GASTROINTESTINAL TRACT.PPTbbbbbbbbbbbbbbb

best

1. The oral cavity and the Gastrointestinal
tract
pathology
Dr. JabessaGemechu
(MD, Assistant professor of pathology)

2. Oral cavity
Salivary glands
Esophagus
Stomach
Small and large intestine
Appendix
Peritoneum

3. ORAL CAVITY
Inflammations
Herpes simplex virus infection
-most are caused by HSV-I
-Usually trivial “cold sores”
-Primary infection commonly in children 2-4 yrs
-severe and diffuse involvement of oral mucosa,
tongue and pharyngeal mucosa may occur acute
herpetic gingivostomatitis
-xizedby formation of clear vesicles
-vesicles rupture to yield extremely painful shallow
ulcers.

7. •histologically intranuclear inclusions and
multinucleate giant cells
•lesions resolve spontaneously within 3-4
weeks
Aphthous ulcers ( canker sores)
•very common superficial ulcerations of the oral
mucosa
•more common in the first two decades
•appear as single or multiple shallow hyperemic
ulcerations covered by thin exudate and
rimmed by a narrow zone of erythema
•lesions spontaneously resolve within a week

10. Oral candidiasis ( trush)
•take the form of a superficial curdy, gray to
white inflammatory membrane
•scraping reveals an underlying erythematous
inflammatory base
•the fungus is a normal inhabitat of the oral
cavity
•causes disease only in individuals who are
diabetic ,neutropenic or
immunocompromised like in AIDS

12. Glossitis
•implies to inflammation of the tongue
•also applied to the beafy-red tongue
encountered in certain deficiency states like
vit.B12, Riboflavin, niacin pyridoxine iron
Xerostomia
•dry mouth, a major feature of sjogren
syndrome

13. Hairy leukoplakia
-Uncommon oral lesion virtually restricted to
HIV patients
-appears as white confluent patches of fluffy
(“ hairy”) hyperkeratotic thickening
-microscopically appear as piled up layers of
keratotic squames based on mucosal
acanthosis
-EBV is now accepted as a major cause

14. Tumors and precancerous lesions
Leukoplakia and Erythroplakia
•Leukoplakiais a white plaque on the oral
mucous membranes that cannot be removed
by scraping and classified clinically or
microscopically as another disease entity
•is a clinical term: until it is proved otherwise
it must be considered precancerous

17. Eryethroplakia ( dysplastic leukoplakia)
•represents a red ,velvety possibly eroded area
within the oral cavity
•epithelial changes are markedly atypical
•associated factors with these lesions
•Cigarettes, pipes cigars, alcohol, ill filling
denture…
•HPV particularly type 16 have been identified in
tobacco-related lesions

18. Squamous cell carcinoma
-represents ~ 95% of cancers of oral cavity
-most common ages 50-70 yrs
-commonly associated with tobacco and alcohol
-HPV serotypes 6, 16, and 18 are associated
-may occur anywhere in the oral cavity but
favored locations are floor of the mouth ,
tongue , hard palate and base of tongue
-prognosis is best with lip lesions , 5 year
recurrence –free rate approaching 90%
-poorest outcome is with tumors in the floor of
the mouth and base of tongue

20. Odontogenic cysts and tumors
Ameloblastoma
•Tumor arising from odontogenic epithelium
•Commonly cystic , locally invasive but has benign
course
Odontoma
•The most common type of odontogenic tumor
•Arise from epithelium but show extensive
deposition of enamel and dentin

21. Salivary glands
Inflammation
•May be of viral, bacterial or autoimmune origin
•Most common form of viral adenitis is mumps which
particularly affects the parotids
•Other glands like pancreas and testes may also be involved
•Inflammatory changes also occur in autoimmune diseases like
Sjögren syndrome
•Nonspecific bacterial sialadenitis particularly involving
submandibular gland usually occur secondary to ductal
obstruction by stones (sialolithiasis)
•The most common offenders are S.aureusand S.viridans

22. Neoplasms
•About 65% -80% arise within the parotid
•10% in the submandibular and the remainder
in the minor salivary glands
•The likelihood of a salivary gland tumor being
malignant is more or less inversely
proportional to the size of the gland.
•the benign tumors most often appear in the
5
th
-7
th
decade and the malignant ones
somewhat latter

23. Benign
Pleomorphic adenoma
•Also called mixed tumor
•~60% occur in the parotid
•Are composed of epithelial elements and
mesenchymal elements
•Mesenchymal elements take the form of
myxoid or chondroid background
•Usually present as painless slow growing ,
mobile descrete mass

26. A carcinoma infrequently arises in a pleomorphicadenoma-
Carcinoma ex pleomorphicadenoma ora malignant mixed
tumor
Incidence of malignant transformation increases with the
duration of the tumor
Warthintumor (papillary cystadenoma
lymphomatosum)
The second most common salivary gland neoplasm
Arise almost always in the parotids and are benign
Composed of cysts lined by double layer of epithelial cells
resting on a dense lymphoid stroma
More common in males

27. Mucoepidermoid carcinoma
•Represent about 15% of all salivary gland
tumors
•Most common form of malignant salivary
gland tumor
Other salivary gland tumors include
•Adenoid cystic carcinoma
•Acinic cell tumor

28. Esophagus
Congenital anomalies
Atresiaand fistula
A.Blind upper and lower esophagealsegment
B.Fistula between blind upper segment and
trachea
C.Blind upper segment ,fistula between blind
lower segment and trachea
D.Blind upper segment only
E.Fistula between patent esophagusand
trachea

29. Stenosis-fibrous thickening of the esophageal
wall with atrophy of the muscularis
Mucosal webs -semicircumferential
protrusions of the mucosa into the
esophageallumen
Those in the upper esophagusare often
designated as webs : those in the lower
esophagusare often designated as Schatzki
rings

30. Lesions associated with motor dysfunction
Achalasia
-characterized by
1.Aperstalisis
2.Partial or incomplete relaxation of the LES
3.Increased resting tone of the LES
Pathogenesis of primary achalasiais poorly
understood

31. •Secondary achalasia may arise in Chagas
disease in which Trypanosoma cruzi causes
destruction of the myenteric plexus
•Classic clinical symptom is progressive
dysphagia
•Regurgitation and aspiration may occur

32. In about 5%, possibility of developing SCC
Other complications include candidal
esophagitis, diverticulaand aspiration with
pneumonia
Hiatalhernia
Is characterized by separation of the
diaphragmatic cruraand widening of the
space between the muscular cruraand
esophagealwall.

33. Two patterns
•Sliding
-constitutes 95% of the cases
-is protrusion of the stomach above the
diaphragm creating a bell shaped dilation
•Paraesophageal
-a separate portion of the stomach usually along
the greater curvature enters the thorax

35. Diverticula
•An outpouching of the alimentary tract that
contains all visceral layers
•False diverticulum is an outpouching of
mucosa and submucosa only.

36. Typical symptoms are regurgitation and a
mass in the neck
Aspiration with resultant pneumonia is a
significant risk
Laceration (Mallory-Weiss syndrome)
longitudinal tears in the esophagusat the
esophagogastricjunction
a consequence of severe retching
Occur most commonly in alcoholics

37. Tears may involve only the mucosa or may
penetrate deeply enough to perforate the
wall.
Account for 5-10% of upper GI bleeding
Boerhavesyndrome is rupture of the
oesophagus and is a rare and catastrophic
event.

38. Esophagitis
Reflux esophagitis
-reflux of gastric contents into the lower esophagus
is the first and foremost cause of esophagitis
Associated causative factors
-decreased efficacy of esophageal antireflux
mechanisms
-presence of a sliding hiatal hernia

39. -inadequate or slowed esophageal clearance of
refluxed material
-delayed gastric emptying
-reduction in the reparative capacity of the
esophageal mucosa
Morphologic changes include
-simple hyperemia
-inflammatory infiltrate
-basal zone hyperplasia
-elongation of lamina propria occur

40. •Clinical manifestation consist of dysphagia ,
heart burn, regurgitation of sour brash,
hematemesis or melena
•Consequences include
–Bleeding
–Stricture
–Tendency to develop Barrett esophagus

41. Barrett Esophagus
a complication of longstanding
gastroesophagealreflux
Characterized by replacement of the distal
esophagealmucosa by metaplasticcolumnar
epithelium as a response to prolonged injury
Grossly or endoscopicallyappear as a red
velvety mucosa
Microscopically the squamous epithelium is
replaced by metaplasticcolumnar epithelium
complete with mucosal glands

44. •Dysplasia may be presnet
•Is associated with 30-40 fold increased risk of
developing adenocarcinoma then the general
population
Infectious and chemical esophagitis
Can occur due to
•Ingestion of mucosal irritants such as alcohol,
corrosive , acids or alkali
•Cytotoxic anticancer therapy

45. Infection after bacteremia or viremia , HSV
and CMV in immunocompromised
Fungal infections in immunocompromised or
debilitated patients –candida
Uremia
Esophageal varices
Collaterals that develop in the region of the
lower esophagus during portal hypertension
The increased pressure in the esophageal
plexus produces dilated tortuous vessels
called varices

46. •Varices develop in 90% of cirrhotic patients
and are most often associated with alcoholic
cirrhosis
•Schistosomiasis is the second most common
cause
•Variceal rupture produces massive
hemorrhage
•Clinically varices produce no symptoms until
they rupture

47. Tumors
Benign tumors
Mostly mesenchymal in origin and include
leiomyomas , fibromas , lipomas
hemangioma . . . .
Epithelial –squamous papilloma
Malignant tumors
Squamous cell carcinoma represent the
largest majority , recently incidence is
declining and adenocarcinomas are
increasing

48. Squamous cell carcinoma
•Occur in adults over 50
•Has male preponderance
•Has higher incidence in east Asia
Associated factors include
–Alcoholic drinks
–Tobacco
–HPV
–Chronic esophagitis

49. About 20% are located in the upper third
50% in the middle third
30% in the lower third
Three morphologic patterns are described
1.Protruded (60%) –polypoidexophytic
lesion
2.Flat (15%)-a diffuse infiltrative form that
spreads within the wall of the esophagus
causing thickening , rigidity and narrowing

50. 3.Excavated (25%) –a necrotic cancerous
ulceration that excavates deeply into
surrounding structures

52. •Most are moderately to well differentiated
•Local extension into adjacent mediastinal
structures occur early
•Tumors in the upper third metastasize to
cervical lymph nodes
•Those in the middle to mediastinal ,
paratracheal and tracheobronchial nodes
•Those in the lower third most often to
gastric and celiac groups of nodes

53. Clinical presentation includes
Dysphagia
Weight loss
Hemorrhage
Adenocarcinoma
Increasing in incidence
Associated with Barrett esophagus
Usually located in the distal esophagus and may
invade the adjacent gastric cardia
May develop nodular masses or may exhibit
diffusly infiltrative or ulcerative features
Histologically most are mucin producing glandular
tumors

54. Stomach
Congenital anomalies
Heterotopia
-rests of normal tissue may be present at any
site in the GI tract
-nodules of normal pancreatic tissue up to
1cm may be present in the gastric or
intestinal submucosa
-gastric heterotopia –small patches of
ectopic gastric mucosa in the duodenum
or in more distal sites

55. Pyloric stenosis
-congenital hypertrophic pyloric stenosis
-M:F –4:1
-present with regurgitation and projectile
vomiting
-physical examination reveals visible peristalsis
and ovoid palpable mass in the region of the
pylorus

56. Gastritis
Inflammation of the gastric mucosa
Acute gastritis
Acute mucosal inflammatory process ,
usually of transient nature
Is frequently associated with
Heavy use of NSAIDs
Excessive alcohol consumption
Heavy smoking
Uremia

57. –Systmic infections
–Severe stress (e.g. trauma, burn, surgery)
–Ischemia and shock
Mechanisms include
-Increased acid secretion with back diffusion
-Decreased production of bicarbonate buffer
-Reduced blood flow
-Disruption of the adherent mucus layer
-Direct damage to the epithelium

58. •Morphologic changes include edema
,vascular congestion ,neutrophilic infiltrate
erosion
•Clinically may be asymptomatic or may
cause variable epigastric pain, nausea and
vomiting or may cause hemorrhage
Chronic gastritis
•Defined as the presence of chronic mucosal
inflammatory changes leading eventually to
mucosal atrophy and epithelial metaplasia
usually in the absence of erosion

59. Major etiologic associations are
Chronic H.pyloriinfection
Autoimmune
Toxic (alcohol, cigarette )
Radiation
postsurgical
Granulomatous conditions (e.g. Crohn disease)
H. Pylori
-most important etiologic agent
-present in 90% of patients with chronic gastritis
affecting the antrum
-H.pyloriis a nonsporing ,gram negative rod

60. Specialized traits that allow H.pylorito
flourish include
Motility
Urease
Adhesin
Autoimmune gastritis
-10% of chronic gastritis
-autoantibodies to gastric gland parietal cells
and intrinsic factor
-leads to loss of acid production
-seen in association with other autoimmune
disorders such as Hashimotos thyroiditis

61. Morphology
Autoimmune gastritis is characterized by
difuse mucosal damage of the body fundic
mucosa with less intense-to-absent antral
damage
Gastritis in the setting of environmental
causes (including infection by H.pylori)
tends to affect the antral and body fundic
mucosa
Inflammatory infiltrate composed of
lymphocytes and plasma cells in the lamina
propria

62. Regenerative changes
-Metaplasiausually intestinal type
-Atrophy
-Hyperplasia(of gastrin producing cells)
-Dysplasia
•Clinical
-usually cause few symptoms like nausea,
vomiting andupper abdominal discomfort

63. Peptic ulcer disease
•peptic ulcers are chronic most often
solitary lesions that occur in any portion of
the GI tract exposed to the aggressive
action of acid-peptic juices
•Occurs in the following sites in order of
decreasing frequency
–Duodenum first portion
–Stomach usually antrum
–Gastroesophageal junction

64. Within the margins of gastrojejunostomy
Duedenum, stomach, or jejunum of patients
with Zollinger-Ellison syndrome
Meckel diverticulum that contains ectopic
gastric mucosa
Pathogenesis
Imbalance between the gastroduodenal
mucosal defence mechanisms and the
damaging forces
Gastric acid and pepsin are requisite for all
peptic ulcerations

66. H. pylori can cause PUD by different
mechanisms
Production of urease,protease and
phospholipasewhich damages gastric mucus
and surface epithelial cells
Recruitment of inflammatory cells
Other factors include
hyperacidity
e.g. Z-E syndrome exhibit multiple
ulcerations due to excess gastrinsecretion
by a tumor and hence excess gastric acid

67. NSAIDssupressmucosal prostaglandin synthesis
Cigarette smoking impairs mucosal blood flow
At least 98% of peptic ulcers are located in
the first portion of the duodenum or in the
stomach
Gastric ulcers are located predominantly
along the lesser curvature
Majority are single
More than 50% have a diameter <2cm,
about 10% are greater than 4cm
Carcinomatousulcers may be less than 4cm
and size does not differentiate a benign from
malignant ulcer

68. •Appear as round to oval sharply punched
out defect with relatively straight walls
•Depth may vary from superficial lesions to
deeply excavated ulcers
•Perforation or erosion of a vessel may occur
•Histologic appearance varies from active
necrosis to chronic inflammation, scarring
and healing
•Chronic gastritis is virtually universal among
patients with PUD

70. C/F
Epigastricburning or aching pain
Few present with complications such as
anemia, frank hemorrhage or perforation
Pain tends to be worse at night and occurs
usually 1 to 3 hrs after meal
Main complications are
Bleeding
Perforation
Obstruction from edema or scarring

71. Acute gastric ulceration
Stress erosions and ulcers
•Encountered in patients with shock,
extensive burn ,sepsis or severe trauma
,increased intracranial pressure and after
intracranial surgery
•Those occurring in the proximal duodenum
and associated with severe burn or trauma
are called Curling ulcers

72. •Gastric ,duodenal and esophageal ulcers
arising in patients with intracranial surgery
injury or tumors are designated as Cushing
ulcer carry a high incidence of perforation

73. Tumors
Benign tumors
Polyps–any nodule or mass that projects above
the level of the surrounding mucosa
Greater than 90% are of hyperplastic nature
5-10% are adenomas which are true neoplasms
Adenoma contains proliferative dysplastic
epithelium and thereby has malignant potential
Can be sessile or pedunculated

74. Gastric carcinoma
•90-95% of malignant tumors of the
stomach
•Next in order are lymphoma (4%),
carcinoids (3%) and stromal tumors(2%)
•Incidence varies widely being particularly
high in countries like Japan, Chile, China. .
•M:F –2:1
•Three major factors are thought to affect
the genesis of gastric cancer

75. 1.Environmental-infection by H.pylori, Diet
(lack of refrigration, consumption of
preserved , smoked and salted foods , lack
of fresh fruit), cigarette smoking
2.Host factors –chronic gastritis, infection
by H. pylori ,partial gastrectomy, gastric
adenomas , Barrett esophagus
3.Genetic –blood type A, family history,
familial gastric carcinoma

76. Morphology
Location
Pylorus and antrum(50-60%), cardia25%,
remaining in the body and fundus
Lesser curvature is involved in about 40% and
greater curvature in 12%
Gastric carcinoma can be classified on the
basis of
1.Depth of invasion
2.Macroscopic growth pattern
3.Histologic subtype

77. 1.Depth of invasion
Early carcinomas –lesion confined to mucosa
and submucosa
Advanced carcinomas –that has extended
below the submucosa into the muscular wall
2. Macroscopic growth pattern
–Exophytic
–Flat or depressed
–Excavated

78. Morphologic types of
Carcinoma Stomach
Fungating
Ulcerating
Diffuse

80. 3.Histologic subtype
Intestinal type –composed of neoplastic
intestinal glands resembling those of
colonic adenocarcinoma
Diffuse type –composed of gastric type
mucus cells which do not form glands but
permeate the wall as scattered individual
cells or clusters
these cells contain abundant mucin and
form signet ring configuration

82. •For obscure reasons gastric carcinomas
frequently metastasize to supraclavicular
LN (Virchows node)
•A notable site of visceral metastasis is to
one or both ovaries-Krukenberg tumor
Clinical feature
•Wt. loss , abdominal pain ,anorexia
,vomiting , altered bowel habit , anemia ,
hemorrhage , dysphagia . .

83. Less common gastric tumors
•Gastric lymphoma –represent 5% of all
gastric malignancies
is related to H. Pylori
•GI neuroendocrine cell tumors ( carcinoids)
•Mesenchymal tumors
–Leiomyoma , leiomyosarcoma , . .
–GI stromal tumors

84. Small and Large intestines
Congenital anomalies
Duplication
Malrotation
Omphalocele–failure of formation of
abdominal musculature with herniationof
abdominal contents into a membraneous
sac
Gastroschisis–portion of the abdominal
wall fails to form with extrusion of the
intestine
Atresiaand stenosis

85. MeckelDiverticulum
-failure of the vitellineduct ,which connects the
lumen of the developing gut to the Yolk sac
produce a MeckelDiverticulum
-is a true diverticulum
-heterotopicrests of gastric mucosa (or
pancreatic tissue) are found in about 50%
-occur in 2% of the population but most remain
asymptomatic
-when peptic ulceration occurs in the small
intestinal mucosa adjacent to the gastric
mucosa bleeding occur

87. Congenital aganglionic Megacolon
(Hirschsprung disease)
•Characterized by the absence of ganglionic
cells in large bowel leading to functional
obstruction and colonic dilation proximal to
the affected segment
•Histologically there is absence of ganglionic
cells in the muscle wall(Auerbach plexus)
and submucosa (Meissner plexus)

88. •Most cases involve the rectum and sigmoid
only
•Proximal to the aganglionic segment , the
colon undergoes progressive dilation and
hypertrophy
•Dilation may achieve large sizes (15-20cm)
Clinical features
•M:F –4:1
•10% occur in children with Down syndrome

89. •Usually manifest in the immediate neonatal
period by failure to pass meconium followed
by obstructive constipation
•Acquired magacolon can occur at any age and
results from Chagas disease, organic
obstruction of bowel , toxic megacolon
complicating UC or CD, functional
psychosomatic disorder

90. Enterocolitis
Diarrhoea and dysentry
•Diarrhoea –an increase in stool mass, stool
frequency or stool fluidity is perceived as
diarrhoea by most patients
•The principal mechanisms of diarrhoea are
–Secretory diarroea –intestinal fluid secretion
–Osmotic diarrhoea –osmotic forces exerted by
luminal solutes leads to diarrhoea

91. –Exudative diseases –mucosal destruction leads
to output of purulent bloody stool
–Malabsorption–improper absorption of gut
nutrients produce voluminous bulky stool
–Deranged motility –improper gut
neuromuscular function may produce
increased stool
Infectious enterocolitis
Viral gastroenteritis
•Rota virus is the most common cause
•Clinically has incubation period of about 2
days followed by vomiting and diarrhoea
for days

92. •Mostly in children
•Norwalk virus cause the majority of cases of
non-bacterial food-borne epidemic
gastroenteritis in older children and adults
•It has incubation period of 1-2days followed
by 12-60hrs of nausea vomiting watery
diarrhoea and abdominal pain

93. Bacterial enterocolitis
Pathogenetic mechanisms
Ingestion of preformed toxin present in
contaminated food (S.aureus, Vibrios,
C.perfringens)
Infection by toxigenicorganisms which
proliferate within the gut lumen and elaborate
an enterotoxin
Infection by enteroinvasiveorganisms which
proliferate invade and destroy mucosal
epithelial cells

94. In case of infection key bacterial
properties are
1.Ability to adhere
2.Ability to elaborate enterotoxins
3.The capacity to invade
Adherence is usually mediated by
adhesins
Enterotoxinsare polypeptides that cause
diarroeae.g. V.cholerae
Invasion e.g. enteroinvasiveE.coliand
shigellapossess a virulence plasmid that
confers capacity for invasion

95. Morphology
•Most bacterial infections exhibit a general non
specific pattern of damage to the surface
epithelium
–Decrease epithelial cell maturation
–Increased mitotic rate (regenerative changes)
–Hyperemia and edema of lamina propria
–Neutrophilic infiltration

96. Clinical features
•Ingestion of preformed bacterial toxins –
symptoms develop within hours ,explosive
diarrhoea, acute abdominal distress . . .
•Infection with enteric pathogens : after
incubation period of several hours to days
diarrhoea , dehydration . ..
•Insideous infection : e.g. yersinia and
mycobacterium

97. Antibiotic associated colitis
(pseudomembraneouscolitis)
Acute colitis characterized by formation of
an adherent inflammatory exudate
(pseudomembrane) overlying site of
mucosal injury
Usually caused by two protein exotoxins
(A&B) of C.difficile,a normal gut comensal
Disease occurs in patients with a
background of chronic enteric disease
after a course of broad spectrum
antibiotic therapy

98. Thought to result due to the flourish of toxin
forming strains after alteration of normal
intestinal floura
Parasites and protozoa
E.histolytica
G.lamblia
AIDS
-diarrheal illness occur in 30-60% of HIV
infected pts
-most cases are due to microorganisms
-AIDS enteropathy is thought to represent some
proportion

99. Malabsorption syndrome
•Malabsorption is characterized by
suboptimal absorption of fats, fat-soluble
and other vitamins ,proteins ,carbohydrates
,electrolytes minerals and water
•Results from disturbance of
–Intraluminal digestion
–Terminal digestion
–Transepithelial transport

100. Consequences of malabsorption affect many
organ systems
Alimentary tract –diarrhea , flatus,
abdominal pain, weight loss. . .
Hematopoetic system –anemia from
,pyridoxine ,folate, VB12 ,deficiency ,
bleeding from v.k deficiency
Musculoekeletal system –osteopenia and
tetany from calcium, Mg . . .deficiency
Epidermis–purpura and petechiae from
vitamin K deficiency, edema from protein ,
dermatitis from vit. A, Zink deficiency

101. •Nervous system –peripheral neuropathy from
vitamin A and B12 deficiency
Features
•Steatorrhea –passage of abnormally bulky,
frothy , greasy stool is a prominent feature
•Other features are wt loss, abdominal
distension.

102. Celiac sprue
•Rare chronic disease
•Characteristic mucosal lesion of the small
intestine and impaired absorption which
improves on withdrawal of wheat gliadins
and related grains
•A.k.a. glutein sensitive enteropathy , non-
tropical sprue
•Mucosa appears flat or scalloped or may be
visually normal

103. •Biopsy show diffuse enteritis with marked
atrophy or total loss ov villi
•Clinical manifestations include diarrhea ,
flatulence ,wt. loss and fatigue
•There is a long term risk of malignanct disease
(more than half of these are intestinal
lymphomas)

105. Tropical Sprue(post infectious sprue)
•Occurs almost exclusively in people living in
or visiting the tropics
•May occur in endemic form and epidemic
outbreaks have occurred
•No specific causal agent has been
associated but bacterial overgrowth by
enterotoxigenic organisms(e.g. E. coli and
Hemophylushas been implicated)

106. •Intestinal changes are extremely variable
ranging from near normal to severe diffuse
enteritis
•Clinically malabsorption becomes apparent
within days or a week of an acute enteric
infection in visistors to endemic locales
•Mainstay of treatment is broadspectrum
antibiotics

107. Whipple isease
•Systemic disease which may involve any organ
of the body but principally affects the
intestine ,CNS and joints
•Cause is gram-positive actinomycete
Tropheryma Whippeli
•Hallmark of Whipple disease is a small
intestinal mucosa laden with distended
macrophages in the lamina propria

108. •The macrophages contain PAS positive granule
and rod-shaped bacilli by electronmicroscopy
•More common in whites in their thirties to
fourties
•M:E 10:1
•Usually present with diarrhea and wt loss
sometimes of years duration

109. Disaccharidase(Lactase ) deficiency
•The acquired one is more common
•Incomplete breakdown of the disacchride
lactose into glucose and galactose leads to
osmotic diarrhea

110. •IDIOPATHIC INFLAMMATORY BOWEL
DISEASE
Crohn disease and ulcerative colitis
•Are chronic, relapsing inflammatory
disorders of obscure origin
Etiology and pathogenesis
•Genetic predisposition
•Infections cause

111. Incriminated agents include Chlamydia atypical
bacteria and mycobacteria…
•Abnormal Host immunreactivity
–Inflammation as the final common pathway

112. CROHN DISEASE
a.k.a terminal ileitis ,regional enteritis ,
granulomatous colitis
-When fully developed it is characterized
pathologically by
1. sharply delimited and typically transmural
involvement of the bowel by an
inflammatory process
2. the presence of non caseating granuloma
3. fissuring with formation of fistulas

114. Epidemiology
occurs at any age, but peak is teens and
twenties with a minor peak in fifties and
sixties
Females are slightly more affected
Smoking is a strong exogenous risk factor
Morphology
Small intestine alone -40%
Small intestine + colon -30%
Colon alone -30%

115. •may involve duodenum, stomach,
esophagus and even mouth but very rarely
•the intestinal wall is rubbery and thick the
result of edema inflammation fibrosis and
hypertrophy
•classic feature is the sharp demarcation of
diseased bowel segments from adjacent
uninvolved bowel

116. •When multiple bowel segments are
involved the intervening bowel is
essentially normal ( skip lesions) and the
mucosa acquires a coarsely textured
cobblestone appearance
•linear ulcers develop
•narrow fissures develop between the folds
of the mucosa often penetrating deeply
leading to fistula or sinus tract formation
•Mucosal inflammation

117. Chronic mucosal damage
Ulceration
Trans mural inflammation affecting all layers
Non caseating granulomas
Clinical features
Variable but disease usually begins with
intermittent attacks of mild diarrhea fever
and abdominal pain
In some patients the onset is more abrupt
with acute right lower quadrant pain fever
and diarrhea

118. •Complications include strictures, fistulas,
malabsorption
•Extra intestinal manifestations include
migratory poly arthritis, sacroilitis ,ankylosing
spondylitis, erythema nodosum, uveitis
•There is an increased incidence of cancer of
the Gl tract ,but is considerably less than
ulcerative colitis

119. ULCERATIVE COLITIS
•an ulceroinflammatory disease limited to
the colon and affecting only the mucosa
and submucosa except in the most severe
cases
•incidence is slightly greater than Crohn
disease
•onset peaks between 20 and 25 years
•UC involves the rectum and extends
proximally in a retrograde fashion to involve
the entire colon in the more severe cases

120. •It is a disease of continuity and skip lesions
like crohn disease are not found
•In10% of patients the distal ileum may
develop mild mucosal inflammation (
backwash ileitis)
•Isolated islands of regenerating mucosa
bulge upward to create pseudopolyps
•Mural thickening does not occur in UC and
the serosal surface is usually completely
normal

122. Clinical features
•present as a relapsing disorder marked by
attacks of bloody mucoid diarrhea that may
persist for days weeks or months, then
subside & recur
•abdominal pain and in minority constipation
•the most feared long term complication of UC
is cancer

125. Hemorrhoids
variceal dilations of the anal and perianal
venous plexuses
common problems which develop
secondary to persistently elevated venous
pressure within the hemorrhoidal plexus
most frequent predisposing influences are
constipation with straining at stool and
the venous stasis of pregnancy
much more importantly but rarely develop
as result of portal hypertension

126. they may develop in the inferior
hemorrhoidal plexus located below
anorectal line –external hemorrhoid
they may also develop in the superior
hemorroial plexus and produce internal
hemorroids
commonly both are affected
secondary effects include thrombosis
,ulceration ,fissure formation and
infarction with strangulation

127. INTESTINAL OBSTRUCTION
may occur at any level
patients present with abdominal pain and
distension vomiting failure to pass flatus…
Major causes of intestinal obstruction
Mechanical obstruction
Adhesions
Hernias
Volvulus
Intussusception
Tumors

128. Inflammatory strictures
Obstuctire gall stones, fecalith, ,foreign body
Congenital strictures, atresias
Bands
Imperforate anus
Pseudo-obstruction
Paralytic ileus
Vascular-bowel in farction
Myopathies and neuropathies ( eg
Hirschsprung)

129. Small intestine tumors
Adenomas
most occur in the region of the ampullaof
Vater
patients with familial polyposiscoli are
particularly prone
Adenocarcinoma
majority occur in the duodenum and jejunum
grow as napkin ring encircling pattern or as
polypoidfungatingmass
those involving ampullaof Vatermay present
with obstructive jaundice
at time of diagnosis most tumors have locally
spread

130. Tumors of the colon and Rectum
Non neoplastic polyps
•non neoplastic polyps ( mostly hyperplastic )
represent about 90% of all epithelial polyps in
large bowel
•inflammatory ( pseudo) polyps represent
islands of inflamed regenerating mucosa
surrounded by ulceration are seen in patients
with longstanding IBD

131. Hyperplastic polyps
•small epithelial polyps
•often multiple and more than half are
found in the rectosigmoid
•histologically they are composed of well
formed glands and crypts lined by non
neoplastic epithelium
•the usual small hyperplastic polyp has
virtually no malignant potential

132. Juvenile polyps
focal hamartomatousmalformations of the
mucosal elements
most frequently occur in the rectum
mainly sporadic lesions ,majority occurring in
children younger than 5
in adults they are referred to as retention
polyps
tends to be large ( 1 to 3cm)
Histology show abundant cysticallydilated
glands
Generally occur singly and have no malignant
potential
A rare autosomal dominant juvenile polyposis
syndromedoes carry a risk of adenomas and
hence adenocarcinoma

134. Peutz-Jeghers polyp
•autosomal dominant syndrome characterized
by multiple hamartomatous polyps scattered
throughout the entire GIT and melanotic
mucosal and cutaneous pigmentation around
oral mucosa face genitalia palms .
•patients with the syndrome have an increased
risk of developing carcinomas of the pancreas
breast lung ovary anduterus

136. Adenomas
Intraepithelial neoplasmsthat range from
small, often pedunculatedto large that are
sessile
occur in 20-30% before40,rising to 40-50%
after age 60
there is well defined familial predisposition
Three subtypes
Tubular adenomas-Tubular glands
Villous adenomas-villous projections
Tubulovillousadenoma-a mixture of the two
adenomatouslesions arise as the result of
epithelial proliferative dysplasia, which may
range from mild to so severe as to constitute
carcinoma in situ

137. •most tubular adenomas are small and
pedunculated : conversely most pedunculated
polyps are tubular
•villous adenomas tend to be large and sessile
and sessile polyps usually exhibit villous
features
•the malignant risk with an adenomatous polyp
is correlated with three independent features
–polyp size ,
–histologic architecture and
–severity of epithelial dysplasia

139. •cancer is rare in tubular adenomas smaller
than 1cm
•the risk of cancer is high ( ~40%) in sessile
villous adenomas greater than 4cm
Clinical features
•may be asymptomatic ,but many are
discovered during evaluation of anemia or
occult bleeding

141. Familial syndromes
Uncommon autosomal dominant disorders
Familial adenomatouspolyposis(FAP)
genetic defect is in the APC gene on 5q21
patients typically develop 500-2500 colonic
adenomas
multiple adenomas may also be present
elsewhere in the alimentary tract
the majority are tubular
progression to colon adenocarcinoma
approach 100%
cancer-preventive measures include
prophylactic colectomy

143. Gardner syndrome
also autosomal dominant
patients exhibit intestinal polyps identical
to those in FAP combined with multiple
osteomas, epidermal cysts and
fibromatosis
Turcotsyndrome is a rare variant marked by
the combination of adenomatouscolonic
polyposisand tumors of CNS
Hereditary non polyposiscolorectal
cancer(HNPCC)
Is characterized by an increased risk of
colorectal cancer and extraintestinal
cancer particularly of the endometriumin

144. Colorectal carcinoma
98% of all cancers in the large intestine
are adenocarcinoma
Peak incidence is 60 to 79 years
If found in young person preexisting
ulcerative colitis or one of the polyposis
syndromes must be suspected
Dietary factors like excess calorie intake,
low unabsorbablevegitablefiber, intake of
red meat and decreased intake of
protective micronutrients

146. Distribution is as follows
Ascending colon 38%
Transverse colon 18%
Descending colon 8%
Sigmoid 56%
Multiple site 1%
about 1-3% occur in patients with familial
syndromes
tumors in the proximal colon tend to grow as
polypoidexophyticmasses and obstruction is
uncommon

147. •carcinomas in the distal colon tend to be
annular encircling lesions
•microscopically all are adenocarcinomas
•when symptomatic produce anemia fatigue
weakness bowel habit change…
•spread by direct extension into adjacent
structures and by metastasis through the
lymphatics and blood vessels
•the most important prognostic indicator of
colorectal carcinoma is the extent of tumor
at time of diagnosis

151. Carcinoid Tumors
•tumors of neuroendocrine cells
•arise in the pancreas or peripancreatic
tissue lungs, biliary tree, liver andmainly in
GIT
•constitute less than 2% of colorectal
malignancies but almost half of small
intestinal malignant tumors
•tendency for aggressive behavior correlates
with the site of origin, depth of local
penetration and size

152. •appendiceal andrectal carcinoids
infrequently metastasize, by contrast ileal
,gastric and colonic carcinoids have higher
chance of spread especially those that have
penetrated halfway through the muscle
wall and >2cm
•depending on the predominant product
they can be called gastrinoma,
somatostatinoma , insulinoma . . .
•appendix is the most common site of gut
followed by small intestine ,rectum,
stomach and colon

153. •clinically may produce local symptoms
owing to angulation or obstruction of the
small intestine
•may produce Zollinger-Ellison syndrome,
Cushing syndrome ,hyperinsulinism
•some neoplasms are associated with a
distinctive carcinoid syndrome( occurs in
1% of patients with carcinoids and in 20%
of those with widespread metastasis)
•most manifestations are thought to arise
from serotonin
•manifestations include cutaneous flushes,
diarrhea tramps nausea,cough wheezing…

154. Gastrointestinal lymphoma
1-4% of all GI malignancies
Primary GI lymphomas sometimes arise as
sporadic but occur more frequently in certain
populations
1. patients with Helicobacter gastritis
2. Natives of the Mediterranean region
3. patients with congenital immunodeficiency
states
4. HIV-infected individuals
5. individuals undergoing immunosuppressive
therapy
6. patients with sprue

155. •sporadic lymphomas are the most common
form in western hemisphere
•arise from the B cells of the mucosa
associated lymphoid tissue ( MALT)

156. Appendix
Acute appendicitis
usually ( 50-80%) associated with
obstruction ( fecalith, less commonly gall
stone, tumor, or ball of worms ( oxyuriasis
vermicularis)
Obstruction can cause ischemic injury which
favors bacterial proliferation with additional
inflammatory exudateand edema

157. Nevertheless a significant minority of
inflamed appendices have no
demonstrable luminal obstruction
Morphology
initially serosawill be transformed to dull
granular red membrane
later fibrinopurulentexudate covers the
serosa
abscess formation leads to acute
suppurative appendicitis

159. •further progress leads to acute gangrenous
appendicitis
•histologic criterion for the diagnosis of
acute appendicitis is neutrophilic
infiltration of the muscularis
•clinical features include
–abdominal pain
–nausea
–vomiting
–tenderness
–Fever…

160. Tumors of the appendix
Carcinoids
Mucocele and pseudomyxomaperitonei
Mucoceleis globular enlargement of the
appendix by inspissatedmucus usually the
result of obstruction

162. Mucinouscystadenomais the most
common mucinousneoplasm
Malignant mucinouscystadenocarcinoma
penetration of the appendicealwall by
invasive cells and spread beyond the
appendix in the form of localized or
disseminated implants produce cellular
proliferation and mucin secretion
pseudomyxomaperitonei

164. Peritoneum
Inflammation
may result from bacterial invasion or
chemical irritation the most common
causes are
sterile peritonitis
–from mild leakage of bile or pancreatic
enzymes
perforation or rupture of the biliarysystem
hemorrhagic poncreatitis, with leadkageof
pancreatic enzymes and digestion of adipose
tissue to produce fatty acids
surgical procedures, reaction to surgically
introduced foreign material such as talk,

165. Infection
the most common disorders leading to
such bacterial dissemination are
appendicitis, ruptured peptic ulcer
,cholecystitis, diverticulitis, strangulation
of bowel, acute salpingitis, abdominal
trauma…
A wide variety of bacterial organisms are
implicated in peritonitis
spontaneous bacterial peritonitis is an
uncommon condition which occurs in the
absence of an obvious source of
contamination

166. •in generalized peritonitis an exudate may
accumulate under and above the liver to form
subhepatic ,subdiaphragmatic abscess.
Miscellaneous conditions
•Sclerosing Retroperitonitis
•Mesenteric cysts

167. TUMORS
virtually all tumors of the peritoneum are
malignant and can be divided into primary
tumors(mesotheliomas) and secondary
tumors
peritoneal mesotheliomasare associated
with asbestos exposure in at least 80% of
the cases
secondary tumors are common and can
occur in any form of advanced cancer