Path Flashcards

Question

Histo in cowden syndrome

Answer 1

stroma rich polyp with cystically dilated crypts risk of colon cancer = gen pop

Answer 2

chronic pancreatitis pancreas is hard w extremely dilated ducts and visible calcifications

Answer 3

hematochromatosis ## Footnote * 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].

Answer 4

* 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

Answer 5

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

Answer 6

nodular regenerative hyperplasia ## Footnote * 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

Answer 7

* 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. •

Answer 8

occult blood in stool change in powel habits "napkin ring" tumors obstruction uncommon

Answer 9

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

Answer 10

micronodular cirrhosis

Answer 11

intraductal papillary mucinous neoplasm pancreas

Answer 12

persistant inflammation of the gallbladder wall almost always associated w gallstones

Answer 13

metastatic carcinoma

Answer 14

portal fibrosis stage 1 ## Footnote * , 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

Answer 15

* 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

Answer 16

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

Answer 17

dilated crypts filled w mucin and inflammatory debris lamina propria expansion by mixed inflammatory infiltrate

Answer 18

* 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

Answer 19

mucinous adenocarcinoma

Answer 20

more than five juvenile polyps in the colon or erectum

Answer 21

* 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

Answer 22

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. •

Answer 23

villous adenoma

Answer 24

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

Answer 25

budd chiari syndrome and veno-occlusve disease ## Footnote * 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.

Answer 26

bacterial infection in the bile ducts

Answer 27

•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

Answer 28

* 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

Answer 29

HBV ## Footnote * 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]. •

Answer 30

mult nodular metastases causing hepatomegaly central necrosis (outgrow blood supply) cells usually resemble primary (not hepatic) tissue

Answer 31

large, pedunculatd arborizing network of CT, SM, glands with normal epithelium

Answer 32

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.

Answer 33

angiosarcoma ## Footnote * 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

Answer 34

lamina propria invasion little or no metastatic potential

Answer 35

gallstones within lumen of gallbladder or in extrahepatic billiary tree most are non symptomatic made of cholesterol or pigmented (Ca-bilirubin)

Answer 36

fewer polyps (average 30) 50% lifetime risk

Answer 37

right colon! 50-60, asymptomatic neoplastic

Answer 38

chronic alcoholism long standing obstruction autoimmune disease idiopathic

Answer 39

* 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

Answer 40

does not metastasize, clinically benign

Answer 41

* 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

Answer 42

epithelial dysplasia nuclear hyperchromasia elongation and stratification sessile or pedunculated tubular, tubulovillous, villous neoplastic

Answer 43

colon, breast, lung any cancer in any site except leukemia and lymphoma

Answer 44

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

Answer 45

APC - left sided!! 70-80%

Answer 46

hepatocyte swelling by failed osmoregulation rupturing of hepatocyte

Answer 47

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

Answer 48

**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

Answer 49

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

Answer 50

* 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

Answer 51

less common (8-13%) ## Footnote * 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

Answer 52

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)

Answer 53

cirrhosis = stage 4 of fibrosis ## Footnote * 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

Answer 54

most common malignancy of the GI tract 2nd to lung cancer deaths in US peaks in 60s and 70s

Answer 55

endoscopic polpectomy adequat if : superficial tumor not close to margin no vascular/lymph invasion not poorly differentiated

Answer 56

serous cystadenoma pancreas

Answer 57

tubular adenoma colon

Answer 58

serration in the upper third mature goblet cells and absorptive cells non neoplastic

Answer 59

benign, no treatment - incidental finding! ## Footnote * 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

Answer 60

APC/Beta catenin --\> chromosomal instability DNA mismatch repair --\> microsatellite instability stepwise accumulation of multiple mutatios

Answer 61

central necrosis or diffuse necrosis (need transplant or die) lobular inflammation parenchymal necrosis bile duct damage and prolf

Answer 62

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

Answer 63

PSC peri-ductal or onion skinning

Answer 64

* 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 •

Answer 65

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

Answer 66

transaminases and bili viruses, alcohol, drugs, metabolic

Answer 67

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

Answer 68

sqamous cell carcinoma increasing incidence HPV lymph node metastasis

Answer 69

HNCCS herediatry nonpolyposis colorectal cancer syndrome

Answer 70

cholestrol supersaturation - high Ch output - decreased bile acid synthesis - gallbladder hypomobility - excessive mucus

Answer 71

–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

Answer 72

pleural effusions pseudocyst diabetes fat malabsprotton stones in panc duct pancreatic calcification pain from perineural fibrosis

Answer 73

ascending colon polyp smooth, rounded protrusion above the surrounding mucosa

Answer 74

* **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.

Answer 75

alk phos, GGT, bili increased drugs, congen, metabolic, immune, trauma

Answer 76

* 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 • •

Answer 77

necrosis and fibrosis repeated episodes of acute panc

Answer 78

* 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

Answer 79

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

Answer 80

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

Answer 81

fatigue iron deficiency mass obstruction uncommon

Answer 82

tumoral masses or nodules which project into the lumen have a stalk epithelial lesions

Answer 83

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

Answer 84

aggressive - high rate of metstases 20% survival at 5 years

Answer 85

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

Answer 86

juvenile polyp

Answer 87

usually asymptomatic/incidental mild abdominal symptoms can rupture **no malignant potential**

Answer 88

tubular structures in abundant desmoplastic stroma solid firm infiltrative tumors w ill defined borders

Answer 89

a single apoptotic hepatocyte in acute hepatitis

Answer 90

well-circumscribed lesion with a central scar central grey-white depressed stellate scar lympocytic infiltrates normal hepatocytes!! no association w cirrhosis

Answer 91

clinically - attacks of hypoglycemia, CNS system manivestation 90% benign functional - hormone production (insulin, glucagon, somatostatin) nonfunctional - larger lesions at diagnosis malignancy - mitotic activity

Answer 92

* 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)**

Answer 93

•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

Answer 94

* 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

Answer 95

biliary infection ileal disease (crohn, resection, CF)

Answer 96

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

Answer 97

100-2500 tubular adenomas 100% risk of carcinoma early detection, prophylactic colectomy

Answer 98

asymptomatic or abdominal symptoms intrahepatic mass mistaken for the carcinoma can rupture rare association with hepatocellular carcinoma

Answer 99

rare, poor survival (1%) major risk factors: gallstones, crhonic infection adenocarcinoma

Answer 100

metastatic disease

Answer 101

serration throughout the full length of the crypt lined by goblet cells wihtout cytologic features of dysplasia neoplastic

Answer 102

acute cholecystitis serosal congestion, fibrinous exudates, edema red purple mucosa edema necrosiss

Answer 103

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**

Answer 104

polyp syndrome - non neoplastic nonherediatry! unknown cause polyps in stomach and small colon diffusely nodular mucosa

Answer 105

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

Answer 106

adenoma - benign carcinoma - malignant

Answer 107

**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

Answer 108

repeated episodes of severe abdominal pain persistant abdominal and back pain recurrent attacks of jaundice vague attacks of indigestion weight loss

Answer 109

chronic cholecystitis chronic inflam and fibrosis of the wall

Answer 110

bile duct adenoma ## Footnote * 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

Answer 111

periductal or onion skinning fibrosis

Answer 112

mucinous cystic neoplasm pancreas

Answer 113

gallbladder congenital dilations can lead to obstructive jaundice, pain, abdominal mass

Answer 114

30% of adults by age 50 60-75% distal to splenic flexure, more proximal with age neoplastic

Answer 115

depth of invasion and lymph node metastasis early detection and resection is a curative therapy

Answer 116

age 20-50 excessive straining, rectal bleeding, mucus discharge anterior rectal wall - prior injury and healing non neoplastic

Answer 117

•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

Answer 118

* 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

Answer 119

chronic pancreatitis fibrosis reduced number of acini chronic inflam infiltrate enlarged persistent islets dilated ducts w proteinaceous material

Answer 120

tubular adenoma

Answer 121

recovery hepatic failure fibrosis (scarring0 cirrhosis (diffuse fibrotic process through liver w formation of nodules and regen hepatocytes surrounded by bands of fibrosis

Answer 122

endoscopic polypectomy is inadequate --\> surgery

Answer 123

* 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

Answer 124

lymph nodes liver lung bone

Answer 125

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.

Answer 126

**•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

Answer 127

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

Answer 128

malabsorption procedure duodeno-jejunal bypass sleeve open at both ends food can pass but sleeve prevents contact w duodenum delays digestions

Answer 129

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

Answer 130

IgG4 infiltrate and in serum ANA

Answer 131

inhibit COX2 - decrease production of prostaglandin - promotes epithelial proliferation

Answer 132

lymphoplasmacytic sclerosing pancreatitis mass like lesions and irregular beading of the pancreatic duct associated w autoimmune conditions

Answer 133

loss of MSH2, MSH6 HNPCC = germline MLH1, MSH2

Answer 134

macronodular cirrhosis

Answer 135

age - 60-80 black, ashkenazi smoking = double risk high fat and meat diet, BMI chronic pancreatitis diabetes

Answer 136

jaundice, back pain, weight loss

Answer 137

* 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

Answer 138

malignant tumors are far less common in SB than everywhere else can have peutz jeghers or adenomas

Answer 139

mucocutaneous lesions, patches of hyperpigmentation

Answer 140

increased in serum in 50-75% of patients w HCC ## Footnote * 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

Answer 141

solid nests, acini, scant stroma large solid well circomscribed w extensive necrosis

Answer 142

mult non cancerous hamartomas in skin, mucus membranes multiple discrete sessile polyp lesions risk of colon cancer = gen population

Answer 143

cholangeocarcinoma ## Footnote * 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