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Pathology of the Large Intestine

• Aiman Zaher, MD

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Objectives

• At the end of this segment, when given a clinical
  presentation, gross specimen, and/or
  photomicrograph, students will be able to
• Compare and contrast the clinical presentations,
  etiologies, pathogenesis, and gross and
  microscopic changes found in developmental,
  inflammatory, circulatory, mechanical, and
  neoplastic disorders of the large intestine.

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Objectives

• At the end of this segment, when given a clinical
  presentation, gross specimen, and/or
  photomicrograph students will be able to
• Predict the clinical complications associated
  with diseases of the large intestine.
• Define the words in the glossary

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Glossary

• Diverticulum
• Polyps
• Pedunculated
• Sessile

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Structure and Function
6

• Gross
• 1.5 meters long
• Cecum, ascending colon, transverse colon,
  descending colon, and sigmoid colon.
• Sigmoid becomes rectum at the level of the third
  sacral vertebra.
• Blood Supply
• Ascending proximal transverse colon superior
  mesenteric artery
• Remainder of colon to rectum Inferior
  mesenteric artery
• Upper rectum Superior hemorrhoidal branch of
  inferior mesenteric artery
• Lower rectum hemorrhoidal branches of iliac or
  internal pudendal artery.

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• The purpose of the colon is to reclaim water and
  electrolytes.
• Histology
• Mucosa is flat without villi
• Numerous straight tubular crypts extending to
  muscularis.
• Surface cells are columnar with numerous goblet
  cells.
• Crypts contain numerous goblet cells, endocrine
  cells and stem cells.
• Paneth cells not as abundant as in small intestine

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Congenital Anomalies
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Congenital Aganglionic MegacolonHirschsprung
Disease

• Absence of ganglion cells (in Auerbachs and
  Meissners plexi) in a portion of the intestinal
  tract
• Due to problems with neural crest cell migration
  or early death of ganglion cells
• Leads to functional obstruction and massive
  intestinal dilatation proximal to the aganglionic
  segment
• Most cases rectum and sigmoid only
• Complications include enterocolitis and
  perforation of the colon or appendix with
  peritonitis
• Manifests in newborns as failure to pass meconium
  and constipation
• Acquired megacolon results from Chagas disease,
  obstruction by neoplasm or inflammation, and as
  complications of inflammatory bowel disease

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Hirschsprung Disease - Morphology
PJGoldblatt, MD
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Inflammatory Disorders
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Antibiotic Associated Colitis(Pseudomembranous)

• Definition
• Acute colitis characterized by formation of an
  adherent inflammatory exudate overlying sites of
  mucosal injury pseudomembrane
• Etiology
• Clostridium difficile
• Normal part of gut flora
• Toxins A and B cause host cell apoptosis
• May occur without antibiotic therapy after
  surgery or debilitating illnesses
• Pathogenesis
• Usually occurs in patients following a course of
  broad-spectrum antibiotics (almost all
  antibacterials implicated)
• Toxin-producing strains flourish when normal
  flora disrupted

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Antibiotic Associated Colitis(Pseudomembranous)
Pathogenesis
Patients with infection
Pseudomembranous colitis
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Pseudomembranous Colitis - Morphology
Gross Plaque-like adhesions of
fibrinopurulent-necrotic debris and mucus,
adherent to damaged mucosa
GRIPE
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Pseudomembranous Colitis - Morphology

• Microscopic
• Surface epithelium is denuded
• Neutrophils in lamina propria
• Damaged crypts distended by mucopurulent exudate
  that erupts out of crypt (volcanic fashion) ?
  adheres to damaged surface ? pseudomembrane

GRIPE
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Antibiotic Associated Colitis(Pseudomembranous)

• Clinical Features
• Adults acute or chronic diarrheal illness
• Diagnosis C. difficile cytotoxin in stool
• Relapse occurs in up to 25
• Treat with Vancomycin

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Idiopathic Inflammatory Bowel Disease

• Collective term for Crohn disease and ulcerative
  colitis, because of their shared features
• Results from inappropriate and persistent
  activation of the mucosal immune system
• Distinct clinicopathologic manifestations
• Crohn disease granulomatous (50) and can be
  found from the esophagus to anus, most often
  intestine and colon transmural
• Ulcerative colitis nongranulomatous, confined
  to colon and rectum, and superficial
• Both have extraintestinal inflammatory processes
  associated

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CROHN DISEASE
ULCERATIVE COLITIS
Continuous lesions rectum to terminal ileum
Skip Lesions
Transmural Inflammation Ulcers, Fissures, 50
Granulomas
Superficial Inflammation, Ulcers, Pseudopolyps
Robbins 6th Edition
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Idiopathic Inflammatory Bowel Disease

• Etiology and Pathogenesis
• Genetic Predisposition
• 15 of IBD patients have affected first-degree
  relatives lifetime risk if either a parent or
  sibling is affected is 9
• HLA-DR1/DQw5 27 of North American white
  patients w/ CD
• HLA-DR2 patients w/ UC
• HLA-B27 pts with IBD ankylosing spondylitis
• Genetics suggest that CD and UC are distinct
  diseases.
• Infectious causes
• Host of organisms have been studied and none
  eluded gene-knockout mice that normaly develop
  IBD do not develop it when they are germ free
• Abnormal Host Immunoreactivity
• Thought that there is too much T-cell activation
  and/or too little control by regulatory T
  lymphocytes
• Inflammation is Final Common Pathway

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Crohn Disease
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AKA terminal ileitis, regional enteritis,
granulomatous colitis
CROHN DISEASE
Characterized by sharply delineated and typically
transmural involvement of the bowel by an
inflammatory process with mucosal damage,
non-caseating granulomas, and fissuring with
fistula formation.
Skip Lesions (segmental)
Skip Lesions Transmural Inflammation Ulcerations,
Fissures, 50 Granulomas

GRIPE
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Crohn Disease

• Any region of bowel sm. intestine (40), small
  large intestine (30), colon (30)
• Epidemiology
• World-wide, but most prevelant in developed
  Western countries
• Any age peak incidence in 2nd 3rd decades and
  minor peak in 6th 7th decades
• FgtM whites 2-5X gtnon-whites
• US Jews 3-5X gt non-Jews
• Smoking is a strong risk factor

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Crohn Disease - Morphology
Granular serosa with creeping fat and thick
wall mesentery also thickened and edematous
GRIPE
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Crohn Disease - Morphology
Skip lesions Bowel wall thick due to
inflammation, edema, fibrosis, and hypertrophy ?
narrow lumen
GRIPE
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Crohn Disease - Morphology
String sign on x-ray from narrowed gut lumen
PJ Goldblat, MD
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Crohn Disease - Morphology
Early lesions are aphthos ulcers in mucosa ?
coalesce into linear ulcers ? cobblestones
GRIPE
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Crohn Disease - Morphology
Histologically - chronic inflammation that is
transmural and contains non-caseating granulomas
50 of time One complication of transmural
inflammation with Crohn disease is fistula
formation. Seen here is a fissure extending
through mucosa at the left into the submucosa
toward the muscular wall, which eventually will
form a fistula. Fistulae can form between loops
of bowel, bladder, and even skin. With colonic
involvement, perirectal fistulae are common.
Web Path
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Crohn Disease

• Clinical Features
• Intermittent attacks of diarrhea, fever, and
  abdominal pain separated by weeks to months that
  are asymptomatic
• Attacks usually caused by periods of physical or
  emotional stress
• May have occult blood loss, leading to anemia,
  but no massive bleeds
• Some may have severe right lower quadrant pain

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Crohn Disease

• Clinical Complications
• Strictures
• Fistulas
• Malabsorption and protein-losing enteropathy
• Extra-intestinal Manifestations
• Migratory polyarthritis
• Sacroilitis
• Ankylosing spondylitis
• Erythema nodosum
• Primary sclerosing cholangitis
• Clubbing of fingertips
• 5-6 fold increase in GI cancer, but less risk
  than in ulcerative colitis

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Ulcerative Colitis

• Definition
• Ulceroinflammatory disease of the colon, limited
  to mucosa submucosa (except in severe cases)
• No granulomas
• Involves rectum and extends continuously
  proximally, leading to pancolitis
• No skip lesions
• Slightly more common than Crohn Disease and
  affects same type of patient
• Associated with nonsmoking, particularly
  ex-smokers

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ULCERATIVE COLITIS
Continuous inflammation beginning in rectum
and extending to the terminal ileum in some cases




Pseudopolyps Ulcers
Robbins 6th Edition
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Ulcerative Colitis Morphology
Starts as predominantly mononuclear inflammation
in lamina propria
GRIPE
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Ulcerative Colitis - Morphology
Crypt abscesses lead to ulcerations that are
linear and broad-based, leaving a raw, exposed
muscularis propria
GRIPE
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Ulcerative Colitis - Morphology
Isolated islands of regenerating mucosa become
hyperplastic ? pseudopolyps
GRIPE
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Ulcerative Colitis - Morphology
Granulation tissue fills ulcer as inflammation
subsides, leading to fibrosis and mucosal
disarray and gland atrophy. Wall is not thickened
and inflammation does not extend beyond the
submucosa.
GRIPE
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Ulcerative Colitis - Morphology
Dysplasia noted that can give rise to adenomas or
invasive carcinoma.
GRIPE
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Ulcerative Colitis - Morphology
Toxic damage to muscularis propria and neural
plexus ? shutdown of neuromuscular function ?
progressive swelling and gangrene ? toxic
megacolon ? rupture ? peritonitis
GRIPE
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Ulcerative Colitis

• Clinical Features
• Relapsing bouts of bloody, mucoid diarrhea,
  persisting for days, weeks or months. Relapse
  after months, years or decades.
• Usually accompanied by lower abdominal pain and
  cramps, relieved by defecation
• Attacks usually associated with physical or
  emotional stress
• 97 have at least one relapse during a 10-year
  period
• 30 require colectomy in first three years of
  onset due to uncontrollable disease
• Clinical Complications
• Cancer
• 20-30X risk with pancolitis of 10gt years
• Associated carcinomas often infiltrative w/out
  obvious masses
• Actual rate of progression to dysplasia CA is
  low
• Toxic Megacolon
• Extraintestinal lesions

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Inflammatory Bowel Disease Extraintestinal Lesions
Uveitis
10
Ankylosing Spondylitis
Primary Sclerosing Cholangitis
3
Erythema nodosum
Malnutrition
Arthritis 25
Deep Vein Thrombosis 6
Pyoderma Gangrenosum
GRIPE
40
Circulatory Disorders
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Angiodysplasia

• Definition
• Tortuous dilations of submucosal and mucosal
  blood vessels in cecum or right colon
• Epidemiology
• lt 1 of adult population, but 20 of significant
  lower GI bleeds (including chronic and
  intermittent or acute and massive bleeding)
• Usually after age 60
• Etiology and Pathogenesis
• Normal distention and contraction of wall may
  occlude the submucosal veins ? focal dilatation
• LaPlaces Law states that tension in the wall of
  cylinder is a function of intraluminal P
  diameter cecum has widest diameter and therefore
  greatest tension
• Vascular degenerative changes

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Angiodysplasia - Morphology
Vessels span mucosa submucosa and contain
smooth muscle, suggesting they are ectatic nests
of pre-existing veins, venules, capillaries
GRIPE
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Angiodysplasia

• Clinical Features
• Manifested as variable bleeding some massive and
  severe.
• Hematochezia

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Hemorrhoids

• Definition
• Variceal dilations of the anal and perianal
  venous plexuses.
• Microscopically, are thin-walled, dilated,
  submucosal vessels
• Types
• Internal superior plexus above anorectal line
• External inferior plexus below anorectal line
• Etiology and Pathogenesis
• 5 of general population
• Rarely under 30 years of age, unless pregnant
• Secondary to persistently elevated venous
  pressure within the plexi
• Chronic constipation and straining
• Pregnancy (venous stasis)
• Liver Cirrhosis Portal Hypertension

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Hemorrhoids - Morphology
GRIPE
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Hemorrhoids

• Clinical Features
• Hemorrhage
• When traumatized ? thrombosis ? recanalization.
• Ulceration, fissures and infarction due to
  strangulation

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Obstructions/ Dilatations
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Diverticular Disease

• Definition
• A blind pouch lined by mucosa that communicates
  with lumen of gut
• Congenital - all three layers of bowel wall e.g
  Meckel diverticulum
• Acquired - lack or have attenuated muscularis
  propria

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Diverticular Disease

• Epidemiology
• Rare lt 30 In Western countries 50 incidence in
  age 60
• Can occur throughout the GI tract, but most
  commonly in the left colon (particularly sigmoid)
• Usually multiple present and the condition
  called, diverticulosis
• Etiology and Pathogenesis
• Focal wall weakness ? intralumenal pressure
• Longitudinal muscle coat incomplete (taenia coli)
  in colon ? leaving regions where nerves and
  arterial vasa recta penetrate connective tissue
  sheaths around vessels are areas for herniation
• ? Peristalsis ? sequester bowel segments ? ?
  intralumenal pressure ? ? inflammation
• Possibly diets low in fiber reduce stool bulk, ?
  peristalsis

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Diverticular Disease - Morphology
webpath
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Diverticular Disease - Morphology
webpath
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Diverticular Disease - Morphology
Thin wall with flattened or atrophic mucosa,
compressed submucosa, and attenuated or missing
muscularis
webpath
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Diverticular Disease

• Clinical Features
• Most asymptomatic
• 20 symptomatic
• Intermittent cramping, lower abdominal
  discomfort, constipation, distention, feeling
  like rectum wont completely empty, alternating
  constipation diarrhea, minimal chronic or
  intermittent blood loss or rarely massive
  hemorrhage
• Clinical Complications
• Obstruction ? Inflammation ? Perforation ?
  Pericolic abscesses ? fibrosis and/or sinus
  tracts ? peritonitis

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Diverticular Disease - Morphology
Perforation
Web Path
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Tumors of the Colon and Rectum
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What is a Polyp?

• A tumorous mass that protrudes into the gut lumen
• Presumably, all polpys start as small, sessile
  lesions without a stalk and then devlop into
  stalked, pedunculated polyps.

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How are polyps formed?

• Non-neoplastic (hyperplastic polyps)
• Abnormal mucosal maturation
• Inflammation
• Architecture
• Neoplastic
• Proliferation and Dysplasia (adenomatous polyps,
  adenomas)
• These are precursors to carcinoma!
• Submucosal or mural tumors give rise to polypoid
  lesions
• Unless otherwise specified, polyps are
  epithelial and arise from mucosa.

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Benign Lesions
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Non-Neoplastic Polyps
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Hyperplastic Polyps

• Patients 60
• Nipple-like protrusions into lumen often
  multiple
• Histology - well-formed glands and crypts lined
  by non-neoplastic cells
• Virtually no malignant potential

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Hyperplastic Polyps - Morphology
GRIPE
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Juvenile Polyps

• Focal hamartomatous malformations in mucosa and
  lamina propria
• Sporadic and majority in children lt 5 yrs
• Large (1-3 cm), round, smooth and lobulated with
  up to 2 cm stalks
• No malignant potential except for a rare
  autosomal dominant juvenile polyposis syndrome
• 50-100 juvenile polyps in GI tract

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Juvenile Polyps - Morphology
Hamartomatous Malformations
GRIPE
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Juvenile Polyps - Morphology
Lamina propria is bulk of lesion with abundant
cystically dilated glands
GRIPE
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Peutz-Jeghers Polyps

• Hamartomatous polpys of mucosa, lamina propria,
  and muscularis mucosa
• Either single or
• Multiple throughout GI tract, as in P-J Syndrome
• melanotic mucosal and cutaneous pigmentation
  around oral mucosa, lips, face, genitalia, and
  palmer surface of hands
• risk of intussusception, causing death
• The polyps have no malignant potential, but
  patients with syndrome have increased risk of
  carcinoma of pancreas, breast, lung, ovary and
  uterus

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Adenomas

• Epidemiology
• Small pedunculated to large neoplasms that are
  sessile
• Prevalence is 20-30 lt 40 yrs to 40-50 gt
  60 yrs
• Familial predisposition for sporadic adenomas (4X
  risk for 1st degree relatives and 4X risk for
  colorectal cancer)

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Adenomas

• Classification
• Tubular adenomas
• Most common
• gt75 tubular architecture, small pedunculated
• Villous adenomas
• Least common
• gt50 villous architecture
• Tubulovillous adenoma
• Mixture of the other two
• 25-50 villous architecture

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Adenomas

• Malignant Risk
• Adenomas arise from proliferative dysplasia that
  varies in severity they are precursors to
  invasive colorectal adenocarcinoma
• Polyp size, histologic architecture, severity
  of dysplasia determines risk of malignancy
• Rare in tubular adenomas lt1 cm
• Up to 40 of villous adenomas gt 4cm
• Usually contains severe dysplasia

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Adenomas - Morphology
Tubular Adenomas 90 occur in the colon occur
singly in 50 of cases Larger are pedunculated,
smaller are sessile Peduncle is fibrous and
vascular Head is normal mucosa to
adenomatous Epithelium can be dysplastic and
evidence of malignancy is invasion of stalk
GRIPE
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Adenomas - Morphology
GRIPE
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Adenomas - Morphology
GRIPE
GRIPE
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Adenomas - Morphology
GRIPE
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Adenomas - Morphology
Villous Adenomas Large polyps, up to 10 cm Found
in older persons in the rectum
rectosigmoid Sessile to velvety to
cauliflower-like Villiform, frond-like extensions
of the muscosa that have dysplastic epithelium
GRIPE
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Adenomas - Morphology
GRIPE
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Adenomas - Morphology
Adenocarcinoma arising in a villous adenoma
GRIPE
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Adenomas - Morphology
Tubulovillous Adenomas Amount of villous
component determines biologic behavior
GRIPE
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Adenomas

• Clinical Features
• Regardless of whether carcinoma is present, the
  only adequate treatment for a pedunculated or
  sessile adenoma is complete resection.
• If adenomatous tissue is left behind, the patient
  still has a premalignant lesion.

78
Familial Syndromes

• Onset in teens to twenties in all syndromes and
  cancer 10-15 years later
• Autosomal dominant diseases
• Familial adenomatous polyposis (FAP)
• Archetype familial adenomatous polyposis syndrome
• Caused by mutations of the adenomatous polyposis
  coli (APC) gene on chromosome 5
• Exhibits innumerable adenomatous polyps that
  carpet the mucosa
• 100 frequency of progression to adenocarcinoma
• Gardner syndrome
• Variation of FAP
• Addition of osteomas (mandible, skull lung
  bones), epidermal cysts, and fibromatosis
• Turcot syndrome
• Rare
• Adenomatous colonic polyposis CNS tumors
  (gliomas)

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Morphologic and Molecular Changes in
Adenoma-Carcinoma Sequence
Robbins, Fig 17-60, 7th edition
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Malignant Lesions
81
Adenocarcinoma

• Epidemiology
• Adenocarcinomas (98 of cancer in colon)
• 10 of all cancer related deaths in US
• Peak incident 60-79 years
• Highest death rates in US and Eastern European
  countries

82
Adenocarcinoma

• Etiology and Pathogenesis
• Must suspect preexisting UC or Polyposis Syndrome
  if found in young person
• Diet implicated
• Excess caloric intake relative to requirements
• Low unabsorbable vegetable fiber ? reduces
  transit time yields scanty stool
• Large quantities of refined carbohydrates ? toxic
  oxidative products held in contact with mucosa by
  slow-moving stools
• Red meat
• High cholesterol ? synthesizes bile acids ?
  converted into carcinogens by bacteria
• Decreased intake of protective micronutrients,
  e.g. Vit A,C,E

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Adenocarcinoma -Morphology
Distribution 22 cecum/ascending 11
transverse 6 descending 55 rectosigmoid 6
other sites
Distal colon Annular (napkin-ring) lesion that
constricts the bowel
Proximal colon Polypoidal and exophytic
GRIPE
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Adenocarcinoma -Morphology
GRIPE
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Adenocarcinoma -Morphology
GRIPE
Web Path
Web Path
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Adenocarcinoma

• Clinical Features
• Asymptomatic for years and then insidious onset
• Right sided
• Fatigue, weakness, iron deficiency anemia
• Lesions are bulky and bleed easily
• Left sided
• Occult blood in stool
• Alternating constipation and diarrhea
• Crampy discomfort in left lower quadrant
• Rectum sigmoid more infiltrative at time of
  diagnosis ? poorer prognosis
• Iron deficiency anemia in an older man is GI
  cancer until proven otherwise.

87
Adenocarcinoma

• Complications
• Weight loss, malaise, weakness are ominous
  signs
• Metastasis by lymph and blood
• In order of metastatic spread regional nodes,
  liver, lungs and bone
• Extent of tumor at time of diagnosis (stage) is
  the most important prognostic indicator.

88
TNM Classification
89
Carcinoid Tumors

• Source
• Endocrine cells throughout GI tract can generate
  bioactive compounds that coordinate gut function
  (gastrin, vasoactive amines, somatostatin
  insulin)
• Epithelial cells that functionally and
  morphologically resemble endocrine cells
• Epidemiology
• Most located in GI tract
• Peak incidence in 50s
• lt 2 of colorectal malignancies, 50 of small
  intestinal malignancies
• Site is important in terms of biologic behavior
  because there is no reliable histological
  difference between benign malignant carcinoids

90
Carcinoid Tumor - Morphology

• Appendix most common site, followed by the small
  intestine, rectum, stomach, and colon
• Rectal tumors about half of those that draw
  clinical attention.
• In appendix, they arise as bulbous lesions at
  tip, causing obstruction.
• Remainder are submucosal or intramural masses
• Characteristic gross appearance solid,
  yellow-tan
• Rectal and appendiceal almost never metastasize,
  but they may show extensive local spread.

91
Carcinoid Tumor - Morphology
Web Path
92
Carcinoid Tumor - Morphology
Monotonous cells with scant pink cytoplasm and
round to oval, darkly stippled nuclei. On
electron microscopy, they contain membrane-bound
secretory granules.
Web Path
Web Path
93
Carcinoid Tumors

• Clinical Features
• Many asymptomatic
• May obstruct
• May be functional e.g. hyperinsulinemia, Cushing
  Syndrome, Zollinger-Ellison Syndrome
• May have Carcinoid Syndrome
• 1 of all patients 20 with widespread
  metastases
• Excess elaboration of serotonin 5-HT and its
  metabolite (5-HIAA) are present in the blood and
  urine of patients
• Symptoms flushing, intestinal hypermotility,
  bronchoconstriction, hepatomegaly, and systemic
  fibrosis

94
Carcinoid Tumors

• Clinical Complications
• Liver metastasis
• 5 year survival 90 (excluding appendiceal)
• 50 if small bowel tumor with liver metastasis
• Wide spread disease will usually cause death

95
Gastrointestinal Lymphoma

• Definition
• Primary GI lymphomas exhibit no evidence of
  liver, spleen, mediastinal lymph node, or bone
  marrow involvement at the time of diagnosis
• Regional lymph node involvement may be present
• Who gets them?
• Sporadic, H. pylori gastritis, Mediterranean
  population, congenital immunodeficiency, HIV,
  Celiac sprue, immunosuppressive therapy

96
Gastrointestinal Lymphoma

• Clinical Features
• Tumors start as plaques then become exophytic or
  infiltrative
• Symptoms vague to prominent weakness and weight
  loss
• Ulcerate leading to bleeding
• Tumors invade and perforate
• Obstruction
• Complications
• Depth of invasion, size of tumor, histologic
  grade and extension determine prognosis
• 85 10-year survival if localized to mucosa or
  submucosa

97
Appendix
Most common acute abdominal condition that a
surgeon is called on to treat.
98
Acute Appendicitis

• Epidemiology
• Mainly adolescents and young adults
• Males slight more often than females
• Etiology and Pathogenesis
• Obstruction by fecoliths (most common),
  gallstones, tumors or parasites
• Obstruction ? mucous secretion ? ? intralumenal
  pressure ? collapse of draining veins ? ischemia
  ? bacterial proliferation ? further inflammation
  with edema ? ?blood flow
• Some have an unknown cause

99
Acute Appendicitis - Morphology
GRIPE
Web Path
Normal Appendix
Early Acute Appendicitis
Scant neutrophils ? mucosa, submucosa
muscularis ? dull red granular serosa,
characteristic of early acute appendicitis
100
Acute Appendicitis - Morphology
Web Path
Fibrinopurulent Exudate
Normal Appendix
Acute Suppurative Appendicitis
Later, abscesses develop, leading to acute
suppurative appendicitis with fibrinopurulent
serosal exudates. Ultimately, the appendix will
develop acute gangrenous appendicitis. Histologic
diagnosis of acute appendicitis is neutrophils in
the muscularis.
101
Acute Appendicitis

• Clinical Features
• Classic signs are periumbilical pain to lower
  right quadrant, nausea and/or vomiting, abdominal
  tenderness in the region of the appendix, mild
  fever and leukocytosis (15-20 thousand)
• Classic signs absent more than present,
  especially in young children and elderly
• Surgical false positives 20-25 of the time, but
  significant mortality rate (2 w/ perforation)
  outweighs this fact.
• Clinical Complications
• Perforation leading to
• periumbilical abscess
• local peritonitis

102
Peritonitis
103
Peritonitis

• Common Causes
• Sterile peritonitis from leakage of bile or
  pancreatic enzymes
• Perforation or rupture of biliary system
• Acute hemorrhagic pancreatitis
• Surgical procedures
• Gynecologic conditions (endometriosis ruptured
  dermoid cysts)

104
Neoplasms

• Mesotheliomas
• Extremely rare
• Same as those found in pleural cavity and
  pericardium
• Associated with asbestos exposure in 80
• Secondary tumors (Metastatic)
• Common
• Diffuse serosal implantation e.g ovarian and
  pancreatic tumors
• Mucinous cystadenocarcinomas of appendix implant
  peritoneum ? mucin pseudomyxoma peritoneii

105
References

• Kumar, Abbas, and Fausto ROBBINS AND COTRAN
  PATHOLOGIC BASIS OF DISEASE, 7th Edition,
  pp.828-870.