Histo Block 3

GI

Tongue

Normal mouth structures

Circumvallate papilla
Taste pore

Taste Bud

Erupting tooth:

ameloblasts deposit enamel, odontoblasts

deposit dentin
the cells sandwich the deposits
Ameloblasts
Enamel
Dentin

Odontoblasts

Dental Papilla

Lip: squamous stratified epithelium

Parotid gland
Salivary glands
Mucous glands dont stain with H & E

Parotid gland

Duct

Serous
cells

Submandibular gland

Duct

Sublingual gland

Duct

Serous cells

Mucous cells

Mucous cells

ESOPHAGUS

Identify the layers of the esophagus and key anatomic features that affect spread
of disease in this region.

Discuss the mechanism for the development of achalasia.

List five causes of esophagitis and their key gross and histopathologic features.

Describe the histopathologic features of Barrett esophagus.

Name the sequelae of Barrett esophagus. Discuss its clinical management.

Describe the gross and microscopic features of squamous cell carcinoma of

esophagus.

Discuss the clinical presentation of squamous cell carcinoma of the esophagus.

Describe the mechanism in the development and the histopathologic features and
sequelae/complications of esophageal varices.

stratified squamous epithelium

Esophagus: normal

Layers

Submucosal glands

Mucosa

Submucosa

Muscularis externa

Circular muscular
layer
Longitudinal Layer

Esophageal varices:
A. Dilated submucosal veins in the lower
esophagus
B. Arise secondary to portal hypertension
1. Distal esophageal vein normally drains into the
portal vein via the left gastric
vein
2, In portal hypertension, the left gastric vein
drains into the esophageal vein, resulting in
dilation (varices).
C. Asymptomatic, but risk of rupture exists
1. Presents with painless hematemesis
2. Most common cause of death in cirrhosis

Trombosed vein/Ruptured varices

Gross: esophageal varices

Dilated submucosal veins

Viral esophagitis:
Usually in immunosuppressed people
On chemotherapy
On steroid
AIDS
Debilitated

Extensive ulceration of esophagus

secondary to Herpes infection.

May occur in non-immunosuppressed

Especially if previous ulceration

Multiple squamous nuclei with viral inclusions;

Ground glass appearance: prolif of viral particles

HPV koiliocytes

Fungal esophagitis

Candida

Silver stain of candida

Eosinophilic esophagitis:
Associated with atopic patients.
Asthma; eczema; food allergies etc.
Often presents with food impaction
of esophagus
Reflux esophagitis (GERD) also has
eosinophilic infiltrate

Pink: eosinophils

Epithelial hypertrophy

Intra-epithelial eosinophils

Achalasia

Destruction of ganglion cells in myenteric

(Auerbach) plexus by an autoimmune process
Failure of LES to relax in swallowing
Megaesophagus dilatation, muscle
hypertrophy
Clinical: Dysphagia for solids and liquids;
Esophageal tests indicate absence of
peristalsis and failure of the lower esophageal
sphincter
Might lead to aspiration pneumonia

megaesophagus

loss of myenteric ganglia

BARRETT ESOPHAGUS WITH

ADENOCARCINOMA:

Normal Esophagus

Barrett esophagus:
Metaplasia of the lower esophageal mucosa
from stratified squamous epithelium to
columnar epithelium with goblet cells; seen in
10% of patients with GERD
May progress to dysplasia and
adenocarcinoma, usually in the lower onethird of the esophagus

Intestinal Metaplasia

The diagnosis is mos

Barretts esophagus
with adenocarcinom

Adenocarcinoma in muscle
Displasia

55 year old male comes in with complaints

of a burning sensation in chest. A biopsy
of his esophagus is taken and presented
here:

Intestinal
metaplasia
Intestinal
metaplasia

Ulceration in
barretts

Esophageal squamous cell carcinoma

-keratin pearls
-smoking
Normal Squamous Mucosa

Invasive Squamous Cell Carcinoma

Squamous pearls

H2 Stomach

List the regions of the stomach and key variations in mucosal cell types within these regions. How do
they contribute to the normal function of the stomach?

Describe the features of acute hemorrhagic gastritis and its clinical presentation.

What are the three main types of chronic gastritis? Describe the key histopathologic features.

List the entities associated with Helicobacter pylori infection. What features of this organism
contribute to the pathophysiology? What are possible long term sequelae of H. pylori infection?

What is the mechanism of autoimmune gastritis and its histopathologic features?

Describe the varied gross appearances of adenocarcinoma of the stomach. Compare

histopathologic features of intestinal versus diffuse infiltrating types.

What is GIST? What role does the c-kit oncogene play in the diagnosis and treatment of this
malignancy?

What is the mechanism for the development of neoplasms of MALT (mucosal associated lymphoid
tissue)?

Describe the histopathologic and clinical features of primary sclerosing cholangitis.

Parietal cell: bigger, pinker

Chief cell: smaller, more basophilic (ER)

Normal stomach

Parietal cell

Chief cell

Stomach
gastroesophageal
junction

Esophagus

Cardiac gland

Pink: pH, parietal cells

Acute hemoragic gastritis

Abnormal disrupted mucosa

Acute Gastritis
secondary to NSAID use
reactive pattern of hypertrophic
and hyperplastic glands
Antral mucosa shows
erosion, but healing

Chronic gastritis I:
AUTOMIMMUNE CHRONIC ATROPHIC
GASTRITIS

Vitamin B12 deficiency

involves mucosa of body of stomach.
Loss of fundic mucosa.
Replacement of mucosa by
elongated pits and metaplastic
changes in pits and glands.
Normal (top); atrophic (bottom)

Chronic gastritis II
Chronic gastritis caused by H pylori:
Presents with epigastric pain that
worsens with meals
Ulcer is usually located on the lesser
curvature of the antrum.
Rupture carries risk of bleeding from
left gastric artery.

H pylori microorganisms

Gastric cancers I:
Adenocarcinoma of Intestinal-type
large, irregular ulcer with heaped up
margins;
most common in antrum
Risk: intestinal metaplasia (e.g., due
to H pylori and autoimmune
gastritis), nitrosamines in smoked
foods (Japan),

Intestinal-type Adenocarcinoma

Gastric cancer II:

Signet-ring carcinoma:

Signet-ring cell: mucin, displaced nucleus

signet ring cells infiltrate the gastric

wall;
desmoplasia results in thickening of
stomach wall (linitis plastica, leather
bottle stomach)

leather bottle stomach: thick, rigid,

flattened rugae

Signet Ring Cells

Gastric cancer II:

Stomach Lymphomas: MALToma or
B-cell lymphoma

MALToma

associated with H. pylori

causes an immunologic overdrive
Jazzed up lymphocytes
Lymphoma B cell type
The normal architecture is replaced
by a diuse proliferation of large
lymphocytes.
B cell lymphoma in lamina propria

Gastric cancer IV:

GI Stromal Tumor (GIST)

Spindle cell

Interstitial Cells of Cajal (ICC): Pacemaker

Function
ICC - intimately associated with autonomic
nerves and bowel wall smooth muscle cells
Appear mesenchymal or spindle on histology
c-kit mutations in 60% of cases
LUQ pain
large tumors

GIST

c-Kit staining

H2 BILIARY TRACT

What is the mechanism for the spectrum of gallstone

formation?

Describe the clinical presentation of inflammatory diseases

of the gallbladder, acute and chronic.

Compare and contrast the causes and histopathologic

features of acute vs. chronic cholecystitis. What are
possible long term complications?

What are risk factors for developing cancer of the

gallbladder and extrahepatic ducts and what is the long
term prognosis?

Deep folds in the mucosa

Gallbladder

Surface epithelium: deep mucosal folds

The wall of the gallbladder lacks a submucosa
or a muscularis mucosa
Rokitansky-Ascho sinuses are deep diverticula in the mucosa
can store and concentrate (removes 90% of water)

Columnar epithelium, no submucosa

Rokitansky-Ascho sinuses

Mixed stone
Stones:
Female Gender
Use of hormone replacement therapy and birth
control pills.
Use of cholesterol-lowering drugs (Clofibrate).
Pregnancy.
Rapid weight loss
Western Diet
Genetics: e.g. pima women

Cholesterol stone

Pigment stones: precipitated

unconjugated bilirubin.

Acute vs chronic Cholecystitis

Complications:
Empyema: bag of pus
Gangrene
Rupture with bile peritonitis
Hepatic or diaphragmatic abscess
Fistula to duodenum with impacted stone

Acute cholecystitis

Chronic cholecystitis: stones, sequel

to acute

Chronic Cholecystitis with

Gallstone impacted in the
Cystic Duct
Lumen

evere! Acute Inflammation

Gallbladder with mostly chronic inflammation

Adenocarcinoma of the gallbladder

uncommon cancer with very poor
outcome
associated with gallstones
risk: age, female gender

Invasive adenocarcinoma
(can see glands beneath the surface)

Glandular displasia

Glandular Dysplasia

Cholangiocarcinoma
Cancer of the extrahepatic bile ducts
painless tumor, jaundice
not associated with stones
more frequent in males
associated with Ulcerative Colitis
(sclerosing cholangitis) and fluke
infections
poor prognosis

Cytology Brush of Extrahepatic Biliary Tree Mass

Morphology very similar to

Pancreas Ductal Carcinoma

H2 Pancreas

Describe the anatomic landmarks relevant to the development of inflammatory and

neoplastic diseases in the pancreas. Recognize the histopathologic features of the
exocrine and endocrine pancreas.

Describe histopathologic features of acute pancreatitis. What are the primary

causes?

What are the clinical manifestations of chronic pancreatitis? Classify the various
causes and their associated risk factors.

Contrast the features of acute and chronic pancreatitis and discuss the possible
complications.

Identify the cellular origins of pancreatic neoplasms and their key histopathologic
features?

Be familiar with the clinical presentation, diagnostic features and treatment of

pancreatic neoplasms, benign and malignant.

Pancreas -normal
Islet of Langerhans

Centroacinar
cell

Intralobular duct

Acute pancreatitis
Symptoms: fever, nausea, vomiting and LUQ
tenderness.
Labs:
elevated serum amylase and lipase
Hypocalcemia (calcium is consumed during
saponification in fat necrosis)
Etiology:
METABOLIC: Alcoholism [most common],
Hyperlipoproteinemia, Hypercalcemia,
Drugs (e.g., azathioprine)
GENETIC [10-20%]: trypsinogen & trypsin inhibitor
MECHANICAL:Gallstones, Trauma (incl operative injury)
VASCULAR:Shock, Atheroembolism,Vasculitis
INFECTIOUS: Mumps
Complications: phlegmon, bacterial infections, abcess,
pseudocyst
Cause: autodigestion of pancreatic parenchyma by
pancreatic enzymes (early activation of trypsin)

Saponification

Gross: necrosis

Fat necrosis

Lymphocytic infiltrate

Alcoholic chronic pancreatitis

Chronic pancreatitis
Abdominal pain, weight loss
Etiology:
ALCOHOLIC ~ 70%
CHOLELITHIASIS ~4%
Autoimmune
Cystic Fibrosis (children)
protein precipitates in small ducts calcify
>obstruction>inflammation and fibrosis

Extensive fibrosis and

glandular atrophy

Alcoholic chronic pancreatitis:

Calcifications

islets of Lagerhans
last guys standing
because far from ducts

Chronic pancreatitis
Autoimmune chronic pancreatitis
Duct system with extensive inflammation

Cystic fibrosischronic pancreatitis

Benign Exocrine pancreatic cancers

-1 benign cystic pancreatic neoplasm
serous cystadenoma of the pancreas

serous cystadenoma of the pancreas

serous cystadenoma of the pancreas

Pancreatic Endocrine carcinomas:

Gross: Large mass

Gastrinoma (Zollinger-Ellison Syndrome)

Insultinoma
Glucagonoma
Somatostatinoma
Vasoactive Int. Polypeptide-oma (VIPoma)

Steve jobs!

Dierent cells of origin for pancreatic

cancers

Gastrinoma: gastric mucosal hyperplasia

Pancreatic Ductal Adenocarcinoma

-most common (96%)
Symptoms:
If tumor is in the body or tail: abdominal pain
and weight loss
if tumor is in the head: painless jaundice
through obstruction of the bile or pancreatic
duct
Risk: age (avg 70), smoking, chronic pancreatitis
-other: male, AA, Ashkenazi Jews
Histo: ~dierentiated adenocarcinoma (invasion,
ducts) with Desmosplasia (fibrosis)
-produce mucins
Treatment: whipple resection (but still low
survival rates)

Perineural invasion

NERVE

Invasive adenocarcinoma
Desmoplasia

Liver
1.

Acute hepatitis

2.

Alcoholic liver disease

3.

Drugs & toxins

4.

Chronic hepatitis

5.

Non-alcoholic fatty liver disease

6. Biliary (cholestatic) disorders

7.

Metabolic liver disease

8.

Cirrhosis

9.

Tumors

Normal liver

Resident macrophages of liver are:

Portal Vein

Kupffer cell

Bile Duct

Hepatic artery

Layer of hepatocytes surrounding each portal

triad and separating it from the surrounding
sheets of hepatocytes
NORMAL PORTAL TRACT / TRIAD

HEPATIC ACINUS
ZONE
ZONE
ZONE

PT

CV

LIMITING
PLATE

Acute viral hepatitis-lobular

(ALT > AST)

SWOLLEN CELLS WITH DROPOUT

(= NECROSIS) & INFLAMMATION

HAV
resolves, no carrier or chronic stage
massive necrosis in 0.1% cases
may be scarring from single episode
HBV
over 90% recover; 1-2% fulminant
5% chronic
cirrhosis and hepatocellular Ca
HCV: rarely seen acutely
70-80% chronic hepatitis
15-25% cirrhosis
risk of developing hepatocellular ca
is ~2% per year with cirrhosis

Acidophil body: dying

hepatocyte surrounded by
normal parenchyma
LYMPHOCYTIC
INFLAMMATION

HC DISARRAY
+ SWELLING

Acute hep 1
LYMPHOCYTES

LOBULAR
DISARRAY
HEPATOCYTE
DISARRAY
- no sinusoids

BALLOONING
DEGENERATION

ACIDOPHILIC BODIES

HEPATOCYTE
NECROSIS
- acidophilic body
or dropout

CMV Hepatitis

Systemic viruses causing acute

hepatitis
EBV, CMV, HSV,

VIRAL INCLUSIONS IN NUCLEI

& CYTOPLASM

EBV (EPSTEIN-BARR) HEPATITIS

(W/ Infectious Mononucleosis)

Herpes simplex virus

SINUSOIDAL INFILTRATES
HC NECROSIS
HSV
INCLUSIONS

NECROTIC FOCUS

Alcohol liver disease

Normal liver
Fatty change
Alcoholic hepatitis
Cirrhosis
HCC
AST>ALT

Gross

<10%
>90%
occasional
25%
5-15% cirrhotics

TAN YELLOW COLOR

Alcoholic Steatosis:
starts in zone 3 (pericentral)
usually macrovesicular

ALCOHOLIC STEATOSIS

Perivenous and chicken wire fibrosis

PORTAL
TRACT

CV

CV

CENTRILOBULAR
MACROVESICULAR
STEATOSIS

Acute alcoholic hepatitis

Acute hepatitis presents as:
jaundice (mixed CB and UCB) with
dark urine (due to CB),
fever, malaise, nausea
elevated liver enzymes (AST> ALT)
Inflammation involves lobules and
portal tracts and is characterized
by apoptosis of hepatocytes

ation

Dropout:
empty space
where necrotic
1
ACUTE
ALCOHOLIC
HEPATITIS
hepatocytes were

STEATOSIS

MALLORY BODIES
HEPATOCYTE
NECROSIS
(DROPOUT)

POLYS

Mallory bodies: damaged intermediate

filaments within hepatocytes

ACUTE
HEPATITIS
Polys:ALCOHOLIC
polymorphonuclear
leukocyte

Mallory bodies
POLYS

MALLORY BODIES

STEATOSIS

Tylenol overdose
Reye syndrome in children (aspirin)
Ebola, etc
PALE AREAS
NECROTIC

HEMORRHAGE

Fulminant hepatitis

COAGULATIVE NECROSIS
Eosinophilic cytoplasm; Loss of nuclei

Centrilobular necrosis

CHRONIC HEPATITIS C
BLUE
Polka
dotPOLKA-DOT
appearanceLIVER

MINIMAL
FOCAL LOBULITIS

Chronic hepatitis
1. PORTAL INFLAMMATION
2. INTERFACE HEPATITIS
Inflammation and hepatocyte necrosis occurring
at the interface between portal tract & lobule
3. Risk of progression to cirrhosis

DENSE PORTAL
LYMPHOCYTIC
INFILTRATES

INTERFACE
HEPATITIS

Fibrous
Septa Joining
Portal & Central
Areas
CHRONIC
HEPATITIS
C
INTERFACE
HEPATITIS

DEVELOPING CIRRHOSIS

ORIGINAL
PORTAL TRACT

PROGRESSIVE
LOBULAR
ENCROACHMENT

DENSE PORTAL
LYMPHOCYTIC
INFILTRATES

PORTO-PORTAL
FIBROUS BRIDGING

Chronic Hepatitis B

PORTAL INFLAMMATION AND FIBROSIS

about 5% acute cases chronic

1. Variable amounts of inflammation
2. Variable amounts of fibrosis cirrhosis
3. Groundglass hepatocytes due to surface Ag
4. Immunoperoxidase staining:
Cytoplasmic surface Ag
Nuclear core Ag

Immunoperoxidase Staining:
Surface Antigen/Nuclear Core Antigen

Groundglass hepatocites (surface

antigen)

INFLAMMATORY BILE DUCT DISEASES

1. Portal inflam with destructive cholangitis

2. Portal fibrosis bridging fibrosis cirrhosis
3. Progressive jaundice, intractable itch
Labs - congugated bilirubin, bile acids
- cholesterol, alkaline phosphatase

Primary billiary cirrhosis:

Autoimmune destruction of intrahepatic bile ducts
1. Classically arises in women (>40 years)
2. Associated with other autoimmune diseases

PLASMA CELL

LYMPHOCYTES

Primary sclerosing cholangitis:

1.
2.
3.

Inflammation and fibrosis of intrahepatic and

extrahepatic bile ducts
Periductal fibrosis like onion-skin
Risk: Male, IBD, especially Ulcerative Cholitis

PERIDUCT
FIBROSIS

Hemochromatosis

Red gross

Excess body iron leading to

deposition in tissues and organ
damage
Tissue damage is mediated by
generation of free radicals.
Due to autosomal recessive defect in
iron absorption (primary) or chronic
transfusions (secondary)

Fe in bile ducts (Fe stain)

brown/redish pigment

Chronic hepatitis

Wilsons disease

Rare autosomal recessive recessive defect in

ATP-mediated hepatocvte copper
Results in lack of copper transport into bile
B. Copper builds up in hepatocytes, leaks into
serum, and deposits in tissues.
Toxic Cu levels in liver, brain & eye (Kaiser
Fleisher rings)
Copper-mediated production of hydroxy! free
radicals leads to tissue damage.
Presents in childhood with chronic hepatitis/
cirrhosis and neurologic manifestations

Keiser Fleisher rings around iris

Cu stain

Non-alcoholic steatohepatitis (NASH)

commonest liver disease in US
1 transaminases in asymptomatic patient
2. Presence of obesity, insulin resistance
syndrome
BIOPSY
1. Steatosis
2 Inflammation and ballooned hepatocytes
3 Pericentral chicken-wire fibrosis bridging,
cirrhosis

ballooned hepatocytes (B) and

hepatocytes expanded by fat vacuoles (F)

Steatosis
NASH (NON-ALCOHOLIC
STEATOHEPATITIS)
L

STEATOSIS
PORTAL
INFLAMMATION

LOBULITIS

Chicken-wire fibrosis

CV

PERICENTRAL ZONE 3
CHICKEN-WIRE FIBROSIS
TRICHROME STAIN

CIRRHOTIC
LIVER

Cirrhosis

abnormal nodules surrounded by fibrosis.

Etiology:
Alcoholic
60 - 70%
Post hepatitis
30 - 40%
Biliary (primary & secondary) 5 - 10%
Hemochromatosis
5%
Cryptogenic ? NASH
10 - 15%

Bile ductule proliferation

A. End-stage liver damage characterized by regenerative nodules of

hepatocytes surrounded by fibrous connective tissue that bridges
between portal tracts.; proliferation of bile ducts.
B. Fibrosis is mediated by stellate cells
C. Clinical features
1, Portal hypertension leads to
i. Ascites (fluid in the peritoneal cavity)
ii. Congestive splenomegaly
iii. Portosystemic shunts (esophageal varices, hemorrhoids, and caput
medusae)
2. Decreased detoxification results in
i. Mental status changes, asterixis, and eventual coma (due to high
serum ammonia)
ii. Gynecomastia, spider angiomata. and palmar erythema due to
estrogen
iii. jaundice
3. Decreased protein synthesis leads to
i. Hypoalbuminemia with edema
ii. Coagulopathy due to decreased synthesis of clotting factors; degree
of deficiency is followed by PT.

SHRUNKEN LIVER
WT 1000 GMS

NODULAR

Bile ductule proliferation

TRICHROME
H&E

COLLAGENOUS

HEPATOCELLULAR CARCINOMA (HCC)

> 90% of primary liver cancers
1. Hepatitis B and C
2. Toxins eg alcohol, aflatoxin
3. Metabolic
- Hemochromatosis, glycogen storage dis A&B
- NASH
4. Hormones eg estrogens
5. CIRRHOSIS FROM ANY CAUSE

Small cell dysplastic change in

hepatocytes may precede it
LARGE CELL
CHANGE
(degenerative)

NORMAL

SMALL CELL
CHANGE
= DYSPLASIA

Bile plugs

HEPATOCELLULAR CARCINOMA

BILE PRODUCTION

Pseudoglandular pattern; bile plugs

ALPHA
FETOPROTEIN
PROVES HCC

PSEUDOGLANDULAR
PATTERN

HEP PAR 1
PROVES LIVER ORIGIN

CHOLANGIOCARCINOMA
Adenocarcinoma malignant glands
with mucin
Vary from well to poorly differentiated
Fibrous stroma, often dense
Invade widely and metastasize
Histologically NO way to tell from
metastatic adenoca
Prognosis poor

DENSE
COLLAGENOUS
STROMA

MALIGNANT GLANDS
= ADENOCARCINOMA

is an adenocarcinoma of the liver

Metastatic liver Cancer

Small cell lung ca

A. More common than primary liver tumors; most common

sources include colon, pancreas, lung, and breast
carcinomas.
B. Results in multiple nodules in the liver (primary ca have 1)
C. Clinically:hepatomegaly with a nodular free edge of the
liver

Gastric carcinoid

Colon ca

Small and large intestine

1. Compare and contrast the key gross and histologic features of the small and large intestines and regional differences.

2. Describe the histopathologic features of celiac disease (sprue) and its pathogenesis.

3. What organism is associated with Whipples disease?

4. Compare and contrast the key gross and histopathologic features of idiopathic inflammatory bowel disease, i.e.,
ulcerative colitis and Crohns disease. List the possible long term sequelae and complications. How are these diseases
managed clinically?

5. Describe the hallmark histopathologic features of antibiotic associated colitis. What is the pathogenesis and what test is
used for its diagnosis?

6. What is the mechanism for the development of diverticular disease of the colon? What are the complications?

7. What are the histopathologic features of hyperplastic and adenomatous polyps. What is meant by the term dysplasia?

8. Describe the familial syndromes and their associated genetic abnormalities. Recall the key elements in the cell signaling
affected by loss of the APC gene (adenomatous polyposis).

9. What are the risk factors for the development of sporadic colon cancer? Describe the molecular changes that occur in
adenoma to carcinoma sequence. What is the two-hit theory of carcinogenesis?

10. What is meant by the term desmoplasia?

11. What is the clinical presentation and what are the morphologic features of acute appendicitis?

Normal small intestine

Normal duodenum: Brunners glands

secrete alkaline secretion to neutralize chyme

crypts of Lieberkuhn

Normal ileum: Peyers patches (lymphoid)

Normal Jejunum: Plica circulares (largest)

Celiac:

Villous atrophy

increased intraepithelial lymphocytes,

villous atrophy
crypt hyperplasia

Serological:

Anti-tissue Transglutaminase Antibody (tTG), IgA.

Anti-Endomysial Antibodies (EMA), IgA.
Anti-Gliadin Antibodies (AGA), IgG and IgA.
Anti-Reticulin Antibodies (ARA), IgA.

Untreated Celiac: Villous atrophy

Peptic ulcer disease:

Solitary mucosal ulcer involving proximal
duodenum (90%) or distal stomach (10%)
Duodenal ulcer is almost always due to
H pylori (> 95%); rarely, ZollingerEllison syndrome
(gastrin-secreting tumor of the pancreas)
Presents with epigastric pain that improves with
meals
Diagnostic endoscopic biopsy shows ulcer with
hypertrophy of Brunner glands.
May rupture leading to bleeding from the
gastroduodenal artery (anterior ulcer)
or acute pancreatitis (posterior ulcer)
Gastric ulcer is usually due to H pylori (75%); other
causes include NSAlDs and bile reflux.
Presents with epigastric pain that worsens with
meals
Ulcer is usually located on the lesser curvature ol
the antrum.
Rupture carries risk of bleeding from left gastric
artery.

Giardia
travel
nausea, vomiting and diarrhea

Contracted by ingestion of water

contaminated with encysted forms
of the parasite
proliferates mainly in
distal duodenum and upper jejunum
due to availability of bile salts
Traveler's diarrhea

Colon-normal
Mucosa

Goblet Cells
The arrows point at:

Submucosa

Tenia coli

Normal and pathologic components

(adenoma?)

Recto-anal junction

Whipples disease

Abnormal small intestinal mucosa

Pathology: Infiltration of various organs with

macrophages containing Whipple's bacillus
Sites
Lamina propria of SI
Mesenteric lymph nodes
Cardiac valves
CNS

Macrophages in lamina propria with

abundant microorganisms (stained)

Abnormal small intestinal mucosa

TEM of microorganism

Crohns

Granuloma (sometimes w/ Giant cells

=fused macrophages)

Classically - transmural Inflammation

"Skip Lesions
Direct extension of local disease
e.g., granulomatous salpingitis

Giant Cell

Transmural inflammation= into bowel wall

Transmural inflammation= into bowel wall

Surface Ulcer
L
u
m
e
n

Chronic Inflammation
into bowel wall

Chronic Inflammation into bowel wall

Granuloma:
inflamation extends to the ileum

ulcerated colon (rectum not spared)

Ulcerative Colitis
A chronic disease of unknown
etiology characterized by
inflammation of the mucosa and
submucosa of the colon

Colon with marked chronic

inflammation of lamina propria

ulcer: lesion that is eroding the mucous membrane

Pseudopolyp
Ulceration

Crypt abscess

Diverticulitis
Diverticulitis
Complications:
Bleeding:
Abscess, Perforation, Peritonitis, Shock
Fistula
Intestinal Obstruction

Diverticulitis
diverticulitis, maybe perforated

Adenocarcinoma
-glands where they shouldnt be

glands infiltrate the circular muscle

Sporadic and familial colon cancer

-polyps/adenoma

Adenomatous polyp (normal colon

at base)

APC gene mutation (Adenomatous

Polyposis Coli )
FAP = Familial Adenomatous Polyposis

FAP
Juvenile polyposis coli

Non-polyposis Colorectal CA

genome instability, MLH1 (mutL

homolog 1) or MSH-2
Nonpolyposis means that
colorectal cancer can occur when
only a small number of polyps are
present (or polyps are not present at
all).
also usually an adenocarcinoma, but
can have dierent features (e.g. clear
cell, etc).

MLH1 staining

Clostridium dicile causes

pseudomembranous colitis

Pseudomembrane colitis

-hospital acquired
-fecal transplant
-telling signs: long course of antibiotics
C Di overgrowth

Pseudomembrane colitis

Normal appendix

Normal appendix

Lymphatic
nodule

Acute appendicitis
Rovsing sign
Can lead to shock
Etiology: obstruction and stasis

Prominent lymphocytic nodules

Acute inflammation in serosa and peri-appendiceal

soft tissue

Ulceration, transmural inflammation

Lumen