CH11 - Exocrine Pancreas, Gallbladder, and Liver Pathology Flashcards
1
Q
What is annular pancreas?
A
Developmental malformation in which the pancreas forms a ring around the duodenum
2
Q
In annular pancreas what is there a risk of?
A
duodenal obstruction
3
Q
What is acute pancreatitis?
A
Inflammation and hemorrhage of the pancreas
4
Q
What is acute pancreatitis due to?
A
autodigestion of pancreatic parenchyma by pancreatic enzymes
5
Q
What does premature activation of trypsin lead to?
A
activation of other pancreatic enzymes
6
Q
What does acute pancreatitis result in?
A
liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of the peripancreatic fat
7
Q
What is acute pancreatitis most commonly due to?
A
alcohol and gallstones;
8
Q
Beside alcohol and gallstones what are some other causes of acute pancreatitis?
A
include trauma, hypercalcemia, hyperlipidemia, drugs, scorpion stings, mumps, and rupture of a posterior duodenal ulcer
9
Q
What are the clinical features for acute pancreatitis?
A
1) Epigastric abdominal pain that radiates to the back 2) Nausea and vomiting 3) Periumbilical and flank hemorrhage 4) Elevated serum lipase and amylase - lipase is more specific for pancreatic damage 5) Hypocalcemia - calcium is consumed during saponification in fat necrosis
10
Q
In acute pancreatitis why is there periumbilical and flank hemorrhage?
A
necrosis spreads into the periumbilical soft tissue and retroperitoneum
11
Q
In acute pancreatitis why is there elevated serum lipase and amylase?
A
lipase is more specific for pancreatic damage
12
Q
What are the complications for acute pancreatitis?
A
- Shock 2. Pancreatic pseudocyst 3. Pancreatic abscess 4. DIC and ARDS
13
Q
In acute pancreatitis why is shock one of the complications?
A
Its due to peripancreatic hemorrhage and fluid sequestration
14
Q
In acute pancreatitis what happens in pancreatic pseudocyst?
A
Its formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes
15
Q
How does a pancreatic pseudocyst present?
A
as an abdominal mass with persistently elevated serum amylase
16
Q
What happens when a pancreatic pseudocyst ruptures?
A
it is associated with release of enzymes into the abdominal cavity and hemorrhage.
17
Q
What is pancreatic abscess often due to?
A
Ecoli
18
Q
How does pancreatic abscess present?
A
with abdominal pain, high fever, and persistently elevated amylase
19
Q
What happens in chronic pancreatitis?
A
Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis
20
Q
What is chronic pancreatitis most commonly due to?
A
Alcohol in adults and cystic fibrosis in children, many cases are idiopathic.
21
Q
What does acute pancreatitis leading to pancreatic insufficiency result in?
A
malabsorption with steatorrhea and fat soluble vitamin deficiencies. Amylase and lipase are not useful serologic markers of chronic pancreatitis.
22
Q
What are the clinical features of acute pancreatitis?
A
- epigastric abdominal pain that radiates to the back 2. Pancreatic insufficiency 3. Dystrophic calcification of pancreatic parenchyma on imaging, contrast studies reveal a [chain of lakes] pattern due to dilatation of pancreatic ducts. 4. Secondary diabetes mellitus 5. Increased risk for pancreatic carcinoma
23
Q
In acute pancreatitis why is there a chain of lakes pattern on contrast studies?
A
It is due to the dilation of pancreatic ducts and dystrophic calcification of pancreatic parenchyma
24
Q
How is secondary diabetes mellitus related to acute pancreatitis?
A
It?s a late complication due to destruction of the islets
25
What is pancreatic carcinoma?
Adenocarcinoma arising from the pancreatic ducts
26
What is pancreatic carcinoma most commonly seen in?
the elderly (average age is 70 years)
27
What are the major risk factors for pancreatic carcinoma?
smoking and chronic pancreatitis.
28
What are the clinical features for pancreatic carcinoma?
They usually occur late in disease. 1. Epigastric abdominal pain and weight loss 2. Obstructive jaundice with pale stools and palpable gallbladder 3. Secondary diabetes mellitus 4. Pancreatitis 5. Migratory thrombophlebitis (Trousseau sign) 6. Serum tumor marker is CA 19-9
29
What tumor is secondary diabetes mellitus associated with?
It?s associated with tumors that arise in the body or tail
30
How does Trousseau sign present?
as swelling, erythema, and tenderness in the extremities (seen in 10% of patients)
31
For pancreatic carcinoma with obstructive jaundice with pale stools and palpable gallbladder what is it associated with?
tumors that arise in the head of the pancreas (most common location)
32
What does surgical resection of the pancreatic carcinoma involve?
en bloc removal of the head and neck of pancreas, proximal duodenum, and gallbladder (Whipple procedure).
33
What is the prognosis for pancreatic carcinoma?
Very poor prognosis; 1-year survival is < 10%
34
What is biliary atresia?
Failure to form or early destruction of extra hepatic biliary tree
35
What does biliary atresia lead to?
biliary obstruction within the first 3 months of life
36
What does biliary atresia present with?
jaundice and progresses to cirrhosis
37
What does cholelithiasis lead to?
(gallstones) Solid, round stones in the gallbladder
38
What is cholelithiasis due to?
precipitation of cholesterol (cholesterol stones) or bilirubin (bilirubin stones) in bile
39
What does cholelithiasis arise with?
(1) supersaturation of cholesterol or bilirubin, (2) decreased phospholipids (e.g., lecithin) or bile acids (normally increase solubility), or (3)stasis
40
What is the most common type of cholelithiasis?
cholesterol stones (yellow) are the most common type (90%), especially in the West
41
How is cholelithiasis usually described?
radiolucent - 10% are radiopaque due to associated calcium
42
What are the risk factors for cholelithiasis?
They are age (40s), estrogen (female gender, obesity, multiple pregnancies and oral contraceptives), dofibrate, Native American ethnicity, Crohn disease, and cirrhosis.
43
What are bilirubin stones (pigmented) composed of?
bilirubin
44
How do bilirubin stones appear?
They are usually radiopaque
45
What are the risk factors for bilirubin stones?
They are extravascular hemolysis (increased bilirubin in bile) and biliary tract infection (eg. E coli, Ascaris lumbricoides, and Clonorchis sinensis).
46
How is Ascitris lumbricoides related to bilirubin stones?
it is a common roundworm that infects 25% of the world's population, especially in areas with poor sanitation (fecal-oral transmission); infects the biliary tract, increasing the risk for gallstones
47
How is Clonorchis sinensis related to bilirubin stones?
It is endemic in China, Korea, and Vietnam (Chinese liver fluke); infects the biliary tract, increasing the risk for gallstones, cholangitis, and cholangiocarcinoma
48
What are the symptoms for gallstones?
they are usually asymptomatic;
49
What are the complications for gallstones?
They include biliary colic, acute and chronic cholecystitis, ascending cholangitis, gallstone ileus, and gallbladder cancer.
50
What is biliary colic?
Waxing and waning right upper quadrant pain
51
What is biliary colic due to?
the gallbladder contracting against a stone lodged in the cystic duct
52
How are the symptoms for biliary colic relieved?
if the stone passes.
53
What may common bile duct obstruction result in?
acute pancreatitis or obstructive jaundice.
54
What is acute cholecystitis?
Acute inflammation of the gallbladder wall
55
What does an impacted stone in the cystic duct result in?
dilatation with pressure ischemia, bacterial overgrowth (E coli), and inflammation
56
How does acute cholecystitis present?
with right upper quadrant pain, often radiating to right scapula, fever with increased WBC count, nausea, vomiting, and increased serum alkaline phosphatase (from duct damage), risk of rupture if left untreated
57
What is chronic cholecystitis?
Chronic inflammation of the gallbladder
58
What is chronic cholecystitis due to?
chemical irritation from longstanding cholelithiasis, with or without superimposed bouts of acute cholecystitis
59
What is chronic cholecystitis characterized by?
herniation of gallbladder mucosa into the muscular wall (Rokitansky-Aschoff sinus formation)
60
How does chronic cholecystitis present?
with vague right upper quadrant pain, especially after eating
61
What is a late complication of chronic cholecystitis?
Porcelain gallbladder is a late complication
62
What is porcelain gallbladder?
1. Shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification 2. Increased risk for carcinoma
63
What is the treatment for porcelain gallbladder?
it is cholecystectomy, especially if porcelain gallbladder is present
64
What is ascending cholangitis?
Bacterial infection of the bile ducts
65
What is ascending cholangitis usually due to?
ascending infection with enteric gram-negative bacteria
66
What does ascending cholangitis present as?
sepsis (high fever and chills), jaundice, and abdominal pain
67
With what is there increased incidence of ascending cholangitis?
Increased incidence with choledocholithiasis (stone in biliary ducts)
68
What is gallstone ileus?
Gallstone enters and obstructs the small bowel
69
What is the gallstone ileus due to?
cholecystitis with fistula formation between the gallbladder and small bowel
70
What is gallbladder carcinoma?
Adenocarcinoma arising from the glandular epithelium that lines the gallbladder wall
71
What is a major risk factor for development of gallbladder carcinoma?
gallstones are a major risk factor, especially when complicated by porcelain gallbladder.
72
How does gallbladder carcinoma classically present?
as cholecystitis in an elderly woman
73
What is the prognosis for gallbladder carcinoma?
poor
74
What is jaundice?
Yellow discoloration of the skin; earliest sign is scleral icterus (yellow discoloration of the sclera)
75
What is jaundice due to?
Increased serum bilirubin, usually > 2.5 mg/dL
76
What does jaundice arise with?
disturbances in bilirubin metabolism
77
What happens to RBC?s in bilirubin metabolism?
RBCs are consumed by macrophages of the reticuloendothelial system.
78
What happens to the protoporphyrin after the reticuloendothelial system?
The protoporphyrin (from heme) is converted to unconjugated bilirubin (UCB)
79
What happens to the unconjugated bilirubin?
The albumin carries UCB to the liver
80
What happens to the UCB (unconjugated bilirubin) in the liver?
Uridine glucuronyl transferase (UGT) in hepatocytes conjugates bilirubin
81
What happens to conjugated bilirubin?
it is transferred to bile canaliculi to form bile, which is stored in the gallbladder
82
Where is bile released?
It is released into the small bowel to aid in digestion.
83
What happens to the conjugated bilirubin when it is in the intestines?
Intestinal flora convert CB to urobilinogen, which makes the stool brown.
84
How is conjugated bilirubin related to why urine is yellow?
Urobilinogen (which is what CB is converted into in the intestines) is also partially reabsorbed into the blood and filtered by the kidney, making the urine yellow
85
What is the etiology for Extravascular hemolysis or Ineffective erythropoiesis?
High levels of UCB overwhelm the conjugating ability of the liver.
86
What are the lab findings for extravascular hemolysis or Ineffective erythropoiesis?
Increased UCB
87
What are the clinical features for extravascular hemolysis or ineffective erythropoiesis?
dark urine due to increased urine urobilinogen (UCB is not water soluble and, thus, is absent from urine)
88
For extravascular hemolysis or ineffective erythropoiesis what is there an increased risk for?
pigmented bilirubin gallstones
89
What is the etiology of physiologic jaundice of the newborn?
Newborn liver has transiently low UGT activity.
90
What is the laboratory finding for physiologic jaundice of the newborn?
increased UCB
91
What is the clinical findings for physiologic jaundice of the newborn?
UCB is fat soluble and can deposit in the basal ganglia (kernicterus) leading to neurological deficits and death.
92
What is the treatment for physiologic jaundice of the newborn?
phototherapy (makes UCB water soluble),
93
What is the etiology for Gilbert syndrome?
Mildly low UGT activity; autosomal recessive
94
What are the laboratory findings for physiologic jaundice of the newborn?
Increased UCB
95
What are the clinical features for physiologic jaundice of the newborn?
Jaundice during stress (e.g., severe infection); otherwise, not clinically significant
96
What is the etiology for Crigler-Najjar syndrome?
Absence of UGT
97
What are the lab findings for Crigler-Najjar syndrome?
Increased UCB
98
What are the clinical features for Crigler-Najjar syndrome?
Kernicterus; usually fatal
99
What is the etiology for Dubin-Johnson syndrome?
Deficiency of bilirubin canalicular transport protein; autosomal recessive
100
What are the laboratory findings for Dubin-Johnson syndrome?
Increased CB
101
What are the clinical features for Dubin-Johnson syndrome?
The liver is dark; otherwise, not clinically significant
102
What is similar to Dubin-Johnson syndrome and how can you tell the difference?
Rotor syndrome is similar to Dubin-Johnson syndrome, but lacks liver discoloration.
103
What is the etiology for biliary tract obstruction (obstructive jaundice)?
Associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, and liver fluke (Clonorchii sinensis)
104
What are the lab findings for biliary tract obstruction (obstructive jaundice)?
Increased CB, decreased urine urobilinogen, and increased alkaline phosphatase
105
What are the clinical features for biliary tract obstruction (obstructive jaundice)?
Dark urine and pale stool, Pruritus, Hypercholesterolemia with xanthomas, Steatorrhea with malabsorption of fat-soluble vitamins
106
In biliary tract obstruction (obstructive jaundice) why is there dark urine?
Its due to bilirubinuria
107
In biliary tract obstruction (obstructive jaundice) why is there pruritis?
due to increased plasma bile acids
108
What is the etiology for viral hepatitis?
inflammation disrupts hepatocytes and small bile ductules.
109
What are the laboratory findings for viral hepatitis?
Increase in both CB and UCB
110
What are the clinical features for viral hepatitis?
Dark urine due to increased urine bilirubin; urine urobilinogen is normal or decreased.
111
How is HAV and HEV transmitted?
Hepatitis A (HAV) and Hepatitis E (HEV) fecal-oral transmission
112
HAV is commonly acquired by
travelers.
113
HEV is commonly acquired from
contaminated water or undercooked seafood.
114
Is HAV chronic or acute?
Acute hepatitis; no chronic state.
115
Is HEV chronic or acute?
Acute hepatitis; no chronic state.
116
In hepatitis what marks active infection?
anti-virus IgM
117
In hepatitis what does antivirus IgG mean?
Its in HAV and HEV, it is protective, and its presence indicates prior infection or immunization
118
What is hepatitis immunization available for?
HAV only
119
What is HEV infection in pregnant women associated with?
fulminant hepatitis (liver failure with massive liver necrosis)
120
How is Hepatitis B (HBV) transmitted?
Parenteral transmission (e.g., childbirth, unprotected intercourse, and intravenous drug abuse [IVDA])
121
What does Hepatitis B result in?
acute hepatitis; chronic disease occurs in 20% of cases
122
How is Hepatitis C (HCV) transmitted?
Parenteral transmission (e.g., IVDA, unprotected intercourse, needle stick); risk from transfusion is almost nonexistent due to screening of the blood supply.
123
What does hepatitis C result in?
acute hepatitis: chronic disease occurs in most cases
124
What confirms HCV infection?
HCV-RNA test confirms infection; decreased RNA levels indicate recovery; persistence indicates chronic disease.
125
How is Hepatitis D (HDV) transmitted?
Dependent on HBV for infection: superinfection upon existing HBV is more severe than coinfection (infection with HBV and HDV at the same time)
126
For HBV what is the first serologic marker to rise?
HBsAG
127
What defines the chronic state of HBV?
HBsAG > 6 months
128
When is there both HBcAG and HBV DNA?
In the acute and maybe in chronic phase
129
What indicates infectivity for the HBV?
Presence of HBeAG or HBV DNA
130
With HBcAB what immunoglobulin is seen in the acute stage of HBV?
IgM
131
With HBcAB what immunoglobulin is seen in the window stage of HBV?
IgM
132
With HBcAB what immunoglobulin is seen in the resolved stage of HBV?
IgG
133
With HBcAB what immunoglobulin is seen in the chronic stage of HBV?
IgG
134
With HBsAB what immunoglobulin is seen in the resolved stage of HBV?
IgG (protective)
135
With HBsAB what immunoglobulin is seen in the immunization stage of HBV?
IgG (protective)
136
What is viral hepatitis?
Inflammation of liver parenchyma, usually due to hepatitis virus
137
What is viral hepatitis usually due to and what are some other causes for it?
EBV and CMV
138
What does the hepatitis virus cause?
acute hepatitis, which may progress to chronic hepatitis.
139
How does acute hepatitis present?
as jaundice (mixed CB ?conjugated bilirubin and UCB ?unconjugated bilirubin) with dark urine (due to CB), fever, malaise, nausea, and elevated liver enzymes (ALT > AST),
140
For acute hepatitis what does acute inflammation involve and how is it characterized?
It involves lobules of the liver and portal tracts, and is characterized by apoptosis of hepatocytes
141
What are the symptoms for acute hepatitis?
Some cases may be asymptomatic with elevated liver enzymes. Symptoms last < 6 months,
142
What is chronic hepatitis characterized by?
symptoms that last > 6 months
143
What does inflammation in chronic hepatitis predominantly involve?
the portal tract
144
For chronic hepatitis what is there a risk of?
progression to cirrhosis
145
What is cirrhosis?
End-stage liver damage characterized by disruption of the normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes
146
In cirrhosis how is fibrosis mediated?
by TGF-beta from stellate cells which lie beneath the endothelial cells that line the sinusoids.
147
What are the clinical features for cirrhosis due to?
1. Portal hypertension 2. Decreased detoxification 3. Decreased protein synthesis
148
For the clinical features of cirrhosis what does portal hypertension lead to?
1) Ascites (fluid in the peritoneal cavity) 2) Congestive splenomegaly/hypersplenism 3) Portosystemic shunts (esophageal varices, hemorrhoids, and caput medusae) 4) Hepatorenal syndrome (rapidly developing renal failure secondary to cirrhosis)
149
For the clinical features of cirrhosis what does decreased detoxification lead to?
1) Mental status changes, asterixis, and eventual coma (due to T serum ammonia); metabolic, hence reversible 2) Gynecomastia, spider angiomata. and palmar erythema due to hyperestrinism 3) jaundice
150
For the clinical features of cirrhosis what does decreased protein synthesis lead to?
1) Hypoalbuminemia with edema 2) Coagulopathy due to decreased synthesis of clotting factors; degree of deficiency is followed by prothrombin time (PT).
151
What happens in alcohol related liver disease?
Damage to hepatic parenchyma due to consumption of alcohol
152
What is the most common cause of liver disease in the West?
Consumption of alcohol
153
What is fatty liver?
it is the accumulation of fat in hepatocytes
154
What does fatty liver result in?
a heavy, greasy liver
155
How does fatty liver resolve?
with abstinence
156
What does alcoholic hepatitis result from?
chemical injury to hepatocytes; generally seen with binge drinking
157
With alcoholic hepatitis what mediates damage?
Acetaldehyde (metabolite of alcohol) mediates damage
158
What is alcoholic hepatitis characterized by?
swelling of hepatocytes with formation of Mallory bodies (damaged cytokeratin filaments), necrosis, and acute inflammation
159
How does alcoholic hepatitis present?
with painful hepatomegaly and elevated liver enzymes (AST > ALT), may result in death
160
What is a long term complication of alcoholic hepatitis?
Cirrhosis, chronic alcohol-induced liver damage;
161
What is the frequency of cirrhosis in alcoholic hepatitis?
occurs in 10-20% of alcoholics
162
What is non-alcoholic fatty liver disease?
Fatty change, hepatitis, and/or cirrhosis that develop without exposure to alcohol (or other known insult)
163
What is non-alcoholic fatty liver disease associated with?
obesity
164
How do you diagnose non-alcoholic fatty liver disease?
Diagnosis of exclusion; ALT > AST
165
Wha is hemochromatosis?
Excess body iron leading to deposition in tissues (hemosiderosis) and organ damage (hemochromatosis)
166
In hemochromatosis what mediates tissue damage?
It is mediated by generation of free radicals.
167
What is hemochromatosis due to?
autosomal recessive defect in iron absorption (primary) or chronic transfusions (secondary)
168
What is primary hemochromatosis due to?
mutations in the HFE gene, usually C282Y (cysteine is replaced by tyrosine at amino acid 282)
169
When does hemochromatosis present?
in late adulthood
170
What is the classic presentation for hemochromatosis?
Classic triad is cirrhosis, secondary diabetes mellitus, and bronze skin; other findings include cardiac arrhythmias and gonadal dysfunction (due to testicular atrophy).
171
What are the lab findings for hemochromatosis?
Labs show increased ferritin, decreased TIBC, increased serum iron, and increased % saturation.
172
For hemochromatosis, what does liver biopsy reveal?
accumulation of brown pigment in hepatocytes
173
For hemochromatosis liver biopsy, what is the accumulated brown pigment in the hepatocytes?
Lipofuscin
174
For hemochromatosis liver biopsy how do you identify the lipofuscin?
Prussian blue stain distinguishes iron (blue) from lipofuscin
175
What is lipofuscin?
it is a brown pigment that is a by-product from the turnover (wear and tear) of peroxidized lipids
176
Where does lipofuscin commonly present?
in hepatocytes
177
In hemochromatosis, what is there an increased risk of?
hepatocellular carcinoma
178
In hemochromatosis, what is the treatment?
It is phlebotomy
179
What is Wilson?s Disease?
Autosomal recessive defect (ATP7B gene) in ATP-mediated hepatocvte copper transport
180
What does Wilson?s Disease result in?
lack of copper transport into bile and lack of copper incorporation into ceruloplasmin which leads to copper build up in hepatocytes which leaks into serum, and deposits in tissues
181
In Wilson?s Disease what leads to tissue damage?
Copper-mediated production of hydroxyl free radicals leads to tissue damage
182
When does Wilson?s Disease present?
in childhood with: 1) cirrhosis 2) neuologic manifestations 3) Kayser-Fleisher rings in the cornea
183
What are the neurologic manifestations in Wilson?s Disease?
behavioral changes, dementia, chorea, and Parkinsonian symptoms due to deposition of copper in basal ganglia
184
In Wilson?s Disease what does the labs show?
increased urinary copper, decreased serum ceruloplasmin, and increased copper on liver biopsy.
185
In Wilson?s Disease what is there an increased risk for?
hepatocellular carcinoma
186
What is the treatment for Wilson?s Disease?
D-penicillamine (chelates copper)
187
What is primary biliary cirrhosis?
Autoimmune granulomatous destruction of intrahepatic bile ducts
188
In whom does primary biliary cirrhosis classically arise?
in women, the average age is 40 years
189
What is primary biliary cirrhosis associated with?
other autoimmune diseases
190
What is the etiology for primary biliary cirrhosis?
It is unknown; antimitochondrial antibody is present.
191
How does primary biliary cirrhosis present?
It presents with features of obstructive jaundice
192
What is a late complication for primary biliary cirrhosis?
cirrhosis
193
What is primary sclerosing cholangitis?
Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts
194
What is the appearance of primary sclerosing cholangitis?
1. Periductal fibrosis with an onion-skin appearance
195
In primary sclerosing cholangitis what is seen in the uninvolved regions?
they are dilated resulting in a beaded appearance on contrast imaging
196
What is the etiology for primary sclerosing cholangitis?
it is unknown, but associated with ulcerative colitis; p-ANCA is often positive
197
What is p-ANCA?
Perinuclear Anti-Neutrophil Cytoplasmic Antibodies
198
How does primary sclerosing cholangitis present?
It presents with obstructive jaundice; cirrhosis is a late complication.
199
What is there an increased risk for with primary sclerosing cholangitis?
cholangiocarcinoma
200
What is Reye syndrome?
Fulminant liver failure and encephalopathy in children with viral illness who take aspirin
201
What is Reye syndrome likely related to?
mitochondrial damage of hepatocytes
202
How does Reye syndrome present?
with hypoglycemia, elevated liver enzymes, and nausea with vomiting; may progress to coma and death
203
What is hepatic adenoma?
Benign tumor of hepatocytes
204
What is hepatic adenoma associated with?
oral contraceptive use; regresses upon cessation of drug
205
In hepatic adenoma, what is there a risk of?
rupture and intraperitoneal bleeding, especially during pregnancy
206
In hepatic adenoma, describe the tumors?
they are subcapsular and grow with exposure to estrogen
207
What is hepatocellular carcinoma?
Malignant tumor of hepatocytes
208
What are some risk factors for hepatocellular carcinoma?
1. Chronic hepatitis (e.g., HBV and HCV) 2. Cirrhosis (e.g., alcohol, nonalcoholic fatty liver disease, hemochromatosis, Wilson disease, and A1AT deficiency) 3. Anatoxins derived from Aspergillus- (induce p53 mutations)
209
In hepatocellular carcinoma, what is there an increased for?
Increased risk for Budd-Chiari syndrome
210
What happens in Budd-Chiari syndrome as a result of hepatocellular carcinoma?
1. Liver infarction secondary to hepatic vein obstruction
211
How does Budd-Chiari syndrome as a result of hepatocellular carcinoma present?
Presents with painful hepatomegaly and ascites
212
What is the prognosis for hepatocellular carcinoma?
Tumors are often detected late because symptoms are masked by cirrhosis; poor prognosis
213
What is the serum tumor marker in hepatocellular carcinoma?
alpha-fetoprotein.
214
How common is metastasis to liver?
It?s more common than primary liver tumors; most common sources include colon, pancreas, lung, and breast carcinomas.
215
What does hepatocellular carcinoma result in?
multiple nodules in the liver
216
How might hepatocellular carcinoma be detected clinically?
it may be detected as hepatomegaly with a nodular free edge of the liver
