Intestines

Diverticular disease
Def:a diverticulum is a blind pouch leading off
the alimentary tract lined by mucosa that
communicates with the lumen of the gut.
Diverticula can be:
congenital or acquired.

 Congenital diverticula involve all the 3 layers of the

bowel wall.[prototype is meckels diverticulum]
Acquired diverticula either lack or have an attenuated
muscularis propria.

Sites-oesophagus,stomach, duodenum,colon-left
side,sigmoid[most common]

 Multiple diverticulae-diverticulosis.
Pathogenesis:
1)focal weakness in colonic wall
2)increased intraluminal pressure.
{Colon-longitudinal muscle coat is not complete
but is gathered as 3 equidistant bands-taenia
coli.}

 Age >60years more common.

C/F
Mostly asymptomatic
Symptoms include-lower abdominal
pain,discomfort,distension,cramping,sensation of
incomplete defecation.alternate diarrhea and
constipation.
Minimal bleeding or massive hemmorhages

 Grossly-small flask like or spherical

outpouchings 0.5-1cm in diameter.
Microscopically-thin wall composed of
flatenned or atrophic mucosa,compressed
submucosa and attenuated or totally absent
muscularis propria
Hypertrophy of circular muscle layer and
prominent taenia coli seen.

 Complications:
-Obstruction
-Perforation
-Leading to inflammatory changesperidiverticulitis.
-Fibrotic thickening[mimicking ca]

Volvulus
Complete twisting of a loop of bowel about its
mesentric base of attatchment.
Produces intestinal obstruction and infarction.
Site:
Most common in large redundant loops of
sigmoid followed by caecum ,small bowel,
stomach,transverse colon.

Intussusception
Def: When one segment of intestine
constricted by a wave of peristalsis, suddenly
becomes telescoped into the immediately
distal segment of bowel.

 In infants and children-usually there is no

underlying pathology[anatomic lesion/defect
in bowel]
Some cases are associated with rotavirus
infection suggesting that localised
inflammation may serve as a traction point for
intussusception .

 In adults an intraluminal mass or tumor act as

a point of traction.
Complications:
Intestinal obstruction-trapping of mesentric
vessels-infarction.

Hirschsprungs disease[congenital aganglionic

megacolon]
Aganglionosis of a portion of intestinal tract.
Migration of neural crest cells arrests at some point
before reaching the anus. This produces an intestinal
segment that lacks meissners and aurebachs myentric
plexus.
It is characterised by absence of ganglion cells and
ganglia in the muscle wall and submucosa of affected
segment.

 Rectum is always affected,involvement of more

proximal colon.
Proximal to the aganglionic segment the colon
undergoes progressive dilatation and
hypertrophy beginning with descending colon.
Proximal innervated colon may become massively
distended-MEGACOLON

Types:
Short segment-rectum and sigmoid
Long segment-entire colon
Diagnosis:failure to detect ganglion cells in intestinal
submucosa samples stained for acetylcholinesterase.
C/F-failure to pass meconium,obstructive constipation.
Complications: enterocolitis with fluid ,electrolyte
disturbance,perforation of colon.

Meckels diverticulum
Failure of involution of vitelline duct which
connects the lumen of developing gut to the
yolk sac.
Seen in 2% of population
Within 2 feet of ileocaecal valve.

Solitary
Antimesentric side
True diverticulum[all the layers present]
May be present as a small pouch or as a blind
segment having lumen greater in diameter
than that of ileum and length upto 6 cm.

 Mucosal lining may be that of normal small intestine

Heterotopic rests of gastric mucosa or pancreatic tissue
can be seen.
Ulceration may occur adjacent to gastric mucosal restsintestinal bleeding.
Other complications of Meckels include:
Intususception
Incarceration
Perforation.

Typhoid
Salmonella typhi
1st week-bacteremia,fever and chills
2nd week-mononuclear phagocyte involvement
with rash,abdominal pain,prostation.
3rd week ulceration of payers patches with
intestinal bleeding and shock.

Salmonella invades intestinal epithelial cells and

tissue macrophages

Tuberculosis

Amoebiasis

Tumors of small intestine

Benign tumors-adenoma,mesenchymal tumors.
Adenomas occur in region of ampulla of vater
c/f occult blood loss
Obstruction
Intussuseption

Gross:ampulla of vater is enlarged,velvety

surface.
Micro:similar to colonic adenomas

Adenocarcinoma
Age-40-70yrs
Common in duodenum
Gross: napkin ring encircling pattern
Polypoid exophytic masses
Micro:similar to adenoca
c/f
Occult blood loss
Obstructive jaundice

Polyps of intestine
Def- Polyp is a tumorous mass that protrudes into
the lumen of the gut.
All polyps start as small sessile lesions without a
definable stalk.Traction on the mass may create a
stalked or pedunculated polyp.
Types non neoplastic
neoplastic

 Non neoplastic polyps may be formed as a

result of abnormal mucosal
maturation,inflammation or architechture
Neoplastic polyps-arise as a result of
proliferation and dysplasia-adenomatous
polyps/adenomas.[precursors of carcinoma]

Non-neoplastic polyps:

Hyperplastic polyp
Hamartomatous polyp
Inflammatory polyp
Lymphoid polyp

Hyperplastic polyp:90% of epithelial polyps

6th and 7th decade
Pathogenesis: decreased epithelial turnover
and accumulation of mature cells on surface.
Grossly these are small <5mm in diameter
,nipple like,hemispheric,smooth,moist
protrusions of the mucosa.
Single or multiple

 Microscopy-well formed glands and crypts

lined by non neoplastic epithelial cells most of
which show differentiation into mature goblet
or absorptive cells.
Serrated epithelial profile and irregular crypt
architechture.
No malignant potential

Hamartomatous polyps:are malformations of

glands and stroma.
Can occur sporadically or in setting of genetic
syndrome.
Include:
Juvenile polyp
Peutz-jeghers polyps

Juvenile polyp:
Focal hamartomatous malformation of mucosal
epithelium and lamina propria.
Sporadic occurrence
<5years of age.

Gross :large[1-3cm],rounded,smooth or slightly

lobulated lesions with a stalks upto 2cm in length.

 Micro: lamina propria comprises the bulk of

polyp enclosing abundant cystically dilated
glands,inflammation is common,surface may
be congested or ulcerated.
In rare autosomal dominant juvenile polyposis
syndrome-multiple 50-100 juvenile polyps in
intestine. Risk of adenomas and adenoca.

Peutz jeghers polyps:

Hamartomatous polyps that involve the mucosal
epithelium,lamina propria and muscularis mucosa.
Single/multiple.
Peutz jeghers syndrome :AD
1)Multiple hamartomatous polyp throughout GIT
2)Melanotic mucosal and cutaneous pigmentation
around lips,oral mucosa,face,genitalia,and palmar
surfaces of hands.

 Micro:an arborizing network of connective

tisse and well developed smooth muscle
extends into the polyp and surrounds normal
abundant glands.

 2 other hamartomatous polyposis syndromes:

Cowden and cronkhite-canada syndrome.
Cowden syndrome-AD
1)Intestinal hamartomatous polyps
2)Facial trichilemmomas
3)Acral keratoses.

Cronkhite-canada syndrome-non hereditary.

Characterised by GIT hamartomatous polyposis and
ectodermal abnormalities.

Neoplastic polyps
Adenomatous polyps are intraepithelial
neoplasms that range from small often
pedunculated lesions to large neoplasms that are
usually sessile.
Familial
3 subtypes:
Tubular adenomas
Villous adenomas
Tubulovillous adenoma

 All adenomatous lesions arise as a result of

epithelial proliferative dysplasia-low grade to high
grade-precursor lesion for invasive colorectal
adenoca.

Risk factors for malignancy:

Polyp size[>1cm]
Architechture[sessile polyps .4cm dia]
Severity of epithelial dysplasia.[common in villous
areas]

Tubular adenomas:
Colon-90%[others in stomach,small intestine]
Smaller ones are-smooth sessile
Larger ones are coarsely lobulated and have slender stalks.
Micro:stalk is composed of fibromuscular tissue and
prominent blood vessels,covered by normal non neoplastic
mucosa.
Asymtomatic,discovered incidentally during evaluation of
anemia or occult bleeding.

Villous adenomas
Elderly persons
larger in size
common in rectum and rectosigmoid area
Sessile,upto 10cm in diameter.
Micro:frond like villiform extensions of mucosa covered by
dysplastic or disorderly columnar epithelium.

Clinically more symptomatic-overt rectal bleeding

They may secrete copius amount of mucoid material rich in protein
and potassium may lead to hypoproteinemia or hypokalemia.

Tubulovillous adenoma:
Intermediate between tubular and villous
lesions.

Familial syndromes
Familial polyposis
AD
Propensity for malignant transformation
Familal adenomatous polyposis-FAP syndrome:
Mutation on APCgene-chromosome5q21
Types :
Classic
Attenuated
Gardner syndrome
Turcot syndrome

Classic FAP 500-2500 colonic adenomas, carpet the

mucosal surface.
Minimum of 100 polyps required for
diagnosis.
Histologically-most of them are tubular
adenomas

Attenuated FAP:
Fewer polyps average 30
Seen in proximal colon
Gardners syndrome:

Intestinal polyps
Multiple osteomas
Epidermal cysts
Fibromatosis

Turcots syndrome:
Adenomatous colonic polyposis
Tumors of CNS

 Hereditary nonpolyposis colorectal cancerHNPCC syndrome/lynch syndrome

AD
Mutations in DNA repair genes microsatellite
instability
Increased risk of colorectal
cancer,extraintestinal cancer-endometrium
Colonic malignancies-are multiple,not
associated with pre existing adenomas.

Inflammatory bowel disease

Chronic inflammatory conditions resulting from
activation of mucosal immune system.
1]crohns disease
2]ulcerative colitis
Etiopathogenesis:
1.genetic susceptibility[HLA association]
2.role of intestinal flora
3.abnormal T cell responses

 Diagnosis:clinical history,radiographic
findings,lab findings,pathologic examination.

Crohns disease/regional enteritis/granulomatous

colitis

Age :2nd-3rd decade

Sex: females
Common in jews
Risk factor-smoking.

Site:affects GIT from oesophagus to anus.

c/f-fever,abdominal pain,intermittent attacks of
diarrhoea,occult or overt blood loss in
stools,asymptomatic periods.

Anemia
Fluid and electrolyte loss.
Wt.loss
Weakness
Strictures
Fistulas
Protein losing enteropathy
malabsorption

Extraintestinal manifestations:
Migratory polyarthritis
Ankylosing spondylitis
Erythema nodosum
Clubbing
Uveitis
amyloidosis

 Morphology:microscopy
1.Mucosal inflammation-focal mucosal ulcers
2.Chronic mucosal damage-villous blunting in small
intestine,crypts show branching,irregularity,pyloric
metaplasia,paneth cell metaplasia.
3.Transmural inflammation-xray-string sign,skip lesions.
4.Non caseating granulomas.
Increase risk of cancer<UC

Ulcerative colitis
Ulcero inflammatory disease limited to
colon,affecting mucosa and submucosa.
Age-20-25 years
Non smokers

 c/f bloody mucoid diarrhoea,low abdominal

pain,cramps,asymptomatic interval ,serious
bleeding,fluid and electrolyte imbalance.
Site:involves rectum and extends in a
retrograde fashion to involve entire colon.pancolitis.

Morphology:microscopy
Ulceration of mucosa along long axis-continuous
Regenerating mucosa form pseudopolyps.
Toxic megacolon[toxic damage to muscularis
propria and neural plexus.
Progression to dysplasia and frank carcinoma.
Rx-response to surgery good.

Colorectal carcinogenesis
Pathogenesis:
2 distinct pathways-have stepwise
accumulation of mutations
1)APC/beta catenin pathway
2)microsatellite instability pathway.

Colorectal carcinoma

98% occur in large intestine.

They present early , treatment is good.
Age:60-79years
M:F ratio 1.2:1
Young individuals pre existing ulcerative
colitis, polyposis syndrome.

 Etiology:
Dietary factors:
1)excess calorie intake
2)low content of vegetable fibre
3)High content of refined carbohydrates
4)Intake of red meat
5)Decrease intake of protective micronutrients

Site:
Caecum/ascending colon-22%
Transverse colon-11%
Descending colon-6%
Rectosigmoid-55%
Others 6%
Single-99%,multiple-1%

 Gross all begin as insitu carcinoma

Proximal colon-Polypoid exophytic masses-can
cause obstruction.
Distal colon-Annular encircling lesions[napkin
ring] margins are heaped up ,beaded and
firm,ulcerated in mid region,lumen markedly
narrowed.

 Micoscopy: R and L side lesions have similar

features.
Tall columnar cells invade the submucosa and
muscularis propria.
Invasive tumors incite a strong desmoplastic
stromal response.
Mucin production in the lumen or interstitium.
This secretion dissects the gut wall and aids in
extension of malignancy and therefore has a
worse prognosis.

 Clinical features:
Right sided lesions-fatigue,weakness,iron defeciency
anemia.
Bulky lesions-bleed
Left side colon-occult bleeding,changes in bowel
habit,crampy ,lower abdominal
discomfort,malena,diarrhea,or constipation.
Detected early due to symptoms.
Rectum and sigmoid infitrative-poor prognosis.
Iron defeciency anaemia in an older male means GIT
cancer.

Metastases
Local-direct invasion into adjacent structures
Distant-through lymphatics and blood vessels.
Order of spread-regional lymph node-liverlung-bone-serosal membrane of peritoneumbrain.

Malabsorption syndromes
Def:defective absorption of-fats
,carbohydrates,proteins,water,electrolytes,min
erals and vitamins.
c/f include wt loss,anorexia,adominal
discomfort,borborygmi,muscle wasting.
Diagnosis by intestinal biopsy.
Diagnostic feature is steatorrhea[abnormal
bulky,frothy,greasy yellow stools]

 Pathogenesis:disturbance in one of the following:

Defects in intraluminal absorption
Defects in terminal absorption
Defect in transepithelial transport
Decreased small intestinal surface area
Lymphatic obstruction
Infection
Iatrogenic

Celiac disease/celiac sprue/gluten sensitive

enteropathy.
Def:mucosal lesion of small intestine and
impaired nutrient absorption.
Common in Caucasians.
Family history,MHC class II

Pathogenesis:sensitivity to gluten
1]T cell mediated chronic inflammatory
reaction
2]autoimmune component
Diagnosis:
Endoscopy-mucosa-flat/scalloped
Serology-antigliadin/anti endomysial
antibodies.

 Biopsy-diffuse enteritis with marked atrophy or

total loss of villi
Surface epithelium shows-vacuolar
degeneration,loss of microvillus brush
border,increase no. of intraepithelial
lymphocytes.
Crypts-increased mitotic activity,hyperplastic and
tortuous.
Changes are marked in proximal small intestine.
Mucosal changes revert to normal by exclusion of
gluten from diet.

 c/f-diarrhoea,flatulence,wt loss,
fatigue.extraintestinal features of
malabsorption.
Complications:
Malignancy-NHL,small intestinal adeno
ca,esophageal SCC.

Tropical sprue/post infectious sprue

Celiac like disease-common in tropics.
Etiology:Enterotoxigenic E coli,Hemophilus
Site:all levels of small intestine.
Defeciency of B12 and folate-megaloblastic
change similar to pernicious anemia
Treatment-antibiotics-broad spectrum.

Whipples disease[Intestinal lipodystrophy]

Etiology-Tropheryma whippelli bacterium-gram
positive actinomycetes
[proliferates preferentially within macrophages and
invoke no significant host immune reaction.]
Site:any organ of body-intestine,CNS,joints
Diagnosis-PAS positive macrophages,containing
rod shape organisms on EM

Micro:
Important feature is small intestinal mucosa laden with
distended macrophages in the lamina propria.
Expansion of villi by dense infiltrate of macrophages
imparts a shaggy appearance to the mucosal surface.
Edema of mucosa thickens intestinal wall
Involvement of mesentric lymph node,lymphatic
dilatation
Bacilli laden macrophages can also be found in synovial
membranes of joints,brain,cardiac valves.Inflammation
is absent but functional impairment present.

c/f
Features of malabsorption
Arthropathy
Lymphadenopathy,hyperpigmentation
Age:4-5th decade
Sex-males

Disaccharidase lactase defeciency;

Located in apical cell membrane of villous
epithelial cells
Incomplete breakdown of dissacharidelactose-osmotic diarrhea.
Lactase defeciency:
1]genetic[seen in infants on milk feeding]
2]acquired[adults-bacterial/viral]

Abetalipoproteinemia:
Inborn error of metabolism.
AR
Inability to synthesise apolipoprotein B
Triglycerides are stored in intestinal epithelial
cells-lipid vacuolation.
Absence of plasma lipoprotein.
Failure to absorb certain essential fatty acids
leads to lipid membrane defects-acanthocytic
erythocytes.