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Gastrointestinal 3 > Pathology > Flashcards

Pathology Flashcards

1
Q

This is a sudden liver illness that is associated with encepthalopathy within 6 months after the initial Dx.

A

Acute liver failure.

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2
Q

This form of acute liver failure is when the encephalopahy develops within 2 weeks of the onset of jaundice.

A

Fulminant liver failure

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3
Q

This form of acute liver failure is when the enceopahlopathy develops within 2 months of the onset of jaundice.

A

Sub-fulminant liver failure

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4
Q

What is the main pathological change in acute liver failure?

A

massive hepatic necrosis

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5
Q

Which drug accounts for 50% of cases of acute liver failure?

A

acetaminophen

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6
Q

Which hepatitis viruses can lead to acute liver failure?

A

HAV, HBV, and HCV

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7
Q

This is the most common cause of hepati failure and is the end point of relentless long term hepatitis ending in cirrhosis.

A

Chronic liver disease

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8
Q

This is the condition when the hepatocytes remain viable but are unable to perform normal metabolic fxn.

A

Hepatic dysfxn without overt necrosis

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9
Q

Generally, this is the failure of the hepatocytes to perform their homeostatic functions.

A

Hepatic failure.

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10
Q

The elevation of what substance in the blood and CNS contributes to hepatic encephalopathy?

A

ammonia levels

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11
Q

What are some common neurological manifestations of hepatic encephalopathy?

A

Rigidity, hyperreflexia, and asterixis

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12
Q

Which cells swell in the brain that may not just be a minor morphological change?

A

astrocytes

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13
Q

True or False: encephalopathy is reversible if the underlying hepatic condition is corrected.

A

True!

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14
Q

This is the condition where there is renal failure in individuals with severe chronic liver disease.

A

Hepatorenal syndrome.

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15
Q

What is the main contributor that causes hepatorenal syndrome?

A

Decreased renal blood flow

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16
Q

What will change with the urine output in hepatorenal syndrome?

A

It’ll decrease

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17
Q

In hepatorenal syndrome, which 2 substances increase in teh blood?

A

BUN and creatinine

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18
Q

This condition is characterized by the triad of chronic liver disease, hypoxemia, and IVPD.

A

hepatopulmonary syndrome (HPS)

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19
Q

In HPS, which mediator is produced more in the lung?

A

NO

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20
Q

What are the 2 main manifestations for HPS?

A

orthodeoxia and platypnea

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21
Q

These are delicate bands or broad scars linking portal tracts with 1 another in cirrhosis.

A

Bridging fibrous septa

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22
Q

These are nodules containing hepatocytes encircled by fibrosis in cirrhosis.

A

Parenchymal nodules

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23
Q

True or False: focal injury with scarring consitutes cirrhosis.

A

FALSE. the parenchymal injury and fibrosis is diffuse.

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24
Q

This condition is the triad of hepatocyte death, ECM deposition, and vascular reorganization.

A

Cirrhosis

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25
Q

What do you lose in cirrhosis which leads to intrasinusoidal HTN?

A

fenestrations of sinusoidal endothelial cells.

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26
Q

Which cells proliferate and are activated, which is the predominant mechnaism of fibrosis in cirrhosis?

A

hepatic stellate cells

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27
Q

Hepatic stellate cells are activated into what cells as a result of PDGFR-beta?

A

myofibroflasts

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28
Q

Portal HTN, hypoalbuminemia, and hyperaldosteronism can lead to what condition where there is excess fluids in the peritoneal cavity?

A

Ascites

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29
Q

True or False: the concentration of solutes in ascites is similiar to that of the blood.

A

True.

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30
Q

This is the condition when a rise is portal system pressure causes reversal of the flow from portal to the systemic circulation.

A

Portosystemic venous shunts

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31
Q

What are the 3 main varices that can result from portsystemic venous shunts?

A

hemorrhoids, esophageal varices, and caput madusae

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32
Q

Long-standing congestion can cause enlargement of what organ?

A

Spleen

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33
Q

What secondary things might be caused when a pt has congestive splenomegaly?

A

hypersplenism with various cytopenias

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34
Q

Bilirubin overproduction, hepatitis, and bile obstruction can all cause what condition?

A

Jaundice.

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35
Q

True or False: unconjugated bilirubin is insoluble in water at physiological pH and cannot be excreted in the urine.

A

True

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36
Q

This is the hemolytic disease of the newborn as a result of an accumulation of unconjugated bilirubin in the brain.

A

Kernicterus

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37
Q

So what form of bilirubin can be excreted in the urine because it’s loosely bound to albumin?

A

Conjugated form

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38
Q

Almost every newborn develops what kind of hyperbilirubinemia?

A

mild unconjugated hyperbilirubinemia

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39
Q

Why can mild unconjugated hyperbilirubinemia in infants be exasterbated by breastfeeding?

A

cuz theres bilirubin-deconjugating enzymes in boob milk

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40
Q

This genetic hyperbilirubinemia is when a UGT1A1 absence causes colorless bile and serum unconjugated bilirubin reaches a very high level.

A

Crigler-Najjar Syndrome Type I

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41
Q

This genetic hyperbilirubinemia is a less severe form of CNS type I, where the UGT1A1 is reduced and can only form monoglucuronidated bilirubin.

A

Crigler-Najjar Syndrome Type II

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42
Q

What does a pt with Crigler-Najjar Syndrome Type I die of in 18 months?

A

Kericterus

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43
Q

This genetic hyperbilirubinemia is a benign condition where there is a mild, fluctuating hyperbilirubinemia because hepatic bilirubin-glucuronidating activity is only 30% of normal.

A

Gilbert syndrome

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44
Q

This AR hyperbilirubinemia is characterized by chronic conjugated hyperbilirubinemia from a defect in hepatocellular excretion of bilirubin glucuronides from the canalicular membrane.

A

Dubin-Johnson Syndrome

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45
Q

Why is the liver darkly pigmented in DJS?

A

from inclusions of bilirubin glucuronides in the cytoplasm of hepatocytes

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46
Q

This rare hyperbilirubinemia is characterized by asymptomatic conjugated hyperbilirubinemia, normal liver morphology, and chronic jaundice.

A

Rotor Syndrome.

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47
Q

This is a pathological condition of impaired bile formation and bile flow, causing an accumulation of bile pigment in the hepatic parenchyma

A

Chelestasis

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48
Q

Whether it’s extra or intra-hepatic causation of cholestasis, what 2 serum enzymes are elevated?

A

alkaline phosphatase & γ-glutamyl transpeptidase (GGT)

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49
Q

What is the appearance of the hepatocytes when dropets of bile pigment accumulates within them?

A

Fine and foamy appearance (feathery degeneration)

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50
Q

Progressive Familial Intrahepatic Colestasis (PFIC) has what type of genetic inheritance?

A

AR

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51
Q

In PFIC-1, when do u get liver failure?

A

before adulthoold

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52
Q

What is the mutated gene in PFIC-1?

A

ATP8B1

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53
Q

True or False: there is decreased GGT activity in PFIC-1.

A

False. it’s pretty much normal

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54
Q

What is the structure that is mutated in PFIC-2?

A

bile salt export pump

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55
Q

Which gene is mutated to cause PFIC-2?

A

ABCB11

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56
Q

True or False: there are normal levels of GGT in PFIC-2.

A

True

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57
Q

When do pt’s progress to cirrhosis in PFIC-2 in their life?

A

in the first decade of life.

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58
Q

Which cancer are PFIC-2 pt’s at risk for?

A

cholangiocarcinoma

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59
Q

Which gene is mutated to cause a defect in the protein MDR3 in PFIC-3?

A

ABCB4

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60
Q

True or False: there are normal levels of GGT in PFIC-3.

A

False. They are high.

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61
Q

Why are serum GGT levels high in PFIC-3?

A

because of an absence of secreted physphatidylcholine in the bile.

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62
Q

What is the cancer associated with HBV?

A

primary hepatocellular carcinoma

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63
Q

This the the name for the empty cytoplasm with scattered eosinophilic remnants in acute hepatitis.

A

Ballooning degeneration

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64
Q

Which calls undergo hypertrophy and hyperplasia as an inflammatory response in acute hepatitis?

A

Kupffer cells

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65
Q

What is the hallmark of chronic hepatitis?

A

deposition of fibrous tissue

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66
Q

This is a chronic and progressive form of hepatitis which is attributed to T-cell-mediated autoimmunity.

A

Autoimmune hepatitis

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67
Q

What 3 things can trigger an autoimmune hepatitis condition?

A

viral infections, drugs, and herbal products.

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68
Q

What are elevated in serum panels for autoimmune hepatitis?

A

IgG autoantibodies

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69
Q

This type of autoimmune hepatitis has a presence of ANA, SMA, AAA, and anti-SLA/LP antibodies.

A

Type 1 autoimmune hepatitis

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70
Q

What 2 things are present in type 2 autoimmune hepatitis?

A

ALKM-1 and ACL-1

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71
Q

Which WBC is present in the portal tracts and hepatic lobules in autoimmune hepatitis?

A

Plasma cells

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72
Q

Chronic drug-induced liver disease is histologically indistinguishable from what other disease?

A

chronic viral hepatitis

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73
Q

So how can u distinguish the 2?

A

serological markers for viral or drug induced hepatitis

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74
Q

What is the most common cause of drug induced acute liver failure?

A

Acetaminophen

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75
Q

This is a rare and potentially fatal syndrome of mitochondrial dysfxn of the liver, brain, and elsewhere after administration of aspirin

A

Reye syndrome

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76
Q

What types of pt’s are at risk for reye syndrome?

A

kids

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77
Q

What is the histological appearance of the hepatocytes in reye syndrome?

A

extensive accumulation of fat droplets within hepatocytes

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78
Q

Hepatic steatosis, alcoholic hepatitis, and cirrhosis are all factors which make up which condtion?

A

alcholic liver disease

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79
Q

This is the condtion where there are clear macrovesicular globules that compress and displace the hepatocyte nucleus.

A

Hepatic steatosis

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80
Q

What is the morphology of the liver in hepatic steatosis?

A

leargy, heavy, yellow, and greasy

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81
Q

This condition is where there is hepatocyte swelling and necrosis from chemical injruy to hepatocytes, typically after binge drinking.

A

Acoholic hepatitis

82
Q

What are the names of the scattered eosinophilic cytoplasmic clumps of cytoketatin within hepatocytes in alcholic hepatitis?

A

Mallory bodies

83
Q

Which WBC surrounds the mallory bodies in alcholic hepatitis?

A

Neutrophils

84
Q

True or False: in cirrhosis, the liver initially is large and fatty but then turns into a brown shrunken nonfatty light liver.

A

True.

85
Q

What type of tissue gets laid down in cirrhosis to cause the “hobnail” appearance on the surface of the liver?

A

fibrous tissue

86
Q

True or False: men are more susceptible to hepatic injury than women.

A

False. Women > men

87
Q

True or False: African Americans are less susceptible to hepatic injury than men.

A

False. They are more.

88
Q

Which gene can be mutated to cause a lack of intolerance to alcohol? (lol Asians)

A

ALDH

89
Q

These are a group of condtions which have a presence of hepatic steatosis in individuals who do not consume alcohol or do so in small quantities.

A

Nonalcoholic fatty liver disease (NAFLD)

90
Q

What is the progressive form of NAFLD called?

A

Non-alcoholic steatohepatitis (NASH)

91
Q

Where do u see fibrosis in NASH?

A

portal tracts aroudn the terminal hepatic venules

92
Q

This condition is characterized by excessive accumulation of body iron, most of which is depositied in the liver and the pancreas.

A

Hemochromatosis

93
Q

What is the mechanism for the overload of Fe to cause hemochromatosis?

A

excessive iron absorption

94
Q

This condtion is an accumulation of Fe in tissues, which occurs because of parental administration of Fe usually in the form of transfusions.

A

hemosiderosis

95
Q

Which protein, which is encoded by the HAMP gene, is the main regulator of Fe absorption, which can cause hemocrhomatosis?

A

hepcidin

96
Q

What does hepcidin do tot he cellulear Fe efflux channel ferroportin (FPN) to cause hemochromatosis?

A

binds to it and internalizes and proteolysis it

97
Q

So if you lack hepcidin, what happens to Fe levels?

A

overload cuz the Fe efflux channels are never internalized and constantly spit Fe into the plasma.

98
Q

What is the morphology of the liver in hemochromatosis?

A

golden-yellow hemosiderin granules are in the cytoplasm of hepatocytes. fibrosis. cirrhosis in a intensly pigmented liver

99
Q

What is the triad of Sx in hemochromatosis?

A

hepatomegaly, skin pigmentation, and DM

100
Q

This condition is an AR disorder where there is impaired Cu excretion into bile and a failure to incorporate Cu into ceruloplasmin.

A

Wilson disease

101
Q

Where does Cu accumulate in Wilsons?

A

liver, brain, and eye mainly.

102
Q

What is the fxn of ceruloplasmin?

A

used in the blood to carry Cu to the liver where it is degrades and the Cu is excreted in the bile.

103
Q

What is the morphology of the lvier in Wilson disease?

A

steatosis with vacuolated nuclei (glycogen or water) and occasionally focal hepatocyte necrosis

104
Q

Though Wilsons can look axactly like acute viral hepatitis, what is the different change in wilsons that isnt in acute viral hepatitis?

A

fatty change.

105
Q

Will ceruloplasmin levels in Wilsons be high or low?

A

low

106
Q

What is the name of the ring that forms aorudn the eyes in Wilsons?

A

Kayser-Fleisher rings

107
Q

The defciciency in this protein can cause pulmonary emphysema as well as liver disease.

A

Alpha 1-antitrypsin (A1AT)

108
Q

What are the types of inclusions in hepatocytes in A1AT deficiency?

A

Round-oval cytoplasmic globular inclusions, which are acidophilic, PAS+

109
Q

At this age, 10-20% of individuals present with cholestatic jaundice in A1AT deficiency.

A

Newborns

110
Q

This form of hepatitis has focal liver cell apoptosis and necrosis, giant cells, and a parenchymal pattern of injury, typicall in kids.

A

Neonatal hepatits

111
Q

This intrahepatic biliary tract disease is characterized by a course fiberous septa that subdivide the liver in a jigsaw like pattern, and has feathery degeneration and formation of bile lakes.

A

Secondary biliary tract disease

112
Q

What is the main cause of secondary biliary tract disease?

A

bile duct obstruction.

113
Q

Which levels of serum proteins are high in secondary biliary tract disease?

A

conjugated hyperbiliruninemia, increased alk phos, bile acids, and cholesterol.

114
Q

What are the Sx to secondary biliary tract disease?

A

prutitus, jaundic, malaise, dark urine, light stools, hepatosplenomegaly.

115
Q

This intrahepatic biliary tract disease is characterized by autoimmune destruction of the bile ducts.

A

Primary biliary cirrhosis

116
Q

Since the bile ducts are destroyed in primary biliary cirrhosis, what histological changes can u see?

A

noncaseating granulomatous inflmmation

117
Q

This intrahepatic biliary tract disease is characterized by an uknown etiology that cuases periductal portal tract fibrosis, with an onion-like appearance of the ducts.

A

Primary Sclerosis Cholangitis

“Penn State Cries because of onions”

also, penn state is a cult. srsly.

118
Q

In this condition, the larger ducts of the intrahepatic biliary tree are segmentally dilated and many contain inspissated (thickened) bile.

A

Caroli disease.

119
Q

In this condition, R sided cardialc decompensation can cause an enlarged, tense, and cyanotic liver.

A

Passive congestion of the liver

120
Q

In this condition, L sided cardiac failure or shock leads to hepatic hypoperfusion and hypoxia, leading to ischemic coagulative necrosis of hepatocytes.

A

Centrilobilar necrosis

121
Q

In this condtion, a combination of hypoperfusion and retrograde congestion causes a mottled appearance reflexing hemorrhage and necrosis in the centrilobular regions (nutmeg).

A

Centrilobular hemorrhagic necrosis

122
Q

This condition is when sinusoidal dilation occurs when efflux of hepatic blood is impeded and can lead to blood-filled cystic spaces

A

Peliosis hepatis

123
Q

Peliosis hepatis is associated with what other conditions?

A

Cancer, TB, AIDS, post-transplant immunodeficiency, steroids, and rarely oral contraceptives.

124
Q

This condition results from obstruction of 2 or more major hepatic veins producing liver enlargement, pain, and ascites, lading to hepatic dmg.

A

Budd-Chiari syndrome.

125
Q

this is the condition where some of the small veins of the liver are obstructed, typically happeining within 3 wks of marrow transplantation.

A

Sinusoidal obstruction syndrome.

126
Q

In this condition, lympohocytes attack the epithelial cells of the liver, resulting in hepatitis with necrosis of hepatocytes and bile duct epithelial cells.

A

acute graft-vs-host disease.

127
Q

In acute graft-vs-host disease, when does the Sx occur after transplant?

A

10-50 days.

128
Q

In chronic graft-vs-host disease, how many days after transplant can u get portal tract inflammation and bile duct destructin?

A

> 100 days

this is so horrible. omg im dying.

129
Q

This is the condition which is characterized by maternal HTN, proteinuria, peripheral edema, coagulation abnormalities, and varying degrees of disseminated intravascular coagulation.

A

Pre-eclampsia

130
Q

This subsection of pre-eclampsia is characterized by hemolysis, eleveated liver enzymes, and low platelets

A

HELLP

131
Q

Women in their 3rd trimester are at risk for what condition, which can lead to hepatic failure, coma, and death?

A

Fatty liver

132
Q

Case: a chick on oral contraceptives is having a cholecyststectomy and you notice a well-demarcated but poorly encapsulated nodule about 6cm in diameter. What is is?

A

focal nodular hyperplasia

133
Q

Case: A young woman presents with cords and sheets of cells in an adenoma biopsy. Which complication could be life threatening for her?

A

Intraperitoneal Hemorrhage during pregnancy

134
Q

This benign neoplasn is when a tumor of a blood vessel and appears as a dsicrete red/blue, soft nodule usually <2cm in diameter.

A

Cavernous hemangioma

135
Q

THis benign neoplasm derives from hepatocytes, occurs more frequently in women who use contraceptives, and are yellow-tan nodules anywhere in the hepatic substance.

A

Hepatic adenomas

136
Q

This is the most common liver tumor of young childhood.

A

Hepatoblastoma

137
Q

What are the 3 forms of hepatocellular carcinomas?

A

unifocal mass, multifocal mass, diffusively infiltrative cancer.

138
Q

What are the 3 risk factors for hepatocellualr carcinomas?

A

chronic hepatitis, cirrhosis, anatoxins from aspergillus

139
Q

This is the 2nd most common HCC of the biliary tree, arising from bile ducts in and out of the liver.

A

Cholangiocarcinoma

140
Q

This type of gallstone is made of crystalline cholesterol monohydrate, and occur with MURICANS.

A

Cholesterol stones

141
Q

This type of gallstone is made of bilirubin Ca++ salts, and occur in non-muricans.

A

Pigment stones

142
Q

Fat fertile females over forty get which type of gallstones?

A

Cholesterol stones.

143
Q

What genetic disorder can u have mutated to cause cholesterol stones?

A

ATP-binding cassette (ABC) transporters

144
Q

Which medical conditions predispose u to pigmented stones?

A

chronic hemolytic syndromes, biliary infections, ileal disease, CF

145
Q

What are the 4 ways u can form cholesterol stones?

A

supersaturation, hypomotility, crystal nucleation, accetion within gallbladder mucous layer

146
Q

the release of what enzymes cause unconjugated bilirubin to increase, leading to pigmented stones?

A

microbial beta-glucoronidases

147
Q

What is the morphology of cholesterol stones?

A

pale yellow, round, glistening, can be severeal cm

148
Q

What is the morphology of black pigmented stones?

A

small, numerous, hard, crumble, radiopaque (cuz of Ca++ and phosphate)

149
Q

Under what conditions do u get brown stones?

A

in infected intrahepatic or extrahepatic ducts (black stones are when its sterile)

150
Q

What is the morphology of brown pigmented stones?

A

pure Ca++ salts of unconj bilirubin, laminated, soft, greasy, radiolucent.

151
Q

This type of acute cholecystitis is caused by chemical irritation and inflammation from gallbaldder obstruction in the absence of bacterial infection.

A

Acute calculous cholecystitis

152
Q

In what pt population is Acute calculous cholecystitis common?

A

diabetics

153
Q

This type of acute cholecystitis is caused by ischemia.

A

Acute acalculous cholecystitis

154
Q

What is unique to the cystic artery to cause acute acalculous cholecystitis?

A

it has no collateral citculation, so anything that causes inflammation can obstrcut the duct.

155
Q

What is the mophology of the gallbladder in acute cholecystitis?

A

large, thickened/edematous/hyperemic walls.

156
Q

What are the Sx of acute cholecystitis?

A

progressive RUQ pain + fever, anorexia, tachycardia, N/V

157
Q

True or False: in chronic cholecystitis, there still has to be obstruction of the gallbladder outflow to cause the pathology.

A

False. it is not a requisite.

158
Q

What happenes to bile to cause chronic cholecysitits?

A

supersaturation

159
Q

What are the outpouchings of the mucosal epithelium through the wall called in chronic cholecystitis?

A

Rokitansky-Aschoff sinuses

160
Q

Extensive dystropic calcification can lead to a really hard gallbladder in chronic cholecystitis. What is this called?

A

porcelain gallbladder

161
Q

This is the term for the presence of stones within the bile ducts of the biliary tree

A

Choledocholithiasis

162
Q

Which groups of people get Choledocholithiasis more commonly?

A

Asians

lol ella

163
Q

This is the term for the bacterial infection of the bile ducts.

A

Cholangitis

164
Q

What are the 2 main etiologies for cholangitis?

A

Choledocholithiasis and Biliary strictures

165
Q

Which gram stain are the bacteria that cause cholangitis?

A

gram -

166
Q

This is the partial or complete extrahepatic biliary tree obstruction within the first 3 months of life.

A

Biliary atresia

167
Q

The fetal form of biliary atresia comes from the aberrant development of what structure?

A

Extrahepatic biliary tree

168
Q

The more common perinatal form of biliary atresia may be assocaited with what 2 factors?

A

viral infection or autoimmunity

169
Q

Type III of biliary atresia is incorrectable because the obstruction of the bile ducts is above what?

A

The porta hepatis

170
Q

What is the most common malignancy of the biliary tract?

A

gallbladder adenocarcinoma

171
Q

What is the morphology of infiltrating gallbladder carcinomas?

A

poorly defined area of diffuse thickening and induration, deep ulceration, scirrhous

172
Q

What is the morphology of exophylic gallbladder carcinomas?

A

growth into lumen, cauliflower mass, necrosis, hemorrhagic and ulceration of the fundus and neck.

173
Q

Agensis of the pancreas can be a result of a mutation in which gene?

A

PDX1

174
Q

What is the most common anomaly of the pancrea, where there isnt a fusion of the detal duct system of the dorsal and ventral pancreatic primordials.

A

Pancreas divisum.

175
Q

Where does the pancreas drain now in pancreas divisum?

A

through the doral duct (of santorini) and small-baliber minor papilla

176
Q

What is it called when pancreatic tissues get depositied in other organs?

A

ectopic pancreas

177
Q

What is called when pancreatic tissue encircles the duodenum and can cause duodenal obstruction?

A

Annular pancreas

178
Q

This condition is when there is inflammation with associated microvascular leakage, fat necrosis, proteolytic destruction of pareatic parencyma, and interstitial hemorrhage

A

Acute pancreatitis

179
Q

What is the morphology of acute necrotizing pancreatitis?

A

red-black hemorrhage with yellow-white chalk foci of fat necrosis

180
Q

What are the Sx to acute pancreatitis?

A

abdominal pain, anorexia, N/V

181
Q

What serum enzymes are increased in acute pancreatitis?

A

amylase and lipase

182
Q

This is inflammation of the pancreas with irreversible destruction of the exocrine parenchyma, fibrosis, and destruction of the endocrine parenchyma.

A

Chronic pancreatitis

183
Q

What is the msot common cause of chronic pancreatitis?

A

long term alcohol abuse

184
Q

What is the morphology of chronic pancreatitis?

A

parenchymal fibrosis, reduced # and size of acini with relative sparing of the islets of Langerhands, and variable dilation of pancreatic ducts.

185
Q

What is the autoimmune destruction of the pancreas called?

A

Lymphoplasmacytic sclerosing pancreatitis

186
Q

Case: you’re doing a cholecystectomy and find a unilocar, thin-walled, glistening cyst on the pancreas. You also notice it has a thin fiberous capsule around it. What type of cyst is it?

A

Congenital cyst

187
Q

What 2 AD diseases contribute to congenital cysts?

A

polycystic kidney disease and von Hippel-Lindau

188
Q

This is a collection of necrotic-hemorrhagic material with enzymes but has NO epithelial lining on the pancreas.

A

Pseudocyst

189
Q

Are congenital cysts and pseudocyts neoplastic or non-neoplastic?

A

non-neoplastic

190
Q

These are benign cysts of glycogen-rich cuboidal cells surrounding small cysts containing clear, thin, straw-colored fluid .

A

serous cystadenomas

191
Q

Serous cystadenomas look like what type of fruit?

A

Grapefruit

192
Q

These cysts are assocaited with invastive carcinomas, arise in the body or tail, are large, and filled with thick mucin and lined by columnar muci-producing epithelium.

A

Mucinous cystic neoplasms

193
Q

These are mucin-producing intraductal neoplasms, and are usually in the head of the pancreas.

A

Intraductal Papillary Mucinous Neoplasms (IPMNs)

194
Q

These are large, well-circumscribed masses with solid and cystic componenets, which grow in solid sheets in the pancreas.

A

Solid-pseudopapillary neoplasm

195
Q

Which genetic pathway does Solid-pseudopapillary neoplasms usually involve?

A

B-catenin/APC pathway

196
Q

This is the condition where non-neoplastic epithelium develops into noninvasive lesions, which can then turn into invasive carcinomas of the pancreas.

A

Pancreatic cancer (infiltrating ductal adenocarcinomas of the pancreas)

197
Q

What is the gene mutation to cause pancreatic cancers?

A

KRAS > p16/CDKN2A > TP53 > others

198
Q

What is a big risk factor for pancratic cancer?

A

Smoking

199
Q

What is the morphology of pancreatic cancer?

A

hard, stellate, gray-white, poorly defined masses that invade

200
Q

This is the cancer that had prominant acinar cell differentiation, formation of zymogen granules and production of exocrine enzymes.

A

acinar cell carcinoma

201
Q

This is the rare childhood cancer of the pancreas where there are squamous cell islands admixed with acinar cells.

A

Pancreatoblastoma

Gastrointestinal 3 (6 decks)

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