Pathology of the oesophagus:a) disorders of motility, diverticula, varicesb) reflux exophagitisc) esophageal carcinoma

Pathology of the stomach:a) gastritisb) peptic ulcer,c) tumors - polyps, carcinoma, lymphoma,

stromal tumors.Appendicitis:

a) acute - morphologic types, evolution, complicationsb) chronic - evolution and complications

Pathology of the small and large intestine:a) vascular disordersb) inflammatory diseases, infections, enterocolitisc) Crohn´s diseased) ulcerative colitise) malabsorption syndromes

Pathology of the intestines:a) neoplasmsb) polyps - non neoplastic, adenomatous - typesc) gastrointestinal polyposis syndromesd) colorectal carcinoma; lymphomase) intestinal lymphomas, stromal tumors

Clinical OverviewEsophagus - most common disorders are reflux esophagitis (due to exposure of the lower esophagus to gastric acid regurgitating upwards from the stomach) and carcinoma, both squamous and adenocarcinoma being important. In children, esophageal atresia and abnormal developmental links with the trachea are important congenital malformations.The stomach is an important site of peptic ulceration, the ulceration being due to breakdown of the normal mechanisms which protect the stomach mucosa from its own acid. The small intestine is the major site of absorption of the basic food materials, and diseases of small intestinal mucosa may lead to malabsorption syndromes; an important cause is celiac disease (gluten enteropathy) which is an immune process leading to destruction of the small intestinal mucosa. The small intestine, particularly ileum, is the most common site for the chronic inflammatory disease called Crohn’s disease. Acute inflammatory disorders of the small bowel are common but transient, being due to bacterial or viral infection. The stomach and colon are usually also involved (infective gastroenteritis).

Most common inflammatory disease of the entire alimentary tract which requires surgical treatment is acute appendicitis, mainly in children and young adults, but occasionally in mature adults and the elderly where the diagnosis may be missed.

The colon may also be involved in the chronic inflammatory condition Crohn’s disease, but is the main site of the chronic intermittent inflammatory disease called ulcerative colitis.

Predisposing factors to colonic cancer - neoplastic polyps in the colonic mucosa (adenomatous polyps).

Colorectal carcinoma there is a well-recognized sequence ofchanges from benign polyp to invasive adenocarcinoma. Colon - mechanical abnormalities diverticular disease and volvulus. Disorders of the anus are a frequent are mainly trivial with distressing symptoms (hemorrhoids, pruritus ani, anal fissure); the only life-threatening disease of the anus is squamous carcinoma.

GIT is susceptible to bacterial and viral infection, producing acute vomiting and diarrhea, the main source for the infection being contaminated or infected food items (‘food poisoning’).

Vascular diseases affecting the alimentary tract are uncommon, with the exception of arterial infarction of the small bowel due to thrombotic or embolic occlusion of the mesenteric vessel, and acute venous infarction of small or large bowel due to some mechanical obstruction to normal venous drainage.

The most common examples of venous infarction of the bowel are strangulation of a loop of small bowel in a hernial sac and volvulus of the large bowel.

Esophagus

Lesions – esophagitis to cancerDysphagia (difficulty in swallowing) esophageal motor dysfunction,Narrowing, or obstructionClinical manifestations1.Heartburn (retrosternal burning pain) –

regurgitation of gastric contents2.Hematemesis3.Melena

Esophagus

Anatomic disorders of the esophagus1.Stenosis- lower esophageal narrowing,

chronic inflammation, GERD2.Atresia, fistula- newborn with

aspiration, paroxysmal suffocation, pneumonia (tracheoesophageal fistula)

3.Webs, rings- dysphagia to solid foods, partially occluding lumen

4.Diverticula- nocturnal episodic regurgitation

Hiatal hernia- dilated segment of the stomach to protrude above the diaphragm

Sliding- 95% of cases, 9% with heartburn (accentuated by bending forward, supine position, obesity)

Paraeophageal- separate portion of the stomach enters the thorax through

a widened foramen, rarely with reflux, can become strangulated/ obstructed

Complications- ulceration, bleeding, perforation

EsophagusAchalasia- incomplete relaxation of the lower

esophageal sphincter to relax during swallowing:1.Aperistalsis2. Incomplete relaxation3. Increased resting tonePrimary- loss of intrinsic inhibitory innervation of the

lower esophageal sphincter and smooth muscle segment

Secondary- Chagas disease (Trypanosoma cruzi) -myenteric plexus of the GIT

Other possible causes- autoimmunity, previous viral infection (unproven)

5% cases result to CA

EsophagusLacerations (Mallory-Weiss syndrome)Longitudinal tear esophagogastric junctionSevere vomiting/ retching – alcoholics/ acute

illnessPathogenesis- incomplete relaxation of the

esophageal sphincter during vomitingTearing of the involved area75% cases have hiatal herniaTears may involve mucosa or penetrate the wall,

infection may lead to an inflammatory ulceration/ mediastinitis

(5 to 10% of upper GI bleeding due to esophageal laceration)

Esophagus

Varices- dilated tortuous vessels, due to collateral by-pass channels caused by cirrhosis, 2/3 of cases, no symptoms until they rupture

Cause of rupture – unclear, possibly erosion of the mucosa, increased tension, vomiting

50% with concomittant liver CA50% cases subsides spontaneouslyMortality – 20 to 30%

EsophagusEsophagitis-Prolonged gastric intubationUremiaCorrosive/ irritant substancesRadiation or chemotheraphyMajor cause – gastroesophageal reflux disease

(0.5% of adult American)Heartburn is a predominant symptomContributory factors1. Less effective anti-reflux mechanisms2. Inadequate clearance of refluxed material3. Sliding hiatal hernia4. Increased gastric volume5. Reduced reparative capacity – prolonged exposure to

gastric juices

EsophagusEsophagitis-MorphologyMild- simple hyperemiaSevere- erosion or total ulcerationCharacteristics of uncomplicated Reflux

esophagitis1.Epithelial layer with eosinophil with or without

neutrophil2.Basal zone hyperplasia3.Elongation of lamina propria papillaeCM – heartburn, chest pain may mimic heart

attackSequelae- bleeding, stricture, Barrett esophagus

EsophagusBarrett esophagus- complication of a long-

standing GERDUp to 10% of patients with persistent symptomatic

reflux disease-replacement of the distal stratified squamous

mucosa by metaplastic columnar epithelium containing goblet cells (more resistant to gastric content)

male: female ratio = 4:1, common among whitesComplications1.Ulcer, stricture2.Cancer – 30 to 40-fold increase

EsophagusEsophageal CASquamous CA- 90% of cases, > age 50, male:female ratio 3:1Adenocarcinoma- increasing incidence, more among whitesMorphologyEarly – small gray-white thickening or elevation of the mucosa3 types1. exophytic, protrude into lumen2. Necrotizing, erodes into the respiratory tree, aorta, elsewhere3. Diffuse infiltrativeInvolvement

Cervical- 20%Middle third – 50%Lower third – 30%

EsophagusEsophageal CAAdenoca-arise from dysplastic mucosa of Barrett esophagusUsually in the distal third Micros- mucin-producing glandular tumorCMInsidous onset, dysphagia and obstruction -weight loss, anorexia, fatigue, weakness-pain related to swallowingSurgical excision is rarely curative – lymphatic

network, adjacent structureAmenable to surgery if confined to mucosa or submucosa

Chronic gastritis-chronic mucosal inflammatory changes lead to mucosal atrophy and epithelial metaplasia-Helicobacter pylori- non-invasive non-spore forming gram negative rod, bacterial enzymes and toxins, release of chemicals by recruited neutrophil-autoimmune gastritis- gland destruction and mucosal atrophy,loss of parietal cellsMorphology- chronic gastritis- inflammatory changes consist of lymphocytic and plasma cell infiltrate in the lamina propria with variable gland loss and mucosal atrophyCM- few or no symptoms, upper abdominal discomfort, n/vMost patients with peptic ulcer have H. pylori infections, risk for gastric CA 5XAutoimmune gastritis, risk for cancer from 2% to 4%

Stomach

Acute gastritis-acute mucosal inflammatory process, usually of transient nature, may be accompanied by bleeding and mucosal erosionPathogenesis-NSAID(aspirin)Excessive alcohol intake, heavy smokingAnti-cancer drugsUremiaSystemic infection (typhoid fever)Severe stress (trauma, burns, surgery)Ischemia and shockSuicide using acid or alkaliMechanical trauma (NGT)

Stomach

Acute gastritisMorphology- localized to diffused involvement, superficial inflammation of the entire mucosa thickness, with bleeding and erosion (acute erosive gastritis)If the noxious event is short lived – complete recovery of the mucosaCM- asymptomatic, epigastric pain with N/V, hematemesis, melena, possible fatal blood loss-major cause of hematemesis (alcoholics)-25% of patients taking aspirin for RA develop acute gastritisGastric ulcerationBreach in the mucosa, could extend to muscularis mucosae into submucosa or deeper

Stomach

Peptic ulcers-chronic, often solitary, due to aggressive action of

acid-peptic juices98% in the first portion of duodenum or stomach

(ratio 4:1)American- 2.5% males, 1.5% femalesGenetic or racial factors- plays no role in its causationDuodenal ulcers- alcoholic cirrhosis, COPD, chronic

renal disease, hyperparathyroidism(hypercalcemia stimulate gastrin production)

Pathogenesis1.Mucosal exposure to gastric acid and pepsin2.H. pylori infectionActual pathogenesis is murky

Stomach

Peptic ulcersHost mechanism that protects the

mucosa from gastric juices1.Mucus – superficial epithelial cells2.Bicarbonate secretion3.Acid and pepsin secreted as “jets”4.Epithelial regeneration5.Robust mucosal blood flow6.Mucosal prostaglandins – maintain

blood flow

Stomach

H. Pylori70% to 90%- patients with duodenal ulcer70% - gastric ulcers-induce inflammatory and immune

response-produce urease (toxin),

phospholipase (mucosal damage)-vacuolating toxin (VacA), cytotoxin-assod

gene A (CagA)- secretes IL-8 -recruits and activates neutrophils

Stomach

Peptic ulcersNSAID- second to H. pyloriRisk factors – increasing age, higher dose,

prolonged use-suppress mucosal prostraglandin synthesis

(more acid, less mucus and less bicarbonate)-impairs angiogenesis- impedes healing of

ulcersOthers1. Smoking- mucosal blood flow, healing2. Alcohol – directly cause PU3. Stress4. Zollinger-Ellison syndrome

(multiple peptic ulcers - gastrin secretion by a tumor)

Stomach

Peptic ulcerMorphologyMucosal defects that penetrates deeper, mostly round, sharply punched out craters 2 to 4 cm.Sites- ant and post wall duodenum, lesser curvatureNo significant elevation or beading of the edges

Micros- vary with activity, chronicity, degree of healingDiff from AGU- absent gastritis in adjacent mucosaCM- epigastric gnawing, burning, boring pain, worse at night, occurs 1 to 3 hours after mealsRelieve by alkali or food (there are many exceptions)Other- n/v, bloating, belching, weight lossBleeding- chief complication, perforation, malignant transformation

PU- chronic and recurrent, impairs quality of life than shorten it Requires 15 years for healing

Stomach

Stomach

Acute gastric ulcerationStress ulceration- multiple lesions1. Severe trauma (surgical procedures, sepsis, grave

illness2. Extensive burns (Curling ulcers)3. Traumatic or surgical injury to the CNS, or

intracerebral bleeding (Cushing ulcers)Pathogenesis – uncertain – systemic acidosis (severe trauma and

burns)- decrease pH of mucosal cells, hypoxia, impaired mucosal blood flow

Cranial lesion – increase ICP stimulate vagal nuclei – increased acid secretion

Morphology – circular and small (less than 1 cm), base dark brown, singly to multiple throughout stomach and duodenum

CM- ICU admitted patients with sepsis, burns or trauma dev AGUTreatment- prophylactic antacid, blood transfusionNeed to correct the underlying conditionGastric mucosa can recover completely if the patient does not die.

Stomach

TUMORSGastric polyps- mass or nodule that project

above the level of the surrounding mucosa, these are uncommon

Types1.Hyperplastic – 80% to 85%2.Fundic gland – 10%3.Adenomatous – 5%

All arise from a setting of chronic gastritis – adematous polyp has a risk of containing an adenoCA

Stomach

TUMORSGastric Carcinoma

Carcinoma – 90% to 95%Lymphomas – 4%Carcinoid – 3%Mesenchymal spindle cell tumor – 2%

High incident – Japan, columbia, Costa Rica, HungaryOne of the leading killer cancer

Morphology- intestinal (gastric mucous cells that have undergone metaplastic dysplasia in the setting of chronic gastritis, better differentiation)

Common type in high risk population, occurs after age 50 years with 2:1 male predominanceDiffuse variant arise from gastric mucous cells, not

associated with chronic gastritisPoorly differentiated, earlier age, no male predominance

Stomach

Gastric CancerMorphologySite

1.Pylorus and antrum – 50% to 60%2.Cardia – 25%3.Body and fundus – 12%4.Lesser curvature – 40%5.Greater curvature – 12%

*ulcerative lesion on the lesser curvature – more likely malignant

Classification1.Depth of invasion2.Macroscopic growth pattern3.Histologic subtype

Stomach

Gastric CancerMorphologyDepth of invasion –

morphologic feature having the greatest impact on clinical outcome

Early GC – lesion confined to the mucosa and submucosa, regardless of the presence

or absence of of perigastric LN

Advanced GC – extended below the submucosa into the muscular wall

*Mucosal dysplasia precursor lesion

Gastric CancerMorphologyUncommon, a broad area of the gastric wall, or entire

stomach, extensive infiltration, rigid and thickened stomach is termed a leather bottle stomach

-linitis plastica, metastatic ca from the breast and lung may generate a similar picture

The earliest LN metastasis may sometimes involve a supraclavicular LN (Virchow’s node)

Unusual intraperitoneal spread to both ovaries – Krukenberg tumor

CM- early is asymptomatic, advanced – may be asymptomatic, abdominal discomfort or weight loss

Only hope for cure is early detection and surgical removalPrognostic indicator – stage of tumor at the time of resection

Gastric Ca- signet ring

Developmental anomalies1.Atresia, stenosis2.Duplication3.Meckel’s diverticulum- failure of involution of

omphalomesenteric duct leaving a persistent blind-ended tubular protrusion 5 to 6 cm long

4.Omphalocele- congenital defect of the periumbilical abdominal wall, membranous sac in which the intestines herniate

5.Malrotation- intestines not in their normal position

6.Hirschsprung disease leading to congenital megacolon

Small and Large Intestines

Developmental anomaliesHirschsprung disease leading to congenital

megacolon- aganglionic segmentLacks Meissner submucosal, Auerbach myenteric

plexuses.Functional obstruction, distension of the colon

proximal to the affected segmentCM- delay in the initial passage of meconium,

followed by vomiting 48 to 7 hoursEnterocolitis, fluid and electrolyte imbalance, perforationAcquired megacolon• Chaga’s disease –trypanosomes• Obstruction by neoplasm, inflammatory stricture• Toxic megacolon complicating CD or UC

Small and Large Intestines

VASCULAR DISORDER

Ischemic bowel diseaseIntensive infarction – occlusion of any of the major arteries- celiac, superior and inferior mesenteric arteriesTransmural – acute occlusion of the major mesenteric

arteryMural or mucosal – physiologic hypoperfusion, localized

anatomic defectPredisposing factors1. Arterial thrombosis – severe atherosclerosis, dissecting aneurysm, systemic

vasculitis,2. Angiographic procedures, aortic surgery, surgical accidents, hypercoagulable disorder3. Oral contraceptives4. Arterial embolism- cardiac vegetation, aortic atheroembolism5. Venous thrombosis- hypercoagulable state-oral contraceptives, intraperitoneal sepsis6. Post-op state hepatocellular CA, cirrhosis, abdominal trauma7. Nonocclusive ischemia- CF, shock, dehydration, vasoconstrictive drugs

(digitalis,vasopresin, propanolol)8. Others- radiation injury, volvulus, stricture, herniation

Small and Large Intestines

CM- most common in the later years of life, transmural sudden onset of abdominal pain, sometimes with bloody diarrhea, need for prompt diagnosis(recent major abdominal surgery, recent MI, atrial fib) mortality rate = 90%

Diarrheal diseases-increase stool mass, stool frequency, stool fluidity, often with pain, urgency, perianal discomfort, incontinence

Dysentery- low volume, painful, bloody diarrhea

MalabsorptionGluten-sensitive enteropathy- Celiac disease- reduced small intestinal absorptiveSurface area- sensitivity to gluten (oat, barley, rye) immune response- damage to surface enterocyte-symptomatic diarrhea and malnutrition from infancy to mid-adulthood,Removal of gluten in diet results in dramatic improvementTropical sprue, whipple disease- arise from intestinal infectionresults in celiac-like disease within few days after acute diarrheal enteric infection-rare, affects intestine, CNS, joint. Hallmark PAS-positive macrophages in the lamina propria. Etio-gram + and culture R actinomycete (tropheryma whippelli) males, 4th to 5th decades of life- -malabsorption, lymphadenopathy, hyperpigmentation, polyarthritis, obscure CNS complaintsCM- bulky frothy, greasy, yellow or gray stool with weight loss, anorexia, Abdominal distention, borborygmi, flatus, muscle wasting

Consequences of malabsorption

IDIOPATHIC INFLAMMATORY BOWEL DISEASE

Crohn disease, ulcerative colitisChronic relapsing disorders of unknown originCollectively called IBD. Normal intestine represents adynamic balance between1. Factors that activate the host immune system –such as

luminal microbes, dietary antigens, endogenous inflammatory stimuli

2. Host defenses that down regulate inflammatory and maintain integrity of the mucosa

IBD is a heterorogenous group of diseases characterized by exaggerated destructive mucosal immune response.

Tissue injury is likely to be initiated by diverse genetic and immunologic

pathways that are modified by environmental influences, including microbes and their products

CROHN DISEASEInvolves any level of the GIT, associated with complication

of immune origin like iritis, uveitis, migratory polyarthritis, it is a systemic inflammatory disease with predominant GIT involvement, peaks 2nd to 3rd decade of life, more among women, whites, Jews

Characterized by transmural involvement with mucosal damage, caseating granuloma 40% to 60% cases, fissuring and fistulae, sinus tract formation. Thick and rubbery wall. “string sign”. Skip lesion. Microscopic- inflammation, crypt abscess, ulceration, chronic mucosal damage.

CM- variable presentation, recurrent diarrhea, crampy abdominal pain, fever lasting days to weeks, melena- 50%, 10-20% symptom free for decades after initial attacks, 20% continuous active disease

Complications- fistula, abdominal abscess, strictures/ obstructionRare- massive intestinal bleeding, toxic dilatation of colon, cancer

ULCERATIVE COLITISulceroinflammatory disease – colon, limited to the mucosa

and submucosa except in severe cases, begins in rectum

Epidemiology- more common than CD, whites, no sex predilection, peaks at age 20 to 25

Morphology- involves rectum or rectosigmoid colon only in 50% of cases, pseudopolyps- isolated islands of regenerating mucosa

Pathologic features- mucosal inflammation, ulceration, chronic mucosal damage

1.Mononuclear infiltrate 2.ulceration 3. granulation tissue 4.submucosal fibrosis and mucosal atrophy

CM- relapsing and remitting disorder- bloody mucoid diarrhea persists for days, weeks, months. Insidious, cramp, tenesmus, colicky abdominal pain relieved by defecation. Fever, weight loss. 10% first attack is the last

ULCERATIVE COLITIS

Colonic diverticulosisDiverticulum- uncommonBlind pouch leaving off the gut, lined by a mucosa. Most diverticulitis are acquired, lacking or having attenuated muscularis propria.Common site for diverculum- colon,

diverticular disease of the colon -diverticulosisCommon among western adults, prevalence is about 50% by age 60-low fiber diet, reduced stool bulk, exaggerated spastic contraction- herniation of the bowel wallPathogenesis1.Exaggerated peristaltic contractions- increase intraluminal pressure2.Focal defect in the muscular colonic wall

Bowel obstruction80% of cases due to; hernias, intestinal adhesions, intussusception, volvulus (small intestines commonly involve due to its small lumen)Hernial sac- protrusion of a pouch-like sac through a weakness or defects in the abdominal cavityUsual sites anteriorly1.Inguinal and femoral canals2.Umbilicus3.Surgical scar

Incarceration- permanently trappedStrangulation- infarction due to compromised blood supplyAdhesions-surgery, infection, endometriosis- intestine are trapped (internal hernia)Intussusception- telescoping of proximal segment into a immediately distal segment - Common in children may be due to excessive peristaltic activity. Adults- Intraluminal mass (tumor)- infarction

Volvulus- twisting of bowel loops about its base of attachment- small intestines

TumorsEpithelial tumors of the intestines are major causes of diseases and death worldwide

Colorectal cancer second only to bronchogenic carcinoma among the cancer killersAbout 5% Americans will develop colorectal cancer, 40% of them will die of the disease

Adenocarcinoma most common colorectal canceraccounts for 70% of all GIT malignancy.

Small intestine uncommon site for tumor, Polyp- mass protrudes into the lumen- 1. pedunculated, (stalk) 2. sessile-formed by abnormal mucosal maturation, inflammation, architecture No malignancy potential (hyperplastic polyp)-those that arise due to epithelial proliferation and dysplasia (adenomatous polyp or adenoma)Precursor of cancer

Small and Large Intestines

Tumors of the small and large intestinesBenign

Hyperplastic polypHamartomatous polyp Inflammatory polypLymphoid polyp

Neoplastic-epithelial lesionsBenign polyps – adenomaMalignant lesions – adenoCA,

carcinoid tumor, angiomaMesenchymal lesions

Gastrointestinal stromal tumors (benign or malignant)Other benign lesions – lipoma, neuroma, angiomaKaposi’s SALymphoma

Tumors of the large intestinesAdenomasSmall to large lesions, mostly sessilePrevalence – 20% to 30% before age 40,

40% to 50% after age 60Most invasive colorectal adenoCA arise from preexisting adenomatous lesionTypes- tubular, villous, tubulovillous

Malignant risk- polyp size, histologic architecture, severity of dysplasia

-Ca is rare in tubular adenoma < 1 cm-Ca is high (40%) in sessile villous adenoma > 4 cm-Severe dysplasia often found in villous areas(maximum diameter chief determinant for having cancer)CM- small ones- asymptomatic, occult bleeding can lead to anemia, occult bleeding – villous adenomaAll adenoma are potentially malignant

Colorectal CA98% of all cancer in large intestines –

adenocarcinoma arise from adenomatous polyps134,000 new cases/ year, 55,000 deaths, 15% of all cancer-related deaths USAEpidemiologyPeak age 60-70, less than 50% seen in less than 50 y/o if seen consider; ulcerative colitis, polyposis syndromeAdenoma are presumed precursor lesionsMales affected 20% more often than femalesHighest incidence rates in developed countriesEnvironmental factors- dietary practice1.Low content of unabsorbable vegetable fiber2.High content of refined carbohydrates3.High fat content4.Decrease intake vitamin A C E – increased fecal retention, altered bacterial flora

Colorectal CAAdenoma-carcinoma sequence- documented by these observation1. Population with high prevalence of adenomas high prevalence of

colorectal ca2. When invasive a is identified at an early stage surrounding

adenomatous tissue is also presentMorphology25%- colorectal ca – cecum or ascending colon25%- descending colon and proximal sigmoid

Tumors at Proximal colon- exophytic mass, obstruction is uncommon Distal colon- annular encircling lesion – napkin ring constriction

Microscopic- adenoCA well-differentiated to undifferentiated

CM-asymptomatic and develops insidiouslyR-sided- fatigue, weakness, iron deficiency anemiaL-sided- occult bleeding, change in bowel habit, crampy left lower

quadrant discomfortMetastasis- regional LN, liver, lungs, bonesSurgically curative in 25% to 30% of casesMost important prognostic indicator of CRC is the stage of the disease

Small intestinal neoplasmsComprises 75% of the length of the GIT, tumor – 3% to 6% of the GITadenoCA- common site- duodenumCM- late, cramping pain, N/V, weight lossCarcinoid tumor- carcinoma-like, tendency for aggressive

behavior1. Site of origin2. Depth of penetration3. Size of tumor90% of ileal, colonic and gastric carcinoid have metastases during

time of diagnosiscan secrete bioactive products or hormones

Morphology – appendix most common site, bulbous swelling of the tip, obliterate the lumen

Solid, yellow-tan appearance, firm due to desmoplasiaRectal and appendiceal carcinoids almost never metastasizeMicroscopic- form discrete islands, trabeculae, strands, glands or

undiffentiated sheetMonotonous appearance with scanty pinkish cytoplasm, round to

oval stippled nuclei minimal variation in cell or nuclei size

Small intestinal neoplasmsCarcinoid syndrome- clinical features

Vasomotor disturbance (skin flushes, cyanosis)

Intestinal hypermotilityAsthmatic attacksHepatomegaly (metastases)Niacin deficiencySystemic fibrosis

GIT- lymphoma- 40% lymphoma are extranodal, 1% to 4% GIT cancer

Western hemisphere- arise from B-cells of mucosa-associated lymphoid tissue (MALT)

Primary GIT lymphoma has better prognosis

Acute appendicitis10% of people will develop AP in USA and western

countries, peak incidence in 2nd and 3rd decadesmale:female ratio = 1.5:1Pathogenesis- inflammation associated with

obstruction in 50% to 80%Fecalith, gallstone, tumor, ball of worms (E.

vermicularis)- obstruction and ischemia

Acute appendicitisMorphologyEarly AP- dull granular red membraneLater stage- fibrinopurulent covering at the serosa

Acute suppurative AP-abscess formation within the wall with ulceration and

necrosis of the mucosa.Acute gangrenous AP- green-black gangrenous

necrosis though the wall up to the serosaCan result in rupture and suppurative peritonitis

Histologic criterion for diagnosis – neutrophilic infitration of the muscularis propria***

Acute appendicitis

CM- classic1.Mild periumbilical discomfort2.Anorexia, N/V3.RLQ tenderness4.Deep constant ache or pain in the R

lower QFever and leukocytosis appear early in the

course

Large number of cases not classic

Acute appendicitisDifferential diagnoses1. Mesenteric lymphadenitis after viral infection2. Gastroenteritis with mesenteric adenitis3. PID with tubo-ovarian involvement4. Ruptured ovarian follicle at ovulation5. Ectopic pregnancy6. Meckel’s diverticulitis

Mortality – appendiceal perforation = 2%Tumors- carcinoids, mucocele non-neoplastic

obstruction of the lumenMucinous tumor – disseminated intraperitoneal cancer Pseudomyxoma peritonei