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Pathoma Ch 11 - Exo Pancreas & Liver > 11.5 - Liver - Cirrhosis & Tumors > Flashcards

11.5 - Liver - Cirrhosis & Tumors Flashcards

1
Q

What cell mediates the fibrosis in cirrhosis? What factor?

A
  • Stellate cells (lie beneath endothelial cells that line the sinusoids)
  • TGF-beta
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2
Q

clinical feature of cirrhosis?

A 
-Portal HTN
=ascites
=congestive splenomegaly and hypersplenism
=portosystemic shunts
=hepatorenal system
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3
Q

Result decreased detox due to cirrhosis?

A
  • mental status changes (ammonia). asterixis, coma
  • Due to excess estrogen: gynecomastia, spider angiomas, and palmar erythema
  • jaundice
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4
Q

Results of decreased protein synthesis?

A
  • hypoalbuminemia

- coagulogpathy (use PT and PTT to measure cirrhosis)

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5
Q

Alcohol liver diseases: manifestations:

A

1) fatty liver: accumulation of fat in liver - resolves with abstinence - greasy-shiny-yellow liver on gross examination
2) alcoholic hepatitis: chemical injury to hepatocytes DUE TO ACETALDEHYDE (binge drinking) -swelling and ballooning of hepatocyte
- mallory bodies=damaged intermediate filaments (hyaline?)
3) cirrhosis - chronic alcohol induced liver damage

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6
Q

Presentation of alcoholic liver disease?

A
  • painful hepatomegaly
  • elevated AST and ALT (*AST>ALT in 2:1 ratio)

S.T for scotch and tonic

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7
Q

Non-alcoholic fatty liver disease

  • what is it?
  • How develops?
  • common association?
A
  • Faty change, hepatitis &/or cirrhosis
  • develops without exposure to alcohol or other known insult
  • usually due to metabolic syndrome/obesity
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8
Q

non-alcoholic fatty liver disease

-Diagnostic finding that is golden?

A

Diagnosis of exclusion: ALT>AST!

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9
Q

Why is AST higher in alcohol related damage?

A
  • AST is found throughout the body and especially mitochondria
  • alcohol is especially toxic to mitochondria = more AST

(aLt - L for Liver - is more liver specific than AST)

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10
Q

hemochromatosis

  • what is it?
  • how is damage caused?
A
  • excess body iron leading to deposition in tissues and organ damage
  • damage is mediated by generation of free radicals (FENTEN REATION)
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11
Q

Hemosiderosis vs Hemochromatosis

A

Sid=just accumulation in tissues

chrom=actual damage occuring

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12
Q

Secondary hemochromatosis causes:

A

THALAS

  • T=transfusions
  • H=hemochromatosis/neonatal
  • A=alimentary - from diet
  • L=liver disease
  • A=anemia
  • S=sideroblastic anemia
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13
Q

Primary hemochromatosis is due to?

A
  • mutations in HFR gene

- C282Y and H63D

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14
Q
  • Mechanism for iron uptake:

- Mechanism for hemochromatosis?

A
  • GI enterocytes pretty much take up all iron from diet
  • they only release it into the blood when there is a need.. otherwise they hold onto it (KEY REGULATORY MECH FOR IRON)

-so in hemochromatosis this regulatory mech isnt working (HFE gene mutation) and the enterocytes pretty much dump all the iron into the blood

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15
Q

Presentation of hemochromatosis:

A

Late adulthood - iron takes time to accumulate in body

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16
Q

Complications of hemochromatosis:

A

Classic triad:

  • cirrhosis
  • secondary diabetes mellitus
  • bronze skin

Others:

  • cardiac arrhythmia
  • gonadal dysfunction
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17
Q

Hemochromatosis - labs

A
  • INC ferritin
  • DEC TIBC
  • INC serum iron
  • INC % saturation
18
Q

Biopsy of hemochromatosis liver:

A
  • Brown pigment in hepatocytes

- prussian blue stain makes iron blue

19
Q

Tx for hemochromatosis?

Inc risk for?

A
  • phlebotomy

- HCC risk

20
Q

Wilsons disease

  • how do you get this disease?
  • what ahppens?
A
  • autosomal recessive defect in ATP7B gene which is ATPmediated hypatocyte copper transport
  • lack of copper transport into bile and lack of copper incorporation into ceruloplasmin
21
Q

Issues with Wilsons disease?

A
  • copper builds up in hepatocytes –> leaks into serum –> deposits into tissues
  • Copper produces free radicals = tissue damage
22
Q

When does Wilsons present?
Symtpoms in patient?
Inc risk?
TX?

A

-childhood

  • neurologic manifestations
  • Kayser-Fleisher rings in cornea
  • HCC risk increased
  • Tx with D-penicillamine (copper chelating agent
23
Q

Wilsons disease- LABS

A
  • INC urinary copper
  • DEC serum ceruloplasmin
  • INC copper deposit on liver biopsy
24
Q

Primary biliary cirrhosis (PBC)

  • what is it?
  • classic patient?
A
  • autoimmune granulomatous destruction of intrahepatic bile ducts (SMALL DUCTS)
  • middle aged women most common
25
Q

Serum marker for Primary biliary cirrhosis?

A

anti-mitochondrial antibody

26
Q

PBC

  • early presentation?
  • late complication?
A
  • obstructive jaundice

- cirrhosis later in course

27
Q

Primary sclerosing cholangitis (PSC)

  • what is it/what happens?
  • classic appearance with imaging?
A
  • inflammation and fibrosis of intrahepatic and extrahepatic bile ducts (LARGE DUCTS)
  • periductal fibrosis - “onion skin” & uninvolved regions look dilated = “beaded” appearance
28
Q

What other condition is usually associated with PSC?

A

Ulcerative colitis (also have P-ANCA+)

29
Q

Serum marker for PSC?

A

P-ANCA +

30
Q

PSC

  • early presenation
  • complication/risks?
A

-obstructive jaundice

  • cirrhosis
  • cholandiocarcinoma
31
Q

Reye Syndrome

  • How to get?
  • mechanism for disease?
A
  • fulminant liver failure and encephalopathy in CHILDREN with viral illness who take aspirin
  • related to mitochondrial damage of hepatocytes
32
Q

Presentation and progression of Reye Syndrome:

A
  • hypoglycemia
  • elevated liver enzymes
  • nausea + vomit

-Coma and death

33
Q

What disease present like a viral illness and you DO/CAN give aspirin for it?

A

Kawasaki syndrome - vasculitis of coronary arteries with conjunctivits and fever + other viral like symtpoms

34
Q

Hepatic Adenoma

  • what kind of tumor-ben/mal?
  • associations?
  • Risk?
A
  • benign tumor of hepatocytes
  • Associate with oral contraceptives - stop drug = less risk
  • Risk of rupture (tumors are subcapsular=easily ruptured) and intraperitoneal hemorrhage - especially during pregnancy
35
Q

Risk factors for HCC?

A
  • chronic hep (HBV, HCV)
  • cirrhosis (ANY CAUSE)
  • aflatoxins (induce p53 mutations) from aspergillus
36
Q

What is budd-chiari syndrome

A

-liver infarct secondary to hepatic vein obstruction -thrombosis (usually can be due to HCC which invades and blocks the hepativ vein

37
Q

Causes of Budd-Chiari syndrome?

A

-HCC

38
Q

Serum marker for HCC?

A

alpha-fetoprotein (AFP)

39
Q

Most common type of liver tumor?

A

Metastasis to the liver!

40
Q

Most common origin sites for mets to liver?

A
  • colon
  • pancreas
  • lung
  • breast carcinomas

Pathoma Ch 11 - Exo Pancreas & Liver (5 decks)

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