Liver Lectures - GI Exam 2 Flashcards
Acute Liver Failure is…
The _________ in a person without ______
Must have _________ and any degree of _____
Duration of illness is typically _______
Acute Liver Failure is…
The sudden loss of hepatic function in a person without pre-existing liver disease
Must have presence of coagulopathy (INR ≥ 1.5) and any degree of encephalopathy
Duration of illness is typically ≤ 24 weeks
_____ causes the majority of acute liver failure in the US. Runners up include ______ and ________
Tylenol misuse causes the majority of acute liver failure in the US. Runners up include unknown causes and idosyncratic drug reactions
Tylenol is rapidly absorbed from the GI tract. Toxicity is ___ related. In order to have liver effects, patients usually have to take >__g
Tylenol is rapidly absorbed from the GI tract. Toxicity is dose related. In order to have liver effects, patients usually have to take >10g
Acetaminophen reaches peak serum levels in _ hours. This can be delayed by _____ such as _______.
A negative blood screen does not rule out Tylenol toxicity.
Acetaminophen reaches peak serum levels in 4 hours. This can be delayed by other drugs such as anticholinergics. A negative blood screen does not rule out Tylenol toxicity.
Acetaminophen Toxicity
Stage 1: (time). nausea, vomiting, lethargy, malaise. Blood labs and CNS are normal.
Stage 2: (time). RUQ pain, hepatomegaly. nephrotoxicity, hepatotoxicity, coagulopathy.
Stage 3: (time): Jaundice, encephalopathy. Max elevated LFT, sometimes >10,000. Hyoglycemia, lactic acidosis, prolonged INR
Stage 4 (time): Clinical recovery is complete, histological recovery lags. No long-term sequela.
Stage 1: 0.5-24 hours. nausea, vomiting, lethargy, malaise. Blood labs and CNS are normal.
Stage 2: 24 - 72 hrs. RUQ pain, hepatomegaly. nephrotoxicity, hepatotoxicity, coagulopathy.
Stage 3: 72 - 96 hours: Jaundice, encephalopathy. Max elevated LFT, sometimes >10,000. Hyoglycemia, lactic acidosis, prolonged INR
Stage 4: 4d-2wks: Clinical recovery is complete, histological recovery lags. No long-term sequela.
Stage 1: 0.5-24 hours. (clinical presentation). Blood labs and CNS are normal.
Stage 2: 24 - 72 hrs. (clinical presentation). nephrotoxicity, hepatotoxicity, coagulopathy.
Stage 3: 72 - 96 hours: (clinical presentation). Max elevated LFT, sometimes >10,000. Hyoglycemia, lactic acidosis, prolonged INR
Stage 4: 4d-2wks: (clinical presentation)
Stage 1: 0.5-24 hours. nausea, vomiting, lethargy, malaise. Blood labs and CNS are normal.
Stage 2: 24 - 72 hrs. RUQ pain, hepatomegaly. nephrotoxicity, hepatotoxicity, coagulopathy.
Stage 3: 72 - 96 hours: Jaundice, encephalopathy. Max elevated LFT, sometimes >10,000. Hyoglycemia, lactic acidosis, prolonged INR
Stage 4: 4d-2wks: Clinical recovery is complete, histological recovery lags. No long-term sequela.
Stage 1: 0.5-24 hours. nausea, vomiting, lethargy, malaise. (objective findings).
Stage 2: 24 - 72 hrs. RUQ pain, hepatomegaly. (objective findings).
Stage 3: 72 - 96 hours: Jaundice, encephalopathy. (objective findings).
Stage 4: 4d-2wks: Clinical recovery is complete, histological recovery lags. No long-term sequela.
Stage 1: 0.5-24 hours. nausea, vomiting, lethargy, malaise. Blood labs and CNS are normal.
Stage 2: 24 - 72 hrs. RUQ pain, hepatomegaly. nephrotoxicity, hepatotoxicity, coagulopathy.
Stage 3: 72 - 96 hours: Jaundice, encephalopathy. Max elevated LFT, sometimes >10,000. Hyoglycemia, lactic acidosis, prolonged INR
Stage 4: 4d-2wks: Clinical recovery is complete, histological recovery lags. No long-term sequela.
If a patient makes it past the ____ stage of acetaminophen toxicity, they are likely to survive.
The ____ stage of acetaminophen toxicity is characterized by Jaundice and hepatomegaly. Also maximally elevated LFTs (>10,000), prolonged INR, lactic acidosis, hypoglycemia.
If a patient makes it past the third stage of acetaminophen toxicity, they are likely to survive.
The third stage of acetaminophen toxicity is characterized by Jaundice and hepatomegaly. Also maximally elevated LFTs (>10,000), prolonged INR, lactic acidosis, hypoglycemia
The Rumack-Matthew nomogram is used to interpret ______ in relation to ______, in order to assess likelihood of _______.
The Rumack-Matthew nomogram is used to interpret serum acetaminophen levels in relation to time since ingestion, in order to assess likelihood of hepatotoxicity.
Acetaminophen can safely be excreted in the urine by exchaning a hydroxyl moiety for a ___ or a ____.
Acetaminophen can safely be excreted in the urine by exchaning a hydroxyl moiety for a glucuronide or a sulfate.
Acetaminophen can be ____ excreted without altering the chemical structure.
Acetaminophen can be renally excreted without altering the chemical structure.
______ can be afixed to ______, a toxic metabolite of acetaminophen, to render it inert. The ____ is then excreted in the urine.
Glutathione can be afixed to NAPQI, a toxic metabolite of acetaminophen, to render it inert. The glutathione+NAPQI is then excreted in the urine.
Once _____ stores are depleted, acetaminophen is converted to _____ by _______ enzymes. Free-_____ is hepatotoxic.
Once glutathione stores are depleted, acetaminophen is converted to NAPQI by CYP/P450 enzymes. Free-NAPQI is hepatotoxic.
(drug) can be used to treat acetaminophen overdose by inhibiting the production of (metabolite). It works best within (time) of ingestion. After that, serum levels are too high for drug to be effective. Normal (labs) at time of administration predict success.
N-acetyl-cysteine (NAC) can be used to treat acetaminophen overdose by inhibiting the production of NAPQI. It works best within 8 hours of ingestion. After that, serum levels are too high for drug to be effective. Normal LFTs at time of administration predict success.
The (edible) can cause ???-mediated damage to the liver. There is no blood test, so you must have a high clinical suspicion in a patient who presents with (4 things). Liver failure occurs within (time). Can treat with (2 drugs); list for transplant.
The death cap mushroom can cause toxin-mediated damage to the liver. There is no blood test, so you must have a high clinical suspicion in a patient who presents with abd pain, vomiting, diarrhea, and a history of ingesting mushrooms. Liver failure occurs within 4-5 days. Can treat with Pen-G or Silymarin; list for transplant.
____ causes of acute liver failure are rare. _____ almost never causes ALF in the US, but ___ can cause ALF in (4 countries), especially in (population). Only treatment is ______.
___ & _____ can also cause viral ALF. Treat with (drug).
Viral causes of acute liver failure are rare. Hepatitis almost never causes ALF in the US, but HEV can cause ALF in Mexico, Russia, Pakistan, and India, especially in pregnant women. Only treatment is supportive care.
HSV and varicella zoster can also cause viral ALF. Treat with acyclovir.
Idiosyncratic drug-related acute liver failure is diagnosed based on a reaction that occurs with (time) of drug exposure. Common culprits are (5 drugs).
Idiosyncratic drug-related acute liver failure is diagnosed based on a reaction that occurs with ~6 months of drug exposure. Common culprits are Carbamazepine, Sulfonamides (eg. augmentin), Isoniazid, NSAIDs, ecstacy.
Complications of ALF can include (5 things). Liver transplantation must be considered.
Complications of ALF can include encephalopathy, cerebral HTN, nephrotixicity, infections, and coagulopathy. Liver transplantation must be considered.
This patient took too much Tylenol. What’s going on in this image?
Acetaminiophen preferentially affects zone 3. Normalish cells are seen near the portal trid. The cells near the central vein in zone 3 are pink and smudgy.
The most common causes of chronic liver disease and cirrhosis are (4 things).
The most common causes of chronic liver disease and cirrhosis are HBV, HCV, Alcohol, and Non-Alcoholic Fatty Liver Disease.
About __% of people infected with HCV will clear the virus on their own. The other ___% will go on to have chronic liver disease. Fibrosis develops over ___ years. Among those with chronic liver disease, __% go on to have cirrhosis. It is the leading cause of (three things) in the US.
About 15-20% of people infected with HCV will clear the virus on their own. The other 80-85% will go on to have chronic liver disease. Fibrosis develops over 15-30 years. Among those with chronic liver disease, 20% go on to have cirrhosis. It is the leading cause of liver cirrhosis, liver-related deaths, and hepatocellular carcinoma in the US.
Four groups should be screened for HCV: (4). The treatment lasts (time) weeks and has few side effects, but it is expensive.
Four groups should be screened for HCV: baby boomers, people who inject drugs, people on hemodialysis, and anyone who received a drug transfusion prior to 1992. The treatment lasts 8-12 weeks and has few side effects, but it is expensive.
Extra-hepatic manifestations of HCV include…
Non-Hodgkins B cell lymphoma
membranoproliferative glomerulonephritis
cryoglobulinemia
porphyria cutanea tarda
Symptoms of cryoglobulinemia include…
joint aches and swelling
skin vasculitis, palpable purpura over shins
peripheral nephropathy
nephrotic syndrome
Cryoglobulins are abnormal ___ that precipitate at ___. ___% of pts with HCV have cryoglobulinemia, and high serum levels can cause sx.
Cryoglobulins are abnormal Igs that precipitate at cooler temperatures. 40-50% of pts with HCV have cryoglobulinemia, and high serum levels can cause sx.
An estimated ___% of patients with HCV will also have ___. ___ is caused by a deficiency in ___ enzyme which causes a build up of toxic metabolites. It presents with ____ and other ___ & ___manifestations.
An estimated 60-90% of patients with HCV will also have porphyria cutanea tarda (PCT). PCT is caused by a deficiency in uroporphyrinogen decarboxylase enzyme which causes a build up of toxic metabolites. It presents with leasions/blisters on sunexposed areas and other liver and nervous system manifestations.
This patient has HCV. What is the disease pictured?
Porphyria cutanea tarda
Interpret the image and name that disease
Lymphocytic infiltrate and fibrosis around the portal tract. More normal looking hepatocytes around the central vein.
HCV
What virus causes lymphocytic infiltrates and fibrosis around the portal tract?
HCV
Which hepatitis carries the greatest risk for developing hepatocellular carcinoma?
HBV
The H_V virus is a _NA virus that incorporates into host _NA, but it is not _____. This makes it very hard to cure, and increases the risk for developing ________. Damage is caused by the __________.
The HBV virus is a DNA virus that incorporates into host DNA, but it is not cytotoxic. This makes it very hard to cure, and increases the risk for developing hepatocellular carcinoma. Damage is caused by the host immune response.
In HBV infection, ___ antigen is present for _ months. Levels of ______ and ___ can vary widely when infected.
In HBV infection, surface antigen is present for 6 months. Levels of HBV DNA and ALT can vary widely when infected.
H_V and H_V both preferentially affect zone _ near the _______. Only H_V has __________ in hepatocytes on histology.
HBV and HCV both preferentially affect zone 1 near the portal tracts. Only HBV has ground glass inclusions in hepatocytes on histology.
ground glass inclusions are cells on right. Speckled looking cells on left are healthy.
Primary Biliary cirrhosis is a presumed ______disease that destroys ______.
Primary Biliary cirrhosis is a presumed autoimmune disease that destroys intrahepatic bile ducts.
_________ is a presumed autoimmune disease that destroys intrahepatic bile ducts.
Primary Biliary cirrhosis is a presumed autoimmune disease that destroys intrahepatic bile ducts.
Primary biliary cirrhosis is often found in conjunction with (3 autoimmune/allergic + 3 more
Primary biliary cirrhosis is often found in conjunction with Sjogren syn, rheumatoid arthritis, dermatologic conditions, dry eyes, dry mouth, osteopenia/osteoporosis, thyroid disease, and celiac disease
The illness script for primary biliary cirrhosis (cholangitis) is a _____ in (age) who presents with (3 signs/sx) though most pts are asymptomatic
The illness script for primary biliary cirrhosis (cholangitis) is a women in her 30s-60s who presents with pruritis, fatigue, and RUQ though most pts are asymptomatic
The illness script for (disease) is a women in her 30s-60s who presents with pruritis, fatigue, and RUQ though most pts are asymptomatic
The illness script for primary biliary cirrhosis (cholangitis) is a women in her 30s-60s who presents with pruritis, fatigue, and RUQ though most pts are asymptomatic
You can diagnose PBC with an elevated (3 labs); you don’t even really need a liver biopsy. Patients will also have a mildly elevated (2 labs). Elevated (lab) is a very late finding in PBC.
You can diagnose PBC with an elevated AMA, ALP, and IgM; you don’t even really need a liver biopsy. Patients will also have a mildly elevated AST, ALT. Elevated bilirubin is a very late finding in PBC.
Anti-mitochondria antibody (AMA) is the serologic hallmark of ___.
Anti-mitochondria antibody is the serologic hallmark of PBC
You find elevated ALP, AMA, GGT, and IgM in a pt. AST and ALT are mildly elevated. Liver biopsy is below. What is this patient’s diagnosis?
PBC
Notice the histiocytic infiltration and destruction of intrahepatic bile ducts.
You find elevated ALP, AMA, GGT, and IgM in a pt. AST and ALT are mildly elevated. Liver biopsy is below. What is this patient’s diagnosis?
PBC
All of the brownish gunk is bile that has backed up in the liver because of the damaged intrahepatic bile ducts.
The treatment for ___ is ursodeoxycholic acid
The treatment for PCB is ursodeoxycholic acid
___________ is a chronic cholestatic liver disease of unknown origin that causes diffue inflammation and fibrosis of the entire biliary tree.
Primary sclerosing cholangitis is a chronic cholestatic liver disease of unknown origin that causes diffue inflammation and fibrosis of the entire biliary tree.
Primary sclerosing cholangitis is a chronic cholestatic liver disease of unknown origin that causes ________. Medican survival is ___ years, annd the only cure is ____
Primary sclerosing cholangitis is a chronic cholestatic liver disease of unknown origin that causes diffuse inflammation and fibrosis of the entire biliary tree. Medican survival is 10-12 years, annd the only cure is transplant
A typical illness script for ___ would be a man in his 40s who has IBD and present with pruritis, fatigue, and jaundice. Would also have mildly elevated LFTs including ALP. Pts can run the gammit from asymptomatic to cirrhotic.
Most patients with ___ have ulcerative colitis (UC), but few pts with UC have PSC
A typical illness script for PSC would be a man in his 40s who has IBD and present with pruritis, fatigue, and jaundice. Would also have mildly elevated LFTs including ALP. Pts can run the gammit from asymptomatic to cirrhotic.
Most patients with PSC have ulcerative colitis (UC), but few pts with UC have PSC
A typical illness script for PSC would be a (gender) in (age) who has (comorbidity) and present with (3 signs/sx). Would also have mildly elevated (labs). Pts can run the gammit from asymptomatic to cirrhotic.
Most patients with PSC have (comorbidity), but few pts with (comorbidity) have PSC
A typical illness script for PSC would be a man in his 40s who has IBD and present with pruritis, fatigue, and jaundice. Would also have mildly elevated LFTs including ALP. Pts can run the gammit from asymptomatic to cirrhotic.
Most patients with PSC have ulcerative colitis (UC), but few pts with UC have PSC
imaging of ___ will show irregular stricturing and bleeding. Imaging modality of choice is ERCP or MRCP.
imaging of PSC will show irregular stricturing and bleeding. Imaging modality of choice is ERCP or MRCP.
stricturing occurs especially in medium to large caliber ducts.
imaging of PSC will show ___. Imaging modality of choice is ____.
imaging of PSC will show irregular stricturing and bleeding. Imaging modality of choice is ERCP or MRCP.
stricturing occurs especially in medium to large caliber ducts.
The histological hallmark of ___ is “onion skin” fibrosis
The histological hallmark of PSC is “onion skin” fibrosis
The histological hallmark of PSC is “_____ ____” fibrosis
The histological hallmark of PSC is “onion skin” fibrosis
Patients who have PSC may also end up with _____ due to the lack of bile. They can also develop ______. Pts who have PSC on UC are at vvv high risk for _______.
Patients who have PSC may also end up with fat soluble vitamin deficiency due to the lack of bile. They can also develop metabolic bone disease (eg. osteoporosis, osteopenia). Pts who have PSC on UC are at vvv high risk for colon cancer.
___ predisposes patients to developing cholangiocarcinoma. The location of the tumor determines the clinical presentation. Tumors can be intrahepatic, klatskin (perihilar where left and right hepatic bile ducts join; acounts for 60-80%) or distal (10-30%) Diagnosis is challenging and tumors are found in 35-40% of liver explants
PSC predisposes patients to developing cholangiocarcinoma. The location of the tumor determines the clinical presentation. Tumors can be intrahepatic, klatskin (perihilar where left and right hepatic bile ducts join; acounts for 60-80%) or distal (10-30%) Diagnosis is challenging and tumors are found in 35-40% of liver explants
PSC predisposes patients to developing ___________. The _____ of the tumor determines the clinical presentation. Tumors can be _____, _____ (perihilar where left and right hepatic bile ducts join; acounts for 60-80%) or _____ (10-30%) Diagnosis is challenging and tumors are found in 35-40% of liver explants
PSC predisposes patients to developing cholangiocarcinoma. The location of the tumor determines the clinical presentation. Tumors can be intrahepatic, klatskin (perihilar where left and right hepatic bile ducts join; acounts for 60-80%) or distal (10-30%) Diagnosis is challenging and tumors are found in 35-40% of liver explants
Acute Liver Failure in the US is most commonly caused
by _____. Acute Liver Failure requires urgent evaluation for ____ and _____.
Acute Liver Failure in the US is most commonly caused
by acetominophen toxicity. Acute Liver Failure requires urgent evaluation for etiology and liver transplantation.
The hitological hallmark of _______ is a mixed inflammatory infiltrate (mostly plasma cells) that affects portal ducts and lobules with hepatocyte damage. Steroids can improve this.
The inflammation is caused by and environmental trigger + genetic predisposition (HLA DR3 and HLA DR4) –> loss of immune tolerance –> T cell mediated attack on hepatocytes
The hitological hallmark of autoimmune hepatitis is a mixed inflammatory infiltrate (mostly plasma cells) that affects portal ducts and lobules with hepatocyte damage. Steroids can improve this.
The inflammation is caused by and environmental trigger + genetic predisposition (HLA DR3 and HLA DR4) –> loss of immune tolerance –> T cell mediated attack on hepatocytesthis.
The hitological hallmark of autoimmune hepatitis is a _____ infiltrate (mostly ___ cells) that affects _______ and _____ with _________ damage. Steroids can improve this.
The inflammation is caused by and environmental trigger + genetic predisposition (HLA DR3 and HLA DR4) –> loss of immune tolerance –> T cell mediated attack on hepatocytesthis.
The hitological hallmark of autoimmune hepatitis is a mixed inflammatory infiltrate (mostly plasma cells) that affects portal ducts and lobules with hepatocyte damage. Steroids can improve this.
The inflammation is caused by and environmental trigger + genetic predisposition (HLA DR3 and HLA DR4) –> loss of immune tolerance –> T cell mediated attack on hepatocytesthis.
The enzymes ______ and ________ metabolise EtOH to acetaldehyde. The acetaldehyde is then metabolised by _____________ to acetate. The __________ pathway upregulates with habitual alcohol use.
The enzymes alcohol dehydrogenase and cytochrome p450 metabolise EtOH to acetaldehyde. The acetaldehyde is then metabolised by acetaldehyde dehydrogenase to acetate. The cytochrome p45002E1 pathway upregulates with habitual alcohol use.
A male patient presents with fever, jaundice, tender hepatomegaly, and anorexia. He admits to drinking 7 alcoholic beverages daily for the last 10 years. You calculate his Maddrey Discrimination index and find that it is 32. A biopsy of his liver is seen below. What is his diagnosis? What can you tell him based on his MD index score?
He has alcoholic Steatohepatitis. His MD index score means his mortality at 1 month is 30% and mortality at 6 months is 50%. We can treat him with 40mg Prednisolone daily; if he responds after one week he will continue on for 1 month
On histology, a liver with ________ will have steatosis, Mallory-Denk bodies, and pericellular (chicken wire) fibrosis. Zone _ will be primarily affected.
On histology, a liver with alcoholic steatohepatitis will have steatosis, Mallory-Denk bodies, and pericellular (chicken wire) fibrosis. Zone 3 will be primarily affected.
Liver biopsy of a pt with _________ will show iron accumulation in hepatocytes.
Liver biopsy of a pt with hereditary hemochromatosis will show iron accumulation in hepatocytes.
The iron looks like brown sludge on H&E. Confirm it’s iron with prussian blue stain.
biopsry isn’t necessary for diagnosis. helpful for determining extent of damage
Liver biopsy of a pt with hereditary hemochromatosis will show ___ accumulation in hepatocytes.
The __ looks like brown sludge on H&E. Confirm it’s __ with ________stain.
Liver biopsy of a pt with hereditary hemochromatosis will show iron accumulation in hepatocytes.
The iron looks like brown sludge on H&E. Confirm it’s iron with prussian blue stain.
biopsry isn’t necessary for diagnosis. helpful for determining extent of damage
The histological hallmark of A1ATD is _____ accumulated in hepatocytes, especially in zone _, that is revealed with ___ stain. There is also nonspecific fibrosis and inflammation.
The histological hallmark of A1ATD is A1AT accumulated in hepatocytes, especially in zone 1, that is revealed with PAS stain. There is also nonspecific fibrosis and inflammation.
In Wilson’s Disease, a defective ____ causes copper to accumulate in the _____ of hepatocytes, because the copper can’t get packaged in the ____ for excretion in the bile.
In Wilson’s Disease, a defective ATP7B causes copper to accumulate in the cytoplasm of hepatocytes, because the copper can’t get packaged in the golgi for excretion in the bile.
On histology, Wilson’s Dz is a ______. It can mimick any of the disease that cause steatosis, cirrhosis, acute hepatitis, chronic hepatitis. In particular, you might see ___ and ___like in AFLD or ____/____/____ like in AIH. A special ___ stain can highlight copper in hepatocytes, but the stain doesn’t work if the copper is too diffuse. Wilson’s disease is an often missed dx.
On histology, Wilson’s Dz is a masquerader. It can mimick any of the disease that cause steatosis, cirrhosis, acute hepatitis, chronic hepatitis. In particular, you might see steatosis and Mallory bodies like in AFLD or periportal inflammation/bridging necrosis/lobular necrosis like in AIH. A special Rhodanine stain can highlight copper in hepatocytes, but the stain doesn’t work if the copper is too diffuse. Wilson’s disease is an often missed dx.
Classic Wilson’s disease looks like (acute/chronic) liver disease in a person ? y.o. with (eyes). Commonly presents between (?-??) y.o.
Children more often present with _____
Adults present with ________ symtoms
Classic Wilson’s disease looks like chronic liver disease in a person <40 y.o. with KF rings. Commonly presents between 8-18 y.o.
Children more often present with liver disease
Adults present with neurological symtoms
Wat dis?
cirrhotic liver
Histologically, a cirrhotic liver will have ____ and ______
Histologically, a cirrhotic liver will have fibrosis and nodular changes
If you’re patient looks like this guy, it’s probably ascites. You should (imaging) to confirm the increased girth is fluid. To confirm the ascites is 2/2 cirrhosis, calculate a _____. A ___ >___ is sensitive for cirrhosis.
If you’re patient looks like this guy, it’s probably ascites. You should u/s to confirm the increased girth is fluid. To confirm the ascites is 2/2 cirrhosis, calculate a serum-ascites albumin gradient (SAAG). A SAAG >1.1 is sensitive for cirrhosis.
______ are the most common benign tumor of the liver. They are usually diagnosed radiographically. They are composed of vascular lining, and if they are large, the might be resected to prevent bleeding.
Hemangiomas are the most common benign tumor of the liver
Focal nodular hyperplasia is the ____ most common benign lesion. They predominantly affect (gender). Grossly, they have a ____. The proliferation is reactive and so has ____ risk of malignancy. Histology shows ______
Focal nodular hyperplasia is the second most common benign lesion. They predominantly affect women. Grossly, they have a central stellate scar. The proliferation is reactive and so has zero risk of malignancy. Histology shows bland hepatocytes, big vessels, and disorganized bile ducts
Hepatocelluar carcinoma is almost always associated with _____. Patients will have elevated (lab). The most common molecular alterations are __ and ______. On histology, will see _____ hepatocytes with funky looking ____. You can treat with resection, ablation, or transplant, but the bigger the lesion, the worse the prognosis.
Hepatocelluar carcinoma is almost always associated with back ground liver disease, esp. hepatitis. Patients will have elevated alpha fetal protein. The most common molecular alterations are TP53 and beta-catenin. On histology, will see thickened plates of hepatocytes with funky looking nuclei. You can treat with resection, ablation, or transplant, but the bigger the lesion, the worse the prognosis.
Cholangiocarcinoma has a lot of disorganized _____ on histology with prominent ____. The most common molecular alterations are ____ or ____. Treatment includes ______ or _____ ______, but prognosis is poor.
Cholangiocarcinoma has a lot of disorganized glands on histology with prominent stroma. The most common molecular alterations are KRAS or IDH1. Treatment includes resection or systemic therapy, but prognosis is poor.
Angiosarcomas occur predominantly in (gender) and are exceedingly rare. They associated w/ exposure to ___ and ______. On histology, it looks like a bunch of _______ The most common molecular mutation is ___. There is ____ therapy.
Angiosarcomas occur predominantly in men and are exceedingly rare. They associated w/ exposure to vinyl chloride (e.g. factory work) and thorotrast. On histology, it looks like a bunch of ugly disorganized blood vessels. The most common molecular mutation is p53. There is no effective therapy.
