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PATHOLOGY OF THE GASTROINTESTINAL TRACT

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  1. PATHOLOGY OF THE GASTROINTESTINAL TRACT Ismail Matalka ,MRCPath Department of Pathology Jordan University of Science & Technology Irbid - Jordan

  2. THE ALIMENTARY (DIGESTIVE) SYSTEM • Oral cavity (including salivary glands) • Esophagus • Stomach • Small intestine • Colon • Appendix • Liver • Biliary tract • Pancreas

  3. ANATOMY & HISTOLOGY OFTHE ORAL CAVITY • Anatomy • Orifice to digestive & respiratory tracts • Lips, buccal mucosa, tongue, soft & hard palate • Teeth & periodontal tissue • Histology • Lined by nonkeratinized squamous epithelium • Minor salivary glands & sebaceous glands in lips & buccal mucosa • Lymphoid tissue

  4. DISEASES OF THEORAL CAVITY • Congenital anomalies, e.g. cleft lip & cleft palate, macroglossia, branchial cleft cysts • Inflammations: Aphthous ulcers, Herpes stomatitis, Candidiasis ... • Pre-malignant lesions: leukoplakia, erythroplasia • Tumors: Squamous cell carcinoma • Salivary gland inflammations • Salivary gland tumors

  5. ULCERATIVE & INFLAMMAT‏ORY LESIONS OF THE ORAL CAVITYAPHTHOUS ULCERS (CANKER SORES) • Extremely common, up to 40% of population • Single or multiple shallow fibrin-coated painful ulcers of oral mucosa, usually <1 cm, may coalesce • Unknown etiology (?viruses, hypersensitivity) • Triggered by stress, fever, menstruation, pregnancy, certain foods; may be familial • May be associated with inflammatory bowel disease & Behcet syndrome • Self limiting in a few weeks

  6. ULCERATIVE & INFLAMMAT‏ORY LESIONS OF THE ORAL CAVITYHERPETIC STOMATITIS • HSV I>>II; person to person transmission • After primary infection it is usually asymptomatic but virus will persist in ganglia in dormant state • Reactivation: fever, sun or cold exposure, URTI, .. • Herpes labialis: cold sores or fever blisters • Vesicular lesion, edema, degeneration of epidermis • Tzanck test: intranuclear inclusions & giant cells • In immunocompromised: virulent dissiminated infection: gingivostomatitis, encephalitis ...

  7. ULCERATIVE & INFLAMMAT‏ORY LESIONS OF THE ORAL CAVITYFUNGAL INFECTIONS • Candida albicans is part of normal flora (30-40%) • Oral candidiasis (moniliasis, thrush): common in: • Diabetes mellitus • Anemia • Antibiotic or glucocorticoid Rx • Immunodeficiencies & debilitating diseases • Soft white cheese-like plaques • Minimal- marked ulceration with inflammatory exudate and fungal microorganisms (pseudohyphae) • In vulnerable patients, disease may spread

  8. ULCERATIVE & INFLAMMAT‏ORY LESIONS OF THE ORAL CAVITYACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) • HIV infection is associated with different lesions in the oral cavity • Candidiasis • Herpetic vesicles • Other oppurtunistic infections • Kaposi’s sarcoma: multifocal vascular tumor, present in 25% of AIDS patients; HSV8 • Hairy leukoplakia: white patches with hairy surface: • caused by EBV • rare, but seen mainly in AIDS • histology shows acanthosis, hyperkeratosis

  9. PRE-MALIGNANT LESIONS OF THE ORAL CAVITYLEUKOPLAKIA • A clinical term used to describe a whitish well- defined mucosal patch or plaque caused by epidermal thickening or hyperkeratosis • Older men; associated with tobacco, chronic friction (dentures), alcohol & irritant foods; HPV link • Microscopically, they vary from hyperkeratosis without dysplasia to mild to severe dysplasia or CIS • Only histologic examination distinguishes these changes • 3-6% transform into squamous cell carcinoma

  10. PRE-MALIGNANT LESIONS OF THE ORAL CAVITYERYTHROPLAKIA • Red velvety areas which may remain level with or slightly depressed in relation to surrounding mucosa • Greater tendency for epithelial cell atypia and marked dysplasia than leukoplakia • Hyperkeratosis is less frequent; red color is due to intense inflammation and vascular congestion • Higher risk (50%) of malignant transformation (the risk corresponds to the degree of atypia) • Erythroleukoplakia: speckled leukoplakia; mixture of erythroplasia and leukoplakia

  11. MALIGNANT TUMORS OF THE ORAL CAVITYSQUAMOUS CELL CARCINOMA • Represent 90% of oral cavity malignancies (3% of all malignant tumors); M>F • Lip>ant. floor of mouth>tongue>palate • Etiology: smoking, smokeless tobacco, protracted irritation (e.g. dentures), chronic dental & oral infections, sunlight, heat, alcohol, atrophy, HPV • Plaque, mucosal thickening or ulcer • Invasive &/or in situ carcinoma; well differentiated to undifferentiated • Spread to local LN (submandibular, high jugular…) • Px: depends on location (e.g. lip), grade, stage • 50% lead to death in 5 years ;overall 5 YS without L.N mets is 40% after chemo & radio ;and 20% with L.N mets

  12. DISEASES OF THESALIVARY GLANDS • Inflammation • Viral sialadenitis • Bacterial sialadenitis • Autoimmune sialadenitis • Sialolithiasis • Tumors • Benign • Pleomorhpic adnoma (mixed tumor) • Warthin’s tumor • Malignant • Carcinoma ex-pleomorphic adenoma • Mucoepidermoid carcinoma • Adenoid cystic carcinoma • Mickulicz’s syndrome

  13. INFLAMMATIONS OF THE SALIVARY GLANDSVIRAL SIALADENITIS • Most common cause is mumps, which usually affects the parotid gland (epidemic parotitis) • 70% bilateral parotid; 20% unilateral; 10% others • Mumps is an acute contagious childhood disease • Paramyxovirus, acquired by respiratory droplets • Usually self limited, but may lead to complications, which are commoner in adults: • Pancreatitis • Orchitis: usually unilateral; rarely leads to infertility • CNS inflammation: rare but serious

  14. INFLAMMATIONS OF THE SALIVARY GLANDSAUTOIMMUNE SIALADENITIS • Sjogren’s syndrome: inflammation of salivary glands & mucus-secreting glands of nasal mucosa (resulting in dry mouth or xerostomia) and lacrimal glands (resulting in dry eyes or keratoconjunctivitis sicca) • 90% are females; parotid enlargment in 50% • May be primary or secondary (60%) to othe autoimmune disease (RA, SLE, polymyositis ..) • Lymphocytic infiltration & fibrosis • RF, ANAs +/-; anti-ribonucleoprotein SS-A & B Abs • High risk to develop lymphomas

  15. INFLAMMATIONS OF THE SALIVARY GLANDSSIALOLITHIASIS & NONSPECIFIC SIALADENITIS • Bacterial • Secondary to ductal obstruction by stones (sialolithiasis) in major excretory duct • Usually unilateral • Pathogenesis: impacted food debris & edema around orifice following injury • Ductal dilatation, periductal inflammation, secondary bacterial invasion & suppuration • Predisposing factors: Hx of major surgery, dehydration, long-term phenothiazines Rx

  16. SALIVERAY GLANDSTUMORS • Relatively uncommon; 2% of tumors in humans • 80% of tumors occur in parotid gland • Equal M:F ratio; all ages [6th - 7th decade] • Most of these neoplasms are benign: 70-80% of parotid tumors and only 50% of submaxillary tumors • c/o: mass at angle of jaw • Wide histologic variations • Benign: Pleomorphic adenoma, Warthin’s tumor • Malignant: Carcinoma ex-pleomorphic adenoma, mucoepidermoid carcinoma, adenoid cystic carcinoma

  17. TUMORS OF THE SALIVARY GLANDSPLEOMORPHIC ADENOMA • aka: mixed tumor: Most common tumor (65-80%) of the salivary glands • Slowly growing well-demarcated, mostly arising from superficial parotid • Pathology: heterogeneous histology with epithelial elements, myxoid stroma, often containing chondroid foci or, rarely, bone • Px: recurrence after surgery: 10% • Malignant transformation: 15% in parotid, 40% in submandibular gland

  18. TUMORS OF THE SALIVARY GLANDSWARTHIN’S TUMOR • aka: Papillary cystadenoma lymphomatosum • Benign slowly growing tumors • 5-10% of all parotid tumors; extremely rare in other salivery glands • Pathology: composed of cystic spaces lined by tall columnar cells overlying abundant lymphoid tissue • Histogenesis: vestigial embryonic remnnants of branchial cleft origin? • Rx: cured by surgical excision

  19. PATHOLOGY OF THE SALIVARY GLANDSMICKULICZ’S SYNDROME • Combination of salivary and lacrimal glands enlargement with xerostomia • May be due to many causes: • Sarcoidosis • Leukemia/lymphoma • Sjogren’s syndrome

  20. THE ALIMENTARY (DIGESTIVE) SYSTEM • Oral cavity (including salivary glands) • Esophagus • Stomach • Small intestine • Colon • Appendix • Liver • Biliary tract • Pancreas

  21. DISEASES OFTHE ESOPHAGUS • Congenital anatomic disorders • Agenesis, atresia, fistula, stenosis • Acquired anatomic/motor disorders • Stenosis, webs & rings, HH, achalasia, ... • Inflammations • Reflux esophagitis • Barrett’s esophagus • Vascular diseases • Tumors

  22. CLINICAL FEATURES OFDISEASES OF THE ESOPHAGUS • Different esophageal diseases share a limited number of symptoms: • Dysphagia: difficulty in swallowing • deranged esophageal motor function • narrowing or obstruction of lumen • Heartburn: retrosternal burning pain • regurgitation of gastric contents • Hematemesis: vomiting of blood • Melena: blood in stools • severe inflammation, ulceration or laceration • Respiratory symptoms: dyspnea, cough,.. • aspiration

  23. PATHOLOGY OF THE ESOPHAGUSCONGENITAL ANATOMIC DISORDERS • Present at birth with vomiting, aspiration (pneumonia, asphyxia), gastric distention • Agenesis: absence of esophagus. Very rare • Atresia: failure of development of a segment of esophagus, which is replaced by a thin non-canalized cord (absence of lumen) with formation of upper & lower pouches; associated with tracheo-esophageal fistula • Stenosis: developmental defect resulting in partial obstruction or narrowing of the esophageal lumen • Rx: Urgent medical & surgical intervention

  24. PATHOLOGY OF THE ESOPHAGUSACQUIRED ANATOMIC DISORDERS • Stenosis : caustic strictures ,post-surgical ,inflammatory, tumours , autoimmune diseases ( Scleroderma ) . • Webs & Rings : Mucosal webs or mucosal and submucosal concentric ring partially occluding the esophagus . • Diverticula : outpouching of the esophageal wall

  25. ACQUIRED ANATOMIC/MOTOR DISORDERS OF THE ESOPHAGUSHIATAL HERNIA • Protrusion of a dilated sac-like segment of stomach above the diaphragm • Separation of the diaphragmatic crura • Incidence: 1-20% of adults; increase with age • Mostly asymptomatic • c/o heartburn & regurgitation of gastric juices in 9% due to LES incompetence; related to position; symptoms are accentuated by positions favoring reflux • Patients with severe reflux esophagitis usually have HH; however, HH & reflux are not the same condition

  26. TYPES OFHIATAL HERNIA • 2 anatomic patterns: • Sliding (axial): 95% of cases; bell-shaped dilation; due to congenital short esophagus, strictures, spasm or long-standing fibrous scarring of esophagus, resulting in traction on stomach • paraesophageal (non-axial or rolling): segement of cardiac stomach dissects alongside esophagus through a defect. May follow traumatic rupture of diaphragm; may strangulate and infarct

  27. ACQUIRED ANATOMIC/MOTOR DISORDERS OF THE ESOPHAGUSACHALASIA • Failure to relax, i.e., incomplete relaxation of LES in response to swallowing, producing functional obstruction & dilation of more proximal esophagus • c/o progressive dysphagia to liquids and solid food, nocturnal regurgitation & aspiration of undigested food, aspiration pneumonia • Abnormal manometric studies: aperistalsis, partial relaxation of LES, & increased basal tone of LES • Pathology: deranged innervation of LES; absent myenteric ganglia in the body of esophagus; normal, hypertrophic , or thining of muscles; associated mucosal inflammation, ulcer or fibrosis

  28. TYPES OFACHALASIA • Two main types: • Primary (sporadic): Commoner. Unknown cause ? Autoimmune. ? Previous viral infection. • Secondary: • Chaga’s disease: Tryponosoma cruzi infection causing destruction of myenteric plexus ganglion cells in the GIT & ureter; megaduodenum, megacolon, megaureter • Diabetes (Autonomic neuropathy); vagus nerve injury .. • Esophageal squamous cell carcinoma in 5% usually in younger age than in patients without this disease

  29. ACQUIRED ANATOMIC/MOTOR DISORDERS OF THE ESOPHAGUSLACERATIONS • aka: Mallory-Weiss syndrome • Longitudinal tears at the esophago-gastric junction • Encountered in alcoholics, after bout of severe retching or vomiting • Pathogenesis: inadequate relaxation of LES muscle during vomiting • May occur in patients without hx of vomiting • HH is found in 75% of patients with MWS • Linear irregular lacerations, few mm-cm in length • Involve mucosa or deeply penetrate & perforate wall • 5-10% of all cases of massive hemetemesis; however, the majority do not cause profuse bleeding

  30. VASCULAR LESIONS OF THE ESOPHAGUSVARICES • Due to portal hypertension, which leads to formation of portal-systemic collateral bypass channels • Collateral veins will develop in the region of lower esophagus when portal flow is diverted through the coronary veins of stomach into the plexus of esophageal submucosal veins into azygous veins • Most common cause of portal hypertension is liver cirrhosis • Rare causes: portal vein thrombosis, hepatic vein thrombosis (Budd-Chiari syndrome), pylephlebitis, tumor compression or invasion into major portal radicals