Lesions of the oral cavity Salivary glands See Oral pathology · abdomen (confusing appendicitis),

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Lesions of the oral cavity Salivary glands See Oral pathology

Transcript of Lesions of the oral cavity Salivary glands See Oral pathology · abdomen (confusing appendicitis),

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Lesions of the oral cavitySalivary glands

See Oral pathology

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Esophagus

• From highly lethal Ca to bland esophagitis.• Dysphagia, heartburn, hematemesis, melena.

• Anatomic and motor disorders:– Stenosis - adults, dysphagia, lower esophagus narrowing due

to reflux and inflammation– Atresia and fistula - newborn with aspiration (absence of

lumen), tracheoesophageal fistula (may be together) – Mucosal webs - acquired mucosal membrane occluding the

lumen– Diverticula - nocturnal regurgitation, acquired outpouching of

the wall

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Esophagus

• Hiatal hernia:• Separation of the diaphragmatic crura and

widening of the space between the muscular crura.• Two patterns:

– 1/axial (sliding) hernia - 95 % of cases, protrusion of stomach through the diaphragm, bell-shaped,

– 2/paraesophageal (rolling) - separate portion of stomach, cause obscure. Heartburn, regurgitation of food, incompetence of sphincter. Obesity! Complications - ulceration, bleeding, perforation.

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Esophagus

• Achalasia:– "Failure to relax" of lower esophageal sphincter in

swallowing– aperistalsis, – partial or incomplete relaxation of the lower

sphincter, – increased resting tone of the lower sphincter– Impaired arrangement of innervation.

– Secondary - destruction of the myenteric plexus - Chagas' disease (Trypanosoma cruzi).

– Progressive dilatation of proximal esophagus, inflammation, thickening, nocturnal regurgitation, young adults, childhood, risk of squamous Ca.

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Esophagus

• Laceration (Mallory-Weiss syndrome):

–Longitudinal tears - chronic alcoholics - inadequate relaxation of the musculature of lower sphincter during vomiting.

–Mucosal tear - bleeding, wall tear - ulcer, mediastinitis

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Esophagus

• Varices:–Porto-caval anastomoses

–Liver cirrhosis - portal hypertension–2/3 of all cirrhotic patients–massive hemorrhage, 40% die

during first episode, 1/2 within 1Y

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Esophagus

• Esophagitis:–gastric intubation, uremia, irritant

foods, alcohol, smoking, radiation, chemotherapy–Higher incidence in Northern Iran and

China–Mild - hyperemia, severe - ulceration–Heartburn, regurgitation, chest pain

(mimicking MI), bleeding, Barrett

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Esophagus

• Barrett's esophagus:– long-lasting reflux, – abnormal metaplastic columnar

epithelium with goblet cells – low pH - ulcers, 30-40x increased

risk of adenoCa.– red, velvety mucosa - up from

gastroesophageal junction or isolated islands in the distal esophagus

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Esophageal tumors

• Benign tumors –papilloma –Leiomyoma–Lipoma –Etc.

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Esophageal carcinoma

–squamous cell Ca–Risk factors:»esophagitis, achalasia, Plummer-

Vinson sy (microcytic hypochromic anemia, atrophic glossitis)»Life style - alcohol, tobacco»Genetic - tylosis (hyperkeratosis of

palms and soles) - Northern Iran»Barrett - adenoCa»Long prodromes, dysplastic

changes.

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Esophageal carcinoma

–Grossly:– 1/polypoid – 2/ulcerative – 3/diffuse

– AdenoCa:– Barrett - distal esophagus

• Weight loss, anorexia, fatigue, pain related to swallowing

• Biopsy, surgery

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Stomach

– From bland gastritis to carcinoma.– Congenital . pyloric stenosis, diaphragmatic

hernia, gastric heterotopia (esophagus, small intestine - Meckel).

– Heartburn, vague pain, hematemesis, melena.

• Gastritis:– Inflammation of gastric mucosa.

• Acute or chronic

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Chronic gastritis Type B

– > frequent x acute– atrophy or metaplasia– Helicobacter pylori, persists for decades– enzymes + toxins + noxious chemicals from

recruited neutrophils– Intestinal metaplasia - dysplasia– Proliferation of lymphoid tissue - ML– Hypochlorhydria

Type A– autoimmune - antibodies x parietal cells – atrophy - loss of acid + intrinsic factor – achlorhydria – pernicious anemia – hypergastrinemia

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Peptic ulcers• Erosion – mucosa• Ulcer – lamina muscularis mucosae and deeper• Acute or chronic• Gastric x duodenal• Loss of balance betwen protective and aggressive

forces• Most frequent cause = Helicobacter p.

– Helicobacter pylori - > 70% gastric ulcers– Only 10-20% patients with Helicobacter pylori develop peptic ulcer.

Unknown interactions.

• Zollinger-Ellison sy - hypergastrinemia• Cigarette smoking, alcohol. corticosteroids, stress

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• Acute ulcers:–Mainly in stomach, rare in duodenum– stress– trauma, surgical injury of CNS,

extensive burns, gastric irritant drugs– Small - up to 1 cm, anywhere in the

stomach, usually multiple. Adjacent mucosa without inflammation

Acute peptic ulcers

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• Chronic u. - several cm– Elevated walls - radial mucosal folds. Gastritis is almost

always associated.• Complications:• penetration - to omentum, liver, pancreas• perforation – peritonitis• bleeding - melena, exsanguination

• Symptoms - burning and boring pain, weight loss, hemorrhage. Pain is worse at night, relieved by alakali or food

Chronic peptic ulcers

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Tumors

• Epithelial tumors predominate

• Polyps:• 1/ hyperplastic - 80 - 85% - not true

neoplasms • 2/ fundic gland polyps - 10% - dilated glands• 3/ adenomatous - 5% - true neoplasms• All more frequent in chronic gastritis.

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Gastric carcinoma–AdenoCa (95%), • Geographical incidence - most

common in Japan, Hungary.• AdenoCa - two forms - • 1/ intestinal type - from intestinal

metaplasia - chronic gastritis - male predominance - nitrites, smoked foods, Helicobacter pylori, pernicious anemia• 2/ diffuse type - in younger, directly

from gastric glands - risk factors unknown

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Gastric carcinoma

• Localization- pylorus, antrum, cardia, remainder of the body and fundus

• Early cancer - mucosa, submucosa• Morphology:

– 1/ exophytic– 2/ flat– 3/ ulcerative

– Leather-bottle stomach - scirhous carcinoma (linitis plastica)

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Gastric carcinoma

• Histology:– 1/ intestinal type– 2/ diffuse - "signet ring" cells

• Metastasis - regional lymph nodes, supraclavicular node (Virchow's). Krukenberg tumor (ovary), liver

• Symptoms - abdominal discomfort, weight loss, pain.

• Therapy – surgery

• Prognosis – very bad in advanced

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Small intestine

• developmental anomalies–Atresia - segmental–Stenosis - segmental –Duplication –Meckel's diverticulum - failure of involution of omphalomesenteric duct, 3-4 cm long, distal ileum, asymptomatic, gastric metaplasia, islands of pancreatic tissue

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Large intestine

• developmental anomalies–Malrotation - cecum in left upper

abdomen (confusing appendicitis), –Hirschprung disease - megacolon

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Hirschprung disease - congenital megacolon

• Aganglionic segment of intestinal wall - 1/5 of cases - longer segment, rarely - the whole colon. Males predominate (4:1). Sometimes extreme dilatation (15-20 cm in diam.) - ulcers, stercoral peritonitis.

• resection of aganglionic segment (frozen sections - intraoperative).x

• Acquired megacolon:• 1/Chagas's disease - trypanosomes destroy the

plexus• 2/obstruction by the tumor• 3/toxic megacolon• 4/functional psychosomatic disorder

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Vascular disorders

• Ischemic bowel disease:• Acute occlusion – infarction. • end-arteries - transmural necrosis

–venous obstruction (thrombosis) - hemorrhagic infarsation.

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Vascular disorders

• Conditions

1/ arterial thrombosis - AS, vasculitis, surgical accidents, oral contraceptives

2/ arterial embolism3/ venous thrombosis4/ non-occlusive ischemia - shock, dehydration, cardiac failure

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Vascular disorders

– Transmural infarction - dark red hemorrhagic, gangrene (bacteria), perforation

– Mural and mucosal - multifocal, ulcerations, inflammation, pseudomembrane

– Symptoms - usually in older patients, transmural - severe pain, bloody diarrhea, shock, high mortality

– Mural and mucosal - abdominal distention, bleeding, pain, may be fatal but may heal

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Vascular disorders• Angiodysplasia:

• Tortuous dilatation of mucosal and submucosal vessels - cecum, 6th decade, bleeding• hereditary hemorrhagic teleangiectasia

(Osler-Weber-Rendu sy)• isolated lesions, cause - mechanical factors

• Hemorrhoids:• Varices - rectum and anus, after the age of

50, pregnancy, obstipation, liver cirrhosis• Complications - bleeding, prolaps,

thrombosis

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Diarrheal diseases

• Bacterial enterocolitis:– Toxins (Staphylococcus aureus, Vibrio, Clostridium

perfringens,, Clostridium botulinum), – Salmonella (typhi, enteritidis) - S. typhi - typhoid

fever – Shigella - distal colon.– Campylobacter jejuni - superficial ulcers. – Yersinia enterocolitica - lymph node granulomas

(lymphadentis mesenterialis).– Vibrio cholerae - small intestine, mucus depleted

crypts.– Clostridium difficile - pseudomembranous colitis.– Clostrdium perfringens - severe necritizing

enterocolitis with perforation (pigbel)

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Diarrheal diseases

• Viral gastroenteritis - (gastritis less pronounced in a case of all gastroenteric cases):

• Rotavirus, Norwalk virus, other viruses (adenovirus, calcivirus, astrovirus)

• Protozoal infection:• Entamoeba histolytica • Giardia lamblia

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Malabsorption syndromes

• Impaired absorption of fats, proteins, carbohydrates, electrolytes, minerals, and water

• Most common - due to pancreatitis, celiac sprue, and Crohn's disease

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Malabsorption syndromes

• Pancreatic insufficiency - chronic pancreatitis, cystic fibrosis.

• Bacterial overgrowth - osmotic diarrhea, steatorrhea

• Lactose intolerance - inherited disaccharidase deficiency - milk intolerance

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Malabsorption syndromes

• Gluten-sensitive enteropathy = celiac sprue– non-infectious - crossreactivity– sensitivity to gluten (grains of wheat, oat,

barley, rye) – epithelial damage

• Tropical sprue - infection (unknown), diffuse enteritis, ATB treatment

• Whipple's disease - intestine, CNS, joints– macrophages laden by Gram+ Tropheryma whippelii– ATB treatment, males, 4-5th decade

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Idiopathic inflammatory bowel disease

• Crohn's disease• Ulcerative colitis

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Idiopathic inflammatory bowel disease

• Crohn's disease • segmental transmural inflammation, fibrosis

and thickening, usually terminal ileum and caecum

• "skips", anywhere in GIT (systemic disease - accompanied by uveitis, sacroilitis, polyarthritis, sclerosing cholangoitis

• Any age, most 2nd - 3rd decade• Symptoms - non-characteristic - pain, fever,

diarrhea, sometimes bleeding, remissions, relapses

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Idiopathic inflammatory bowel disease

• transmural, mucosal damage, granulomas, fissures and fistulae

• ulcers in mucosa, mucosal inflammation, granulomas

• dysplastic changes, higher risk of Ca• Complications - fistulae to other

bowel loops, urinary bladder, vagina, skin, abdominal abscesses, intestinal strictures

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Idiopathic inflammatory bowel disease

• Ulcerative colitis • limited to mucosa and submucosa. • Starts in rectum, extends proximally

(whole colon)• Systemic disease - migratory polyarthritis,

uveitis, sclerosing cholangitis• Any age, peak 20-25 years• Symptoms - pain, bloody mucosal

diarrhea, weight loss Extraintestinal manifestations - migratory polyarthritis

• Dg - endoscopy, biopsy

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Idiopathic inflammatory bowel disease

• Ulcerative colitis • Granulomas & skip lesions absent, little fibrosis• Rectum+sigmoideum - 80%, entire colon 10%. • Bleeding, edema, inflammatory pseudopolyps• ulcers - longitudinal, sometimes gangrene, mucosal

atrophy• Diffuse inflammatory infiltrate, crypt abscesses• ulcer healing - submucosal fibrosis• Dysplastic changes, high risk of Ca (duration &

extent of disease play a role)

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Colonic diverticulosis

• Congenital - all three layers - Meckel.• Most - acquired - anywhere in GIT, mostly in

sigmoid colon• nerves and vessels penetrate internal (circular)

muscular layer - defects• Older age, Western countries (low fiber diet)

• Symptoms - asymptomatic, discomfort• diverticulitis - pain, abscess formation. • Treatment - high-fiber diet, diverticulitis - surgery

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Colonic diverticulosis

• Two factors:– 1/ peristaltic contractions - elevation of

pressure– 2/ focal defects of muscular wall

• Appearance - up to 1 cm, usually sigmoid, adjacent to teniae, thin-walled

• Complications - inflammation - diverticulitis, perforation - peritonitis, adhesions

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Bowel obstruction

• Hernias - protrusion of pouchlike, serosa-lined sac of peritoneum - hernial sac. Inguinal, femoral, umbilical canal, surgical scars.

• Retroperitoneal hernia - Treitz ligament. Segments of viscera trapped,

• Incarceration – ischemia – necrosis (hemorrhagic infarction), ileus

• Acute abdomen !

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Bowel obstruction• Intussusception - proximal segment

to distal

• Volvulus - twisting of the loops or other structures (ovary) - small bowel usually - obstruction, infarction

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Tumors• High incidence of colorectal Ca in Czech

Republic• Vast majority- large intestine

• Polyps – Sessile– Pedunculated– non-neoplastic - inflammatory – Hyperplastic– adenomatous polyps– Mesenchymal– lymphoid

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Tumors

• Non-neoplastic polyps - increase with age, 90% of all polyps, hyperplastic - small (up to 5 mm), singly or multiple, no malignant potential!

• Juvenile polyps - hamartomatous, cystic glands, children younger than 5 years. In adults - retention polyps - long stalk, occur in rectum

• Peutz-Jeghers polyps - hamartomatous - smooth muscle within mucosal stroma

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Adenomas• Small to large, large intestine, dysplastic

changes• Majority of all adenoCa arise from adenomas• Symptoms - asymtomatic, occult bleeding,

bleeding, anemia. Polyp in Vater's ampulla - biliary obstruction. All adenomas potentially malignant

• Three types:– 1/tubular– 2/villous– 3/tubulovillous

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Adenomas• Tubular - most common, pedunculated, • branching glands, dysplasia – biopsy• sometimes intramucosal Ca - invasive -

growth into the stalk• Villous - larger, sessile - up to 10 cm in diam.,

higher risk • Tubulovillous - admixture.

• Risk of Ca - size, histology, grade of dysplasia

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Familial polyposis syndromes

• Autosomal dominant, familial adenomatous polyposis (FAP) - Gardner sy - more than 100

• Most - tubullar adenomas• Risk of Ca - 100% by mid life.• Hereditary nonpolyposis colorectal

cancer (HNPCC) - autosomal dominant (Lynch's sy) - high risk of colorectal Ca and endometrial Ca

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Colorectal carcinoma• Large intestine (98%), 6 - 7th decade• Higher risk - adenomas, ulcerative colitis• M>F• High – USA, Europe• Low – India, South America, Africa. Japan

• Dietary causes:– 1/ low-fiber– 2/ high content of refined carbohydrates– 3/ high content of animal fat– 4/ low vitamin A, C, and E

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Colorectal carcinoma

Distribution of Ca • proximal colon - polypoid, fungating mass. • Sigmoid&rectum - circular, stenosing• Both penetrate – up to the serosal surface• Symptoms - silent, fatigue, iron deficiency anemia• Right sided – bleeding• Rectal – stenosis• Meta - regional LN, liver, lungs, bones• Detection - occult bleeding test, colonoscopy, biopsy,

CT - spread (metastases)• Therapy – surgery, radiation, chemotherapy

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Small intestinal tumors

• Only 3-6% of GIT tumors• AdenoCa - unusual, circular growth -

duodenum (ampula), LN spread

• Carcinoid - producing hormones (serotonine)

• derived from neuroendocrine cells • low-grade malignant, local infiltrative growth,

meta rare• Small bowel, appendix, rectum, bronchi

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Small intestinal tumors• Carcinoid• yellow-tan, desmoplasia• Mitoses rare• Asymptomatic - hormones metabolized in

liver• Carcionid sy - (cutaneous flushes,

diarrhea, asthma, heart fibrosis (pulmonary + tricuspid valve) - hepatic metastases.

• GIT malignant lymphoma - usually non-Hodgkin, MALToma, H. pylori!

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Appendix

• Acute appenicitis - acute abdomen. oxyuris vermicularis

• Mucocele - dilatation of the lumen by mucus - non-tumorous obstruction (fecalith) - mucosal atrophy

• rarely mucocele ruptures - mucoperitoneum

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Appendical tumors

• Carcinoid• Mucinous cystadenoma • cystadenoCa• Pseudomyxoma peritonei =

mucus+tumor cells, implantation metastasis

• Jelly – like material in peritoneal cavity