalcemia.
_ Drugs : NSAID , cortisone .
_ Functional dyspepsia : it’s a persistent dyspepsia with no organic cause
( –ve endoscopy & the patient is Helicobacter pylori – negative ).
Diagnosis :
History analysis:
- What type of discomfort does the patient feel ? e.g. heartburn , distension…
- Is this discomfort related to meal ?
- Time to meal :
_ During meal : Esophageal cause : Reflux esophagitis.
_ ½ H after meal : Gastric cause e.g. Peptic ulcer .
_ 2-3 H after meal : Duodenal cause e.g. Duodenal ulcer.
_ 8 H after meal : Intestinal cause : obstruction .
- Type of meal :
Fat : Cholecystitis Meat : Cancer stomach . Starch : Gastric ulcer .

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-Associated symptoms .
Investigations : for the cause
Patients with persistent dyspepsia need to be referred for endoscopy if they
are over 50 years old , or they have associated weight loss , dysphagia , GIT
bleeding or previous gastric surgery .
Treatment :
_ Diet : eat little & often , Avoid fatty food, tea, coffee , smoking, alcohol.
_ Symptomatic treatment .
_ Treatment of the cause .

-Plummer vinson syndrome→esophageal web+iron deficiency anemia+young female.

-Schatski ring→complete ring at the squamocolumner junction of esophagus

-Mallory Weiss Syndrome

- It is a linear mucosal tear at the esophageo-gastric junction produced by
a sudden increase in the intra-abdominal pressure.
- It usually occurs after a bout of coughing, retching or after an alcohol
binge. It is diagnosed by endoscopy.
- The hemorrhage stops spontaneously. Rarely surgery with oversewing of
the tear may be required

Esophageal carcinoma

Cancer esophagus is one of the most lethal of all cancers.

Predisposing factors:
- It is more common in old males (60-70 years).
- Smoking, alcohol, achalasia or reflux and Barrett's esophagus. i.e.
columner metaplasia of the lower esophagus (see later).
- Tylosis (hereditary disorder of squamous epithelium) with hyperkerosis of palms and
soles.
- Corrosive strictures. - Plummer-Vinson $.

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Pathology:
Macroscopically: The lesion is usually ulcerative & it extends around the
. wall of the esophagus, causing narrowing.
Microscopically: It is usually squamous cell carcinoma.
Also adenocarcinoma may arise in columnar epithelium
of Barrett's esophagus, due to longstanding reflux.
Spread: Direct, haematogenous or through lymphatics.

Cllilical Features:
- Progressive dysphagia, first to solids and eventually to fluids.
- Weight loss, due to dysphagia and anorexia.
- Mediastinal syndrome.
- Late the esophageal obstruction causes difficulty in swallowing and coughing with
pulmonary aspiration.
investigations:
1. Barium swallow: - Irregular filling defect with shouldering sign.
- Rat-tail appearance may occur.
2. Esophagoscopy: with biopsy.
3- CT scan of chest & abdomen for size of the tumor & spread outside the esophagus.
treatment:
A. Surgical resection: If the tumor has not infiltrated outside the esophageal wall
followed by chemotherapy and radiation, but unfortunately most patients presented late.
B. Other methods of restoring swallowing, in cases of metastatic disease:
1. Radiotherapy is limited for squamous cell carcinoma of the upper and middle third.
2. Chemotherapy (5-fluouracil and cisplatin) can be used with radiotherapy.
3. Palliative maneuvers: stent application or by-pass operation to allow fluids and soft
food to be eaten or local destruction of the tumour by laser.

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Stomach & duodenum

Physiological aspect :
- HCL is secreted by the parital cells of the stomach through the action of hydrogen-
Potassium ATPase ( proton pump )
- Function of HCL :
_ Converting pepsinogen to pepsin , initiating the first stages of protein digestion.
_ Antibacterial barrier.
- HCL secretion is stimulated by :
_ Vagus ( directly & via increasing gastrin )
_ Gastrin.
_ Histamine.
- HCL secretion is inhibited by : MCQ
_ Somatostatin _ Secretin _ Cholecystokinin
N.B.
Parietal cells _ secrete HCL & intrinsic factor.
Peptic cells ( chief ) _ secret Pepsin.
G cells _ secret Gastrin.
Peptic ulcer
Definition :
- Ulceration of mucosa which is exposed to acid peptic juice.
- The following sites are affected :
o Duodenum.
o Stomach.
o Jejunum ( after gastrojejunostomy )
o Esophagus.
o Meckel’s diverticulum ( contains ectopic gastric tissue )

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Etiology :
It occurs when stomach acid penetrates the stomach and/or duodenal lining.
- It’s a mix of :
o Hyperacidity : duodenal ulcer.
o Decreased mucosal resistance : gastric ulcer.
1- Helicobacter pylori infection ( duodenal > gastric )
2- Traditional NSAIDs : ( gastric > duodenal ).
3- Rare causes : Zollinger Ellison syndrome ( _ acid production )

1- Helicobacter pylori :
- Responsible for the majority of peptic ulcer ( 90% of DU , 70% of GU ).
- [Link] is a gram -ve spiral bacillus transmitted by feco-oral or through
mouth to mouth such as kissing.
- Many people have [Link] infection, but not everyone who has an infection
will develop a peptic ulcer.
- Pathogenesis of [Link] :
_ _-↓ somatostatin. _ _-↑ gastrin release.
_- Produce cytotoxins causing mucosal inflammation.
2- Non steroidal anti-inflammatory drugs ( NSAIDs ) :
- NSAIDs act by inhibiting cyclo-oxygenase enzyme ( COX ) leading to decrease
prostaglandin _ mucosal erosions & ulceration.
- Notice that prostaglandin play a big role in gastric protection.

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Disorder associated with peptic ulcer :

- Cirrhosis. - CRF.
- COPD. - Coronary diseases.

Clinical picture :
Symptom : Epigastric pain
- Character : burning , gnawing or dull ache.
- Site :
o DU : above the umbilicus & to the right of the midline.
o GU : epigastric & in the midline.
Sudden onset of severe generalized pain may indicate perforation.
- Duration : variable from few minutes to several hours.
- Relation to meal :
o DU : 2 - 3 h after meals.
o GU : precipitated by food ½ h after meals
So, in DU : pain awakes the patient from sleep ( the most important symptom )
- Relie
ving factors :
o DU : antacid or food , so appetite _ ( patient eats frequently to relief pain)
o GU : fasting , vomiting ( some patients learn to induce vomiting for pain relief )
- Associated symptoms :
anorexia , vomiting & weight loss in GU.
Signs : may be -ve
- Localized tenderness at the site of ulcer ( severe tender suggests a perforation)
- Physical examination is critically important for discovering evidence of ulcer
complications.
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Complications : _
o GIT bleeding : most common complication ( 15% ) , may be the first symptom.
o Perforation : The second most common complication.
o Pyloric obstruction.
Investigations : _
o Endoscopy : The best to detect the ulcer

o Occult blood in stool.

o Investigations for H. Pylori : antibodies , culture & sensitivity test

Treatment :
i. Diet :
o Frequent small meals.
o Avoid spicy food , smoking , alcohol.
ii. Medical treatment :
1. Antacid : ( symptomatic relief in mild cases )
e.g. mixture of Aluminum & Mg hydroxide ( Maalox )
2. H2 blockers : ( for 4-8 weeks )
They block H2 receptors _ reduction of acid secretion.
_ Cimetidine : 200 mg four times/d . SE : reversible gynecomastia & impotence.
_ Ranitidine ( Zantac ) : 150 mg twice /d or better 300 mg at bed time.
_ Famotidine : 20 - 40 mg/d.
3. Proton pump inhibitors ( PPI ) : ( for 4 - 6 weeks )
- They inhibit H - K ATPase enzyme ( proton pump ) _ _ H+ secretion _ _ HCL secretion.
_ Omeprazole ( Losec ) : 20 mg / d.
_ Lansoprazole : 30 mg / d.

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_ Pantoprazole : 40 mg / d.

4. Sucralfate : ( for 4 -6 weeks )

- It’s a mucosal protective agent ( coating agent )
- Dose : 1 gm / qid.
- Not given with antacid.
5. Anticholinergic drugs :
Pirenzepine ( gastrozepine ) : selective M1 blocker.
6. Eradication of H. Pylori : ( triple therapy for 2 weeks )
- No single agent is effective in eradication this organism.
- Triple therapy is used for 2 weeks e.g.
_ omeprazole tab+clarithromycin+metronidazole or amoxicillin
- Eradication of H. Pylori may lead to dramatic decrease in ulcer recurrence
to less than 5%.
7. Avoid NSAIDs :
If NSAIDs must be continued , either use selective COX-2 inhibitors as
Lomoxicam ( Xefo ) or use traditional NSAIDs plus a strong acid inhibitor.
iii. Surgical treatment :
o Indication :
Recurrent bleeding , Perforation , Pyloric obstruction , Malignancy.
o Operations : Partial gastrectomy , Vagotomy.
iv. Treatment of complications :
o Bleeding :
- Ranitidine or Omeprazole infusion.
- Endoscopic injection of adrenaline.
- Blood transfusion.
o Perforation : IV fluid , analgesic & antibiotic then surgery.
o Pyloric obstruction : surgery.

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Acute gastritis
Acute superficial inflammation of gastric mucosa, sometimes associated with multiple
small mucosal erosions. Acute gastric ulcerations occur in the same setting as erosions
(erosive gastritis), but ulcers are larger.

Causes:
1- Gastric irritants: Spices, Aspirin, NSAID, Cortisone, alcohol. ... etc.
2- Stress Ulcers:
- Hge, shock, cardiac infarction.
- Cerebral trauma, stroke (Cushing ulcer).
3- Curling ulcer secondary to burns.
4- CMV and herpes simplex in immunocompromised patients.
5- Accidental ingestion of caustic substances such as strong alkali
.
Complications:
- Hematemesis.
Clinical picture
- Epigastric pain & tenderness.
- Nausea, vomiting.
- Hematemesis, melena.
investigations: Upper endoscopy.
Treatment:
1. Correct general condition.
2. Treat the cause.

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Chronic gastritis
It is a chronic inflammation of gastric mucosa which can lead to mucosal atrophy
including loss of parietal and chief cells with subsequent metaplasia which
constitutes a background for carcinoma.
Causes:
1. Autoimmune (type A) leading to pernicious anaemia.
2. Helicobacter (type B) i.e. bacterial.
3. Chemical (type C) i.e. biliary reflux (post gastrectomy).
Clinical picture:
- Asymptomatic.
- Epigastric discomfort.
- Nausea, vomiting.
- Pernicious anemia (Autoimmune type).

Investigations:
- Upper endoscopy with biopsy.
- Parietal cell antibodies and intrinsic factor antibodies in autoimmune gastritis.
treatment:
-ttt cause -symptomatic ttt

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Gastric carcinoma
Age>65yrs,>in males
Risk factors:
1. H. pylori chronic gastritis.
2. Nitrosamines.
3. Autoimmune & atrophic gastritis.
4. Adenomatous gastric polyps.
5. Spicy food, diets high in salt.
6. Spirits, Smoking
Pathology:
Macroscopic (mostly in the antrum)
- Cauliflower mass.
- Malignant ulcer.
- Diffuse infiltrating mass which may result in the picture of linitis plastica
in barium meal study.
Clinical features:
• Gross hematemesis is unusual, but anemia from occult blood loss is frequent.
• Ascites or jaundice due to liver involvement.
• Bone, brain metastases also occur. Krubenberg tumour (metastasis to ovaries)
• Hard lymph node in the left supraclavicular fossa (Virchow's node)

investigations:
1. Endoscopy + Biopsy (8-10 biopsies should be taken from around the ulcer)
2. Barium meal: Irregular filling defect, Linitis plastica (infiltration throughout the
entire stomach).
3. CT, ultrasound demonstrate masses and liver secondaries.
4. Endoscopic ultrasound is more accurate.

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Treatment:
A. Operable: radical and total gastrectomy with lymphadenectomy + esophago-
jejunostomy with post operative chemotherapy plus radiation.
B - Inoperable cases
-Palliative ttt

Malabsorption Syndrome

- Definition:
Failure of absorption of one or more of the nutrient (fat, proteins, CHO, minerals.)
- Steatorrhea (fatty_stool) remains the main mark of malabsorption.
Causes:
I- Gastric Causes:
1-Gastrectomy.
2-Atrophic gastritis.
3-Cancer stomach → achlorhydria (_HCl)→Bacterial Contamination of intestine.
4-Zollinger-Ellison's syndrome → hyperchlorhydria (_HCl) → inhibits pancreatic lipase.
II- Hepato-biliary Causes :
1- Liver Cirrhosis
2- Chronic hepatitis.
3- Biliary obstruction. 4- Biliary fistula.
III-Pancreatic Causes :
1- Chronic pancreatitis 2- Cystic fibrosis
3- Cancer head of pancreas. 4- Pancreatectomy.
IV- Intestinal Causes : (the most common)
A) Primary causes:
1- Tropical sprue: unknown etiology but may be:
- Bacterial, viral , parasitic infection. - Folic acid deficiency.

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2- Coeliac disease: ( Non-tropical sprue , Gluten sensitive enteropathy)

- autoimmune disorder in which there is an abnormal reaction to gluten (protein found in
wheat) →Ag. Ab reaction →damage of intestinal mucosa.(subtotal villous atrophy mainly
in duodenum and jejunum
Etiology:
• Most of patients have HLA-DQ2.
- C/P : The peak incidence in adults is in the third and fourth decades, female> male.
• The main presentation is malabsorption syndrome.
• Dermatitis herpetiform is (blistering subepidermal eruption of the skin)
• There is increased incidence of auto-immune thyroiditis &type1 DM.
• Other associated diseases include inflammatory bowel disease, liver disease & fibrosing
alveolitis.
- Complications : small intestine carcinoma , ↑incidence of
lymphoma,infertility,hypocalcemia,iron deficiency anemia,megaloblastic anemia.
- Investigations:
1- IgA antigliadin antibodies,antitransglutaminase abs.,antiendomysial abs.
2- Jejunal biopsy → villous atrophy
- Treatment : The only effective treatment is lifelong gluten free diet.

B) Secodary to intestinal diseases:

1- Short gut syndrome: extensive intestinal resection →↓absorptive surface.
2- Stagnant (blind) loop syndrome: Stagnation of intestinal content e.g.
strictures of small intestine , Diverticulosis → bacterial overgrowth →
mucosal injury & nutrients utilization .
3- Systemic diseases: DM , amyloidosis, hypothyroidism , CHF.
4- Infection: -Bacterial over growth.
-TB enteritis, Giardia, Strongeloides,
5- Inflammation: Crohn's disease , Irradiation.
6- Iatrogenic: Antacids , Biguanides , Cholestyramine , .

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7- Lymphatic obstruction:
_ Lymphoma.
_ Whipple's disease : (mainly affects MAN)
Malabsorption Syndrome, Arthritis , Neuropathy & lymphadenopathy,clubbing.
Clinical picture:
I. General manifestations:
1- loss of weight. 2- fatigue.
3- fever 4- clubbing of fingers.
II. Intestinal manifestations:
1- Steatorrhea: Stool is Pale, bulky, offensive, floats on water, greasy, glistening.
2- Diarrhea: malabsorption usually results in diarrhea.
3- Audible intestinal sounds (borborygmi).
4- Distension, colic.
III. Nutritional deficiency:
↓protein → muscle wasting, edema, recurrent infections
↓ Fat → loss of weight.
↓CHO →hypoglycemia

↓ Minerals: Iron →anemia.

Na → Muscle cramps, hypotension.
K → arrhythmia.
Ca, Mg →tetany.
Iodine → Goitre.
↓ Vitamins: A → night blindness, follicular hyperkeratosis.
D → Rickets, osteomalacia.
E → infertility.
K → Bleeding tendency.
C → Scurvy
B1 →Beri – Beri.

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B2 →glossitis – gastritis.
B3 → Diarrhea, Dermatitis, Dementia.
B6 → peripheral neuritis.
B12 → Megaloblastic anemia.
IV. C/P of the cause: Coeliac disease , history of surgical operation ……….
Investigation:
I- Biochemical investigation:
1- Estimation of fecal fat: (n : 6 gm/d)
- in steatorrhea → total fat is increased ( > 6 gm/d )
↓ split fat →intestinal disease - ↓ Non split fat → pancreatic disease
2- Pancreatic function tests.
3- D-xylose test:
25g of D-xylose given to pt.
o Normally : 5 hours urine should contain at least 5 gm provided that
normal renal functions.
o In malabsorption syndrome : 5 hours will contain less than 5 gm

II- Hematological Investigations :

1- Blood picture: Anemia. (Microcytic anemia due to iron deficiency or macrocytic
anemia due to vitamin B12 or Folate malabsorption.
2- Plasma proteins : hypoproteinemia.
3- Serum electrolytes.
4- Prothrombin time: may prolonged because of malabsorption of vitamin K.
III- Radiological investigations:
1- CT 2- MRI 3- U.S.
4- Barium meals:
_ Dilatation of intestinal lumen. _ Loss of normal feathery appearance

IV- Investigations for bacterial overgrowth :

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1) 14 C- Xylose breath test :

O 14 C-Xylose is given orally then measure the 14 CO2 in the breath.
O In bacterial overgrowth : ↑ 14 CO2 in the breath because more bacteria
will act on 14 C- Xylose.
2) Aspiration of jejunal content then culture.

Treatment:
1- Treatment of the cause:
T.B enteritis : anti TB drugs.
Tropical sprue : antibiotic ( tetracycline ) & folic acid.
Coeliac disease :
- The only effective treatment is lifelong gluten free diet.
- cortisone.
2- Diet: Low fat, low fibers, non irritant diet.
3- Parentral vitamins, minerals, fluid.
4- Symptomatic treatment :
e.g. Anti diarrheal drugs : Difenoxylate , Loperamide

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IRRITABLE BOWEL SYNDROME ( IBS )

Definition:
It's a functional disturbance of colonic motility with no organic cause .
Etiology : unknown , psychological disturbance play a role.
Clinical picture: long history with long free interval
o Recurrent pain :over any part of the colon (especially in left iliac fossa).
o The pain is by food & __ by defecation .
o There is constipation or diarrhea .
o Abdominal distension is common .
o Patient with IBS often complain of anxiety , depression & tension headache.
Investigations : - no +ve finding .
Treatment :
-Reassurance .
-Diet : high fiber diet & bran , Avoid coffee , tea , smoking

-Tricyclic antidepressant e.g. amytriptyline (Tryptizole) 10-25 mg or nortiptyline 75mg in

diarrhea-predominant.
-Tegaserod which is serotonin receptor agonist it activates serotonin
receptors in GIT (zelmac), 6mg/12hr, it can be used also in constipation - predominant.

Factors that can trigger irritable bowel syndrome:

-GI infection. - Antibiotic therapy.
-Psychological stress. - Mood disorders
-Eating disorders.

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INFLAMMATORY BOWEL DISEASE

( Crohn's disease & ulcerative colitis )
Etiology:
_ Is still questionable.
_ Most probably autoimmune
_ Genetic factor: play a great role.
_ Infections (T.B, measles): not confirmed.
_ Psychological factor may play a role.

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Treatment:
Medical treatment :
1- Sulfasalazine: reduce inflammation especially in ulcerative colitis.
-1 gm /6 h reduced to a maintenance dose of 2 gm/ day for 2 years after remission .
2- Steroid (prednisone) : 60mg/d. This is the main treatment for active disease
3- ImmunoSuppressants: Azathioprine ( Imuran ).
4-infliximab→in perianal crohns disease
5- Symptomatic :
- Antibiotics for 2ry infection : Metronidazole & ciprofloxacin.
- Anti diarrheal drugs.→lopiramide(c/I in active disease)
Surgical treatment : ( Indications )
- Failure of medical treatment. - Severe complications→toxic
megacolon,fistulas,perianal abscess

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Acute Pancreatitis
Etiology :
o gall stones → obstruction of pancreatic duct ( the most common cause )
o Alcohol. o Viral infection e.g. mumps, Coxsackie B.
o Hyperlipidemia. o Hypercalcemia. o Idiopathic.
NB : Gall stones → back regurge of trypsin enzyme (autodigestion)
Symptoms :
o Abdominal Pain: epigastric pain radiating to the back and relieved by pending forward
o Nausea & vomiting.
Signs : Unexpectedly, abdominal signs are minimal in comparison with the severity of
pain.
o Tenderness & rigidity : at first in the upper abdomen, later on become generalized.
o Cullen sign: umbilical ecchymosis.
o Grey turner's sign: ecchymosis in flanks.
Complications:
o Multiple organ failure ( MOF ) : HF, Renal failure, Respiratory failure.
o Abscess. o Pancreatic ascites. o HypoCalcemia.
o DIC. o Diabetes mellitus.
o Obstructive jaundice : due to edema of the head of the pancreas.
Poor prognostic indicators : (ranson`s criteria)
o PaO2 < 60mmHg .
o Age > 55 years.
o Neutrophils: WCC > 16,000 /mm3.
o Calcium < 8mg %.
o Renal: Urea > 100mg %.
o Enzymes: LDH > 350 ; SGOT > 250 U.
o Albumin < 3gm%
o Sugar: Glucose > 200 mg % .

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Investigation:
1. Pancreatic enzymes :
o Amylase ( N : 75-150 somogyi unit ) : ↑↑( in blood , urine , peritoneal fluid )
o Lipase : ↑↑ , more specific than amylase.
NB : Serum_amylase_is_ raised_ in_ other_ conditions_ [Link] peptic ulcer_
Ectopic pregnancy, alcoholics, salivary gland disease…)
2. Peritoneal aspiration : contains high amylase.
3. Blood picture : leucocytosis , anemia in hemorrhagic pancreatitis.
4. X ray, US, CT : gall stones , swollen pancreas , calcification,necrosis.
5. ECG : to exclude myocardial infarction.
Treatment :
- Nasogastric suction.
- IV nutrition.
- Antibiotics.
- Analgesics : pethidine ( no morphine as it induces spasm of the sphincter of Oddi )
- Somatostatin infusion.
- Treatment of complications e.g. Respiratory support , cortisone.
- Surgery for pancreatic abscess & ERCP may be needed.
Prognosis : death rate is about 10%.

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Chronic Pancreatitis
Chronic pancreatitis is an inflammatory condition characterized by irreversible damage to
the exocrine & later to the endocrine tissue of the pancreas.
Etiology : Like Acute pancreatitis but :
o Chronic alcoholism is the commonest cause.
o Gall stones are unlikely to cause chronic pancreatitis.

Clinical picture : Triad of :

i- Recurrent abdominal Pain: radiate to the back.
ii- DM
iii- Steatorrhea ( malabsorption $ )
Investigation:
o Like acute pancreatitis.
o CT is the most sensitive for detection of pancreatic calcification.
o ERCP : shows irregular dilation and structuring of the pancreatic ducts.
Treatment :
1. Stop alcohol
2. Pancreatic enzyme replacement : taken as enteric coated tablets.
3. symptomatic treatment :
_ pain : Analgesics.
_ Treatment of DM.
_ Treatment of steatorrhea.

-Cancer Head of Pancreas

_ painless obstructive jaundice.
_ loss of weight.
_ Anorexia.
-Cancer Body of Pancreas
_ Pain: radiate to back.
_ Jaundice: rare.

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-Gastrinoma: zollinger Ellison syndrome

- The tumor arises from G cell of the pancreas secreting excessive amount of gastrin. It
may arise from the duodenum.
- It leads to peptic ulcers in the stomach, duodenum and jejunum (the ulcers are large,
deep and multiple).
- Diarrhea occurs due to low pH in upper intestine.
- A high gastrin level confirms the diagnosis.
- Isotope scans, ultrasound and CT can demonstrate the tumor.
- Treatment is with a proton pump inhibitor, octreotide is also used.
- These tumors are malignant and the patients die from the malignancy rather
than gastrointestinal problems.
- Surgery is reserved for removal of the primary tumor only.

Familial adenomatous polyposis

It is an autosomal dominant disease characterized by adenomas of the colon

(neoplastic polyposis) when osteomas of the jaw, sebaceous cysts and colonic
polyps are present the condition is called Gardner's syndrome.
Pathology:
- There are 100 or more adenomas in the colon usually 1000 and
sometimes 5000. The rectum is usually involved.
- The polyps appear at adolescence and become malignant within 15
years and the patient usually dies before the age of 40.
Clinical features:(Symptoms usually begin in the mid 30s)
- Abdominal pain.
- Diarrhea, blood and mucous in stool.

Investigations:- Ba enema shows multiple small filling defects throughout the colon.

- Upper GI endoscopy as gastric, duodenal and periampullary polyps are

also common.

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- All relatives must be examined by annual sigmoidoscopy after the age of

10 years.
Treatment:
Total colectomy with ileorectal anastomosis with follow up to detect cancer so
it is safer to remove the rectum also (proctocolectomy and ileostomy).

Colonic cancer
Age & sex: Male, old age (60-65 years).
Risk factors:
1. Familial polyposis.
3. Excessive consumption of meat and animal fat.
5. Ulcerative colitis.
2. Family history.
4. Low dietary fibers.
5-hereditary nonpolyposis colorectal cancer.(lynch syndrome)
NB aspirin and NSAID decrease risk of colonic cancer
Pathology:
Macro:
1. Cauliflower mass. 2. Malignant ulcer. 3. Infiltrating mass.
Micro: Adenocarcinoma
Modified duke`s staging:
- Stage A: Cancer confined to the bowel wall.
- Stage B: Cancer extending beyond the bowel wall, but without metastasis
- Stage C: Cancer involving lymph nodes.
- Stage D: Cancer with distant metastases.
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Clinical picture: (The majority are a symptomatic until advanced)

• Alteration in bowel habits with or without abdominal pain is common with left sided
colonic lesions.
• Rectal and sigmoid carcinomas usually bleed.
• Carcinoma of the caecum may become large and still remain asymptomatic. It can
present as an iron deficiency anemia.
• Intestinal obstruction may occur in elderly.
• Clinical examination →abdominal mass or normal.

-investigations:

-Carcinoembryonic antigen (CEA)→high in 70%

-stool for occult blood→positive

-ct scan for staging

-colonoscopy

Treatment:

-operable cases duke`s A &B→resection

-nonoperable cases duke`s C→chemotherapy

NB. Symptoms of GIT diseases →look at practical part.

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