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ecture Notes of 
nternal medicine 





Gastroenterology 

Biliary system 

Pancreas 



Dr. Osama Mahmoud Mohamed 

Assistant Professor of Internal Medicine 
Ain Shams University 



Index 



Diseases of The Mouth 1 

Stomatitis 1 

Diseases of The Tongue 3 

Diseases of The Salivary Blantts 4 

Diseases of esophagus 5 

- Structure of the esophagus 5 

- Hiatus Harnia 5 

- Esophageal Achalasia 7 

- Carcinoma of the Esophagus 8 

Gastro-Esophageal Reflux Disease (GERD) 9 

Miscellaneous disorders of the esophagus 1 1 

Diseases of the Stomach and Duodenum 13 

- Anatomy of the stomach & duodenum 13 

- Peptic Ulcer 13 

Pharmacology of drugs used in peptic ulcer 20 

- Acute Gastritis, Erosions & Acute Ulcerations 22 

- Chronic Gastritis 23 

Cancer Stomach 23 

- Miscellaneous disorders of the stomach & duodenum 25 

Diseases ol intestine 28 

- Malabsorption Syndrome (Intestinal Failure) 28 

- Dysentery 33 

- Intestinal Amoebiasis 34 

- Bacillary Dysentery (Shigellosis) 35 

- Intestinal Bilharziasis 36 

- Inflammatory Bowel disease 37 

- Functional bowel disorders 42 

- Megacolon 44 

- Cancer Colon 44 

- Diverticular Disease of the Colon 45 



Familial Adenomatous Polyposis , 46 

- Neuroendocrine Tumors of the Gastrointestinal Tract Pancreas 47 

Carcinoid Tumours 48 

Intestinal Obstruction 49 

- Acute Appendicitis, Meckel's Diverticulum 51 

Gall Bladder &Billiary System 52 

- Gallstones 52 

- Acute Cholecystitis 54 

- Chronic Calculous Cholecystitis 55 

Miscellaneous diseases of the biliary system 56 

The Pancreas 53 

- Acute Pancreatitis 59 

- Chronic Pancreatitis 62 

- Carcinoma of the Pancreas 63 

Pancreatic islet tumors 64 

Mute Abdomen 65 

Protein Losing Enteronattiy ez 

Motility disorders ot GIT 67 

SIT Bleeding 67 

diseases ol Peritoneum 68 

- Acute Peritonitis 68 

Tuberculous Peritonitis 68 

Malignant Ascities and Tumors of Peritoneum 70 

Retroperitoneal fibrosis 70 

Functional Gastrointestinal Disorders 71 

GIT involvement in systemic diseases 71 
Bttra-gastrointestinal or multi system manifestations ot 

GIT disorders 72 

Systemic manifestations oi pancreatic diseases 72 

Immune mediated GIT diseases 72 



GIT 



Diseases of the Mouth 



Stomatitis 



- The mouth contains many of commensal micro organisms. So, oral hygiene 
is essential. Negligence of oral hygiene may lead to bacterial proliferation 
causing stomatitis. 

- Stomatitis may also occur when resistance to the commensal population is 
lowered e.g. in the immune-compromised host. 

- Stomatitis may also occur due to nutritional deficiency. 

1 - Ulcerative Stomatitis (Vincent's infection) 

Clinical Picture 

- It occurs in adults with malnutrition and poor dental hygiene. 

- There are ulcers on the gum, palate, lips and the inner aspects of 
cheeks. 

- Halitosis. 
Investigations 

- A stained smear shows spirochetes and fusiform bacilli. 
Treatment 

- Metronidazole or penicillin. 

2- Viral Stomatitis 

- Herpes simplex may cause herpes labialis in normal persons. 

- It can lead to severe stomatitis in immune-compromised patients. 

- Coxsackie virus causes herpangina with acute pharyngitis, ulcers of the soft 
palate and pharyngeal mucosa. 

3- Candidiasis (Moniliasis) 

Etiology 

- The fungus Candida albicans is a normal commensal in the mouth. It 
may proliferate to cause thrush in babies and in debilitated patients. 

- Also thrush is common in patients receiving prolonged treatment with 
antibiotics and in patients who are immunosuppressed by 
corticosteroids or AIDs. 




GIT 

Clinical picture 

- White patches on the tongue and buccal mucosa. 

- In severe infection the pharynx and esophagus can be affected 
causing dysphagia. 

Treatment 

- Cause. 

- Lozenges or suspension of nystatin. 

- Systemic antifungal in severe infection. 

4- Stomatitis due to nutritional deficiency 

- This occurs due to deficiency of niacin, riboflavin, folic acid and vitamin B 12 . 

- When the deficiency is acute and severe the tongue is red and painful 
because of atrophy of the papillae. 

- Angular stomatitis often accompanies glossitis especially in severe riboflavin 
and iron deficiency. 



* Angular thelitis (angular stomatitis) 

It is erythema or crusting of the labial angles is also caused by Candida. It is 
associated with intra oral candidasis. It is treated with topical with or without 
systemic antifungal drugs, iron and vitamin supplements. 

* Cheilitis 

Painful vertical fissures mainly of lower lip caused by malnutrition. It may 
occur in Crohn's disease or with exposure to sunlight and wind. 



5- Recurrent aphthous ulceration 

Etiology (Affecting 20% of the population) 

- Unknown etiology. 

- Emotional stress may precipitate the attack. 

- May occur during the premenstrual phase. 

- May occur in association with Crohn's disease, ulcerative colitis or 
Behcet's disease. 

- Nutritional deficiencies with or without Gl disorders are occasionally 
found. 

- The ulcers are recurrent at intervals of days to a few months. 

Clinical picture 

- Multiple shallow rounded ulcers, they are painful. 



* Minor ophthous ulcers are < 10mm with grey white centre with thin 
erythematous halo and heal with 14 days without scarring, 

* Major aphthous ulcers > 10mm persist for weeks or months and heal with 
scarring. 



GIT 




Treatment 



Hydrocortisone hemisuccinate lozenges. 

Topical anesthetics. - Colchicine 



Skin dis e ase s associated with mouth ulcerations: 

- Erythema multiforme (Stevens Johnson $). 

- Lichen planus. - Pemphigus vulgaris. 
Drugs causing mouth ulcerations: 

- Antimalarials. - a-methyl dopa. 

- Penicillamine and gold salts. 
Mou th ul c eration w it h systemic d isorders: 

- Inflammatory bowel disease. - Behcet's disease. 

- SUE. - Reiter's disease 
Malignant tum or s of th e mouth: 

- It is a squamous cell carcinoma. 

- Tobacco, alcohol consumption and leukoplakia are predisposing 
factors. 

- Treated by surgical excision and/or radiotherapy. 
Diseases of g ums: 

- Acute necrotizing gingivitis (Vincent's gingivitis). 

- Gingival swelling or hypertrophy may occur due to hereditary gingival 
fibromatosis, drugs (phenytoin, cyclosporine and nifidipine), 

pregnancy, scurvy and acute leukemia. 



Diseases of the tongue 

(See also the clinical part) 

Glossitis: 

■ It may be involved in stomatitis due to nutritional deficiency. 

■ Glossitis is a red, smooth, sore tongue seen in B 12 , folate and iron 
deficiency. 

Leukoplakia: 

It is a chronic lesion (white, firm smooth patches). 
It usually starts at the side of the tongue. 
Early it is not painful but later become tender. 
It is associated with alcohol and smoking. 
It may precede the development of carcinoma. 
Isotretinoin may reduce disease progression. 

Black hairy tongue: (unknown etiology) 

It is due to proliferation of chromogenic microorganisms causing brown 

staining of elongated filiform papillae. 

- 




GIT 

Functional disorders: 

■ Glossodynia (painful tongue) and glossopyrosis (burning sensation in the 
tongue) if the tongue looks normal the cause may be depression. 

■ Bad taste in the mouth is sometimes due to drugs or sinusitis but it may 
reflect anxiety or depression. 

Tumors of the tongue 

- Squamous cell carcinoma. - Kaposi's sarcoma in AIDs. 

Diseases of the Salivary Glands 

Ptyalism (excessive salivation) 

Causes 

1- Psychogenic. 2- Prior to vomiting. 

2- Secondary to oral pathology e.g. stomatitis. 

Xerostomia (dryness of the mouth) 

- Dehydration. - Psychogenic. 

- Sjogren's $. - Radiotherapy. 

- Drugs e.g. anticholinergics and antihistaminics. 

Sialadenitis (inf lamination of salivary glands) 

Acute sialadenitis may be due to mumps (parotitis) or bacteria. 

Salivary calculi 

These occur occasionally in the submandibular gland or its ducts. 

Clinical picture 

- Painful swelling of the submandibular gland after eating. 

- Stones can sometimes be felt in the floor of the mouth. 

Invsestigations 

- Sialography. - Plain X-ray will show the stone. 

Treatment 

- Surgical removal. 

Neoplasm of salivary glands 

- The majority occur in the parotid gland. 

- The pleomorphic adenoma is the commonest which may turn malignant. 

- Malignant tumors usually result in lower motor neurone lesion of facial 
nerve. 



Sarcoidosis can involve salivary gland, e.g. in cases of Heerfordt's and 
Mikulicz syndromes (see chest diseases). 



GIT 



M> 



Diseases of Esophagus 

Structure of the esophagus) 

• It is a hallow muscular tube, about 25 cm long connecting the pharynx 
to the stomach, it has no significant absorption or secretory function. 

• It is lined by stratified squamous epithelium except near the gastro- 
esophageal junction lined by columnar epithelium. 

• The esophagus is separated from the pharynx by the upper 
esophageal sphincter (UES) which is normally closed by the 
cricopharyngeus muscle contraction. 

• The lower esophageal sphincter (LOS) consists of an area of the distal 
end of the esophagus with a high resting tone to prevent reflux. 

• The relaxation and reduction of LOS tone that occurs during 
swallowing is under the control of vagus and other hormonal 
mechanisms. The presynaptic neurotransmitter is acetylcholine. The 
postsynaptic neurotransmitters which cause relaxation are nitric oxide 
and vasoactive intestinal peptide. 

■ The act of swallowing begins with propulsion of the chewed bolus into the 
posterior oropharynx by the tongue. 

■ During the next phase of swallowing several actions occur : 

- The soft palate elevates to close the nasopharynx. 

- The epiglottis close over the larynx. 

- The UES relaxes. 

- The pharyngeal constrictors contract to propel the bolus into the 
esophagus. 



Hiatus Hernia 



This describes the herniation of a part of the stomach into the chest. 

I. Sliding hiatus hernia 

There is herniation of the gastro-esophageal junction through the 
esophageal hiatus in the diaphragm into the thorax. 

This will affect the valvular mechanism of the gastro-esophageal 
junction leading to reflux of gastric Contents into the esophagus. 



GIT 



km: 




Clinical Features: 

Heart burn (Pyrosis): It is a burning retrosternal pain occurring in 
lying down gr leaning forward, it is severe during sleep. 

- Dysphagia may occur due to esophageal stricture. 

Bleeding e.g. haematemesis, melena or presented with iron 
deficiency anemia due to esophagitis. 

- It may be asymptomatic. 

Investigations: 

1 -Barium swallow. 2- Upper endoscopy. 

Treatment: 

I. Medical 

- Weight reduction, also meals should be small. 

- Sleeping in semi-sitting position. 

- H 2 blockers and proton, pump inhibitors. 

- Prokinetic drug: Domperidone (motilium). 

IL...S..U.rS.G.rX:. Indicated in resistant cases, (fundoplication) see later. 

Cardio-oesophageal junction (b) 

Hernial sac 




(a) The oesophagastric anatomy in a stiding hiatus hernia 
(b) The anatomy in a para-oesophageal hernia 

II. Paraesophageal or Rolling Hernia 

- A small part of the fundus of the stomach rolls up alongside the 
esbphagus through the hiatus. 

- The gastro-esophageal junction remains in normal position, so there is 
no reflux. 

- It may lead to mediastinal syndrome if severe. 

- Also gastric volvulous or strangulation may occur. 

- Surgery is indicated in severe cases. 




GIT 

Esophageal Achalasia 

It is a motility disorder of the esophagus characterized by failure of relaxation 
of the lower esophageal sphincter with aperistalsis in the body of the esophagus 
(atony). 

Pathogenesis; 

1) Degeneration in the myenteric nerve plexus of the esophageal wall. 

2) Lesion in the nitric oxide containing neurons. 

ClllliCOl f€«ltlll'€S£ (The disease is more common in middle-aged females). 

- Intermittent dysphagia to fluids & to solid foods. 

- Retrosternal chest pain occurs with vigorous non peristaltic contraction of 
the esophagus. 

- Putrefaction of the retained food leads to halitosis. 

- Chest infections may occur due to aspiration during sleep, due to 
regurgitation. 

- Weight loss is usually not marked. 

Investigations: 

1. Chest x rav showing : 

■ Absence of gases in the fundus of the stomach. 

2. Barium swallow: 

■ Dilated esophagus, the lower end gradually narrows (bird's beak 
deformity). 

3. Upper endoscopy: For diagnosis & to exclude cancer esophagus, 

in achalasia the endoscope can pass easily 
through the narrowing without resistance. 

4. Manometry: It shows aperistalsis with failure of the lower 

esophageal sphincter to relax. 

Te'catmcnt: 

1 . The treatment of choice is endoscopic dilatation. 

2. Endoscopic botulinum toxin injection in the lower esophageal sphincter. 

3. Laparoscopic cardiomyotomy if these measures fail (Heller's operation). 
i.e. division of the muscle at the lower end of the oesophagus, it can be 
done laparoscopically. 

4. In old age Ca Ch blockers (Nifedipine) can be tried initially. 

_____ - - 



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 $. 

Pathology: 

Macroscopicallv: 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. 

Clinical 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. Esophagoscopv: 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. 

_ - 



GIT 




Gastro-Esophageal Ref 1uh Disease IGERD1 



Definition: 

Reflux of gastric contents into the esophagus which allows prolonged contact 
of these contents with the lower esophageal mucosa. It is the most common 
disorder of the esophagus. 

EtiOlOgy aild PatllO<I€Ii€SiS: (failure of antireflux mechanisms) 

1 . The resting lower esophageal sphincter (LOS) is low and fails to increase 
when lying flat. 

2. Decrease esophageal clearance of acid due to poor esophageal 
peristalsis. 

3. Delayed gastric emptying. 

4. Hiatus hernia may impair the pinchcock mechanism of the diaphragm. 

5. The lower esophageal sphincter tone fails to increase when intra 
abdominal pressure is increased by tight clothes or pregnancy. 

Factors associated with increase pel Sum: 

- Obesity - Pregnancy 

- Fat, peppermint - Chocolate 

- Coffee (Caffeine) - Smoking 

- Anticholinergics - Ca Ch blockers 

- Nitrates - Hiatus hernia 

Clinical picture: 

1 . Heart burn: It is the most cardinal symptom of GERD, it is due to direct 

stimulation of the hypersensitive esophageal mucosa. 

2. Chest pain: similar to angina (due to reflux or esophageal spasm). 

3. Odynophagia: (painful swallowing). 

4. Dysphagia: due to disturbed motility or structure. 

5. GIT bleeding, Iron deficiency anaemia (esophagitis). 

6. Pulmonary, cough, aspiration pneumonia may occur. 

Investigations: 

GERD is a clinical diagnosis & many patients can be treated without 
investigations 

1. Endoscopy, to confirm the presence of esophagitis. 

2. 24 hour intraluminal pH monitoring of the esophagus. 

3. Esophageal manometry. 

4. Barium study: It may show a hiatus hernia. 




GIT 

Complications: 

Stricture of esophagus. 

- Esophageal ulceration. 

- Barrett's esophagus: columnar metaplasia of the lower esophagus. 

It is a premalignant leading to adenocarcinoma. 

- Reflux induced laryngitis. 

Treatment: 

I. Simple lifestyle measures: 

50% of patients can be treated by: 

• Cessation of smoking, loss of weight and simple antacids. 

• Avoid alcohol, fatty meals & drugs e.g. nitrates. 

• Avoid heavy meals especially before sleep. 

• Raising the head of the bed at night. 

• Avoid any other precipitating factor. 

II. Pharmacological therapy: 

JLJD^QlgSJCedyCG-g^^C acidity- (Prolonged therapy is usually needed) 

- Antacids: Mg trisilicate and aluminium hydroxide, also 

alginate containing antacids forming a gel with 
gastric contents reducing reflux. 

- H 2 blockers. Ranitidine (Zantac®) (300mg at bed time) 

- Proton pump inhibitors: Omeprazole (20-40mg/day), 

Lanzoprazole (30mg/day) or pantoprazole (20- 
40mg/day). They inhibit the gastric hydrogen-potassium 
ATPase. 

2JPyo^sJii^«asesjesophageal 
peristalsis and LOS 

pressure (prokinetic) • 

- Cisapride (Prepulsid): 
not available now !?. It ""£ 
leads to arrythmia. 

- Metoclopramide or 
Domperidone. 

III. Surgery: '■ % 

- Nissen fundoplication (antireflux " f ~ 

surgery) is performed laparoscopi- / 

cally for severe cases with repair of 
hernia if present. The gastric fundus 
is warraped around the abdominal 
oesophagus. 




- ^* 'i^> 



jd-*" 



10 



GIT 



A 



GERD 


Myocardial Ischemia 


- Burning pain produced by bending, 
stooping or lying down. 


Compression or crushing pain. 


- Pain seldom radiates to the arm. 


- Pain radiates into neck, shoulder and 
both arms. 


- Pain precipitated by drinking hot 
liquids or alcohol. 


- Pain produced by exercise. 


- Relieved by antacid, t by nitrates. 


- Relieved by rest and nitrates. 


- No dyspnea. 


- Dyspnea may present. 



Miscellaneous disorders of the esophagus 



GEObCIS (Globus hystericus is an old name) 

- Persistent or intermittent sensation of a lump or foreign body in the throat, 
this sensation is present between meals. Absence of dysphagia on 
swallowing. 

- In the majority, it is probably a functional disease. 

- In the treated by reassurance with antiureflux therapy. 

Diffuse esophageal spasm (liypci'inotllity) 

- It is a severe form of abnormal esophageal motility. Usually it causes 
retrosternal chest pain and dysphagia. It can accompany GERD. 

- Ba swallow may show corkscrew esophagus. A variant of diffuse 
esophageal spasm is the nutcracker (super-squeeze) esophagus. 

- It can be treated by nitrates, Ca ch. blockers. 

- Occasionally balloon dilatation or even myotomy is necessary. 

Esopliagltis 

- Reflux esophagitis (see GERD). 

- Infection by Candida, herpes simplex and CMV in immuno-compromised 
patients. This can be treated by antifungal and antiviral. 

- Pills induced esophagitis results from tetracycline, iron, NSAIDs, KCI 
tablets, tetracyclines and other antibiotics, (drink sufficient fluid more than 
120ml) with oral medications to prevent esophagitis. 



11 



GIT M ffl&& 

Mallory Weiss $ 

- 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. 

Perforation of the esophagus 

- This may occur at endoscopy, it is small and can be treated 
conservatively by antibiotics and I.V fluid. 

- Also, it may occur spontaneously due to sudden increase in intra 
esophageal pressure e.g violent vomiting, straining (Boerhaave's $). 
There is severe chest pain, abdominal pain and shock. It needs surgery. 

Esophageal rings (lower esophagus) or webs (upper 

esophagus) are composed of fibrous tissue causing dysphagia and 
can be treated by balloon or bougie dilation. There is an assocfation 
between esophageal web, Iron deficiency anaemia, glossitis and angular 
stomatitis (plummer Vinson syndrome). Dilatation of the web is rarely 
necessary, iron therapy for iron deficiency anaemia. Lower esophageal 
(Schatzki ring) treated by dietary advice, but dilatation is occasionally 
necessary. 



12 



kit iBBr 

Diseases of the Stomach and Duodenum 



Anatomy of the stomach 6 duodenum 



The stomach is divided into an upper part (the fundus), the mid part or body 
and the antrum which extends into the pyloric region. 

There are two sphincters; the gastro-esophageal and the pyloric sphincters. 

The mucosal lining of the stomach formed of folds or gastric rugae. 

The upper two thirds of the stomach contain parietal cells secreting HCI and 
chief cells secreting pepsinogen. The antrum contains mucous secreting cells 
and G cells which secrete gastrin. 

Mucus secreting cells secrete mucous and bicarbonate which is trapped in 
the mucus gel. 

The mucosal barrier is formed by the surface membrane of mucosal cells and 
the mucus, this protects gastric mucosa from damage by aspirin, NSAID, 
alcohol and bile salts. 

Prostaglandins stimulate mucus secretion; this is suppressed by aspirin and 
NSAID which inhibit cyclooxygenase. 

The duodenum is C-shaped and the pancreas sits in its concavity. The 
duodenal mucosa contains Brunner.s glands, which secrete alkaline mucus. 
This along with the pancreatic and biliary secretions helps to neutralize the 
acid secretion from the stomach when it reaches the duodenum. 



Peptic Ulcer 



■ HCI is secreted in the stomach by the parietal cells through the action of the 
Hydrogen-potassium ATPase (proton pump). 

■ Secretion of HCI is under neural and hormonal control. Both stimulate acid 
secretion through the direct release of histamine stimulating the parietal 
cells. Acetylcholine and gastrin also release histamine. 

■ Somatostatin inhibits both histamine and gastrin release decreasing acid 
secretion. 

■ Gastrin is secreted by G cells in the antrum, it stimulates HCI secretion. 

Definitions 

It is an ulcer in the duodenum, stomach, lower esophagus or in the Jejunum 
after gastrojejunostomy with exposure to acid-peptic juices with a defect in the 
mucosa that extends through the muscularis mucosa into the submucosa or 
deeper. 



13 



GIT 






Etiology of peptic ulcer: 

The proteolytic enzyme pepsin and gastric acid were initially identified as the 
key factors involved in the pathogenesis of peptic ulcer. So the concept of no 
acid, no ulcer has been widely used and accepted for many years, recently, 
the role of factors other than acid and pepsin in the pathogenesis of peptic 
ulcer has been recognized, e.g. : - 

1 ■ Helicobacter pylori (H. pylori): 

■ H. pylori is a spiral-shaped, gram negative, urease producing 
organism. 

■ The organism is found under the mucus layers in close to gastric 
epithelial cells. 

■ It is transmitted by faeco-oral or oral-oral (saliva) routes. 

■ 30-60% of western populations are affected and the prevalence is 
higher in underdeveloped countries. The older populations are more 
liable. 

- Increase gastrin release. 

- Increase pepsinogen secretion. 

- Cytotoxin release. 

- An alteration in the mucus protective layer. 

- Decrease in somatostatin from the antral cells (somatostatin 
inhibits both histamine and gastrin release). 



The organism produces urease enzyme which splits urea producing ammonia 
which raises the pH around it to protect itself. 



2. non-steroidal a»ti-inf lamm atory drtrosCHSAIPs): 

■ Prostaglandins have important several mechanisms to protect 
gastric mucosa. They stimulate bicarbonate & mucus secretion from 
the gastric mucosa. Also they increase the microvasculature of the 
mucosa. All these mechanisms are called the mucosal barrier. 

■ NSAIDs act by inhibiting cyclo-oxygenase enzyme (COX) leading to 
decrease prostaglandins at the site of inflammation. 

■ NSAIDs decrease gastric and duodenal prostaglandins, so mucosal 
erosions & ulcerations will occur. 

■ The cyclo-oxygenase enzyme (COX) has 2 types, COX-2, which is 
present at sites of inflammation and COX-1, which is present in the 
stomach. 

■ So COX-2 inhibitors will not affect the gastrointestinal mucosa. 



GIT 







3. Smoking: 



Decreases ulcer healing. 

Increases the incidence of recurrence. 



ft Other factors: 



Reflux is responsible for ulcers at lower esophagus. 
Gastrinoma (Zollinger-Ellison syndrome). 
Peptic ulcer (PU) is more common in men than women. 
Familial incidence especially in duodenal ulcer (DU). 
Peptic ulcer is more common with blood group O. 



PU and gastritis occurs in cirrhotics due to decreased destruction of gastrin & 
histamine by the liver and decreased mucosal viability due to congestive 
gastropathy. Gastritis and PU also common in uremics (see nephrology). 



Symptoms? 

1 ■ Epigastric pains 

.Character;. Burning, stabbing, or dull ache. 

Site -..(patient points to the epigastrium) 

- The patient can indicate its site with two or three fingers (the 
pointing sign). 

- Back pain suggests penetrating ulcer. 

RelajtimLtojmealsL(variable) 

- Duodenal ulcer: it is worse when the patient is hungry & at night. 

- Gastric ulcer: It occurs 0.5-1 hr after meals. 

Night pain : Pain wakes the patient from sleep suggests DU. 

PainreHef: 

- Duodenal ulcer: Food, antacids and vomiting. 

- Gastric ulcer: fasting, antacids and vomiting. 

2* tf atlSCai may accompany the pain. 

3« Vomitings It is infrequent but often relieves the pain. Some patients 
learn to induce vomiting for pain relief. 

ft. CI bleeding: 

- It may be manifested by hematemesis or melena. Also chronic 
undetected blood loss may occur leading to anemia. 

5. APPCtitCS Is variable: 

- Duodenal ulcer: It increases in most cases. Also the patient may 

identify the pain as hunger pain and obtains relief 
by eating, weight gain may occur. 

- Gastric ulcer: Patient suffers from sitophobia for fear of pain, 
weight loss may occur. 

15 



GIT 






6. Heart blll'li: It occurs due to acid regurgitation. Water brash also may 

occur. 

7. Episodic pain (Periodicity): 

This will occur especially in duodenal ulcer. The pain occurs in (on 
again/off again) episodes lasting 2-3 weeks at a time, three or four 
times in a year. Between episodes the patient feels well. 

8. Manifestations of complications: (See Later) 

In some patients the ulcer is completely silent, presenting for the first time 
with complication 

Signs: (May l>c negative) 

-Tender epigastrium. - Signs of anemia. 

- Signs of peritonitis with perforation. 

Investigations: 

I. Upper endoscopy: 

- For exclusion of GERD or malignancy & to differentiate 
between benign & malignant gastric ulcers. 

- All gastric ulcers should be biopsied. 

II. Barium isicais fiess comm only used tlian endoscopy) 

£aMric.ulcer;. 

- Ulcer niche on the lesser curvature with serial films. 

- Notch on the greater curvature opposite the niche. 

.Duo.de.naL.U.lcer- deformity of the duodenal cap with serial films. 

III. Investigations for Hel icobacter pylori: 

1. Serum antibodies: detect IgG antibodies (sensitive and specific) 

but are not useful for eradication. 

2. Urease test: biopsies are added to a urea solution; in positive cases 

the urease splits urea to release ammonia giving color 
change in the indicator, as ammonia raises the pH of 
the solution. 

3. Culture: biopsies obtained can be cultured. 

4. Histology: H. pylori can be detected histologically by (Giemsa) 

stained sections of gastric mucosa obtained by biopsy. 

Non invasive method to diagnose H. pylori is 13 C urea breath test by measuring of 
13 C0 2 in the breath after ingestion of C urea. It is a quick, easy screening test. 



D.D. * Pancreatitis * Cholecystitis 

* GERD, Cancer stomach * Inferior wall myocardial ischaemia or infarction. 




GIT 

Complications: 

1. Hemorrhage, haematemesis, melena or anaemia 

2. Fibrosis and obstruction 

a) Gastric outlet obstruction. b) Hour-glass stomach. 

3. Perforation: (common in duodenal ulcer) 

This causes generalized peritonitis, or subphrenic abscess. Plain 
chest X ray showing pneumoperitoneum. 

4. Penetration: Pain usually is sudden and radiates to the back, with 

rise of serum amylase. 



MallHllclllCyS In gastric ulcers?? (Malignant gastric ulcer is mostly 

malignant from the start). 



Treatment: 

1 ■ Medical Treatment: 

The aim of medical treatment is to relief pain, induce ulcer healing and 
to prevent recurrence and complications. 

I.Diet : 

- Soft bland diet. It is better to be small and frequent. 

- Avoid irritant foods and smoking. 

- Avoid excessive milk intake as it may increase acidity due to 
its calcium content. 

2Jiz_WcKkers: (for 4-6 weeks to ensure ulcer healing) 

- Ranitidine (Zantac®) 300 mg/D. 

- Famotidine (Antodine®) 20-40 mg/D. 

3. Proton Pump Inhibitors (PPIs): (for 4-8 weeks) 

- Omeprazole (Losec®) 20 mg/D. 

- Pantoprazole (Controloc®) 40 mg/D. 

- Lanzoprazole (Lanzor®) 30 mg/D. 

.4.. Eradication. ofJHUPjjori: (Triple therapy for 2 weeks) 

- A proton pump inhibitor e.g omeprazole 20-40mg/D 

- Also 2 antimicrobials are used; Metronidazole 400mg/TID 
plus amoxycillin 750mg /TID or clarithromycin 500mg/TID are 
used. Heli-cure is a drug in the market containing tinidazole, 
omeprazole and clarithromycine, it is given one tab/1 2hr for 2 
weeks 

5. - Avoid NSAIDs, or use selective COX-2 inhibitors. 

- Cessation of smoking. 



17 



S%m. 



GIT 




II. Surgical Treatment off PU indicated In: 

1. Failure of medical treatment. 

2. Recurrent uncontrollable hemorrhage. 

3. Perforation or penetration. 4. Pyloric obstruction. 
5. Possible malignancy (See gastric carcinoma). 

Types gLsurgery 

1. Partial gastrectomy: 

- Billroth I -> the lower part of the stomach is removed and 

stomach remnant is connected to duodenum (a) 

- Billroth II -> the remnant of the stomach is connected to 

the first loop of jejunum (polyagastrectomy) (b). 

2. Highly selective vagotomy (c) 



w* 



(a) 



id 



(b) 







i ( 


V 


-^ v 


$* 



v„ 



-jrrf 



r 



»\ O i, \ - 



- "V*"Y 



/ 



i 












Partial gastrectomy - reduction of partial cell mass by removal of 

part of the stomach, (a) billroth I gastrectomy, (b) Polya (or Billroth II) 

gastrectomy, (c) Vagotomy - can be either (i) truncal, or (ii) highly 

selective with preservation of the antral and pyloric innervation. 




Roux-en-Y gastrojejunostomy 

Model illustrating a Roux- 
en-Y gastrojejunostomy. 



• Reduction of the parietal cell mass by removal of part of the stomach (partial 
gastrectomy) [see (a), (b)] 

• Elimination of the cephalic phase of acid secretion by division of the vagus 
[see (c)] 



18 



git m m* 

III. Treatment off Complications: 

1. Hemorrhage: 

- Omeprazole: by I.V infusion or ranitidine infusion. 

- Endoscopic injection of adrenaline or use of heater probe or 
laser therapy. 

- Blood transfusion: to restore the blood volume rapidly. 

- Surgery: for resistant cases. 

2. Perforation or penetration: nasogastric suction, IV fluids, 

antibiotics & analgesics, surgery is performed to repair 
the perforation with omental patch and drain the 
abdomen. 

3. Pyloric obstruction: see later. 

Complications of surgery 

1 ) Early Dumping Syndrome (postprandial vasomotor symptoms) 

- Nausea, distention associated with sweating, faintness, palpitation 
and flushing that occur following gastrectomy. It occurs .particularly 
after sweet foods (after 30 minutes). 

It is due to rapid gastric emptying of food into jejunum, which is 
followed by rapid influx of fluid to dilute the osmotic load, Also 
release of serotonine and VIP is incriminated. 

- This is treated by symptomatic treatment and ingestion of small 
meals with avoidance of fluids at meal time. Surgery may be 
indicated, e.g. Billroth II -^ Billroth I. 

2) Late Dumping Syndrome 

- Hypoglycemia in the second hour after eating due to rapid 
absorption of glucose causing hyperglycemia -> hyperinsulinemia. 

3) Diarrhea 

- This occurs after vagotomy due to motility disorders . 
It can be treated by loperamide. 

Cholestyramine may be helpful in cases of increased excretion 
of bile acids. 

It may occur due to bacterial overgrowth in the blind loop of a 
polyagastrectomy, antibiotics are helpful. 

4) Vomiting 

- It is due to trapping of food as a result of altered anatomy. 

- Treatment is symptomatic. 

5) Nutritional Complications (maldigestion and malabsorption) 

Iron deficiency anemia due to poor iron absorption. 

- B12 deficiency with long term gastritis with j, intrinsic factor. 

- Osteomalacia, protein malnutrition. 

8) Bezoar (see later). 7) Stagnant Loop Syndrome (see later). 
. _ 




GIT 

8) Alkaline or bile reflux Gastritis (Biliary gastritis ): 

Due to excessive reflux of bile and pancreatic and intestinal 
secretions into the stomach, it may result from gastric resection or 
bypassing the pylorus. It is unresponsive to antacids, sucralfate is 
better. Surgical diversion of pancreaticobiliary secretions away from 
gastric remnant with a Roux-en-Y gastrojejunostomy (See before). 

In recurrent ulcer after surgery, eradication of H pylori is important, also Zollinger 
Ellison syndrome must be considered. 

Pharmacology of Drugs used in Peptic Ulcer 

A. Acid neutralizing drugs: 

1. Antacids; 

Aim to increase pH above 4 so inhibits pepsin activity so relieves pain, 
also they accelerate healing. 

.Classification: 

1) Systemic: (NaHC0 3 ) Potent, rapidly acting but not used 

because of systemic alkalosis. 

2) Non systemic: (non absorbable & so don't disturb acid-base 

balance) 

- Mg oxide & hydroxide: reacts quickly but causes diarrhea 

- Mg trisilicate: reacts slowly to form Mg chloride. 

- Ca carbonate: reacts quickly to form CaCI, which is 
absorbable. It causes constipation and when combined 
with milk -> hypercalcaemia (milk alkali syndrome) with 
hypercalcemia and hyperphosphatemia. 

2. H» receptors antagonists: (for 4-6 weeks) 

They inhibit histamine receptors-inhibit both basal &stimulated gastric 
secretion accelerating healing: 

Cimetidine 

Side effects (Antiandrogen) : 1- Impotence. 2- Gynaecomastia. 

Dose : 200 mg four times / day (with meals & at bed time) 

Ran|t|d|jne__jmdLJFamp^ -> As cimetidine but with minimal side 

effects and do not cause impotence or 
gynecomastia. 
Dose : 

- Ranitidine: 1 50 mg twice/day or better 300 mg once at bed 

time. 

- Famotidine: 20-40 mg/day 

"~ 20 



M 



GIT 

3. Pi*oton pmnp Inhibitors: for 1 -8 weeks 

Omeprazole 20-40 mg/P, Lansoprazole 30mg/d 

- The final phase of H + secretion by parietal cells is helped by 
an enzyme called (H + , K + -ATPase) which serves as a proton 
pump exchanging potassium for hydrogen. 

- Omeprazole is specific to inhibit this enzyme so decreasing 
HCI secretion. It leads to hypergastrinaemia. 

B. Cytonrotectlve and coating agents: 

1 B 5*l<l'alf at€ (Gastl^Ofalt),, it is a complex salt of sucrose sulphate 

and aluminum hydroxide. 
Mechanism: 1 - It inhibits H + diffusion to the base of ulcer. 

2- Stimulates mucous and bicarbonarte secretion. 

3- It enhances mucosal defense and repair. 

4- Increases endogenous tissue PG so help healing. 

Dose: 1 gm. tab.1 hr. before each meal. It is good for biliary gastritis. 

It should be avoided in patients with chronic renal 
insufficiency to prevent aluminum induced neurotoxicity. 

2. Prostaglandin Ei analogue (Misoprostol) 

Mechanism: 1- Stimulates mucosal blood flow. 

2- Increases mucosal defense and repair. 

3- Increases mucous and bicarbonate secretion. 

It is mainly used as a cytoprotective agent in prevention of NSAID 
associated gastric ulcers. 200ug tab 2-4 times/D (Misotec). 

The main side effects are diarrhea and abdominal pain. 

C, Anticho linergic drugs !», 

P ir enzepine (gastrozepine), it is of limited value 

It is an anticholinergic 

-> i gastric secretion & delays gastric emptying. 

Side effects : - Dryness of mouth. 

- Tachycardia 

- Retention of urine. 

NB: Recently there are 3 muscarinic receptors Ml, M2, M3. 
Gastrozepine is selective on M1 so it is specific to stomach with 
fewer side effects. 

P. Bismut h containing preparations; 

Stimulate 

E, Therap y off H pylori (see before) 

— 



Acute Gastritis, 



GIT 




Erosions & Acute Ulcerations 



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. 

Etiology 

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 

(Lye) 

Pathology 

Mucosal edema and hyperemia with influx of neutrophils into the epithelial 
layer. Sloughing of the superficial epithelium (erosion) and haemorrhage may 
occur. 

Mechanisms 

1 . Increase acid production with back diffusion. 

2. Decrease production of surface bicarbonate buffer. 

3. Decrease mucosal blood flow. 

4. Direct damage to mucosal epithelium. 

Complications 

- Hematemesis. - Chronicity. - Perforation. 

Clinical Picture 

- Epigastric pain & tenderness. 

- Nausea, vomiting. 

- Hematemesis, melena. 

IllVCStigatiOllS: Upper endoscopy. 

Treatment 

1. Correct general condition. 

2. Treat the cause. 

3. Local measures. 

- Gastric wash by cold saline & antacids by Ryle tube. 

- IV ranitidine or omeprazole. Misoprostol can be used. 

4. Gastrectomy with failure of medical treatment. 



22 



GIT 



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). 

4. Chronic abuse of NSAID or aspirin. 

Clinical picture: 

- Asymptomatic. - Nausea, vomiting. 

- Epigastric discomfort. - Pernicious anemia (Autoimmune type). 

Investigation: 

- Upper endoscopy with biopsy. 

- Parietal cell antibodies and intrinsic factor antibodies in autoimmune 
gastritis. 

Treatment: 

- Cause. - Symptomatic treatment. 



Carcinoma of the Stomach 



Sex 6 Age -> > 45 
Predisposing 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 



Benign gastric ulcers have not been shown to develop into gastric 

cancer. 

Diets high in vegetables and fruits and low in salt protect against gastric 

cancer. 



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. 



23 



GIT 





Ulcerated mass 



Narrowed lumen from 
locally Infiltrating cancer 




Polypoid carcinoma 



"Linitls plasties" appearance of 
diffusely .Infiltrating carcinoma 



Diagrammatic representation of various presentations of gastric carcinoma. 

Microscop ic -> Adenocarcinoma (More than 90% of cases). 
-> Gastric lymphoma (fewer than 5%). 

Complications 

1. Spread : 

Direct to duodenum, esophagus, & surrounding organs. 
Blood -> Liver via portal circulation. 
Lymphatic -> para-aortic lymph nodes, 

Virchow's lymph nodes may occur. 
Peritoneal seeding (Transcoelomic spread) may occur with either 
diffuse nodules and ascites or deposits on the ovaries in females 
(Krukenberg tumour). 

2. Obstruction of: (Pylorus -> vomiting, Esophagus -> dysphagia). 

3. Perforation. 

Clinical picture 

■ Epigastric pain which is not differentiated from the pain of peptic ulcer 
disease. Both being relieved by food and antacid. 

■ Most patients have advanced disease at the time of presentation and also 
have nausea, anorexia and weight loss. 

■ Dysphagia can occur with tumors involving the fundus. 



24 




GIT 

■ 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 suprackavivular fossa (Virchow's node) 



Paraneoplastic syndromes with cancer stomach : 

* Trousseau's $ (thrombosis). * Acanthosis nigricans. 

* Membranous nephropathy. * Dermatomyositis. 

* Seborrheic keratosis (Laser-Trelat sign). 



Investigations : 

1. Endoscopy + Biopsy (8-10 biopsies should be taken from around the 

ulcer) 

2. Ba 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. 

Treatment 

A. Operable: radical and total gastrectomy with lymphadenectomy +■ 
esophago-jejunostomy with post operative chemotherapy 
plus radiation. 

B - Inoperable cases 

1 . Pyloric obstruction -> Palliative gastrojejunostomy. 

2. Cardiac obstruction -> Celestin tube. 

3. Laser ablation. 

4. Narcotics, celiac plexus block. 



Miscellaneous disorders of the stomach & duodenum 



A) Functional gastro-duodcnal disorders 

I. Gastropai'csls 

Causes: 

- Autonomic neuropathy e.g DM & uremia. 

- Scleroderma. 
Polymyositis. 

After gastric surgery. 

— — — 



_ git mm f" 

Clinical picture: 

Epigastric fullness and early satiety. 

- Anorexia, nausea and vomiting. 
Investigations : 

- Endoscopy. 

Radioisotope gastric emptying study. 
Treatment: 

- Cause. 

- Prokinetic drugs e.g. domperidone (Motelium). 

- Erythromycin is a macrolide antibiotic that stimulate smooth muscle 
motilin receptors located at all levels of the Gl tract (it mimic the effect 
of Gl peptide motilin) leading to prokinetic effects. It is of limited 
efficacy because of tachyphylaxis and side effects. 

II. Noil ulcer dyspepsia (Functional dyspepsia): 

It is a chronic dyspepsia (pain or upper abdominal discomfort) in absence 
of organic disease. Other symptoms include early satiety, fullness, 
bloating and nausea. 

Aetiolog y: (Mucosal, motility or psychiatric disorder) 

C/P: (as above plus) : 

There are two groups : 

- Ulcer like dyspepsia in which upper abdominal pain is dominant. 

- Dysmotility like dyspepsia in which upper abdominal discomfort 
(non painful) sensation is dominant. 

Investigation: (to exclude organic diseases) : 

- Endoscopy is important to exclude mucosal pathology. 

- Abdominal sonar may detect gall stones which are rarely 
responsible for the dyspeptic symptoms. 

Treatment: 

- Antacids, H 2 blockers. 

- Prokinetics e.g. domperidone given before meals. 
Low dose amitriptyline may be of value. 

- H pylori eradication is controversial. 



26 



git f gKmr 

B. Duodenal diverticulum 

- It is an outpouching of the duodenal mucosa. 

- Usually it is asymptomatic but it may perforate retroperitoneally, it may 
obstruct the bile or pancreatic ducts or it may bleed. 

- It is treated surgically. 

C. Bczoars 

- These are plant material present in the stomach in cases of gastroparesis or 
after gastric surgery. 

- There is pain, nausea and vomiting. Palpable epigastric mass may be 
present. 

- Diagnosis is by plain X-ray and endoscopy. 

- Treatment is by disruption at endoscopy or by enzyme ingestion. 

D. Pyloric obstruction or stenosis (gastric 
outflow obstruction} 

Causes (the obstruction may be prepyloric or in the duodenum) 

1- Active duodenal or gastric ulcer with surrounding edema. 

2- Healing of duodenal or gastric ulcer with scarring. 

3- Gastric malignancy. 

4- External compression due to pancreatic carcinoma. 

Clinical picture 

- Projectile vomiting, huge volume, the vomitus contains particles of 
yesterday's food. 

- O/E there a succession splash. 

- Persistent vomiting with loss of acid leading to metabolic alkalosis. 



- Barium meal. 

- Endoscopy. 

Treatment 

- Fluid and electrolyte replacement with nasogastric suction via a 
nasogastric tube. 

- Surgical intervention. 



GIT I HIIp 

Diseases of Intestine 




(Intestinal r-aikire) 
Definition: 

The malabsorption syndrome refers to a clinical condition in which a number 
of nutrients and minerals are not normally absorbed, however lipids almost 
always fail to be absorbed leading to steatorrhea (fatty stool). 

Causes 6 classification of malabsorption syndrome: 

I. Inadequate digestion 

AlJPG^t^MJ^ectojm^istejtpj^hej^ 

B) Deficiency or inactivation of pancreatic lipase. 
1 - Exocrine pancreatic insufficiency 

a) Chronic pancreatitis. 

b) Cystic fibrosis. 

c) Pancreatic resection. 

2- Ulcerogenic tumor of the pancreas e.g. Zolinger Ellison 
syndrome (gastrinoma). 

II. Reduced intestinal telle salt concentration: 

A) Liver disease, e.g. parenchymal liver disease or cholestasis. 

B) Abnormal bacterial proliferation in the small intestine. 

The bacterial proliferation leading to deconjugation of bile salts. 

QlJDmgsisjg^^^ 

• Neomycin. 

• Calcium carbonate. 

• Cholestyramine. 

ill, inadequate absorptive surfaces 

e.g. multiple bowel resections in cases of regional enteritis (short 
gut syndrome). 

IV. Lymphatic obstruction: 

• Primary intestinal lymphangiectasia. 

• Whipple's disease. 

• Lymphoma. 



28 



* 



GIT 

V. Cardiovascular diseases: 

Due to congestion and hypoxia of intestinal mucosa e.g. in cases 
of constrictive pericarditis and congestive heart failure. 

VI. Endocrine and metabolic diseases: 

• D.M due to bacterial proliferation. 

• Hyperthyroidism due to rapid gastric emptying and intestinal 
transit. 

• Adrenal insufficiency and hypoparathyroidism. 

VII. Intestinal Causes: (the most common) 

1 . Coeliac disease (gluten-sensitive enteropathy). 

2. Tropical sprue, Whipple's disease. 

3. Lymphatic obstruction e.g. intestinal Lymphangiectasia 
(Whipple's disease) or intestinal lymphoma. 

4. Inflammation: T.B & Crohn's. 

5. Parasites: Giardia Lamblia. 

6. Irradiation enteritis. 

7. Amyloidosis. 

8. Disarcharidase deficiency. 

Clinical Picture: 

I. Gastrointestinal manifestations: (Steatorrhoeal: 

1 . Generalized malnutrition and weight loss due to malabsorption of 

fat, carbohydrate and protein -> loss of calories. 

2. The stools are bulky, offensive, greasy & glistening. 

3. Diarrhoea, due to impaired absorption with increased secretion 
of water as the unabsorbed bile acids and fatty acids decrease 
absorption of water and electrolytes. 

4. Flatus due to bacterial fermentation of unabsorbed carbohydrate. 

5. Abdominal pain due to distention or inflammed bowel. 

II. Genitourinary: 

• Nocturia due to delayed absorption of water. 

• Azotemia and hypotension due to fluid depletion. 

III. Hematopoietic: 

• Anemia due to impaired absorption of Iron, vitamin B12 & folic acid. 

• Bleeding tendency due to vitamin K malabsorption. 

IV. Musculoskeletal: 

• Bone pain due to protein depletion leading to osteoporosis and 
also due to calcium malabsorption leading to osteomalacia. 

• Tetany and parathesia due to hypocalcemia. 

• Weakness due to anaemia and hypokalemia. 



29 




GIT 

V. Nervous system: 

• Night blindness due to vitamin A deficiency. 

• Peripheral neuropathy due to B12 and thiamine deficiency. 

VI. Skin: 

• Hyperkeratosis and dermatitis due to vitamin A deficiency. 

VII. Manifestations of the cause: 

• e.g. Regional enteritis, Whipple's disease, Celiac disease, or 
tropical sprue. 

Coeliac disease (gluten-sensitive enteropathy or 

non tropical sprue] 

Etiology: 

• Gluten is contained in the cereals e.g wheat, rye, barely & oats. 

• It can be fractionated to produce a, p & y gliadin peptides. 

• a gliadin is injurious to small intestinal mucosa. 

• The exact mechanism of damage to small intestine is not known, 
(immune mechanisms !?) 

• Most of patients have HLA-DQ2. 

Pathology: 

• There is subtotal villous atrophy, mainly in the proximal small bowel. 

Clinical Picture: 

• The peak incidence in adults is in the third and fourth decades, 
female > male. 

• The main presentation is malabsorption syndrome. 

• Dermatitis herpetiformis (blistering subepidermal eruption of the skin) 

• There is increased incidence of auto-immune thyroiditis & IDDM. 

• Other associated diseases include inflammatory bowel disease, liver 
disease & fibrosing alveolitis. 

Investigations: 

1 . Endomysial antibodies (IgA) (sensitive & specific). 

2. Jejunal biopsy: appearance of subtotal villous atrophy. 

3. Other tests for absorption. 

Treatment: 

Gluten-free diet produces rapid clinical and pathological improvement. 

Complic ations: Increased incidence of some tumors: 

- Intestinal lymphoma. - Carcinoma of S.I. 

- — 



GIT 







vmus 



Tropical Sprue 

Etiology: 

• It occurs in residents or visitors to tropical areas 

• The etiology is not known, but it is likely 
to be infective. 

Clinical Picture: Normal **-V. '.-MHM J *** 

• Malabsorption syndrome. 

• The onset is sometimes "acute and 
occurs either a few days or many years 




Villus 



after being in tropics. ». /_/ * •! !• • H ^^ 

_ m _ _ a r Partial villous [ ♦ *-» « " 

Pathology: ^mi 

• There is partial villous atrophy. 
Treatment: combination of : - 

• Tetracycline: 1 gm/D for up to 6 months. \U\ \\' "til )'• Crypl 

• Folic acid: 5 mg/day. SuWola , „l 

• Vitamin B 12 is given to all acute cases. atT °P h y I • 

Blind (stagnant! loop syndrome 

[Intestinal bacterial overgrowth) 

Causes 

l-_St_l^ctural abnormalities producing stasis of intestinal contents: 

• Small bowel diverticulae. 

• Strictures e.g. regional enteritis. 

• Billroth II gastrectomy with afferent loop stasis. 

2r„F|stulas- 

• Gastrocolic. • Jejunocolic . 

3- Hy porno tility of intestine: 

• Scleroderma. • Diabetes mellitus. 

• Hypothyroidism. 

4- Miscellaneous: 

• Hypogammaglobulinemia. 

• Gastric hypochlorhydria e.g. subtotal gastrectomy, pernicious 
anemia or prolonged use of H 2 receptor antagonist. 

Bacterial overgrowth may lead to deconjugation of bile salts affect the process of 
digestion and absorption. Also there is B12 deficiency probably due to uptake of 
vitamin B12 by microorganisms. 

C/P : manifestations of the cause + malabsorption $. 

Investigations: 

bacterial count of jejunal aspirate and glycocholic acid breath test (see later), 
ft treatment of the cause, antibiotics, surgery. 



31 




GIT ' '' 



Whipple's Disease 



This is a rare disease affecting males, it is caused by bacilli called (Tropheryma 
whippelii). There is obstruction of lymphatic drainage causing fat malabsorption. 

Clinical Picture: (Multisystem disease) 

• Steatorrhea • Weight loss, fever. 

• Abdominal pain • Pericarditis, meningitis 

• Lymphadenopathy • Arthritis precedes intestinal symptoms 

Investigations: 

• Biopsy, electron microscope showing macrophage infiltrating the villi. 

• The organism is also diagnosed by PCR. 

Treatment : dramatic improvement with antibiotic e.g. ampicilin, tetracycline or 
chloramphenicol. 

Investigations of Malabsorption Syndrome: 

I. Biochemical Investigations: 

1. Quantitative determination of stool fat (faecal fat) 

- Normally, faecal fat is less than 6 gm/24h. 

- In steatorrhoea, faecal fat is increased. 

2. D-xylose absorption test: 

- We give 25 gm D-xylose (pentose) orally and 5 hours urinary 
excretion of D-xylose is estimated. 

- Normally: 5 hours urine should contain > 4.5 gm and peak 
blood level more than 30 mg/dl. In malabsorption urinary and 
blood levels are below normal. 

4„t. Glucose .tpteraiicejtest;. 

- Flat curve in intestinal malabsorption. 

- Normal or diabetic curve in pancreatic malabsorption. 

II. Hacmatolog icai Investigations: 

1. Blood picture: 

- Iron deficiency leads to: Microcytic hypochromic anemia. 

- B12 or folic acid deficiency leads to: Macrocytic 
normochromic anaemia. 

2iJPl3MaLa^J[pjtein.S: There is hypoproteinaemia. 

3. Estimation of serum electro lytes: 

- Diminished Ca, P, Fe, Na, K, CI & magnesium. 




GIT 

III. Radiological Investigations: 

Barium meal & follow through study of S.I.: 

Will show the "Malabsorption Pattern": 

- Loss of the normal feathery appearance of jejunum. 

- Segmentation or clumping of barium. 

IV. Schilling test for vitamin B i » absorption: <see hematology) 

V. Intestinal Biopsy: 

- Jejunal biopsy showing the mucosal appearance. 

VI. Tests for Bacterial Overgrowth: 

1. 14 C - g lycochqlic acid breath test: 

- Patient is given radioactive 14 C labeled glycocholic acid orally. 
If there is bacterial overgrowth, bacteria will deconjugate the 
bile acid with release of 14 C-glycine, which is metabolized and 
appears in the breath as 14 C02. 

- Normally, there is <10 3 organisms/ml. if there is >10 5 
organisms/ml, this indicates bacterial overgrowth. 

Treatment of malabsorption syndrome: 

I. Treatment of the cause: 

1 . Surgery for strictures or fistulae. 

2. Antituberculous drugs for T.B enteritis. 

3. Flagyl for giardia, antibiotics for Whipple's disease and tropical sprue. 

4. Gluten free diet for celiac disease. 

5. Antibiotics and surgery for stagnant lobe syndrome. 

II. Parenteral fluids and feeding with supplements of the deficient 

elements. Total parentral nutrition can be used. 



Dysentery 



Dysentery is an acute inflammation of the large intestine characterized by diarrhea 
with blood and mucous in the stool. Tenesmus also occur with rectal involvement. 

Causes: 

1. Amoebic dysentery. 3. Bilharzial dysentery 5. Cancer rectum. 

2. Bacillary dysentery. 4. Ulcerative colitis. 6. Diverticulosis. 



33 



GIT 




Intestinal Amoebiasis 



Etiology and Pathology: 

- Amoebiasis is usually caused by entamoeba histolytica. Cysts of 
E. histolytica survive well outside the body and are ingested in water or 
uncooked food which has been contaminated by human feaces. 

- In the colon the vegetative trophozoite forms emerge from the cysts. 
Under certain conditions the amoebae invade the mucous membrane 
of the large bowel. The lesions are usually maximal in the caecum. 

- A localized granuloma (amoeboma), presenting as a palpable mass in 
the rectum or causing a filling defect in the colon on radiography. 

- Amoebae may enter a portal venous radical and carried to the liver 
where they multiply rapidly and destroy the parenchyma causing an 
amoebic abscess. 

Clinical Presentations: up is highly variable) 

I. Asymptomatic cvst passers. 

They pass cysts in stools leading to spread of infection. 

II. Acute Amoebic D ysentery: 

Acute onset of colitis with the following: 

- Diarrhea with mucus and blood. Bloody diarrhea may occur. 

- Tenesmus, flatus & abdominal discomfort. 

- Tenderness over the caecum & sigmoid colon. 

- The right iliac pain may simulate acute appendicitis. 

- The general condition is good but headache, nausea & anorexia 
may occur. 

III. Chronic intestinal amoebiasis: 

This takes the form of recurrent short attacks of diarrhoea or dysentery, 
alternating with normal bowel habits. Abdominal distension with 
constipation may occur. 

Complications: 

1 . Hepatic amoebiasis with amoebic liver abscess. 

2. Amoeboma (mass of fibrotic granulomatous tissue most commonly 

in the caecum or rectosigmoid region). 

3. Haemorrhage and stricture. 

Investigations: 

1. Stool examination: showing vegetative or cyst forms. 

2. Si gmoidoscopy: Flask shaped ulcers. 

3. Abdominal sonar or CT: For diagnosis of amoebic liver abscess. 

4. Serological tests : Antibodies are detectable by immuno- 

fluorescence in the serum of patients. 

. _____ __ 



G/7__jMpr 

Treatment: 

- Invasive intestinal amoebiasis responds to oral metronidazole 800 
mg/8 hours for 5 days (tissue and luminal amoebicidal). 

- Diloxamide (furamide) 500 mg/8 hours for 10 days to eliminate 
luminal cysts (luminal amoebicidal). 

- Stools are re-examined 4 weeks later. 



Tinidazole (fasigyn - protozole) single dose of 2 gm daily for 3 days. 

It is tissue and luminal amoebicidal. It can be used instead of metronidazole. 



Bacillary Dysentery 



[Shigellosis) 



Etiology: 

(bacilli belong to the genus Shigella) 

- Shigella bacilli which are Gram -ve & non-motile. 

- There are 4 groups of shigella: S. dysenteriae, S. flexneri, S. boydii, 

S. sonnei. 

Epidemiology and Mode of Infection: 

- Bacillary dysentery is endemic allover the world. 

- Feco-oral transmission by contaminated food or by flies, but contact 
through unwashed hands after defecation is the most important 
factor. 

Clinical Picture: 

(children under 5 years are predominantly affected, the incubation period is 

usually 48 hours) 

Abdominal pain. Watery Diarrhea wit h Fever and malaise . 

- Severe cases showing bloody diarrhea with mucus, tenesmus and 

severe cramping abdominal pain. 

- Dehydration may occur in severe conditions. 

- Tenderness along the course of colon. 

- Nausea, vomiting and headache may occur. 

- Arthritis, conjunctivitis, urethritis occasionally complicate bacillary 

dysentery (Reiter's Syndrome). 

Investigations: 

1. Stools: 

Excess WBC's & RBC's. Faecal culture demonstrates the organism. 

2. Sigmoidoscopy: 

The colonic mucosa is red and swollen with pseudomembrane. 

___ - — 



git J B MM5y 

Tl'CatmClltZ (shigellosis is an acute self limiting intestinal infection) 

1. Fluid replacement: Excess oral fluids & IV fluids in severe conditions 

2. Antibiotics (GIT antiseptic): Ciprofloxacin 500 mg twice daily or 

trimethoprime 200 mg/12 hrs for 5 days in severe cases. 

3. Antispasmodics: in cases with severe abdominal colics only !?. 



Drugs which decrease intestinal motility, e.g. diphenoxylate (lomotil) & antispasmodics are 
better to be avoided as they may decrease the intestinal wash of the organisms. 



Intestinal Bilharziasls 



Etiology: 

It is mainly due to S. mansoni, it may be caused by S. haematobium. The 
colon is predominantly affected. It may be asymptomatic. 

ClilllCal PiCtUrC (see tropical diseases) 

I. Colonic and hepatic bilharziasis. 

- There is bilharzial dysentery. 

- Bleeding per rectum. 

- Anemia & clubbing may be present with intestinal polyps. 

- Hepatosplenomedaly with portal hypertension. 

- A localized granulomatous reaction in the intestine (bilharziomajmay 
' be felt in left Uiac fossa. It may be mistaken for a colonic tumor. 

II. Manifestations of complications: See tropical diseases. 

llftVCStifJdtlOllS: (see details in tropical diseases) 

1. Stools examination: for bilharzial ova. 

2. Blood picture: for anemia & eosinophil. 

3. Serological tests: see tropical diseases. 

4. Sigmoidoscopy & rectal biopsy for ulcers or polyps 

5. Barium enema: For polyps in the colon. 

Treatment: 

/. Antibilharzial drugs: S$q tropical diseases. 

I{. Symptomatic treatment and treatment of complications. 

III. Colonoscopic polypectomy. It can control the number of colonic 
polyps. 

. ■ . — 



22_jMpr 

Inflammatory Bowel Disease 



There are two major forms of inflammatory bowel diseases; Crohn's disease which 
can affect any part of the Gl tract & ulcerative colitis which affects only the large 
bowel. Both of them are chronic non specific inflammation. 

There is overlap between these two conditions, so it is necessary to distinguish 
between these two conditions as there are differences in their management. 

Biology: unknown 

1. Familial: The condition is more common amongst relatives of the 
patients than in the general population. 

2. Genetic: there is HLA B27 relation in patients with inflammatory bowel 
disease and ankylosing spondylitis. 

3. Auto-immune!? 

4. Diet: high sugar intake has been found in patients with Chron's 
disease. Smoking is protective in ulcerative colitis and worsens Crohn's 
disease 

5. Infective agent!? 



I. Ulcerative Colitis 



Pathology: 

Site of involvement 



• It can affect the rectum alone (proctitis), or extends proximally to 
involve the sigmoid and descending colon. 

• It may involve the whole colon. 

• Inflammation of the distal terminal ileum may occur (backwash ileitis). 

Macroscopi c cha ng es 

• Diffuse inflammation limited to the mucosa. 

• There is extensive ulceration, with the adjacent mucosa appearing as 
inflammatory polyps. 

Microscopic changes 

• Crypt abscesses is the characteristic lesion, which will progress to 
ulceration. 

37 



GIT / < 

Clinical Picture: 

- Age: This occurs at any age but most frequently between 20-40 years. 

- Sex: women are affected more than men. 
^ Intestinal Manifestations 

- Bleeding per rectum. 

- Diarrhea (bloody diarrhea) with mucous. 

- Tenesmus, when the disease is confined to the rectum. 

- Abdominal discomfort. 

- Remissions & exacerbations. 

- Abdominal examination: The abdomen may be slightly distended or 
tender on palpation. 

- Rectal examination: It may show blood. 

11. Extra-intestinal Manifestations: (occur in Crohn's and ul c erative 
colitis}. 

Joints: Eye: 

- Sacroiliitis. - Uveitis. 

- Ankylosing spondylitis. - Conjunctivitis. 

- Monoarthritis. - Episcleritis. 

Skin: Kidney and gall bladder: 

- Erythema nodosum. - Stones. 

- Pyoderma gangrenosum. 
Liver and biliary tract 

- Fatty liver. - Autoimmune hepatitis. 

- Sclerosing cholangitis. - Liver cirrhosis. 
Misallaneous 

- Amyloidosis. - Hypercoagulable state. 

Investigations; 

1 . Stool examination and culture: To exclude other causes of diarrhea. 

2. Blood e xamina tion: 

- Anemia of chronic disease (normchromic, normocytic) 

- There is often raised ESR, CRP and total leucocytic count during 
exacerbation. 

^•Barium enema: 

- Loss of haustrations with narrowing of the lumen. 
4. Sigmoidoscopy: 

- The mucosa is edematous, friable and bleeds. 

- Ulcers & pseudo-polyps. 

- Biopsy showing crypt abscesses 

Normocytic normochromic anemia of chronic disease, t ESR, | CRP and t TLC 
usuall y occur in both types of inflammatory bowel disease. 

. . — 



GIT I J\ 

Treatment: 

A, General Me asu r es: 

1 . Diet: low residue diet. 

2. Blood transfusion: In cases of severe bleeding 

3. Fluid therapy for dehydration and electrolyte disturbances. 

B. Medical treatment: 

/- Sulphasalazine (Salazopyrin): 

- Sulphasalazine consists of a 5-aminosalicyclic acid (5- 
ASA) attached to sulphapyridine as a carrier; this 
combination is broken down in the colon by bacteria to 
release the active agent 5-ASA which acts locally. 

- Oral 5-ASA only is not effective because it is absorbed 
from the small intestine and therefore does not reach the 
colon. 

- Sulphasalazine is started at a dose of 3-4 gm/D reduced to 
a maintenance dose of 2 gm/D. in mild cases it may induce 
a remission, but its main role is to reduce the number of 
relapses when taken long term. 

//- Corticosteroids: 

They can be used as follows. 

- Mild attacks and proctitis can be treated with local rectal 
steroids as retention enemas. Also mesalamine enemas 
are useful. 

- Moderate attacks are treated with oral prednisolone 
30-40 mg daily. 

- Severe attacks treated with high dose, 60 mg prednisolone 
daily. 

///- Other drugs: 

Medications for diarrhea (loperamide or codeine 
phosphate). 

- Antibiotics for secondary bacterial infection and 
septicaemia with gram negative bacteria. 

- Azathioprine (Immuran): for cases not responding to steroids. 

- Cyclosporine should be tried before advocating colectomy. 



Maintenance of Remission: All patients are maintained on 5-ASA compound for 

many years after remission. Patients who 
frequently relapse despite 5-ASA are treated with 

_ __ thioprines (azathioprine). ___ 

___ 39 



GIT 

Medical management of fulminant ulcerative colitis : 

- IV fluids. - Blood transfusion. 

- Antibiotics. - Nutritional support. 

- IV cyclosporine or infliximab. - IV methylprednisolone 60mg/d. 

- Heparin for prophylaxis of venous thrombosis. 




C Surg i c al T reatment; 

- The main indication is poor response to medical treatment 
or occurrence of complication. 

- Proctocolectomy with terminal ileostomy or colectomy with 
ileo-rectal anastomosis. 

II. Crohn's Disease 

(Regional enteritis) 
Biology: 

Similar to ulcerative colitis, but it occurs more in smokers. It usually affecting 
young adult 

Pathology: 

- The disease may affect any part of GIT from the mouth to the anus, but it 
has a particular tendency to affect the terminal ileum & ascending colon. 

- The disease may affect multiple areas with relatively normal bowel in- 
between ("skip lesions"). It may also involve whole of the colon. 

Macroscopic: 

- The involved small bowel is usually thickened & narrowed. 

- There are deep ulcers and fissures in the mucosa giving a cobblestone 
appearance. 

- Fistulae & abscesses may occur. 
Microscopic: 

- The inflammation extends through all layers of the bowel (transmural). 

- There is chronic inflammatory cells with lymphoid hyperplasia, granulomas 
may occur in 50 % of patients. 

Clinical Pictures 

- Diarrhea, Abdominal pain and weight loss. Constitutional symptoms of 
malaise, low grade fever, nausea and vomiting. 

- The patient may present with acute right iliac fossa pain mimicking acute 
appendicitis. The condition is also similar to terminal ileitis caused by 
yersinia. 

- The presentation of Crohn's colitis is usually similar to ulcerative colitis. 

- Abdominal examination is often normal, although tenderness and right iliac 

fossa mass may be present. 

_ _ _ — 




GIT 

Investigations: 

.1. Barium follow-through for small bowel: 

May show alteration in mucosal pattern, with deep ulceration, areas of 
narrowing in the ileum (string sign). Skip lesions with normal bowel in- 
between are also seen. 

2 Barium enema: 

May show colonic disease, it is usually patchy with deep ulceration 
(late). 

3 Qolpnoscopy. 

It is performed if colonic involvement is suspected with biopsies. 

4 Mitraspnpgraphy & CT: (particularly spiral CT) 

To detect abscesses, masses, thickened bowel wall & mesentery or 
other extraluminal problems. 

Treatment: 

1. General measures: for diarrhea, abdominal pain, anemia, and electrolyte 

disturbances. 

2. Corticosteroids: for moderate/severe attacks 30-60 mg prednisone/day. 

3. Sulphasalazine: for colonic involvement. 1gm/8hr. 

4. Immunosuppressive agents: Cyclosporine can be tried, azathioprine 

is helpful to maintain the steroid induced 
remission. 

5. Monaclonal antibodies against TNF (infliximab) i.e. biological therapy. 

6. Metronidazole (800 mg three times daily) and Cotrimoxazole (two 

tablets twice daily) are useful in severe perianal disease, 
possibly owing to their antibacterial action. 



Maintenance of remission: Some patients can come off all therapy!?. 

other require a small dose of steroids 
and/or long term azathioprine therapy. 



7. Surgery. Consists of resection & end-to-end anastomosis or stricturoplasty. 
The indications of surgery are: 

Failure of medical treatment. 

Complications: obstruction, perforation, fistula, stricture or abcesses. 

Complications of inflammatory bowel disease 

1= Perforation of the intestine leading to abscesses and peritonitis. 

2- Stricture of S.I and short gut $ in Crohn's disease. 

3- Hemorrhage and anaemia. 

4- Toxic meaacolon is more common in ulcerative colitis. 

5- Carcinoma of the colon. 6- Amyloidosis kidney. 

. — 



GIT fff*^ 

Functional bowel disorders 



Functional bowel disease is a general term used to include the irritable bowel 
disease, pain/gas/bloat syndrome and functional diarrhea. 

Pain/gas/bloat syndrome 

There is abdominal pain and distension. The abdominal pain is exacerbated 
by eating and not relieved by opening the bowels and not associated with diarrhea 
or constipation. The abdominal distension is not restricted to the upper abdomen, 
also there is postprandial fullness. It is treated by selective serotonine reuptake 
inhibitor paroxetine (Seroxat) combined with prokinetic drug e.g. domperidone or 
smooth muscle relaxant e.g. mebeverine (duspataline or colospasmin). 

Functional diarrhea 

There is diarrhea in absence of abdominal pain. The first stool of the day is 
usually formed, the later ones are looser or watery. There is urgency of detection. 

It is important to exclude other causes of diarrhea either functional or organic. 

It is treated by Loperamide (Imodium) and tricyclic antiodepressant at night 
e.g. clomipramide (Anafranil) 10-30 mg. _____ 



♦ Features against functional diarrhea are large volume stool, rectal bleeding, 
nutritional deficiency and weight loss. 

♦ Chronic diarrhea without pain is caused by many diseases (see causes of 
diarrhea in the practical parts). 



Irritable bo%vel syndrome 

PCflllltlOlM 

It is a functional bowel disorder in absence of structural pathology. 

Etiology: 

The etiology is uncertain:- 

(1) Psychological disturbances e.g. anxiety and somatisation are evident. 

(2) Altered Gl motility. (3) Visceral hypersensitivity 
(4) Luminal feptors e.g. abnormality in gut flora. 

Clinical Picture: (long history with long symptom free intervals) 

1 . Recurrent abdominal pain: it is classically situated in the left iliac fossa. 

2. The pain is decreased by defecation or passing flatus. 

3. There is constipation or diarrhea with feeling of incomplete evacuation. 

4. The stools may be ribbon like with passage of mucus. 

5. Abdominal distention is extremely common. 

6. Abnormal stool passage e.g. straining or urgency. 

7. Tenderness over the sigmoid colon. 

8. Features of irritable person usually present. 



42 



GIT JMP ^, 

Diagnostic criteria (Rome criteria) 

Abdominal discomfort or pain that has two of three of the following 
features: 

■ Relieved with defecation, and/or 

■ Onset associated with a change in frequency of stool, and/or 
■ Onset associated with a change in form or appearance of stool. 



o Abnormal stool frequency i.e. > 3 / day and < 3 / week, 
o Abnormal stool form (hard, loose, watery, lumpy). 

Non GI features of irritable bowel syndrome: 

Dysmenorrhoea. - Premenstrual tension. 

Headache. - Bad breath. 

Unpleasant taste in the mouth. - Poor sleeping, fatigue. 
Urinary symptoms e.g. frequency, urgency. 

Factors that can trigger irritable bowel syndrome: 

GI infection. - Antibiotic therapy. 

Psychological stress. - Mood disorders 

Eating disorders. - Pelvic surgery 

Investigations; No positive findings. 

- Recurrent pain in the right hypochondrium is usually not due to gall bladder 
disease, but to the irritable bowel syndrome. 

- Recurrent pain in the right iliac fossa is not due to chronic appendicitis, but to 
the irritable bowel syndrome. 

Treatment: 

1 . Patients must be reassured of the benign nature of the condition. 

2. A high fiber diet and bran are helpful. 

3. Smooth muscle relaxants for pain e.g. Mebeverine. 

4. Selective serotonin reuptake inhibitor paroxetine (Seroxat) in constipation 
predominant. 

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

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



Other GI symptoms suggestive of psychosomatic [functional! disorders: 

• Nausea alone. • Halitosis. • Abdominal bloating. 

• Vomiting alone. • Belching. Chronic right hypochondrial pain. 



Chronic left iliac fossa pain. 



43 



GIT 



Megacolon 




I- HirSChSPrUUg'S dlSCaSC: (usually presents in the first years of life) 

• This is a familial disorder due to congenital absence of the myenteric 
nerve plexus in the wall of the pelvic colon and upper rectum. The 
involved segment constitutes a functional obstruction but the normal 
proximal colon becomes dilated. 

• Constipation, abdominal distention and vomiting since birth. 

• There is persistent abdominal swelling and the rectum is empty on 
digital examination. 

• Barium study showing wide dilatation of the colon. 

• Rectal biopsy can confirm the diagnosis. 

• Treatment is by excision of the abnormal segment of colon and rectum. 

II- Acquired megacolon In the adult, causes: 

• Psychogenic megacolon: 

- Disregard for urge to defecate. - Antidepressant drugs. 

• Prolonged laxative abuse due to degeneration of myenteric plexus. 

• Scleroderma, hypothyroidism due to chronic constipation. 

• Toxic megacolon in ulcerative colitis. 

• Most patients managed by treatment of the cause, prokinetics, subtotal 
colectomy may be needed. 



Cancer Colon 



AgC 6 Sex: Male, old age (60-65 years). 

Predisposing factors 

1 . Familial polyposis. 

3. Excessive consumption of meat and animal fat. 

5. Ulcerative colitis. 



2. Family history. 
4. Low dietary fibers. 



The risk of developing adenoma and carcinoma is reduced among aspirin and 
NSAID users !?. 



Pathology 

Macro 

1 . Cauliflower mass. 
Micro: Adenocarcinoma 



2. Malignant ulcer. 



3. Infiltrating mass. 



Modified Puke's classification off colorectal carcinoma 

- 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. 



44 



GIT 



m 



ClllllCal PiCtllPCS (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 is usually unhelpful, a mass may be palpable and 
hepatomegally may present with liver metastases. 



Any change in bowel habit or bleeding per rectum must be investigated 
especially in old age. 



Investigations 

1. Barium enema (double contrast). 

2. Lower Gl Endoscopy + Biopsy. 

3. Carcinogenic embryonic antigen may be helpful. 

4. CT and abdominal sonar for hepatic metastases. 

Treatment 

Operable Cases -> Resection with end to end anastomosis. Right 

sided tumours are removed by right 
hemicolectomy and those on the left by a 
resection tailored to the segment of bowel 
involved. 

Chemotherapy+ radiotherapy plus palliative 
surgery e.g Colostomy. 



Inoperable Cases-} 



Diverticular Disease of the Colon 



Pathology 

- There is pouches of mucosa extrude 
through the muscular wall through 
weakened areas near blood vessels form 
diverticula. 

- This is more common in the sigmoid colon 
due to high intraluminal pressure. The 
disease may be related to the low fiber 
diet with longstanding constipation. 

- Diverticulitis occurs when faeces obstruct 
the neck of the diverticulum -> stagnation 
-> bacterial multiplication -» inflamm- 
ation. This may lead to perforation, 
abscess, fistulae and peritonitis. 



Mesocolon 
Circular muscle 
Diverticulum 




Taenia 
(longitudinal muscle) 

The human colon In dhmrtlculosft 



45 



Ml 

GIT ( XW 

ClilllCdl l>iCt(ll*€ (old age with longstanding constipation) 

1- It is asymptomatic in 90% of cases. 

2- Recurrent pain in left iliac fossa. 

3- Alternating constipation and diarrhea. 

4- Bleeding per rectum. 

5- Diverticulitis leads to symptoms and signs similar to appendicitis but on 
the left side. 

Complications 

- Perforation with peritonitis. 

- Fistula with urinary bladder with dysuria and pneumaturia. 

Investigations 

- t ESR, t TLC. 

- Spiral CT of the lower abdomen showing the diverticulae. 

Treatment 

- Mild early diverticular disease can be treated by dietary fibers and 
agents to regulate the bowel motions. 

- Acute attacks of diverticulitis can be treated with metronidazole and 
cephalosporin. Few cases may require resection of the diseased 
segment. 



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. 

CHlliCal PiCtlll ft e (Symptoms usually begin in the mid 30s) 

- Abdominal pain. 

- Diarrhea, blood and mucous in stool. 



46 



GIT 




m 



Investigations 

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

- Upper Gl endoscopy as gastric, duodenal and periampullary polyps are 
also common. 

- All relatives must be examined by annual sigmoidoscopy after the age of 
1 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). 

Other Won Neoplastic Gastrointestinal polyposis syndromes 

- Peutz-Jeghers $ (colonic polyps + pigmentation of lips and fingers). 

- Turcot' $ (colonic polyps + malignant central nervous tumors). 

- Cronkhit-canada $ (colonic polyps + hair loss and hyperpigmentation). 

- Cowden's disease (colonic polyps + orocutaneous hamartomas, thyroid 
tumors). 



Neuroendocrine Tumors of the 



Gastrointestinal Tract and Pancreas 



Biologic considerations 

A striking feature of neuroendocrine tumors is the preservation of highly 
differentiated cell function. Tumor cells contain secretory granules and maintain the 
capacity for amine precursor uptake and decarboxylation (APUD); a process 
essential for production of monoamine neurotransmitters such as serotonin, 
dopamine and histamine. These cells also synthesize and secrete peptide 
hormones. 

Distribution of APUD tumors (APUDomas): 

- GIT: Carcinoid. 
Pancreas: Islet cell tumors. 

- Thyroid: Medullary carcinoma. 

- Skin: Melanoma. 

- Adrenal gland: Pheochromocytoma. 

- Lung: Carcinoid tumor and small cell carcinoma, 
(see the different types of APUDomas in different chapters). 



47 



GIT / f f f P^ 

Carcinoid Tumors 



These tumors originate from the enterochromaffin cells (APUD cells of the 
intestine). They make up 10% of the neoplasms of small intestine. 

Sites 

- Appendix. 

- Terminal ileum. 

- Rectum. 

Clinical picture 

* Clinically most carcinoid tumours are asymptomatic until metastasis are 
present. 

- So carcinoid syndrome occurs in only 5% of patients with carcinoid 
tumors when liver metastases occur. 

- Flushing on the face and neck. 

- Abdominal pain and recurrent watery diarrhea. 

- Wheezy chest. 

- Paroxysmal hypotension. 

- Endocardial fibrosis leads to T.S and P.S., T.I. 

- Examination of the abdomen reveals enlarged liver. 

- The diarrhea and cardiac complications are due to 5-HT. 

- The cutaneous flushing is due to kinins e.g. bradykinin causing 
vasodilatation, bronchospasm and increased intestinal motility. 

Investigations: 

- High level of 5-HT metabolite in urine, 5-hydroxyindole acetic acid 
(HIAA). 

- Abdominal sonar, CT for hepatic metastases. 

Treatment 

- Octreotide (somatostatin analogue) alleviates the flushing and diarrhea. 

- Interferon and other chemotherapeutic drugs can reduce tumor growth!? 

Prognosis 

- Most patients survive up to 5-1 years after diagnosis. 

_ __ . — 



GIT 



Intestinal obstruction 




It is termed as failure of passage of intestinal contents. 

I- Mechanical obstruction 

Causes 



* Luminal 



- Colonic tumours. 

- Gall stone ileus. 

* Mural 

- Stricture. 

- Hematomas from trauma. 

* Extramural 

- Adhesions from prior surgery. 

- Strangulated hernia. 

- Metastatic tumours. 



Foreign bodies. 
Meconium ileus. 

Intussusception. 
Ischaemia. 



Volvulus. 
Endometriosis. 



Obstruction of the bowel leads to bowel distension above the block, with 
increased secretion of fluid into the distended bowel. Bacterial infection 
occurs in the distended stagnant bowel. In strangulation the blood supply is 
impeded with gangrene, perforation and peritonitis unless urgent 
interference in undertaken. 



Diagnosis 



Abdominal colic, vomiting and constipation without passage of flatus. 

The vomiting is profuse in upper gut obstruction and may be absent 
in lower gut obstruction. 

Examination showing abdominal distension with increased bowel 
sounds, marked tenderness suggests strangulation. 

X-ray abdomen (Eract position) showing distended loops with air 
fluid levels in small bowel obstruction. In large bowel obstruction the 
caecum and ascending colon are distended, barium enema can 
diagnose colonic obstruction. 

CT scan can localize the lesion. 



Treatment 



IV fluids. 



Intestinal decompression with nasogastric suction or small bowel 
intubation. 



49 



g> 



GIT_ 

Laparotomy with removal of the obstruction in some cases of small 
bowel obstruction. If the bowel is gangrenous due to strangulation 
resection of the affected segment is required. 

In large bowel obstruction due to malignancy colorectal stents can 
be inserted. Volvulus of the sigmoid can be treated by passage of 
sigmoidoscope or a rectal tube to un-kink the bowel, recurrent 
volvulus may require sigmoid resection. 



II- Adynamic obstruction or paralytic ileus 

It is a nonobstructive lack of propulsion through the intestinal tract. 
Causes 

- Recent abdominal surgery. 

Electrolyte disturbance especially hypokalemia. 

- Chemical or bacterial peritonitis. 

- Severe intra abdominal inflammation, e.g. pancreatitis. 
Diagnosis 

- Abdominal distension with diminished bowel sounds. 

- X-ray abdomen shows diffuse intestinal gas. 

Treatment 

- Bowel rest (Nothing by mouth with nasogastric suction). 

- Treatment of the cause. 

- Neostigmine I.V. may be required. 



intestinal pseudoobstruction: 

Primary: 

- Visceral myopathy. - Visceral neuropathy. 

Secondary: 

- Collagen disease: scleroderma - polymyositis. 

- Endocrine disease: DM - Hypothyroidism. 

- Amyloidosis. - Drugs: tricyclic antidepressants. 

Diagnosis: Plain x ray abdomen showing a gas filled large bowel. 

Treatment: Treatment of the cause, prokinetic and cholinergic agents e.g. 

neostigmine. 



50 



GIT 



£> 



Acute appendicitis 



It is a common and curable cause of acute abdomen. It occurs in males > 
females between 1 0-30 years of age. 

Pathogenesis 

- The primary event is an obstruction of the appendiceal lumen by a 
fecolith, inflammation, foreign body or neoplasm. This lead to 
increased intraluminal pressure with infection leading to appendiceal 
necrosis and perforation. 

Diagnosis 

- Pain in the right lower quadrant which is vague and may be around 
umbilicus initially but becomes localized to MC Burney's point with 
rebound tenderness. 

- Rectal tenderness occur in pelvic appendicitis, also retrocecal 
appendicitis causes psoas muscle pain on hip extension. 



There is leucocylosis, CT and sonography are helpful. 



DP 

- Gastroenteritis. 

- Grohn's disease. 

- Oyarian Torsion. 

- Amoebic colitis 

Treatment: Appendictomy 



Mesenteric adenitis. 

Meckel's directiculum. 

Pelvic inflammatory disease (PID). 

Yersinia terminal ileitis. 



Meckel's diverticulum 

It is the most common congenital abnormality of the Gl tract, 
affecting 2-3% of the population. 

The diverticulum projects from the wall of the ileum about 60cm from 
ileocaecal valve. 

It is usually symptomless but about 50% contain gastric mucosa so 
peptic ulcers can occur and may bleed or perforate. 

Acute inflammation of the diverticulum may occur giving picture 
similar to appendicitis. 

Treatment is surgical removal laparoscopically. 



51 



_^____^_ git JBpr 

Call Bladder & Biliary System 

Anatomy of the biliary system (sec Hematology) 



The right & left hepatic ducts arise 
from the right & left lobes of the liver & 
unite to form the common hepatic duct, 
which is joined by the cystic duct from the 
gall bladder to form the common bile duct. 

The common bile duct passes 
behind the first part of the duodenum & 
enters its second part through a common 
channel at the ampulla of Vater. 



Heister's spiral valve 




Duodenal 
papilla 



Pancreatic duct 

Ampulla of Vater 
Sphincter of Oddi 



Gall Stones 



PrCValCIICC Gall stones are present in 10-20% of the population. 

Risk factors for cholesterol gall stones: 

- F > M. - Contraceptive pill, octreotide. 

- Obesity. - DM. 

- Rapid weight loss. - Increasing age. 

- Multiparity. - Diet (high in animal fat). 

- Liver cirrhosis. - TPN (| gall bladder emptying) . 

Etiology 6 types 

I. Cholesterol gall stones: 80%: 

1. Excess cholesterol in bile, due to increase in hydroxy-methyl- 
glutaryl-CoA (HMG-CoA) reductase which catalyses the 
cholesterol synthesis. 

2. Diminished bile salts synthesis in bile. 

II. Bile pigment stones : 20% : 

1. Black pigment stones: (contain calcium salts of bilirubin) 

caused by chronic haemolysis, e.g. spherocytosis. 

2. Brown pigment stones: (cholesterol, calcium salts of fatty acids 

and Ca bilirubinate) 

caused by stasis of bile in common bile duct e.g. by 
stricture, sclerosing cholangitis. 



52 



; GIT ( B Br 

Clinical Picture: 

1. The majority of cases (approximately 80%) are asymptomatic (silent) 
gall stones, discovered accidentally by abdominal sonar. 

2. A gall stone may impact in the neck of the gall bladder or in the cystic 
duct giving biliary pain or cholecystitis. 

3. Obstruction of common bile duct leading to pain, jaundice, cholangitis 
(bacterial infection). 

4. Biliary pain usually occurs in the epigastrium and right hypochondrium. 



Fatty, fertile, females above 40 years have the same chance of having gall 
stones as the rest of population. 



Complications of gall stones: 

- Pancreatitis, cholecystitis. 

- Obstructive jaundice (stone in C.B.D) and cholangitis. 

- Gall stones may erode gall bladder wall to the intestine leading to 
obstruction mainly in the terminal ileum (gall stone ileus) and biliary 
enteric fistula. 

- Increase risk of carcinoma of the gall bladder may be causally 
related!?. 

Treatment 

I. Non surgical Treatment of gall stone 

a. Medical dissolution (for cholesterol stones) by o ral bile acids. 

Indication: (patient selection) 

- Radiolucent stones. - Stones of diameter < 15mm. 

- Moderate obesity. - No acute symptoms. 
Methods: 

- Chenodeoxycholic acid 12 mg/kg/day. 

- Or ursodeoxycholic acid 8-12 mg/Kg/day. 

- Or combination of both. 
Duration: 1 -2 years. 

b. Ex tra corpor eal sho ck wave lithotri psy. 

c. Contact di sso l u tion therapy with methyl eth e r. 

II. Other medical measures 

Treatment of cholec ystitis: see later then cholecystectomy. 

Treatment of biliary pain: antispasmodics, NSAID or opiates e.g. 
pethidine. Morphine can be used In severe pain with 
concurrent use of atropine to reduce the increased tone 
of the sphincter of Oddi which is induced by morphine. 

III. Cholecystectomy either laparoscopic or bv 
minilaparotomv. 

— 



GIT 



Acute Cholecystitis 




Etiology 6 Pathophysiology 

- In over than 90% of cases the gall bladder contains gall stones, the 
initial event is obstruction to gall bladder emptying. 

- There is initially sterile inflammation, then becomes infected. 

- So, G.B. may distend with mucus (mucocoele) or pus (empyema). 

- Rarely, acute gangrenous cholecystitis occurs with perforation leading 
to peritonitis. 

Symptoms: 

1- Severe pain 

- In the right hypochondrium or epigastrium. 

- It can radiate to the back & right shoulder. 

- Pain lasts for hours (continuous, increasing in intensity oyer 24 hours). 

2° Nausea & vomiting may occur. 

Signs: 

2) Fever. 

3) Jaundice occurs in some cases, due to edema or stone in common bile duct. 

4) Positive Murphy's sign 

- Right hypochondrial tenderness being worse on inspiration. 

- There is guarding & rebound tenderness. 

Investigations: 

1- Blood count showing leucocytosis, raised CRP. 

2- Bilirubin, AST, ALT & alkaline phosphatase: may show mild elevation, 
significant elevation indicates bile duct obstruction. 

3- Ultrasound 

- Sonographic Murphy's sign (local tenderness over visualized GB) 

- Distension of G.B. 

4- Radionuclide scan e.g. (HI DA scan), It can also identify cystic duct 
obstruction. 

Differential Diagnosis: 

1 - Retrocaecal acute appendicitis. 5- Perforated peptic ulcer. 

2- Acute pancreatitis. 6- Right basal pneumonia 

3- Acute right pyelonephritis. 7- Myocardial infraction. 

4- Hepatitis. 8- Hepatic abcess. 

__ . - . — 



GIT 

Treatment: 

I. Medical: 

- Bed rest, nothing by mouth, IV fluids. 

- Relief of pain with an opiate. 

- Antiemetic as domperidone suppositories. 

- Third generation cephalosporin, quinolone or amoxicillin. 

II. Cholecystectomy: 

- Urgent surgery: in cases with complications. 

- Elective surgery: done after stabilization with medical therapy. 




Chronic Calculous Cholecystitis 



It is a chronic cholecystitis with gall stones 

Pathology: 

- Usually there are stones in the gall bladder. 

- Shrunken gall bladder with thickened wall is found on ultrasound 
examination. 

Clinical features: (usually vague) 

- Indigestion, upper abdominal discomfort or distension. 

- There are recurrent attacks of right upper abdominal pain. 

- Local tenderness & positive Murphy's sign is usually present. 



Most patients with chronic hypochondrial pain suffer from functional bowel disease. 



investigations: 

Ultrasonography reveals thick gall bladder wall and gall stones. 

Differential Diagnosis: 

1 . Functional bowel disease. 

2. Peptic ulcer. 

Treatment: 

1) Cholecystectomy (minilaparotomy). 

2) Laparoscopic cholecystectomy: is a new trend with mortality less 
than 0.1%, and the patient can leave hospital in 24-48 hours. 



55 




GIT 

Post-cholvcvstectomv syndrome 

- Some patients continue to complain of right hypochondrial pain, flatulence, 
indigestion & intolerance to fatty foods, despite a normal image of the biliary tract. 

- In the majority of patients, the original diagnosis was incorrect & the patient was 
suffering from functional bowel disorder, the gall stones being an incidental 
finding. 

- The occurrence of severe pain with jaundice or abnormal liver chemistry suggests 
a retained stone in C.B.D & this can be confirmed by sonar. 



Miscellaneous diseases of the biliary system 



Primary Sclerosing Cholangitis (PSC) 

PSC results from inflammation and fibrosis of the intrahepatic and 
extrahepatic bile ducts leading to narrowing throughout the biliary system. 

Etiology 

- Unknown, immunological mechanisms have been suggested. 

- 70% of patients have inflammatory bowel disease (usually ulcerative colitis). 

Clinical picture 

- Asymptomatic. 

- Pruritis, jaundice and occasionally abdominal pain. 

- Liver cirrhosis and portal hypertension can develop. 

investigations 

- ERCP showing multiple strictures with beading of bile ducts. 

- ANCA antibodies are positive in 80% of cases. 

Treatment 

- It is unsatisfactory. 

- Steroids, azathioprine, methotrexate and ursodeoxycholic acid may be 
helpful to some patients. 

- Biliary strictures can be dilated or stented at endoscopy. 

- Liver transplantation should be considered in advanced cases. 

__ — 



GIT 



Biliary dyskinesia 




It is a clinical syndrome of right upper quadrant symptoms (recurrent 
epigastric and right upper quadrant pain). 

Manometric study showing increased tone of sphincter of Oddi. 

It is treated by nitrates or calcium channel blockers or by surgical 
sphincterotomy of sphincter of Oddi. 

Caroli's syndrome 

It is a congenital segmental dilatation of the intrahepatic biliary system. 
Recurrent attacks of cholangitis with liver abscesses may occur. 
Complications include biliary stones and cholangiocarcinoma. 
Antibiotics for cholangitis, segmental liver resection for localized disease. 

Haemobilia 

It is a bleeding into common bile duct. 

It can occur due to hepatic trauma, tumor or liver biopsy. 

Blood enters the biliary tree and produces either cholestatic jaundice or 
gastrointestinal bleeding. 

Carcinoma at papilla of Vater 

40% of adenocarcinoma of the small intestine arise in relation to the papilla of 
Vater. 

There are pain, anemia (GIT bleeding) and weight loss. It is diagnosed by 
endoscopy with biopsy. 

It must be differentiated from cancer head of pancreas and 
cholangiocarcinoma. 

Treatment is resection. 



Acute cholangitis 



It is due to bacterial infection of the bile ducts secondary to common duct 
stones, strictures, neoplasms or following ERCP. 

Symptoms are fever with rigors, abdominal pain and jaundice (Charcot's 
triad). 

There is leucocytosis with positive blood culture (usually E coli). 

It is treated by amoxicillin with gentamycin I.V, Ceftazidime is also used, then 
treatment of the obstruction. 



57 



GIT 



The Pancreas 



Anatomy: 



The pancreas is a retroperitoneal organ extends across the posterior 
abdominal wall from the second part of the duodenum to the spleen. 
The head is encircled by the duodenum, the body which forms the 
main bulk of the organ ends in a tail that lies in contact with the spleen. 

The pancreas consists of exocrine and endocrine cells. 

The main pancreatic duct joins the common bile duct to enter the 
duodenum as a single duct at the ampulla of Vater. 



Inferior vena cava 
Aorta 



Bile duct 



Ampulla 
of Vater 



Duodenal papilla 



Duodenum 




Uncinate process of pancreas 






Spleen 
Main pancreatic duct 

Body of pancreas 



Superior mesenteric arteryand vein 



Important surgical relations of the pancreas. 



Function: 



Exocrine function 

- Pancreatic acini synthesize digestive enzymes e.g. amylase, lipase 
and proteases (trypsinogen and chemotrypsinogen). 

Endocr ine function 

Islets of langerhans contain four main types of cells: 

- B cells produce insulin. 

- a cells produce glucagon. 

- D cells produce somatostatin. 

- PP cells produce pancreatic polypeptide (PP). 

- Enterochromaffin cells produce serotonin. 



58 



GIT fl f_P^ 

Investigations for diagnosis of pancreatic disease 

1. Exocrine part 

- Serum amylase and lipase are raised in pancreatitis. 

- Faecal fat high in steatorrhea (malabsorption). 

2. Endocrine part 

- Serum level of insulin, glucagon. 

- Glucose tolerance test. 

3. Visualization of the pancreas 

- Plain X-ray for pancreatic clarification in chronic pancreatitis. 

- Sonar for calcification and pancreatic cysts. 

- CT scan for all pancreatic diseases. 

- ERCP to examine ductular system. 

- Angiography to detect tumors. 



Acute Pancreatitis 



This is an acute inflammatory process of the pancreas which may involve 
peripancreatic tissue. 

Etiology (risk factors): 

1- Gallstones. 2- Hyperlipidaemia (T triglycerides). 

3- Alcohol. 4- Iatrogenic e.g. ERCP. 

5- Drugs -> steroids, azathioprine 6- Pancreatic tumors. 

-> lasix, sodium valproate. 

7- Infections e.g. mumps & coxsackie. 8- Idiopathic, hypercalcemia. 

Pathogenesis: 

♦ Reflux of bile up the pancreatic duct associated with occlusion of ampulla by 
gall stone with autodigestion of the pancreas by proteolytic enzymes e.g 
trypsin released in the pancreas -> leading to proteolysis edema, vascular 
damage & fat necrosis with edematous pancreatitis in mild cases & 
hemorrhage and necrosis in severe cases. 

♦ Alcohol alone can damage the pancreas. 

♦ Pancreatitis can also occur in other condition that impair drainage of 
pancreatic duct e.g. pancreatic tumour. 



59 



GIT m gfr 

Clinical Picture: 

1. Abdominal pain: epigastric or upper abdomen, it may radiate to the back 

between the scapulae. 

2. Nausea & vomiting in most cases. 

3. Tenderness, guarding & rigidity of the abdomen may occur. 

4. Ecchymosis of the abdominal wall: 

- Cullen's sign: periumbilical ecchymosis. i 

- Grey Turner's sign: ecchymosis in the flanks, f ^ are s/ ns 

Local pancreatic complications with mild attacks of pancreatitis, but systemic 
complications occur only with severe attacks. 

Complications: 

1. Pancreatic: 

- Pancreatic abscess & pancreatic ascites. 

- Pancreatic ascites reflects involvement of peritoneal surfaces by 
the inflammatory process and rarely rupture of a pancreatic duct 
with entering of pancreatic juice into the peritoneal cavity may occur 

- Pseudocysts evolve from acute fluid collections 4 weeks or more 
after the start of the attack. 

2. Hepatobiliary: Obstructive Jaundice due to obstruction of CBD 

& portal vein thrombosis. 

3. Intestinal: Paralytic ileus & G.I. hemorrhage. 

4. Systemic: 

- Metabolic: Hypocalcaemia & hyperglycaemia. 

- Haematological: Disseminated intravascular coagulopathy. 

- Renal: Acute renal failure. 

- Cardiovascular. Circulatory failure (hypovoelemic shock). 

- Respiratory. Acute respiratory failure (ARDS). 

Signs Indicate severe pancreatitis 6 poor prognosis (Ranson's signs) 

1. WBC's: raised (more than 16,000/mm3). 

2. Blood glucose: raised (more than 200 mg/dL). 

3. Arterial 2 : diminished (less than 60 mmHg). 

4. Plasma albumin: diminished (less than 3 gm /100 ml). 

5. Serum transferases: raised (more than 200 units/L). 

6. Serum calcium: diminished (less than 8 mg/dL). 

7. Serum LDH: raised (more than 600 u/L). 

9. Blood urea: raised (more than 100 mg/dL). 

10. Age above 55 years. 

' 60 



GIT 



A. 



Mortality is approximately 1% with < 3 Ranson's signs, 10% to 20% with 3-5 signs 
and greater than 50% with > 6 signs. Another method to assess the severity of 
acute pancreatitis called APACHE scores, If the score > 8 (severe pancreatitis) and 
if < 8 (fatal outcome is unlikely). 

APACHE means Acute Physiologic and Chronic Health Evaluation. 



Investigations: 

1 . Elevated serum amylase, also serum lipase is elevated. 

2. Plain X-ray abdomen: ileus & may be pancreatic calcification in 

acute on top of chronic pancreatitis. 

3. Ultrasound & CT: swollen pancreas, fluid collections & gallstones 

may be present. 

4. Peritoneal aspiration: contains high amylase. 

5. MRI 



Serum amylase is elevated > 5 folds on the first day then fall rapidly because of 
renal clearance. Onset (2-12 hours), peak (12-72), return to normal after 3-4 
days. So Late presentation may give false negative results. 24 hour urinary 
amylase may be helpful. 

A persistently raised serum amylase suggests the occurrence of pseudocyst or 
pancreatic abscess or a non pancreatic cause. 

Serum amylase is elevated also in cases of intestinal obstruction, perforated 
peptic ulcer, cholecystitis and in alcoholics (raised salivary amylase). 



Treatment: 



1 . Nasogastric suction I to reduce vomiting & abdominal distension and to 

2. Nil by mouth J put pancreas to rest. 

3. Fluid and electrolyte replacement. 

4. Analgesia with an opiate (other than morphine) e.g pethidine or tramadol 
as morphine causes spasm of the sphincter of Oddi. 

5. Somatostatin infusion may be useful (it put the pancreas to rest). 

6. Management of shock. 

7. Peritoneal lavage. 

8. Protease inhibitor and kallikreinin inactivator e.g aprotinin (Trasylol 
vials). 

9. Platelet activating factor antagonist (Lexipafant). 

10. Surgery for pancreatic abscess, endoscopic sphincterotomy in cases of 
gall stones in common bile duct. 

— _ — 



GIT 



Chronic Pancreatitis 




It is a chronic inflammatory disease of the pancreas characterized by 
irreversible damage of the pancreas with permanent impairment of function. 

Etiology: 

1 . Chronic Calcifying pancreatitis, the most common. 

It is caused by chronic alcoholism. 

2. Hereditary Pancreatitis. 

3. Tropical Pancreatitis in region where there is protein & fat malnutrition. 

4. Obstructive Pancreatitis due to obstruction of pancreatic duct e.g stricture. 

Clinical picture: 

1 . Abdominal pain: in the epigastrium and upper abdomen with radiation to 

the back. 

2. Marked weight loss, due to anorexia. 

3. Steatorrhoea occurring when the secretion of pancreatic lipase is reduced 

by 90%. 

4. Diabetes Mellitus commonly with calcified pancreatitis. 

Complications: 

1 . Pancreatic pseudocyst. 

2. Pancreatic ascites, when there is a communication between the panc- 

reatic duct & the peritoneal cavity. 

3. Obstructive Jaundice. 

Investigations: 

1 . Serum amylase is of little value, it may be raised during pain episodes. 

2. Plain X-ray of the abdomen may show calcification of pancreas. 

3. Ultrasound & CT: abnormalities in pancreatic size & calcification in most 

cases. 

4. Estimation of exocrine function of the pancreas e.g. measurement of 

duodenal enzymes. 

5. Blood sugar. 

Treatment: 

1 . It should be to stop drinking alcohol. 

2. The pain needs to be controlled often with narcotics. 

3. Diabetes is treated by insulin. 

4. Steatorrhoea is treated by low fat diet and pancreatic supplements. 

5. Surgery may be indicated in cases of intractable pain. 



62 



GIT 




- It affects males more than females above age of 60. 

Predisposing factors 

- Smoking. - High dietary fat. - Chronic pancreatitis. 
Occupational exposure to petroleum products. 



Alcohol probably does not affect the risk. 

Fruits and vegetables are probably protective due to their high fibre 

and vitamin C. 



Pathology 

- ^ 90% of pancreatic tumors are adenocarcinomas and arise from the duct 
•epithelium. 

- 70% of cases the tumor arising from the head of pancreas. 

-» The tumors spreads locally to duodenum, peritoneum. Liver and spleen 
are also affected. 

Clinical picture 

f - Caf'CfflOfJia Of the Stead presents with painless jaundice. 

Epigastric or upper abdominal pain radiating to the back occurs 
at sometime in the course of the disease. Anorexia & weight loss 
also occur. 

2- Carcinoma Of the body OP the tall presents with abdominal pain, 

anorexia and weight loss. It may be relieved by sitting forward. 

Jaundice is rare. Glucose intolerance may occur. 



Courvoisier's sign: 

Dilatation of gall bladder may occur with cancer head pancreas, this is usually 
not found with gall stone disease due to the associated chronic inflammation 
with fibrosis of the wall of gall bladder. 



Investigations 

- Tumor markers as CEA (carcinoembryonic antigen) and CA19-9 
(carbohydrate antigen). CA is more specific and more sensitive 

- Spiral contrast enhanced CT. 

- Barium meal showing displacement of the stomach and duodenum. 

- ERCP. 

- Fine needle aspirate or tru-cut biopsy if there is difficulty in distinguishing 
cancer from chronic pancreatitis. 

Treatment 

- Whipple operation (removal of the duodenum and the head of the 
pancreas) i.e pancreaticoduodenectomy is only attempted in localized 
tumors of the head. 

- In the majority of cases the management is palliative palliation wi;<< 
bypass procedure e.g. stent in CBD to allow drainage or bypass surgery 

anasto mosis of CBD with jejunum (choiedojejunostomy) and analgesia . 

— 63 



GIT fflB f^ 

Periampullary tumors 

- These arise from the papilla of vater, terminal parts of the pancreatic or 
common bile ducts or from the duodenal mucosa adjacent to the papilla. 
Usually the tumor is an adenocarcinoma. 

- Most patients present with obstructive jaundice which may occasionally 
be intermittent. 

- Iron deficiency anemia may occur due to bleeding from the tumor. 

- The diagnosis is made by ERCP, CT scan. 

- The treatment is Whipple resection or transduodenal excision. 

- This tumor is of good prognosis in comparison with carcinoma of the 
pancreas. 



Pancreatic Islet tumors 



I. Gastrinoma (Zollliigcr-Ellisoii 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. 

II. Vipomas 

- Tumors secreting VIP and leading to secretory diarrhea through stimulation 
of c-AMP leading to dehydration. 

- Plasma level of VIP is very high. 

- Octreotide is effective, resection may be required. 

III. Glucagonomas 

- These are a-cell tumors that produce glucagon. 

- There are erythematous rash, cheilosis, diarrhea and DM. 

- The diagnosis is made by measuring glucagon in the serum and CT 
abdomen. 

- Surgery to decrease the tumor size. 

- Chemotherapy is of little value. 

IV. Somatostatinomas 

- They produce DM, steatrrhoea, weight loss and gall stones. 

V. Insulinoma (see endocrine). 

_ . — 



GIT 



Acute Abdomen 



This term is used to define a group of abdominal conditions (that cause the 
patient to be hospitalized within a few hours of the onset of pain) in which surgical 
treatment must be considered to treat perforation, peritonitis, obstruction and 
vascular and other intraabdominal catastrophes, so early surgical consultation 
should be obtained. 

Causes 

Acute abdomen is caused by sudden inflammation, perforation, obstruction or 
infarction of various intra-abdominal organs. However many extra abdominal and 
medical conditions such as pneumonia, myocardial infarction, nephrolithiasis and 
metabolic disorders may lead to acute abdominal pain, or picture mimic acute 
abdomen (see later). 

• Bowel 

- Acute appendicitis. 

- Perforated viscus e.g. peptic ulcer. 

- Diverticular disease. 

- Intestinal obstruction and strangulation. 

- Meckel's diverticulum. 

- Terminal ileitis by bacterial infection (Yersinia). 

• Vascular 

- Mesenteric occlusion. - Rupture aortic aneurysm. 

• Gynaecological 

- Ruptured ectopic pregnancy or ovarian cyst. 

- Acute salpingitis. 

• Miscellaneous 

- Cholecystitis. - Acute pancreatitis. 

- Acute mesenteric adenitis. 

Clinical Picture 

History 

1- Sudden onset of pain suggests perforation of viscus, rupture 
aneurysm, torsion of ovarian cyst or acute pancreatitis. 

2- Back pain suggests pancreatitis, rupture of an aortic aneurysm or 

renal disease. 

- 65 



GIT 




3- Inflammatory conditions e.g. (appendicitis) produce a more gradual 
onset of pain. With peritonitis the pain is continuous and may be 
made worse by movement. 

4- Vomiting may occur with any abdominal conditions but if persistent 
it suggests intestinal obstruction. 

5- Ask about other symptoms as change in bowel habit, urinary 
symptoms and gynaecological history. 

Examination 

1- Abdominal tenderness, muscle guarding and rigidity are signs of 
peritonitis. 

2- Inflammation of pelvic peritoneum may produce tenderness on 
rectal examination. 

3- Absent bowel sounds suggest peritoneal involvement, strangulation 
or ischemia or ileus. 

4- Search for specific S&S according to the cause. 



Visceral abdominal pain is experienced in that region of the abdominal wall 
innervated by spinal nerves with the same segmental origin of the diseased 
viscus. 

Parietal abdominal pain results from irritation of the peritoneum innervated by 
spinal nerves supplying the overlying abdominal wall, so parietal pain is 
localized to the area of abdomen affected. 



Investigations 

- Blood picture: f TLC in inflammatory conditions. 

- Serum amylase is high in acute pancreatitis. 

- X-ray to detect air under diaphragm due to perforated viscus or multiple 
fluid level in intestinal obstruction. 

- Sonar for cholecystitis, appendicitis. 

- Spiral CT for pancreatitis, appendicitis. 

- Laparoscopy. 

Treatment 

- Specific treatment according to the cause. 



Medical conditions which may mimic acute abdomen 


- Myocardial infarction. 


- Sickle cell disease. 


- Pleurisy. 


- Vasculitis. 


- Irritable bowel $. 


- FMF. 


- Diabetic ketoacidosis, Addisonian crisis. 


- Gastroenteritis. 


- Henoch Schonlein purpura. 


- Herpes zoster. 



66 



GIT 




Protein Losing Enteropathy 

It is an increased protein loss across an abnormal gastrointestinal mucosa 



causing hypoalbuminaemia. 

Causes 

- Gastric carcinoma. 

- Atrophic gastritis. 

- Intestinal lymphangiectasia. 

- Whipple's disease. 

- Inflammatory bowel disease. 

- Celiac and tropical sprue. 



TB enteritis. 
Cancer colon. 
Congestive heart failure. 
Constrictive pericarditis. 
Esophageal carcinoma. 
Scleroderma 



Motility disorders of GIT 



Esophagus: Achalasia, esophageal spasm, scleroderma, reflux. 

Stomach: gastroparesis. 

Intestine: 

- Small or large intestinal diverticulosis. 

- Megacolon. - Irritable bowel disease. 

- Intestinal pseudoobstruction. 



a 



y 



See 
Before 



J 



BIT Bleeding 

[see the practical part] 

Causes of upper GIT bleeding 

- Oesophageal: varices - oesophagitis - cancer - Mallory weiss $. 

- Gastric: Gastric erosion - peptic ulcer - congestive gastropathy 

carcinoma. 

- Duodenal ulcer. 

Blood disease or vascular malformations. 

Causes of lower GIT bleeding 

- Inflammatory bowel disease. - Cancer colon. 

- Hemorrhoids. - Diverticulitis. 

- Angiodysplasia. - Ischaemic colitis. 

- Anal fissure. - CMV colitis. 

- Blood disease. 



67 



GIT 




Diseases of Peritoneum 



Acute Peritonitis 



Etiology 

- Bacterial peritonitis due to perforation of GIT or penetrating wound. 

- Chemical peritonitis due to spillage of pancreatic enzymes, gastric acid or 
bile as a result of injury or perforation of the intestine or biliary tract. 

- Sterile peritonitis due to SLE and FMF. 



The most common causes of bacterial peritonitis are appendicitis, 
perforations associated with diverticulitis and peptic ulcer. 



Clinical Picture 

- Abdominal pain, tenderness, rebound tenderness and rigidity of the 
abdominal wall. 

- Peristalsis may be present early but usually disappears with progression of 
illness. 

Investigations 

- X ray to detect air under diaphragm. 

- Serum amylase for pancreatitis. 

- Diagnostic paracentesis, abdominal CT and sonar. 

Treatment 

- Nasogastric tube 

- IV fluids 

- Antibiotics (infective peritonitis) 

- Peritoneal lavage 

- Specific treatment of the cause. 



Tuberculous Peritonitis 



Etiological types 

1) Primary: occurs in children due to ingestion of infected milk. The bovine 

bacilli are the cause of infection in 80%of cases. 

2) Secondary: due to reactivation of a tuberculous focus in the abdomen 
often a lymph node, tuberculous enteritis, & pulmonary tuberculosis. 

~~ ~ ^g 



git mm f" 

Pathological types: 

1. Ascitic type : free fluid in the peritoneum with no adhesions. . 

2. Loculated type: adhesions divide the peritoneal cavity into many loculi. 

3. Adhesive form: causing adhesions of the intestinal loops. 

Complications: 

1) Intestinal obstruction (adhesive). 

2) Intestinal fistula. 

Clinical picture: 

Onset: usual ly gradual. 

Symptoms 

1 . Symptoms of toxaemia. 

2. Constipation or diarrhea. 

3. Abdominal pain. 

Examination may show the following: 

1 . Unilateral shifting dullness. 

2. Abdominal tenderness with mild rigidity of the abdomen. 

3. Palpable masses, (rolled omentum). 

4. There is a doughy sensation on palpation of the abdomen. 

5. No lower limb edema. 

Abdominal sonar: -> Free or encysted ascites. 

Tapping of the ascitic fluid: 

1 . Straw-colored. 

2. Rich in proteins & lymphocytes. 

3. Z.N., culture or PCR for the organism. 

Plain X-rav abdomen: - Calcified mesenteric L.N. 

CT and sonography: showing mesenteric thickening and lymph node 

enlargement. 

Laparosc o pic examination for peritoneal tubercles and biopsy. 
TPCatlllCllt: -» Antituberculous treatment for 18 months to two years. 



69 



^ git nfgr 

IVBaligiiant Ascites anil Tumors of Peritoneum 

Aetiology: 

1 . Primary tumors of the peritoneum as mesothelioma. 

2. Secondary to malignancy o\ stomach, liver or ovaries. 

Clinical picture: 

1) Massive rapidly accumulating ascites. 

2) Abdominal examination shows: 

- Distention with ascitic fluid which is usually massive. 

- Abdominal masses. 

3) Usually there is no LL edema. 

Investigations: 

1 ) Examination of the ascitic fluid: 

- Hemorrhagic. 

- Malignant cells. 

2) Abdominal sonar, CT abdomen and laparoscopic peritoneal biopsy. 

Tl fe €atlll€IIt: Palliative treatment. 



Retroperitoneal fibrosis 



The etiology is usually unknown, but it may be associated with methysergide 
therapy and occasionally with carcinoid syndrome. It usually occurs in middle age, 
with malaise, fever, and weight loss. There is anemia and raised ESR. CT 
abdomen is diagnostic. The common complication is urinary tract obstruction due to 
ureteric involvement. It may require surgery. 



70 



functional Gastrointestinal disorders IFGID) 

- Group of Gl disorders in absence of abnormalities in digestion, absorption or 
structural lesions. 

- FGID may be a form of dysregulation of brain - gut function, psychological 
stress can exacerbate the symptoms. 

U Functional esophageal disorders : 

- Globus -> see before. 

- Functional chest pain of presumed esophageal origin 

- It is midline chest pain (not burning in nature) in absence of GERD, 
achalasia or cardiac cause. 

- It is treated by acid suppression, nitrates, calcium channel blockers, 
amitriptyline 10mg are effective. 

- Rumination syndrome 

- Persistent or recurrent effortless regurgitation in absence of 
nausea, vomiting, heartburn or abdominal discomfort. 

2. Functional gastroduodenal disorders ; 

- Functional dyspepsia (non ulcer dyspepsia) 

It includes upper abdominal pain/discomfort, fullness, early satiety, 
bloating and nausea, there are two groups : 

- Ulcer like dyspepsia i.e. pain in the upper abdomen. 

- Dysmotility like dyspepsia i.e. discomfort (non painful) sensation in 
the upper abdomen. 

It is treated by reducing intake of fat, coffee, alcohol and smoking. H 
pylori eradication is often used with prokinetics. 

- Aei*ophavla (It is usually unconscious) 

- It is treated by explanation, reassurrance and treatment of 
associated psychiatric disorder. 

- Functional vomiting 

- It is characterized by occurance on at least separate days in a 
week with absence of criteria of eating, psychiatric, gut, brain or 
metabolic abnormalities. It is treated by anti-nausea drugs and 
antidepressants. 



3« Functional bowel disorders* 

Irritable bowel syndrome. 
- Pain / gas / bloat syndrome. 
Functional diarrhea. 



See before 



GIT involvement in systemic diseases 



Rheumatoid disease -> gastritis (NSAID). 
SLE -> mesenteric vasculitis. 



71 






GIT 

- Scleroderma -> dysphagia, malabsorption (bacterial overgrowth). 

- Polymyositis -> dysphagia. 

- Vasculitis -> mesenteric vascular occlusion. 

- Diabetes mellitus -> gastroparesis, diarrhea and constipation (autonomic 
neuropathy). 

- Thyrotoxicosis -> diarrhea. 

- Hypothyroidism -> constipation. 

- Addison's disease -> nausea, vomiting and diarrhea. 

- Chronic renal failure -> gastroparesis & constipation (autonomic neuropathy), 
peptic ulcer. 

- Systemic amyloidosis -> malabsorption syndrome. 

Extra-gastrointestinal or multisystem 
manifestations of GIT disorders 

- Chronic atrophic gastritis -> pernicious anemia. 

- Pyloric obstruction -> electrolyte disturbances. 

- Malabsorption syndrome -> anemia, osteoporosis, peripheral neuropathy, 

(see before). 

- Whipple's diseased arthropathy. 

- Coelic disease -> IgA nephtopathy??. 

- Intestinal ameobiasis -> ameobic hepatitis 

- Inflammatory bowel disease -> arthropathy, uveitis, erythema nodosum, renal 
stones, sclerosing cholangitis. 

- Carcinoid tumors -> flushing, bronchospasm, pulmonary stenosis, tricuspid 
stenosis and regurge. 

- GIT bleeding -> iron deficiency anemia. 

- Familial polyposis -> see before. 

Systemic manifestations of pancreatic diseases 

- Acute Pancreatitis -> DIC, acute renal failure, hypovolemic shock, ARDS. 

- Chronic Pancreatitis -> malabsorption, DM. 

- Cancer pancreas and pancreatic islets tumors-> see before. 

Immune mediated GIT diseases 

- Autoimmune gastritis. - Coelic disease. 

- Inflammatory bowel disease. - Food allergy -> see immunology. 



72 



References 



Harrison text book (Principles of Internal Medicine). 

Cecil Textbook (Textbook of Medicine). 

Kumar (Clinical Medicine). 

Davidson's (Principles and Practice of Medicine). 

Henry/Thompson (Clinical Surgery). 

Robbins (pathologic basis of disease). 

Cecil Essentials of Medicine. 

The National Medical Series for Independent Study 

(Medicine). ^_^^__^ 



Author's avaiIadIe books 



1- Hepatology. 

2- Gastroenterology. 

3- Endocrinology. 

4- Rheumatology. 

5- Cardiology. 

6- Nephrology. 

7- Hematology. 

8- Neurology and psychiatry. 

9- Infectious diseases, tropical diseases, immunology, 
nutrition, genetics, geriatric, toxicology and therapeutics. 

10- Respiratory diseases. 

11- Clinical medicine (symptoms and examination). 

■ Cardiology. 
- Chest. 

■ Abdomen. 

■ Neurology. 

■ General. 






Computerized By: Dr. Yahia M. Makkeyah 



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