PATHOLOGY OF GASTROINTESTINAL SYSTEM · Type II - combined chronic duodenal and gastric ulcer Type III –pre-pyloric ulcer within 2 cm of pyloric Type IV - ulcer high on a small

C h ro n i c S i a l o a d e n i t i s , P l e o m o r f i c A d e n o m a , G i a n t C e l l E p u l i s Ra d i c u l a r C y s t , C h ro n i c G a s t r i t i s , , G a s t r i c U l c e r, U l c e r a t i ve C o l i t i s , C ro h n ’ s d i s e a s e, H e p a t i t i s , L i ve r C i r r h o s i s , C h ro n i c C h o l e c y s t i t i s , A c u t e H e m o r r ha g i c N e c ro s i s O fPa n c r e a s

General medicineINST ITUTE OF PATHOLOGICAL ANATOMY, FACULTY OF

MEDICINE , COMENIUS UNIVERS ITY, BRATISLAVA

PATHOLOGYOF GASTROINTESTINAL SYSTEM

ORAL CAVITY DISEASESIALOADENITIS

= acute or chronic inflammation of a predominantly porogenicnature

Etiology

• viruses (mumps, CMV), bacteria and yeast

Acute sialoadenitis

• catarrhal, purulent inflammation, abscesses

Complications

• Abscess (possibility of rupture low due to thick fascia)

• fistulation, purulent thrombophlebitis of superficial veins andphlegmona of the neck

ORAL CAVITY DISEASESIALOADENITIS

Chronic sialoadenitis

• The last stage of acute prolongated inflammation

Microscopic findings

• Atrophic (duct enlargement, duct epithelial hyperplasia,acini atrophy and ligament replacement, chronicinflammatory infiltrate)

• Productive (fibrosis to hyalinization) sclerosis of thesalivary gland without enlargement of the ducts

Incorrectly referred to as a tumor - Küttner's tumor!

Chronic sialoadenitis (HE) histotopogram

Dialted ducts

Chronic inflammatory

infiltrate

Chronic sialoadenitis (HE) 259

Dialted ductus

Fibrosis

Chronic inflammatory infiltrate

Chronic sialoadenitis (HE) 259

Dialted ductusChronic inflammatory

infiltrate

Serous acini

Mucinous acini

ORAL CAVITY DISEASESJÖGREN SYNDROME

• Autoimmune disease with affection of salivary and lacrimal glands

• Primary SS (sicca syndrome) - xerostomia, xerophtalmia

• Secondary SS - xerostomia, xerophtalmia + other autoimmunediseases

Diagnostics

•Autoantibodies, sialography and / or scintigraphy of the salivarygland, salivary gland functional examination, eye examination, lipbiopsy - small salivary glands

•Microscopic findings

• Benign lymphoepithelial lesion (myoepithelial sialoadenitis),destructive lymphocytic infiltrate, atrophy to squamous metaplasiaof the acinari epithelium

• Hyperplasia of the duct epithelium, obliteration of the lumen

Possible transition to malignant B-line lymphoma !!!

Sjogren syndrome (HE)

Proliferation of

lymphoid tissue

Loss of secretory

cells

ORAL CAVITY DISEASEMIKULICZ’S DISEASE

• Benign lymphoepithelial lesion

• Probably an autoimmune disease

• slow one- or two-sided enlargement of the salivary gland, painless, lasting years


Sclerosis

Myoepithelial cell bands

Lymphoid tissue

ORAL CAVITY DISEASEPLEOMORPHIC ADENOMA

= benign tumor - most common of all salivary gland neoplasms

• most commonly affects parotis, women, 30-60y

• slow-growing, painless and firm mass with the face deformations

Macroscopic findings

• smooth or lobulated, well-encapsulated tumor that is clearly demarcated from the surrounding normal salivary gland


• fibrous capsule

• epithelial structures (solid isles) present in stroma (myxoid, mucoid or chondroid) = myxochondroepithelioma

• myoepithelial cells

Unclear biological prognosis - incomplete encapsulation and transcapsular growth – recurrence, 1% malignant transformation

Pleomorphic adenoma (HE) 98

Epithelial component

Mesenchymal component

- chondorid

Mesenchymal

component - myxoid

ORAL CAVITY DISEASEGIANT CELL EPULIS

• proliferative, chronic, reparative focal connective tissueproliferation of the gingiva

• benign lesion, reactive hyperplasia!!

• causes: chronic irritation, mostly on the anterior parts of themaxilla, may recur unless predisposing factors removed

• most often near premolars

Macroscopic finding

• localize tumor like gingival enlargement, pedunculated orsessile swelling, dark red, often ulcerated

Microscopic finding

• multinucleated osteoclast-like giant cells in a rich vascularstroma

Giant cell epulis (HE) 138

Spindeled cells

Giant cells

Capillaries

ORAL CAVITY DISEASERADICULAR CYSTS

= radicular / periodontal / periapical

• most common cyst of the jaws

• chronic inflammation → epithelial proliferation(rests of Malassez) in periapical granuloma →cyst lining (nonkeratinized stratified squamousepithelium)

• fibrous capsule with lymphocytes and plasmacells

• destruction of the bone of the jaws

• higher risk of squamous cell carcinoma

• treatment - enucleation

Radicular cyst (HE) 143

Cyst cavity

Cyst capsule Cyst capsule – non-keratinizing squamous epithelium

Fibrous capsule with chronic inflammatory infitlrate

BARRETT’S ESOPHAGUS

• intestinal metaplasia occurs on the esophageal mucosa due to gastroesophageal reflux

• change of squamous epithelium into cylindrical goblet epithelium

• intestinal metaplasia is precancerosis of stomach adenocarcinoma

• Barrett's esophagus has a 40-fold higher risk of malignancy

• Localization - lower part of the esophagus at the transition to the stomach

Risk factors

• reflux, smoking, alcohol, hiatus, motility disorder

Diagnostics

• endoscopic examination with biopsy specimen collection

BARRETT’SESOPHAGUS


• gastric-type epithelialmetaplasia above the gastro-esophageal passage, chronicinflammatory infiltrate insubmucosa

• cylindrical epithelium withgoblet cells on the left andsquamous epithelium on the right

Squamous epitheliumCylindrical epithelium

GASTRITIS

Etiology

• high doses of NSAID, alcohol, smoking, cytostatics, systemic infections (eg. salmonellosis), severe stressconditions, ischemic damage and shock, ionizing radiation, mechanical trauma, inappropriate diet

Diagnostics

• endoscopic examination with biopsy sample collection (always describe which part of the stomach thesample is taken from!)

Complications

• gastric ulcer, pernicious anemia

Clinical findings

• from asymptomatic manifestations to severe blood loss in gastric ulcer at ac. gastritis

• asymptomatically or with mild symptoms such as e.g. stomach pain, nausea and nausea gastritis

GASTRITISACUTE GASTRITIS

= acute inflammatory process with gastric mucosal damage from hyperemia to erosions and ulcers


• mucosal hyperemia, edema, Neu and Lym infiltration, epithelial regeneration may also occur

• healing occurs through regeneration or becomes chronic

GASTRITISCHRONIC GASTRITIS

= chronic inflammatory disease of gastric mucosa with transition to atrophy and intestinal metaplasia

Classification by etiology

Type A – autoimmune type, • Affects the stomach body

Type B – bacterial type

• Affects the antrum, H.pylori

Classification by morphology

1. Superficial or deep• Depending on the depth of the lymphocyte-plasmatic infiltrate

2. Athrophic gastritis with / without intestinal metaplasia• Precancerosis in case of metaplasia

GASTRITISCHRONIC GASTRITIS


• non-specific picture !!! (normal / edematous /atrophic mucosa) macroscopic image may notcorrelate with microscopic !!!


• alternation of atrophic and hyperplastic mucosa,chronic inflammation, sclerosis of the stroma,intestinal metaplasia

Chronic gastritis (HE) 216

Chronic inflammation

Atrophy and destruction of glands

Chronic gastritis type B – H. Pylori

GASTRODUODENAL ULCER DISEASE

• occurrence of one or more ulcers of the stomach or duodenum

Localisation

Type I - small curvature mediogastrically

Type II - combined chronic duodenal and gastric ulcer

Type III – pre-pyloric ulcer within 2 cm of pyloric

Type IV - ulcer high on a small whore near GE junction

• Duodenal ulcers are 4 times more common (80%) than gastric, they also bleed more often

• Duodenal ulcer - 95% in the bulbus of duodenum on the front and / or back wall (kissing ulcer)

• Ulcers in the large curvature - suspected malignancy

Diagnostics

• Xray, Xray + contrast, endoscopic examination, biochemistry

GASTRODUODENAL ULCER DISEASE

Special types of ulcers

• Cushing's ulcer - in trauma or CNS surgery (vagus irritation - HCl hypersecretion)

• Curling ulcer - in burns (hyperhistaminemia - hypersecretion HCl)

• Zollinger-Ellison Syndrome - ↑ gastrin production (stimulates HCl secretion) in pancreatic gastrinoma

• Stress ulcer - impaired mucosal perfusion

Ulcerations types

• Acute ulcers - funnel-shaped defect with sharp edges, often multiple, with black bottom (digested blood)

• Chronic ulcer - round defect with embedded edges, light base (cleared by enzymes and HCl, red-pink - granulation tissue, white – fibrous tissue), solitary, radial convergence of surrounding mucous membranes

GASTRODUODENAL ULCER DISEASEGASTRIC ULCER

Etiology

• mucosal barrier damage, hyperacidity at elevated serum gastrin levels, digestion ofgastric mucosa

Complications

• bleeding, obstruction, penetration, perforation, ulcarscarcinoma

Clinical findings

• pain (visceral) in the epigastrium after eating (antacids do not usually relieve)

• anorexia, feeling of fullness, heartburn, occasional vomiting with the admixture ofbile, for fear remain hungry

• affects older individuals

GASTRIC ULCER


4 histologic layers:

• necrotic zone (fibrin exudate, tissue detritus, PMNL)

• superficial exudative zone(coagulation necrosis)

• granulation tissue zone

• scarring zone

Multiple gastric ulcers

Gastric perforation

Chronic antral ulcer Perforation of chronic ulcer

Acute peritonitis due to ulcer perforation

Gastric ulcer (HE) histotopogram

Normal mucosa

Ulcer

Necrotic zone

Exudative zone

Granulation tissue zone

Gastric ulcer ( HE ) 64

Normal mucosa

Necrotic zone

Exudative zone

Granulation tissue zone

DUODENAL ULCER

Clinical findings

• fasting epigastric pain (often wakingthe patient at night - night hungrypain)

• food and antacids bring relief

• typical seasonal occurrence withexacerbations in spring and autumn(duration 1-2 weeks),

• affects younger individuals

Duodenal ulcer with penetration to pancreas (HE) histotopogram

Duodenal mucosa

Muscel layer duodenum

Penetrating ulcer

Pancreas

Erosion of vessel with

over imposed thrombus

INFLAMMATORY BOWEL DISEASE (IBD)

Crohn’s disease Ulcerous colitis

Localization Whole GIT, most common ileum rectum and colon

X-ray abdomenSegmental involvement (alteration of inflamed and healthy

segments)

Continual involvement from rectum

orally

Thickening of the intestinal wall Straightening of the haustra

Endoscopy Discontinued changes, focal linear ulcerationsHemorrhagic mucosa, diffuse continual

inflammation, pseudo-polyps

Histology Inflammation of all layers of intestinal wall (transmural) Inflammation of mucosa and submucosa

Typical epitheloid granulomas, lymphocytic infiltrate Criptitis, crypt abscesses

Clinical pictureAbdominal pain, loss of weight, diarrhea with blood and

mucusBloody diarrhea with tenesmi

Complication Fistule formation, stenosis, abscesses Increased risk of carcinoma

INFLAMMATORY BOWEL DISEASE (IBD) ULCEROUS COLITIS

• a rare autoimmune type of inflammation

• mainly affects the rectum and the descending part of the colon

• the average age of the patients is 11 years

Etiology

•multifactorial, genetic factors, immunological factors, exogenous factors

Complications

• iridocyclitis, glaucoma and cataract bag result from corticosteroid treatment, primary sclerosingcholangitis, “overlap syndrome”, thromboembolic complications, toxic megacolon, colorectal cancer

Diagnostics

• endoscopy, colonoscopy, USG

ULCEROUS COLITIS

Macroscopic findings• ulcers, pseudopolyps, haustraldisappearance, bowel shortening

Microscopic findings• edema, lymphoplasmocyte infiltrate,crypt abscesses, goblet cellsincreased, later decreasing,increased endocrine cells, vasculardamage, muscle abnormalities

Ulcerous colitis (HE) histotopogram

Superficial ulcerations of mucosa

Regeneration of mucosa – inflammatory pseudo-polyp

Ulcerous colitis – crypt abscess (HE) 250

Lympho-plasmocytic infiltrate

INFLAMMATORY BOWEL DISEASE (IBD)CROHN’S DISEASE

• chronic non-specific inflammation up to the formation of granulomas

• affects the entire thickness of the intestinal wall, segmental involvement

• it mainly affects the terminal ileum and / or colon

Etiology

• unclear, multifactorial, genetic factors, immunological factors, exogenous factors

• it is believed to be a dysregulation of the immune response to common bacterial antigens

Diagnostics

• laboratory diagnostics - occult bleeding, ASCA, CRP, FW antibodies

• imaging methods - X-ray, USG, CT

• endoscopic examination - colon, gastro, capsule endoscopy

INFLAMMATORY BOWEL DISEASE (IBD)CROHN’S DISEASE


wall thickening, stenosis, mucous ulcers withsurrounding swelling, appearance of"cobblestones", fissures, fistulae


transmural inflammation (Ly, plasmocytes,macrophages), granulomas, ulcerations andfissures, submucosa edema, later intestinal fibrosis

Crohn’s disease (HE) 330

Inflammatory infiltrate – lymphocytes,

plasmocytes, macrophages

Fissure

Crohn’s disease (HE) 330

Fissure Graulomas

Mucosa

Transmural

inflammatory

infiltrate

COLORECTAL CARCINOMAS

• the third most common malignancy in the world

Etiology

• sporadic form (90%)

• hereditary form (10%) - Lynch syndrome, familial adenomatosis of the colon

• risk factors - age, obesity, smoking, eating habits

Precancerous lesions

• Adenomatous colon polyps with low grade / high grade dysplastic changes


Diagnostics

• colonoscopy with sampling, laboratory examination, USG, others by extent

Clinical findings

• excessive flatulence, alteration of the defecation stereotype, colic pain or subileouscondition, bleeding from tumor to GIT, either microscopic or macroscopic, anemiasymptoms, acute peritonitis, tenesms



• exophytic (polyposis) - mainly riskof obstruction of intestinal lumen(ileus) or invagination

• excavated (exulcerated) - the riskis mainly bleeding and perforationof the intestinal wall

• flat (infiltrating) - can long beclinically silent


• mainly adenocarcinoma (G1-G3)

CHRONIC HEPATITIS

Etiology

• most often viral etiology, other infections, toxic substances - alcohol, drugs


• necrosis (piecemeal) = portions of periportal hepatocytes are necrotic

• portal tract lesions (inflammatory infiltrate - lymphocytes, plasma cells, macrophages; bile ductproliferation)

• intralobular lesions (steatosis, Mallory hyaline, hyperplasia of Kupfer's cells)

• fibrosis

Diagnostics

• HBsAg + a HBcAg + (immunohistochemical evidence)

Chronic hepatitis (HE) 136, 128

Inflammatory infiltrate

– lymphocytes, plasma

cells, macrophages Necrosis of hepatocytes



Mallory’s hyaline



hepatocytes

Piecemeal necrosis of

hepatocytes

LIVER CIRRHOSIS

= irreversible, diffuse, chronic, progressive process leading to lobular and vascular disorganization of liver architecture into nodular (end stage of various diffuse liver diseases)

Classification:A: According to etiology:• Alcoholic cirrhosis (alcoholic liver damage), most common• Post-necrotic cirrhosis (chronic hepatitis C, B, B+D)• Biliary cirrhosis (long lasting obstruction of biliary ducts)• Toxic cirrhosis (toxic damage of liver – paracetamol, amatoxin,…)• Metabolic diseases (Wilson’s disease, Alfa-1-antitrypsine deficiency, hemochromatosis, CF, prfyria,…)• Autoimmune hepatitis• Cryptogenic (idiopathic)

B: According to morphology• Micronodular• Macronodular• Mixed

C: According to the activity• Active (continuous hepatocellular necrosis and inflammatory infiltrate)• Inactive (without evidence of necrosis and inflammatory infiltrate)

LIVER CIRHOSIS

Macroscopic finding

• tough consistency, rounded edges, thickened capsule

• node size – micronodular (nodules to 3 mm)

- macronodular (nodules over 3 mm)

- mixed

Microscopic finding

• necrosis, regeneration, joining of individual portal fields,fibrosis, pseudolobules, pseudo-canaliculi, bile lakes and thrombi

Complications

• portal hypertension, bleeding, icterus, liver failure, renal failure,hyperestrism, encephalopathy

Bile lakes

Steatosis

Pseudolobules

Micronodular cirrhosis

Nodular change of parenchyma

Thickened capsule

Micronodular cirrhosis (HE) 62, 63

Fibrous septa

Proliferated biliary ducts

Pseudolobules


Micronodular cirrhosis (HE) 62, 63

Fibrous septa with chronic inflammatory infitlrate

Proliferating biliary ducts

Pseudo-cannaliculi – biliary ducts without lumen

Micronodular cirrhosis (van Gieson)

Pseudolobules

Pseudolobules

Pseudolobules

Pseudolobules

Pseudolobules

Fibrous septa

Micronodular cirrhosis(FH)

PseudolobulesPseudolobules

Pseudolobules

Fibrous septa

CHRONICCHOLECYSTITIS• It results from either gradual development or

from acute cholecystitis

Etiology

• bacteria (streptococci, Escherichia coli,staphylococci)

Clinical finding

• biliary dyspepsia - upper abdominal pressure,episodic abdominal pain locally or diffuse,pyrosis, anorexia, flatulence, meteorism, nausea,steatorrhea,

• attacks of repeated biliary pins

CHRONIC CHOLECYSTITIS


• rigid thick wall, often presence of stones !!

• fibrosis of the wall with inflammatory exudation, the mucous membrane is reddened, sometimescovered with ulcers, sometimes completely absent

• for a longer period of time a retraction occurs → an image of a puckered gallbladder

• in obstruction → hydrops - bile discoloration after absorption of bile dyes, calcium salts fall out andgive the gallbladder a milk color,

• salts can also be deposited in the wall → "porcelain gallbladder“


• thickened muscle, proliferation of fibrous tissue, lymphocytic infiltrate, epithelial entrapment deep intomuscle (Rokitansky-Aschoff sinus)

Chronic cholecystitis (HE) 99


Thickened muscle layer

Rokitansky-Aschoff sinuses

Chronic cholecystitis (HE) 99

Rokitansky-Aschoff sinuses


CHOLESTEROLOSISGALLBLADDER

• a common non-neoplastic disease inwhich lipid accumulation occurs inthe gallbladder mucosa

• steatosis due to lysosomaldysfunction

Macroscopic finding

• strawberry gallbladder

Microscopic finding

• In the thin ligament of laminapropria mucosae are present foamymacrophages distorting the mucosalalgae

Cholesterolosis of the gallbladder (strawberry gallbladder)

ACUTE HEMORRHAGIC NECROSIS OF THE PANCREAS

• digestion by own pancreas enzymes (trypsin - pancreas necrosis, phospholipase A - fat necrosis (Balser’snecrosis), elastase - vascular necrosis)

• prognostically worst sudden abdominal event

Etiology

• gallbladder, biliary tract and Vater’s papilla disease - acute biliary pancreatitis

• alcoholism - acute ethylic pancreatitis

• postoperative pancreatitis, after ERCP - acute iatrogenic pancreatitis

• hyperlipidemic pancreatitis, post-traumatic pancreatitis; pancreatotoxic induced pancreatitis (ATB), infections -parotitis virus, viral hepatitis, inappropriate diet

Complication

• Pulmonary - atelectasis, pneumonia, hypoxia, ARDS;

• Metabolic - hyperglycemia, hypocalcaemia, acidosis, hyperTAG;

• KVS - tachycardia, hypotension, arrhythmia, shock;

• Renal - oliguria, azotemia;

• Hematological - DIC;

ACUTE HEMORRHAGIC NECROSIS OF THE PANCREAS


• swelling of the pancreas, fat necrosisand pancreatic parenchyma necrosis,hemorrhagic ascites


• necrosis (pancreas parenchyma, fat),bleeding, polymorphonuclearleukocytes

bleeding

PMNLFat necrosis

Balser’s (fat) necrosis on acute pancreatitis

Acute hemorrhagic necrosis of pancreas (HE) histotopogram

Pancreas parenchyma

bleeding

inflammation

Acute hemorrhagic necrosis of pancreas (HE) 130

inflammation

Pancreas parenchyma

Fat necrosis

bleeding

Acute hemorrhagic necrosis of pancreas (HE) 130

Fat necrosis

Documents

PATHOLOGY OF GASTROINTESTINAL SYSTEM · Type II - combined chronic duodenal and gastric ulcer Type III –pre-pyloric ulcer within 2 cm of pyloric Type IV - ulcer high on a small