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histology of PBC

1. florid duct lesion

2. granulomatous inflammation

•Histology of PBC: the pt has high antimitochondrial antibodies.  He has a granulomatous inflammation [top right image – black arrow points to the granuloma].  You have a destruction of the bile duct – the bile duct is no longer intact in the top left image [black arrow]. 
•In the bottom image you can see the jigsaw puzzle cirrhosis – very unique for PBC.


risk for cholesterol gallstones


female (estrogens) - OCPs

obesity and metabolic syndromes

rapid weight loss 

gallbladder stasis 


inflammatory polyps histo


epithelial changes with inflammatory infiltrates in lamina propria 

non neoplastic 


intragastric balloon 


restricts food intake for 60 months - 20-40 lbs lost 



secondary to elevated venous pressures 

straining at defecation or pregnancy or portal htn

thin walled dilated submucosal vessels beneath anal or rectal mucosa 


Types of bile duct epithelial lsions

bile duct adenoma - benign

cholangiocarcinoma - malignant


invasive adenocarcinoma

if lesion penetrates muscularis mucosa 

metastatic potential


anal condyloma 

squamous papilloma caused by HPV 

papillary gorwth 

enlarged keratinocytes w central hyperchromatic wrinkled nucleus 



in food can cause damage

•The primary food contaminants are aflatoxins, which are especially seen in developing countries

•If peanuts in particular go bad, it can cause a certain fungal infestation that can produce aflatoxins and AFB1

•This aflatoxin can directly cause a mutation in the p53 tumor suppressor gene

•The 249ser gene mutation is very unique for aflatoxic damage

•This aflatoxin toxin can react synergistically with HBV infection

•Aflatoxin in the liver, in human cells, can induce much more damage related to HBV infection

•In another sense, this can also mean that aflatoxin prevalence parallels that of HBV infection

•In the area that has high HBV infection, you have high incidence of the toxin


stellate cells 

in space of disse

•Stellate cells, under normal conditions, are very quiet; they store some fat and minerals

•When the activate, they become fibroblasts and produce collagen, which can eventually cause fibrosis leading to cirrhosis, which we will discuss later


carcinoid tumors 


from endocrine stem cell in crypt 

more indolent than carcinoma 

can make many bioactive things 


hereditary non-polyposis colon cancer 

i.e. lynch syndrome 

increased risk of many cancers 

colorectal cancers often multiple at young age in right colon

inherited germline mutations in DNA repair caretaker 

most common syndromic form of colon cancer 


sessile polyps

tumoral masses or nodules which project into the lumen, usually refers to epithelial lesions 

sessile polyps have a broad pase 



•Histology of PBC: the pt has high antimitochondrial antibodies.  He has a granulomatous inflammation [top right image – black arrow points to the granuloma].  You have a destruction of the bile duct – the bile duct is no longer intact in the top left image [black arrow]. 
•In the bottom image you can see the jigsaw puzzle cirrhosis – very unique for PBC.


hyperplastic polyps etiology and location

non neoplastic! 

age 60-70, asymptomatic 

*left colon and rectum 



precursor of colorectal adenocarcinoma 

tubular, villous, tubulovillous 

risk of malignancy with size, architecture, dysplasia 

familial, higher chance with age 


pathogenesis of hepatocellular adenoma


female hormones (contraceptoves) 


acute cholecysitis

acute inflammation of the gallbladder 

90% from obstruction of the neck of the cystic duct by stones (calculus cholecystitis) 

10% from ischemia of systic aretey 

sepsis, immunosuppression, trauma, diabetes, nfection


budd chiari syndrome

hepatic venous outflow obstruction

blockage of 2 major hepatic veins 

passive congestion and centrilobular necrosis 

•This is a typical presentation for Budd-Chiari Syndrome.
•[top left image] Here is a thrombus.  If the vessel is blocked, you cause congestion of blood. The blood spills over from the sinusoids and damages the hepatocytes.
•[bottom left image] This is partial.  You can see the thrombosis [black arrow].  If you block the left hepatic vein, you cause damage to the left lobe [the darker left portion of the liver shown].
•Histologically, you can see the ischemia in the liver parenchyma [right images].  The hepatocytes are gone b/c the oxygen is depleted.  There are no nutrients, causing damage.


juvenile polyp

hamartomatous non-neoplastic polyps 

30-50% of patients develop AC by age 45

usually sporadic in kids under 5

usually in rectum 

in adults: "retention polyp"

can mean there is a rare polyposis syndrome


colon polyp:

tubular adenoma 


epithelial cells fail to mature as migrate to crypt surface

crowded disorganized rounded glands, numerous goblet cells and enlarged hyperchromatic nuclei 


dysplastic change

before hepatocellular carcinoma

•In 10 to 30 years, you can have a clear preneoplastic change (pre-neoplasia)

•It does not necessarily have to go through an adenomatous change; the adenoma is a different animal

•That is called a dysplastic change

•You will see high- or low-grade dysplasia before HCC

•There may be another 3-5 years before the hepatocytes become dysplastic

•Most of the time, the process will stop here à the patient will not develop cancer

•However, a certain percentage of patients pass that boundary over another 5-10 years and progress on to hepatocellular carcinoma (neoplasia)


neoplastic lesion

•If the proliferation goes out of control without a boundary or limits, you get neoplastic disease

•Benign disease



•Malignant disease


•Primary hepatocytic carcinoma, ductal carcinoma, cholangiocarcinoma


histo in cronkhite-canada syndrome 

mortality in 50-60% 

cystically dilated crypts w marked inflammation

mucosa adjacent to polyps also shows cystic dilation


Histo in cowden syndrome 

stroma rich polyp with cystically dilated crypts 

risk of colon cancer = gen pop


chronic pancreatitis 

pancreas is hard w extremely dilated ducts and visible calcifications 



•You do a biopsy on this pt.  This is what you see in the liver biopsy.
•This is the brown colored deposit [black arrow in left image].  It is iron. 
•If you are not sure, do an iron stain [right image]. 


angiosarcoma risk factors

•Some major risk factors in the United States include exposure to vinyl chloride

•This used to be used in the plastic industry, but no longer

•If there is contamination in the water, this can potentially cause development of angiosarcoma

•Exposure to thorium dioxide, which was previously used as contrast for radiology, is also associated with angiosarcoma

•Now we know this is associated with this disease, so it has been banned

•Arsenic and arsenite can also cause angiosarcoma, particularly in developing countries where these can contaminate food


nodular regernative hyperplasia pathogenesi

similar to FNH - adaptive parenchymal hyperplasia due to heterogenous distribution of blood flow

•Top left: wedge resection with a multiple nodular appearance

•The yellowish tissue is liver parenchyma

•There is some bile staining (green)

•Bottom left: the trichrome stain shows a nodule almost separated by incomplete septa

•It is not like cirrhosis

•Cirrhosis, by definition, is a completely separate nodule

•Top right: high power view shows a nodular appearance

•There is a central area; a central vein

•Around the area are the proliferative hepatocytes

•There is still a portal tract with a bile duct à it is hyperplastic, not neoplastic

•Bottom right: reticulin stain highlights the hepatocytes

•This is classic for nodular regenerative hyperplasia (NRH)

•This is not a neoplastic process


nodular regenerative hyperplasia 

•Top left: wedge resection with a multiple nodular appearance

•The yellowish tissue is liver parenchyma

•There is some bile staining (green)

•Bottom left: the trichrome stain shows a nodule almost separated by incomplete septa

•It is not like cirrhosis

•Cirrhosis, by definition, is a completely separate nodule

•Top right: high power view shows a nodular appearance

•There is a central area; a central vein

•Around the area are the proliferative hepatocytes

•There is still a portal tract with a bile duct à it is hyperplastic, not neoplastic

•Bottom right: reticulin stain highlights the hepatocytes

•This is classic for nodular regenerative hyperplasia (NRH)

•This is not a neoplastic process


•See the pink globules [black arrow in left image] – protein structures within the hepatocytes.
•If you do a special stain PASD, you would see the pink proteins [black arrow in right image], which are glycoproteins, stuck in ER and cannot be transported outside of the ER for further processing. 
•Another hereditary disease is a1-antitrypsin deficiency.  It is another autosomal recessive disorder.  The gene is on chromosome 14, encoding a protease inhibitor. 
•The abnormal protein that is produced cannot be folded properly.  Proteins are synthesized in the ER, but this mutated protein cannot be processed well.  It is stuck in the ER and cannot get out.  It forms a globule.
•Wild type genotype is normal; most common mutant is PiZZ.
•Histologically, will see round globules depositing in hepatocytes.


adenocarcinoma on left side of colon symptoms

occult blood in stool

change in powel habits 

"napkin ring" tumors 

obstruction uncommon 


endoscopic gastroplasty

endoscopy with stitch device that stitches stomach closed to make it smaller



micronodular cirrhosis


intraductal papillary mucinous neoplasm



chronic cholecystitis

persistant inflammation of the gallbladder wall

almost always associated w gallstones 


metastatic carcinoma


portal fibrosis stage 1

•, there’s a significant amount of portal fibrosis (collagen) here

•It’s stage 1 because you don’t see any fibrosis above the portal tract


pathology and degrees of HCC

•The degree of cellular differentiation is very important for patient prognosis

•If the tumor cells have very similar cytology to the hepatocytes, they are well-differentiated

•The cells can be recognized as hepatocytic in origin

•The other extreme is poorly differentiated—you cannot tell that the tumor cells came from liver; you cannot recognize the liver at all

•In the middle is moderately differentiated

•This is very important for the hepatologist to know when the patient is diagnosed with HCC

•Other important pathologic features for this disease include vascular invasion

•All hepatic surgeons know that if the patient has vascular invasion, the patient has a very poor prognosis

•The lesion may contain bile



•Top left: well-differentiated hepatocellular carcinoma

•This is obviously from the liver; it looks like hepatocytes

•Bottom: poorly-differentiated HCC

•You cannot tell that this tumor is derived from the hepatocytes

•Top right: moderately differentiated

•This looks like a tumor, but you can still recognize that this is hepatocellular in origin

•There is cribriforming, a very high N/C ratio

•Well-differentiated carcinoma has a very good prognosis

•After resection, you probably do not need chemotherapy

•For a poorly-differentiated carcinoma, the patient needs adjuvant therapy (post-surgical treatment); this may be chemotherapy or radiation


mucinous cystic neoplasm


slow growing mass in the tail of the pancreas 

cystic cavities villed w mucin 

cysts lined by columnar mucin-producing epithelium associated w dense stroma

no commnication w pancreatic ducts 

can progress to invasive adenocarcinoma 


histology of polyps in juvenile polyposis

dilated crypts filled w mucin and inflammatory debris 

lamina propria expansion by mixed inflammatory infiltrate 



•Angiosarcoma is a malignant type of hemangioma

•This is a very uncommon disease

•It is a malignant tumor arising from the endothelial lining

•Grossly, it is usually a grey-white tumor with hemorrhagic areas

•It affects the vessel

multicentric with both lobes involved 70% of the time

grey white tumor with hemorrhagic areas


mucinous adenocarcinoma


syndrome criteria for juvenile polyposis 

more than five juvenile polyps in the colon or erectum 


Types of vascular lesions

•Hemangioma: people think of this as a hamartomatous change, but most people think of this as proliferation of the endothelial lining

•Angiosarcoma is a malignant type of hemangioma



lymphoid aggregate (sometimes seen in hep B)

bile duct epithelial cell proliferation

•You have a lymphoid aggregate [black arrow in left image], which is clinically a very important hint for the diagnosis of Hep C infection.  If you see this plus bile duct epithelial cell proliferation [green arrows in right image] – normally you have one, but here you have multiple – this is very typical for Hep C.



villous adenoma


pathogenesis of focal nodular hyperplasia 

parenchymal hyperplasia 

•Parenchymal hyperplasia resulting from abnormal blood flow

•In certain areas, there is an arterial abnormality with a thicker wall; more blood comes to the area with more oxygen and nutrients

This particular area has a high proliferative potential and can form very large lesions

•This is associated with female hormone stimulation: estrogen

•This is due to high estrogen receptor protein expression in the affected area

•These receptors respond to hormone stimulation


budd chiari syndrome and veno-occlusve disease 

•This is a typical presentation for Budd-Chiari Syndrome.
•[top left image] Here is a thrombus.  If the vessel is blocked, you cause congestion of blood. The blood spills over from the sinusoids and damages the hepatocytes.
•[bottom left image] This is partial.  You can see the thrombosis [black arrow].  If you block the left hepatic vein, you cause damage to the left lobe [the darker left portion of the liver shown].
•Histologically, you can see the ischemia in the liver parenchyma [right images].  The hepatocytes are gone b/c the oxygen is depleted.  There are no nutrients, causing damage.



bacterial infection in the bile ducts 


•portal fibrosis with septal formation

In stage 2, in addition to the fibrosis in the portal tract, you see some fibrosis penetrating into the liver parenchyma

•We call this septal formation



pathogenesis of hemangioma

•It is a congenital disease that is sometimes characterized by hormone-promoted growth

•As a result, you need to closely monitor pregnant women with hemangiomas

•The hemangioma can grow to be very large and compress the fetus, particularly late in pregnancy



•There is a specific histology associated with Hep B.
•For Hep A, it is not chronic so we don’t usually do biopsy.  If you do a biopsy, you see acute hepatitis, which has no specific features.
•Hep B has a unique feature: ground glass cytoplasm.  This [black arrow in left image] is ground glass cytoplasm, which contains lots of viral hepatitis surface antigens.  If you do an immunostain for the surface antigens, they will show up like this [black arrow in right image].



pathology of metastatic carcinoma 

mult nodular metastases causing hepatomegaly

central necrosis (outgrow blood supply) 

cells usually resemble primary (not hepatic) tissue 



histology of polyps in peutz-jeghers 

large, pedunculatd 

arborizing network of CT, SM, glands with normal epithelium 



autoimmune hepatitis 

prominent plasma cell infiltrate 

central lobular necrosis/bridging necrosis 

increase in serum auto ab titers

•Autoimmune hepatitis is unique clinically b/c it normally occurs in young women and postmenopausal women.  Men can have it but at a much smaller percentage.
•Histologically, it shows prominent plasma cell infiltrate [left image].  Plasma cells produce antibodies – that’s why it is autoimmune.  They produce antibodies against the human antigen.
•Another feature is the central lobular necrosis or bridging necrosis [right image].  This is the central vein [see label].  There are tissue and cells surrounding the central vein which is damaged and collapsed. 
•To make a diagnosis, you have to have an autoantibody increase in the serum, ANA, SMA and some other autoantibodies.
•[Inaudible student question: “What is the difference…”]  Answer: No, these are plasma cells [points to left image].  Plasma cells are mature lymphocytes.  If an antigen stimulates the lymphocytes, they turn into plasma cells which produce antibodies.  This is why it is autoimmune, different from Hep B or Hep C or drug toxicity.  [Student:  “They still look the same to me.”]  Plasma cells are morphologically different from lymphocytes, which have small nuclei and very limited amount of cytoplasm.  Plasma cells have a lot of cytoplasm and contain antibodies.  Pathologists can look at these and immediately tell they are plasma cells.



•Histologically, the tumor is extensively infiltrating, anaplastic-like, with spindle cells derived from blood vessels

•The tumor is growing around the sinusoids

•You cannot recognize any hepatocytic architecture; the hepatocytes are all damaged, or have been replaced by the malignant cells

•This can sometimes form a solid mass, infarct, atrophy and fibrosis


intramucosal carcinoma in adenoma

lamina propria invasion

little or no metastatic potential 




within lumen of gallbladder or in extrahepatic billiary tree 

most are non symptomatic 

made of cholesterol or pigmented (Ca-bilirubin)


Attenuated FAP

fewer polyps (average 30) 

50% lifetime risk


sessile serrated adenoma location and etiology

right colon! 

50-60, asymptomatic 



etiology of chronic pancreatitis

chronic alcoholism 

long standing obstruction

autoimmune disease 



•Bottom: the high power view shows a poorly differentiated hepatocellular carcinoma

•Compare to normal hepatocytes in the hyperplastic lesion; these hepatocytes have lost their normal, recognizable architecture

•It has a clustered, infiltrative pattern

•There is a single artery at bottom left, but with no bile duct


high grade dysplasia - carcinoma in situ (in adenoma)

does not metastasize, clinically benign


hepatocellular adenoma

•This is also well-demarcated, but there is no central scar

•capsulated!! unlike FNH


•One very important feature of this disease is that there is no normal portal triad

•Because this is a neoplastic disease, this disease has an unpaired artery without a bile duct companion

•No bile duct, only an artery

We have a prominent vessel and draining vein


adenoma polyps histo

epithelial dysplasia 

nuclear hyperchromasia 

elongation and stratification

sessile or pedunculated

tubular, tubulovillous, villous 



most common primary sites of metastatic carcinoma of the liver

colon, breast, lung

any cancer in any site except leukemia and lymphoma


intraductal papillary mucinous neoplasm


mucin-producing epithelial neoplsm from major pancreatic ducts or branches 

more common in the head of the pancrease and in men

can progress to invasive carcinoma 


most common mutation in sporadic colon cancer? 

APC - left sided!! 



ballooning degeneration

hepatocyte swelling by failed osmoregulation

rupturing of hepatocyte 


dietary factors in adenocarcinoma

low intake of veggie fiber --> decreased stool bulk/altered bowel microbiota --> increase synthesis of toxic oxidative by-products of bacterial metabolism 

high intake of carbs and fat --> enhance hepatic synthesis of cholsterol and bile acids --> converted in carcinogens by intestinal pacteria 



microsattelite instability 

caretaker patheway 

DNA mismatch repair pwathway 

HNPCC  = germline MLH1, MSH2 

can be acquired

1. germline or somatic mutations of mismatch repair genes 

2. alteration of 2nd allele 

3. microsatellite instability/mutator phenotype 


stage 3

portal to portal bridging fibrosis 

2 portals connected by thin fibrous bands

•In bridging fibrosis, you can see the fibrosis trying to form nodules but they’re not completely separated yet.

•This is stage 3


familial adenomatous polyposis mutation

APC gene 



How does alcoholism lead to HCC? 

•Alcoholism causes damage directly and indirectly

•Indirectly, alcohol can be metabolized by CYP450 (2E1) and produce intermediate components called reactive oxygen species (ROS)

•These ROS are very active and can damage the proteins and DNA, causing DNA instability

•Side note: this is important in lipid metabolism, but causes damage in this context

•There is also production of an intermediate factor called acetaldehyde, which can also cause protein and DNA damage

•DNA damage can cause cellular transformation, which can persist and eventually cause the mutation that leads to oncogenesis


intrahepatic cholangiocarcinoma

less common (8-13%) 

•If there is intrahepatic cholangiocarcinoma, the patient presents clinically with abdominal pain, gradually growing mass lesions, and progressive jaundice

•Again, this is very nonspecific

•Prognosis is very bad

•This disease is very hard to pick up early on

•When you identify this disease, it is usually later stage


anal intraepithelial neoplasia



neoplastic proliferation of squamous cells confied to anal mucosa 

high N/C ratio 


mitotic figures above basal layer (more immature cells in high grade)



cirrhosis = stage 4 of fibrosis

•In stage 4, there’s going to be cirrhosis

•As comparison, this is normal (left)

•The surface is very smooth with normal contour. Histologically, it has normal architecture.

•In cirrhosis, you can see the formation of nodules

•If you did a biopsy, you’ll see these nodules surrounded by fibrotic bands


colonic adenocarcinoma

most common malignancy of the GI tract 

2nd to lung cancer deaths in US 

peaks in 60s and 70s


management if carcinoma occurs in a pedunculated adenoma? 

endoscopic polpectomy adequat if :

superficial tumor not close to margin 

no vascular/lymph invasion

not poorly differentiated 


serous cystadenoma 



tubular adenoma 




hyperplastic polyps histo

serration in the upper third 

mature goblet cells and absorptive cells 

non neoplastic 


bile duct adenoma 

benign, no treatment - incidental finding! 

•These bile duct adenomas are often recognized during laparoscopic examination such as during cholecystectomy

•Clinically, bile duct adenoma can mimic carcinoma

•If you do a CT scan and are not aware that the patient has this, you may think that the patient has carcinoma

•These are grey-white firm nodules that are usually well-demarcated, but not necessarily

•They are usually composed of circular bile duct-like structures with fibrous stroma


2 pathways of colorectal carcinogenesis 

APC/Beta catenin --> chromosomal instability 

DNA mismatch repair --> microsatellite instability 

stepwise accumulation of multiple mutatios


histo of drug toxicity

central necrosis or diffuse necrosis (need transplant or die) 

lobular inflammation

parenchymal necrosis

bile duct damage and prolf


tubular adenoma

most in colon (90%) 

low grade dysplasia = adenoma 

smaller - sessile and smooth 

larger - pedunculated, lobulated 

stalk = fibroconnective tissue and vessels covered by non neoplastic mucosa



peri-ductal or onion skinning


histology of fulminant hepatitis 

•This is what you see from the biopsy

•The liver parenchyma is totally gone; this is near total necrosis with the liver parenchyma totally destroyed

•You may have a few remaining hepatocytes, but they aren’t functioning and the patient isn’t going to survive

•The patient is on life support and needs a liver transplant


colon polyp? 

hyperplastic polyp 

non neoplastic 

delayed shedding of epithelial cells result in crowding and tufting toward surface of the crypt 

elongated crypts with tufting serrated surface lined y mature goblet cells and absoroptive cells 


labs increased in hepatocellular injury/hepatitis

transaminases and bili 

viruses, alcohol, drugs, metabolic


chronic pancreatitis 

inflammatory process of pancreas resulting in irreversible losss of exocrine and endocrine function


sqamous cell carcinoma 

increasing incidence


lymph node metastasis 


what is the most common syndromic form of colorectal cancer? 


herediatry nonpolyposis colorectal cancer syndrome


cholelithiasis factors and mech 

cholestrol supersaturation

- high Ch output 

- decreased bile acid synthesis 

- gallbladder hypomobility 

- excessive mucus


pathogenesis of HCC

–Nearly always develops in the setting of chronic hepatitis or cirrhosis resulting from the following risk factors
•Viral infection (HBV, HCV)
•Chronic alcoholism
•Food contaminants (primarily aflatoxins)
•Genetic disorders (hemochromatosis, Wilson’s,  tyrosinemia).
Repeated cycles of cell death and regeneration, resulting in genetic alterations.

Viral gene integration into human genome


complications of chronic pancreatitis 

pleural effusions



fat malabsprotton

stones in panc duct

pancreatic calcification

pain from perineural fibrosis


ascending colon polyp

smooth, rounded protrusion above the surrounding mucosa


Treatment of HCC

Resection: if localized and well-demarcated, particularly in the early stages, you can resect the tumor

•Some of these patients have a very good prognosis, especially if the pathology says it is well-differentiated

•Follow these patient with testing (AFP)

Chemoembolization: if the tumor is very large and non-resectable, chemoembolization

•If the patient wants a transplant, chemoembolization is often used first

Radioablation: this is one modality used to treat patients who have a diffuse lesion that cannot be resected

•If the patient has a diffuse lesion and chemotherapy is not effective, radioablation is an option

•Liver transplantation: this is a promising modality of treatment

•This has a very high survival rate, much higher even than resection alone

•Treatment options rely on correct pathological diagnosis and staging: well-differentiated, poorly-differentiated, vascular invasion, clear margins, etc.


labs in billiary tract injury

alk phos, GGT, bili increased 

drugs, congen, metabolic, immune, trauma 


kuppfer cells

•Kupffer cells are also very important; kind of act as macrophages, which engulf damaged cells, particularly hepatocytes (such as in Hepatitis)

•The can also engulf certain things like ions and small mineral compounds


mechamism of acute pancreatitis for chronic pancreatitis 

necrosis and fibrosis 

repeated episodes of acute panc 


Major differences between FNH and Hepatic Adenoma

•FNH is a hyperplastic lesion; there are portal triads present

•Hepatic adenoma is a neoplastic lesion without portal triads; it has unpaired arteries

•These are otherwise very similar in terms of their clinical presentation and epidemiology

•Clinical follow-up is also very similar


acinar cell carcinoma


like normal acinar cells, form zympgen granules and produce exocrine enzymes (trypsin and lipase) 

metastatic fat necrosis caused by the releae of lipase into the circulation



hamartomatous (non neoplastic) - juvenile polyps 

risk of gastric, SB, colonic, pancreatic AC 

sporadic and syndromic 

 is an autosomal dominant genetic diseasecharacterized by the development of benign hamartomatous polyps in the gastrointestinal tract and hyperpigmented macules on the lips and oral mucosa (melanosis).[1] 

entire GI tract! meanotic skin and mucosal pigmentation

higher risk of carcinoma: pancreas, breast, lung, ovary, uterus 



adenocarcinoma on right side of colon symptoms


iron deficiency 


obstruction uncommon


pedunculated polyps

tumoral masses or nodules which project into the lumen

have a stalk 

epithelial lesions


mallory hyaline 

collapsed, dense condensation of cytoskeletal proteins in the cytoplasm of hepatocytes


clinical course of angiosarcoma

aggressive - high rate of metstases 

20% survival at 5 years


extrahepatic cholangiocarcinoma 

symptoms associated w bile obstruction and mass

klastskin tumor - located at bifurcation of right and left hepatic ducts

•This can be identified early on because they block the bile duct and cause jaundice

•The symptoms are usually associated with bile duct obstruction and mass lesion

•Klatskin tumors are located at the bifurcation of the main hepatic duct

•If that area is blocked, no bile can be secreted

•This can immediately cause abdominal pain and jaundice à the image shows the sclera of the patient are yellow

•If found early on, this indicates the need for surgery

•Surgery is not a cure, but you can at least resect the tumor


what is concisdered a hamartomous polyp? 

tubulovillous adenoma

cloacogenic polyp

sessile serrated adenoma

juvenile polyp

juvenile polyp


clinical course of focal nodular hyperplasia 

usually asymptomatic/incidental 

mild abdominal symptoms

can rupture

no malignant potential


histology of ductal adenocarcinoma

tubular structures in abundant desmoplastic stroma 

solid firm infiltrative tumors w ill defined borders 


acidophil body

a single apoptotic hepatocyte 

in acute hepatitis


focal nodular hyperplasia 

well-circumscribed lesion with a central scar

central grey-white depressed stellate scar 

lympocytic infiltrates 

normal hepatocytes!!

no association w cirrhosis


pancreatic neuroendocrine tumors (PEN)

clinically - attacks of hypoglycemia, CNS system manivestation

90% benign

functional - hormone production (insulin, glucagon, somatostatin)

nonfunctional - larger lesions at diagnosis 

malignancy - mitotic activity



•Hyperplasia is proliferation of cells with limits

•Hyperplasia is either epithelial or fibroblastic proliferation

•There is a boundary; at a certain number of cells or certain number of divisions, these cells stop proliferating

•In the liver, you can have hepatocytic proliferation like:

•Focal nodular hyperplasia (FNH)

•Nodular regenerative hyperplasia (NRH)


Nodular Regernerative Hyperplasia 

•Hepatocellular nodules distributed throughout the liver in the absence of fibrous septa between the nodules 

Diffuse nodular lesions throughout the liver

•The hepatocytes are plump and very enlarged

•The reticulin stain highlights changes in the hepatocellular architecture, which takes on a nodular appearance


•These are a few examples of hepatocellular carcinoma

•Top left: single nodule, appears well-demarcated

•Top right: another nodule

•Two nodules are separated by a thin septa

•This is not well-demarcated à it has a very irregular border

•Bottom left: several nodules, diffuse changes

•Bottom right: large nodule with satellite lesions

•This is a sign of intrahepatic metastasis

•There are different types, shapes and demarcations


risk for pigment gallstomes

biliary infection

ileal disease (crohn, resection, CF)



the presence of stones in the bile duct of the biliary tree


Classic FAP

100-2500 tubular adenomas 

100% risk of carcinoma 

early detection, prophylactic colectomy 


clinical course of hepatocellular adenoma

asymptomatic or abdominal symptoms

intrahepatic mass mistaken for the carcinoma 

can rupture

rare association with hepatocellular carcinoma


carcinoma of the gallbladder 

rare, poor survival (1%) 

major risk factors: gallstones, crhonic infection



What is the most common malignancy in the liver? 

metastatic disease


sessile serated adenoma histo 

serration throughout the full length of the crypt 

lined by goblet cells wihtout cytologic features of dysplasia 



acute cholecystitis 

serosal congestion, fibrinous exudates, edema

red purple mucosa edema necrosiss


serous cystadenoma 

multicystic neoplasms that usually occur in the tail of the pancreas

cysts are small, lined by glycogen rich cuboidal cells with clear, thin, straw colored fluid 

amost always benign



cronkhite-canada syndrome

polyp syndrome - non neoplastic 

nonherediatry! unknown cause 

polyps in stomach and small colon 

diffusely nodular mucosa 



mechanism of alcohol for chronic pancreatitis 

increases protein concentrations in the pancreatic juice --> obstruction

free radicals cause membrane lipid oxidation, fusion of lysosomes and szymogen granules, acinar cell necrosis and fibrosis 

toxic: alchol directly has toxic effects on acinar cells 


Types of hepatocellular lesions

adenoma - benign

carcinoma - malignant


chromosomal instability 

gatekeeper pathway 


FAP, germline APC inactivation 

can have multigene acquaired in activation

1. "first hit" = germline or somatic mutations of cancer suppressor genes

2. methylation abnormalities - inactivation of normal alleles 

3. protoncogene mutations  



clinical features of chronic pancreatitis 

repeated episodes of severe abdominal pain

persistant abdominal and back pain

recurrent attacks of jaundice 

vague attacks of indigestion

weight loss 



chronic cholecystitis 

chronic inflam and fibrosis of the wall 


bile duct adenoma

•Top right: if you take one slice from the tissue at left, you see clusters of bile ducts

•This is benign bile duct proliferation

•Bottom: high power view

•This is benign

•The proliferative index is very low; there are no mitotic figures

•This is a benign lesion


Histology of PSC

periductal or onion skinning fibrosis 


mucinous cystic neoplasm



choledochal cyst


congenital dilations 

can lead to obstructive jaundice, pain, abdominal mass


adenoma polyps etiology and location

30% of adults by age 50 

60-75% distal to splenic flexure, more proximal with age 



most important prognostic factor for CRC?

depth of invasion and lymph node metastasis

early detection and resection is a curative therapy 


inflammatory polyps mechanism, etiology and location 

age 20-50

excessive straining, rectal bleeding, mucus discharge 

anterior rectal wall - prior injury and healing

non neoplastic 


•focal nodular hyperplasia


If you section one piece of tissue and look at it histologically for microscopic evaluation, what do you see?

•Top left: well-circumscribed lesion

•Top right: a central scar composed of fibrous tissue à by definition, a scar is fibrotic tissue that replaces normal parenchyma

•In the middle, there are some thicker-walled blood vessels

•This is a vein or artery à it is a thicker-walled vessel

•Bottom left: on the edge of focal nodular hyperplasia, you see some inflammation and bile duct proliferation

•Bottom right: if you do a special stain, you can highlight the fibrous tissue


•This hemangioma was resected

•This is typical of a hemangioma à there is very hemorrhagic, sponge-like tissue

•The tissue shows a lot of vasculature filled with blood

•Bottom: the vasculature becomes large, sclerotic and fills with blood


•These are usually solitary lesions, but there may be multiple lesions

•Typically these are less than 3 cm in size, but can become very large à these are called giant hemangiomas


•Virtually all consist of vascular spaces

•These are mostly venous-type



chronic pancreatitis


reduced number of acini

chronic inflam infiltrate 

enlarged persistent islets 

dilated ducts w proteinaceous material 


what is the most common neoplatic polyp in the bowel that has the potential to progress to cancer? 




tubular adenoma

tubular adenoma


possible outcomes of liver injury


hepatic failure 

fibrosis (scarring0 

cirrhosis (diffuse fibrotic process through liver w formation of nodules and regen hepatocytes surrounded by bands of fibrosis 


management if carcinoma in a sessile adenoma 

endoscopic polypectomy is inadequate --> surgery 


Clinical course of nodular regernative hyperplasia 

•Clinically, this is usually associated with portal hypertension

•Patients can present with ascites and splenomegaly

•Again, NRH is also associated with other conditions, such as lupus and Budd-Chiari disease

•Certain people think this has malignant potential, but this is still controversial

•To the lecturer, this will probably never become HCC because it is hyperplastic, not neoplastic


metastatic patterns of colon cancer

lymph nodes





wilson's disease

copper depsition in liver 

•This is what you see if you do a biopsy.  Slightly different from hematochromatosis.
•You see darker, brownish deposits in the left image.
•If you use a copper stain [right image], you will see the very brown, granular copper deposits.



•Cholangiocarcinoma usually occurs in non-cirrhotic liver, which distinguishes it from HCC

•HCC usually occurs in a cirrhotic liver except in the case of HBV, which has oncoproteins that can integrate into the human host and can induce HCC without cirrhosis

•The etiology of HCC is usually related to cirrhosis

•The tumor is composed of a tree-like tumorous mass and is firm; it has a gritty, tumor surface


•This is a type of adenocarcinoma with a marked desmoplastic reaction

•Demoplasia is a fibroblastic reaction to tumor invasion

•Early, you can identify lymphatic and vascular invasion

•This is rarely bile stained because it does not produce bile


villous adenoma

larger and more ominous than tubular adenoma 

rectum and rectosigmoid 


finger like extension 

all degrees of dysplasia 

carcinoma will directly invade the bowel wall 


duodenal sleeve

malabsorption procedure

duodeno-jejunal bypass sleeve 

open at both ends 

food can pass but sleeve prevents contact w duodenum 

delays digestions


histology of acute hepatitis

1. portal and interface inflammation (portal tract filled w lymphocytes)

2. lobular inflammation

3. bile duct damage

4. no significant fibrosis


serum/infiltrate in autoimmune chronic pancreatitis 

IgG4 infiltrate and in serum



aspirin in CRC

inhibit COX2 - decrease production of prostaglandin - promotes epithelial proliferation


autoimmune chronic pancreatitis

lymphoplasmacytic sclerosing pancreatitis 

mass like lesions and irregular beading of the pancreatic duct 

associated w autoimmune conditions


mutations in Lynch syndrome 

loss of MSH2, MSH6

HNPCC  = germline MLH1, MSH2 


macronodular cirrhosis 


risk factors for pancreatic ductal adenocarcinoma? 

age - 60-80

black, ashkenazi 

smoking = double risk 

high fat and meat diet, BMI

chronic pancreatitis 



symptoms of ductal adenocarcinoma 

jaundice, back pain, weight loss 


•This is a hepatocellular adenoma

•Adenomas are usually asymptomatic; normally we do not remove an adenoma surgically unless it is enlarged, the patient wants to have it taken out, or wants to get pregnant

•This particular lesion also responds to hormonal stimulation

•Left image: in contrast, to FNH, this lesion is capsulated

•It is an enucleated tumor with a capsular surface

•Right image: if you cut it in cross-section, you can see the lesion is very well circumscribed and encapsulated

•The central area has some kind of hemorrhage


small bowel neoplasm

malignant tumors are far less common in SB than everywhere else 

can have peutz jeghers or adenomas 


syndrome criteria for peutz-jeghers syndrome

mucocutaneous lesions, patches of hyperpigmentation 




increased in serum in 50-75% of patients w HCC

•The patient requires a certain exam, including a check of his or her serum alpha-fetoprotein

•50-75% of patients have elevated alpha-fetoprotein

•This is a very good marker used to screen patients who may have HCC


histo of acinar carcinoma

solid nests, acini, scant stroma 

large solid well circomscribed w extensive necrosis


Cowden syndrome

mult non cancerous hamartomas in skin, mucus membranes 

multiple discrete sessile polyp lesions

risk of colon cancer = gen population 



•If you do a resection, you will see a large, irregular lesion that is not well-demarcated with a smaller satellite lesion

•There is intrahepatic metastasis

•Right image: there is a very proliferative bile duct-like structure

•Left: the high-power view shows an infiltrative pattern and a desmoplastic reaction

•This is a fibroblastic reaction of the glands

•Bottom right: desmoplastic reaction

•Top right: intravascular invasion

•This is typical for cholangiocarcinoma