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Path Flashcards

1
Q

histology of PBC

A
  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.
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2
Q

risk for cholesterol gallstones

A

older

female (estrogens) - OCPs

obesity and metabolic syndromes

rapid weight loss

gallbladder stasis

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3
Q

inflammatory polyps histo

A

reactive/regenerative

epithelial changes with inflammatory infiltrates in lamina propria

non neoplastic

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4
Q

intragastric balloon

A

restrictive

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

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5
Q
A

hemorrhoids

secondary to elevated venous pressures

straining at defecation or pregnancy or portal htn

thin walled dilated submucosal vessels beneath anal or rectal mucosa

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6
Q

Types of bile duct epithelial lsions

A

bile duct adenoma - benign

cholangiocarcinoma - malignant

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7
Q

invasive adenocarcinoma

A

if lesion penetrates muscularis mucosa

metastatic potential

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8
Q

anal condyloma

A

squamous papilloma caused by HPV

papillary gorwth

enlarged keratinocytes w central hyperchromatic wrinkled nucleus

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9
Q

aflatoxins

A

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
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10
Q

stellate cells

A

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
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11
Q

carcinoid tumors

A

neuroendocrine

from endocrine stem cell in crypt

more indolent than carcinoma

can make many bioactive things

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12
Q

hereditary non-polyposis colon cancer

A

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

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13
Q

sessile polyps

A

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

sessile polyps have a broad pase

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14
Q
A

PBC

  • 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.
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15
Q

hyperplastic polyps etiology and location

A

non neoplastic!

age 60-70, asymptomatic

*left colon and rectum

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16
Q

adenoma

A

precursor of colorectal adenocarcinoma

tubular, villous, tubulovillous

risk of malignancy with size, architecture, dysplasia

familial, higher chance with age

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17
Q

pathogenesis of hepatocellular adenoma

A

idiopathic

female hormones (contraceptoves)

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18
Q

acute cholecysitis

A

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

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19
Q

budd chiari syndrome

A

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.
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20
Q

juvenile polyp

A

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

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21
Q

colon polyp:

A

tubular adenoma

neoplastic/premalignant

epithelial cells fail to mature as migrate to crypt surface

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

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22
Q

dysplastic change

A

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)
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23
Q

neoplastic lesion

A
  • If the proliferation goes out of control without a boundary or limits, you get neoplastic disease
  • Benign disease
  • Adenoma
  • Hemangioma
  • Malignant disease
  • Metastasis
  • Primary hepatocytic carcinoma, ductal carcinoma, cholangiocarcinoma
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24
Q

histo in cronkhite-canada syndrome

A

mortality in 50-60%

cystically dilated crypts w marked inflammation

mucosa adjacent to polyps also shows cystic dilation

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25
Q

Histo in cowden syndrome

A

stroma rich polyp with cystically dilated crypts

risk of colon cancer = gen pop

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26
Q
A

chronic pancreatitis

pancreas is hard w extremely dilated ducts and visible calcifications

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27
Q
A

hematochromatosis

  • 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].
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28
Q

angiosarcoma risk factors

A
  • 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
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29
Q

nodular regernative hyperplasia pathogenesi

A

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
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30
Q
A

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
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31
Q
A
  • 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.

•

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32
Q

adenocarcinoma on left side of colon symptoms

A

occult blood in stool

change in powel habits

“napkin ring” tumors

obstruction uncommon

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33
Q

endoscopic gastroplasty

A

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

safe

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34
Q
A

micronodular cirrhosis

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35
Q
A

intraductal papillary mucinous neoplasm

pancreas

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36
Q

chronic cholecystitis

A

persistant inflammation of the gallbladder wall

almost always associated w gallstones

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37
Q
A

metastatic carcinoma

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38
Q
A

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
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39
Q

pathology and degrees of HCC

A
  • 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
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40
Q

mucinous cystic neoplasm

A

pancreas

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

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41
Q

histology of polyps in juvenile polyposis

A

dilated crypts filled w mucin and inflammatory debris

lamina propria expansion by mixed inflammatory infiltrate

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42
Q

angiosarcoma

A
  • 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

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43
Q
A

mucinous adenocarcinoma

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44
Q

syndrome criteria for juvenile polyposis

A

more than five juvenile polyps in the colon or erectum

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45
Q

Types of vascular lesions

A
  • 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
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46
Q
A

HCV

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.

•

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47
Q
A

villous adenoma

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48
Q

pathogenesis of focal nodular hyperplasia

A

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
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49
Q
A

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.
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50
Q

cholangitis

A

bacterial infection in the bile ducts

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51
Q
A

•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

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52
Q

pathogenesis of hemangioma

A
  • 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
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53
Q
A

HBV

  • 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].

•

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54
Q

pathology of metastatic carcinoma

A

mult nodular metastases causing hepatomegaly

central necrosis (outgrow blood supply)

cells usually resemble primary (not hepatic) tissue

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55
Q

histology of polyps in peutz-jeghers

A

large, pedunculatd

arborizing network of CT, SM, glands with normal epithelium

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56
Q
A

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.
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57
Q
A

angiosarcoma

  • 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
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58
Q

intramucosal carcinoma in adenoma

A

lamina propria invasion

little or no metastatic potential

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59
Q

cholelithiasis

A

gallstones

within lumen of gallbladder or in extrahepatic billiary tree

most are non symptomatic

made of cholesterol or pigmented (Ca-bilirubin)

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60
Q

Attenuated FAP

A

fewer polyps (average 30)

50% lifetime risk

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61
Q

sessile serrated adenoma location and etiology

A

right colon!

50-60, asymptomatic

neoplastic

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62
Q

etiology of chronic pancreatitis

A

chronic alcoholism

long standing obstruction

autoimmune disease

idiopathic

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63
Q
A
  • 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
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64
Q

high grade dysplasia - carcinoma in situ (in adenoma)

A

does not metastasize, clinically benign

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65
Q

hepatocellular adenoma

A
  • This is also well-demarcated, but there is no central scar
  • capsulated!! unlike FNH

neoplastic!!

  • 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

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66
Q

adenoma polyps histo

A

epithelial dysplasia

nuclear hyperchromasia

elongation and stratification

sessile or pedunculated

tubular, tubulovillous, villous

neoplastic

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67
Q

most common primary sites of metastatic carcinoma of the liver

A

colon, breast, lung

any cancer in any site except leukemia and lymphoma

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68
Q

intraductal papillary mucinous neoplasm

A

pancreas

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

69
Q

most common mutation in sporadic colon cancer?

A

APC - left sided!!

70-80%

70
Q

ballooning degeneration

A

hepatocyte swelling by failed osmoregulation

rupturing of hepatocyte

71
Q

dietary factors in adenocarcinoma

A

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

72
Q

microsattelite instability

A

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
73
Q
A

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
74
Q

familial adenomatous polyposis mutation

A

APC gene

75
Q

How does alcoholism lead to HCC?

A
  • 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
76
Q

intrahepatic cholangiocarcinoma

A

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
77
Q

anal intraepithelial neoplasia

A

AID

HPV

neoplastic proliferation of squamous cells confied to anal mucosa

high N/C ratio

desaturation

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

78
Q
A

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
79
Q

colonic adenocarcinoma

A

most common malignancy of the GI tract

2nd to lung cancer deaths in US

peaks in 60s and 70s

80
Q

management if carcinoma occurs in a pedunculated adenoma?

A

endoscopic polpectomy adequat if :

superficial tumor not close to margin

no vascular/lymph invasion

not poorly differentiated

81
Q
A

serous cystadenoma

pancreas

82
Q
A

tubular adenoma

colon

83
Q

hyperplastic polyps histo

A

serration in the upper third

mature goblet cells and absorptive cells

non neoplastic

84
Q

bile duct adenoma

A

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
85
Q

2 pathways of colorectal carcinogenesis

A

APC/Beta catenin –> chromosomal instability

DNA mismatch repair –> microsatellite instability

stepwise accumulation of multiple mutatios

86
Q

histo of drug toxicity

A

central necrosis or diffuse necrosis (need transplant or die)

lobular inflammation

parenchymal necrosis

bile duct damage and prolf

87
Q

tubular adenoma

A

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

88
Q
A

PSC

peri-ductal or onion skinning

89
Q

histology of fulminant hepatitis

A
  • 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

•

90
Q

colon polyp?

A

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

91
Q

labs increased in hepatocellular injury/hepatitis

A

transaminases and bili

viruses, alcohol, drugs, metabolic

92
Q

chronic pancreatitis

A

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

93
Q
A

sqamous cell carcinoma

increasing incidence

HPV

lymph node metastasis

94
Q

what is the most common syndromic form of colorectal cancer?

A

HNCCS

herediatry nonpolyposis colorectal cancer syndrome

95
Q

cholelithiasis factors and mech

A

cholestrol supersaturation

  • high Ch output
  • decreased bile acid synthesis
  • gallbladder hypomobility
  • excessive mucus
96
Q

pathogenesis of HCC

A

–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

97
Q

complications of chronic pancreatitis

A

pleural effusions

pseudocyst

diabetes

fat malabsprotton

stones in panc duct

pancreatic calcification

pain from perineural fibrosis

98
Q
A

ascending colon polyp

smooth, rounded protrusion above the surrounding mucosa

99
Q

Treatment of HCC

A
  • 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.
100
Q

labs in billiary tract injury

A

alk phos, GGT, bili increased

drugs, congen, metabolic, immune, trauma

101
Q

kuppfer cells

A
  • 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

•

•

102
Q

mechamism of acute pancreatitis for chronic pancreatitis

A

necrosis and fibrosis

repeated episodes of acute panc

103
Q

Major differences between FNH and Hepatic Adenoma

A
  • 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
104
Q

acinar cell carcinoma

A

pancreas

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

105
Q

peutz-jeghers

A

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

intussusception

106
Q

adenocarcinoma on right side of colon symptoms

A

fatigue

iron deficiency

mass

obstruction uncommon

107
Q

pedunculated polyps

A

tumoral masses or nodules which project into the lumen

have a stalk

epithelial lesions

108
Q

mallory hyaline

A

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

109
Q

clinical course of angiosarcoma

A

aggressive - high rate of metstases

20% survival at 5 years

110
Q

extrahepatic cholangiocarcinoma

A

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
111
Q

what is concisdered a hamartomous polyp?

tubulovillous adenoma

cloacogenic polyp

sessile serrated adenoma

juvenile polyp

A

juvenile polyp

112
Q

clinical course of focal nodular hyperplasia

A

usually asymptomatic/incidental

mild abdominal symptoms

can rupture

no malignant potential

113
Q

histology of ductal adenocarcinoma

A

tubular structures in abundant desmoplastic stroma

solid firm infiltrative tumors w ill defined borders

114
Q

acidophil body

A

a single apoptotic hepatocyte

in acute hepatitis

115
Q

focal nodular hyperplasia

A

well-circumscribed lesion with a central scar

central grey-white depressed stellate scar

lympocytic infiltrates

normal hepatocytes!!

no association w cirrhosis

116
Q

pancreatic neuroendocrine tumors (PEN)

A

clinically - attacks of hypoglycemia, CNS system manivestation

90% benign

functional - hormone production (insulin, glucagon, somatostatin)

nonfunctional - larger lesions at diagnosis

malignancy - mitotic activity

117
Q

hyperplasia

A
  • 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)

118
Q

Nodular Regernerative Hyperplasia

A

•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
119
Q
A
  • 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
120
Q

risk for pigment gallstomes

A

biliary infection

ileal disease (crohn, resection, CF)

121
Q

choledocholithiasis

A

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

122
Q

Classic FAP

A

100-2500 tubular adenomas

100% risk of carcinoma

early detection, prophylactic colectomy

123
Q

clinical course of hepatocellular adenoma

A

asymptomatic or abdominal symptoms

intrahepatic mass mistaken for the carcinoma

can rupture

rare association with hepatocellular carcinoma

124
Q

carcinoma of the gallbladder

A

rare, poor survival (1%)

major risk factors: gallstones, crhonic infection

adenocarcinoma

125
Q

What is the most common malignancy in the liver?

A

metastatic disease

126
Q

sessile serated adenoma histo

A

serration throughout the full length of the crypt

lined by goblet cells wihtout cytologic features of dysplasia

neoplastic

127
Q
A

acute cholecystitis

serosal congestion, fibrinous exudates, edema

red purple mucosa edema necrosiss

128
Q

serous cystadenoma

A

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

VHL

129
Q

cronkhite-canada syndrome

A

polyp syndrome - non neoplastic

nonherediatry! unknown cause

polyps in stomach and small colon

diffusely nodular mucosa

130
Q

mechanism of alcohol for chronic pancreatitis

A

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

131
Q

Types of hepatocellular lesions

A

adenoma - benign

carcinoma - malignant

132
Q

chromosomal instability

A

gatekeeper pathway

CIN

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
133
Q

clinical features of chronic pancreatitis

A

repeated episodes of severe abdominal pain

persistant abdominal and back pain

recurrent attacks of jaundice

vague attacks of indigestion

weight loss

134
Q
A

chronic cholecystitis

chronic inflam and fibrosis of the wall

135
Q
A

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
136
Q

Histology of PSC

A

periductal or onion skinning fibrosis

137
Q
A

mucinous cystic neoplasm

pancreas

138
Q

choledochal cyst

A

gallbladder

congenital dilations

can lead to obstructive jaundice, pain, abdominal mass

139
Q

adenoma polyps etiology and location

A

30% of adults by age 50

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

neoplastic

140
Q

most important prognostic factor for CRC?

A

depth of invasion and lymph node metastasis

early detection and resection is a curative therapy

141
Q

inflammatory polyps mechanism, etiology and location

A

age 20-50

excessive straining, rectal bleeding, mucus discharge

anterior rectal wall - prior injury and healing

non neoplastic

142
Q
A

•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
143
Q
A
  • 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
  • Macroscopic:
  • 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
  • Microscopic:
  • Virtually all consist of vascular spaces
  • These are mostly venous-type
144
Q

pancreas:

A

chronic pancreatitis

fibrosis

reduced number of acini

chronic inflam infiltrate

enlarged persistent islets

dilated ducts w proteinaceous material

145
Q

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

inflam

cloacogenic

hyperplastic

tubular adenoma

A

tubular adenoma

146
Q

possible outcomes of liver injury

A

recovery

hepatic failure

fibrosis (scarring0

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

147
Q

management if carcinoma in a sessile adenoma

A

endoscopic polypectomy is inadequate –> surgery

148
Q

Clinical course of nodular regernative hyperplasia

A
  • 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
149
Q

metastatic patterns of colon cancer

A

lymph nodes

liver

lung

bone

150
Q
A

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.
151
Q
A

•Grossly:

  • 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

•Histology:

  • 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
152
Q

villous adenoma

A

larger and more ominous than tubular adenoma

rectum and rectosigmoid

sessile

finger like extension

all degrees of dysplasia

carcinoma will directly invade the bowel wall

153
Q

duodenal sleeve

A

malabsorption procedure

duodeno-jejunal bypass sleeve

open at both ends

food can pass but sleeve prevents contact w duodenum

delays digestions

154
Q

histology of acute hepatitis

A
  1. portal and interface inflammation (portal tract filled w lymphocytes)
  2. lobular inflammation
  3. bile duct damage
  4. no significant fibrosis
155
Q

serum/infiltrate in autoimmune chronic pancreatitis

A

IgG4 infiltrate and in serum

ANA

156
Q

aspirin in CRC

A

inhibit COX2 - decrease production of prostaglandin - promotes epithelial proliferation

157
Q

autoimmune chronic pancreatitis

A

lymphoplasmacytic sclerosing pancreatitis

mass like lesions and irregular beading of the pancreatic duct

associated w autoimmune conditions

158
Q

mutations in Lynch syndrome

A

loss of MSH2, MSH6

HNPCC = germline MLH1, MSH2

159
Q
A

macronodular cirrhosis

160
Q

risk factors for pancreatic ductal adenocarcinoma?

A

age - 60-80

black, ashkenazi

smoking = double risk

high fat and meat diet, BMI

chronic pancreatitis

diabetes

161
Q

symptoms of ductal adenocarcinoma

A

jaundice, back pain, weight loss

162
Q
A
  • 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
163
Q

small bowel neoplasm

A

malignant tumors are far less common in SB than everywhere else

can have peutz jeghers or adenomas

164
Q

syndrome criteria for peutz-jeghers syndrome

A

mucocutaneous lesions, patches of hyperpigmentation

165
Q

alpha-fetoprotein

A

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
166
Q

histo of acinar carcinoma

A

solid nests, acini, scant stroma

large solid well circomscribed w extensive necrosis

167
Q

Cowden syndrome

A

mult non cancerous hamartomas in skin, mucus membranes

multiple discrete sessile polyp lesions

risk of colon cancer = gen population

168
Q
A

cholangeocarcinoma

  • 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

GI2 (7 decks)

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