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GI Exam 2 > More Liver Pathology > Flashcards

More Liver Pathology Flashcards

1
Q

Whcih region of liver structure affected first with hepatic injury?

A

ZONE 3 - zone around the central vein - already low in O2 and P450s need O2!! –> drug induced injury

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2
Q

What are intrinsic drug reactions? characteristics?

A
  • predictable
  • dose-dependent
  • short latency
  • specific lesions
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3
Q

What are idiosyncratic drug reactions? characteristics?

A
  • unpredictable
  • dose dependent
  • variable latency
  • variable lesions
  • hypersensitivity
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4
Q

What kind of drug induced liver disease morphology with tetracycline?

A

microsteatosis

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5
Q

What kind of drug induced liver disease morphology with methotrexate?

A

macrosteatosis

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6
Q

What kind of drug induced liver disease morphology with acetaminophen?

A

necrosis

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7
Q

What kind of drug induced liver disease morphology with isoniazid and halothane?

A
  • hepatitis -

- bridging necrosis (with halothane)

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8
Q

What kind of drug induced liver disease morphology with amiodarone?

A

fibrosis

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9
Q

What kind of drug induced liver disease morphology with steroids and erythromycin?

A

cholestasis

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10
Q

Drink some alcohol - immediate change that happens to liver?

A
  • steatosis - fatty liver change that is REVERSIBLE

- perivenular fibrosis

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11
Q

Severe Drinking of alcohol - change that happens to liver?

A
  • hepatitis
  • liver cell necrosis
  • inflammation
  • mallory bodies
  • fatty change - starts out microvesicular and fat coalesces into macrovesicles
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12
Q

Repeated/heavy drinkers - what change that happens to liver?

A

Cirrhosis

  • fibrosis
  • hyperplastic nodules - micronodular
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13
Q

Macro-view of the alcoholic fatty liver?

A

ITS YELLOW - FAT IS YELLOW

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14
Q

what kind of nodular cirrhosis occurs with alcoholic cirrhosis?

What kind of fatty liver change occurs with alcoholic cirrhosis?

A

Micronodular - due to bridging fibrosis

macrovesicular

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15
Q

What are mallory bodies?

A

glob of protein - hylaine! that aggregates in certain diseases
ex) alcoholic hep and wilsons disease

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16
Q

megamitochondria seen in which liver disease?

A

alcoholic hepatitis

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17
Q

Chicken wire fibrosis in space of dis occurs in which liver disease?

A

alcoholic hepatitis long-term abuse

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18
Q

Alcoholic steatohepatitis Clinical/LABS:

A
  • fever
  • leukocytosis
  • jaundice
  • INC AST and ALT (AST»ALT)
  • INC AP (inc with cholestasis)
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19
Q

Alcoholic liver AST to ALT relationship

A

AST will be almost twice as high as ALT

AST - A.”S.T.” for scotch and tonic

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20
Q

Non-Alcoholic steatohepatitis- what risks?

A
  • insulin reisistance/metabolic syndrome (obesity, diabetes, hyperlipidemia)
  • drug hepatotoxicity (tamoxifen (macrovesicular), nifedipine)
  • pregnancy (microvesiculuar)
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21
Q

Liver infarction:

-common?

A

rare bc of dual blood supply!

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22
Q

Ischemic hepatitis, shock liver or hypoxic hepatitis - THINK WHAT PROBLEMS?

A

**LEFT SIDED/VENTRICULAR HEART FAILURE

heart surgery

shock - centrilobular coagulative necrosis (around central veins - ZONE 3 drup); elevated transaminases; jaundice

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23
Q

Extrahepatic portal vein thrombosis due to:

A

1) abdominal infection & inflamm
- appendicitis
- diverticulitis
- pancreatitis
2) hypercoagulability
3) surgery

extra ==> send emboli to the liver

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24
Q

Intrahepatic portal vein thrombosis due to?

A

Issues inside the liver

1) cirrhosis
2) malignancy
3) stasis
4) pregnancy
5) idiopathic PH

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25
Q

Clinical presentation of portal vein hypertension?

A 
-abdominal pain
portal hypertension (ascites, varices, splenommegaly)
-Bowel infarct
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26
Q

Infarct of Zahn happens with which liver condition?

A
  • not a true infarct bc the cells dont actually die - just atrophic hepatocytes
  • INTRAHEPATIC portal vein thrombosis
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27
Q

Budd Ciari syndrome involves what?

A

hepatic vein obstruction - the LARGER VEINS

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28
Q

Hepatic vein obstruction conditions:

A

1) Cardiac MORE COMMON - BACK PRESSURE FROM R SIDED FAILURE; constrictive pericaditis; congenital heart issues
- venous passive congestion
- centrilobular hemorrhagic necrosis
- cardiac sclerosis
2) Budd-Chiari syndrome

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29
Q

First sight of hepatic vein obstruction?

A

DILATED SINUSOIDS

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30
Q

Nutmeg liver seen with which condition- what is it?

A
  • hepatic vein obstruction

- blood backs up and makes nutmeg looking liver

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31
Q

Damage to what zone in the liver?

A

Zone 3 but this time the cause is NOT hypoxic but rather HIGH BACK-PRESSURE RELATED

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32
Q

Definition of Budd CHiari syndrome:

A

clotting or obstruction of the hepatic vein and or IVC!

33
Q

Acute Bud Chiari Syndrome clinical signs:

A
  • abdominal pain
  • hepatomegaly
  • ascites
  • jaundice
  • liver failure
34
Q

Chronic Bud Chiari syndrome clinical signs:

A

portal hypertension

  • cirrhosis
  • obliterative hepatocavopathy (rare)
35
Q

Obliterative hepatocavopathy - what is it: causes?

A

IVC obstruction due to membranous webs that causes edema of the abdominal wall, tortuous abdominal venous pattern, and edema of legs

36
Q

Veno-occlusive disease:
how does it happen?
what happens?

A

VOD - complication following bone marrow transplant or ingestion of certain plant alkaloids
-nonspecific vasculitis arrising in response to an inflammatory challenge = sinusoid obstruction- obstruction of central veins

37
Q

Hereditary hemochromatosis
what is it?
what gene involved??

A
  • abnormal continuous iron absorption through the gut
  • deposition of iron throughout the body

-MUTATION IS HFE GENE**

38
Q

What are the mutant alleles in hereditary hemochromatosis

A

C282Y and H63D

39
Q

Early hereditary hemochromatosis

-where are the deposits?

A

-Fe in periportal hepatocytes

40
Q

Advanced hereditary hemochromatosis

-where are the deposits?

A

Fe in Kupffer cells, bile duct epithelium, and fibrous septa

41
Q

What does Hereditary hemochromatosis progress to?

A
  • pigmented micronodular cirrhosis

- HCC

42
Q

Labs/Diagnosis of Hereditary hemochromatosis?

A
  • INC serum Fe > 300mg/dL
  • inc Transferrin saturationg>2X
  • INC serum ferritin>2X
  • INC hepatic Fe index>2

–> if transferrin and ferritin are both high then genetic testing for C282Y or H63D*

43
Q

hereditary hemochromatosis

-disease outcomes:

A
  • diabetes
  • cardiomyopathy
  • hypogondism
  • skin pigementation
  • pseudo-gout
44
Q

hereditary hemochromatosis on microscopy-

A

A lot of brown pigment deposition in stuff

or iron looks blue with prussian blue stain

45
Q

Secondary iron overload -

mnemonic to remember outcomes

A

THALAS

  • T-Transfusions
  • H-hemochromatosis, neonatal
  • A-alimentary (bantu siderosis) - from diet
  • L-Liver disease
  • A-Anemia, congenital (thalessemia)
  • S-Sideroblastic anemia

Most commonly due to anemia

46
Q

Secondary hemochromatosis vs hereditary?

A

-not as much in hepatocytes but a lot more in kupffer cells

47
Q

Coppuer function -

A

essential for pigment formation, neurotransmitter production, peptide formation, connective tissue biosynthesis and antioxidant defense –THINK WILSONS DISEASE

48
Q

Wilson Disease

  • What is the problem
  • where is the accumulation?
  • who affected?
A

-TOO MUCH COPPER - hereditary (autosomal recessive) - body retains copper

-BRAIN-LIVER- EYE**
Some in basal ganglia

younger disease 6- 20 yo but sometimes in 40yo+

49
Q

What is the protein that copper binds to?

A

ceruloplasmin

50
Q

What are the labs in WIlsons disease?

A
  • DEC serum ceruloplasmin250microg/g tissue
  • inc urinary copper up to 100microg/24 rs
  • Kaiser fleischer rings
51
Q

Main Organs damaged in wilsons disease?

A

BRAIN
LIVER
EYE

52
Q

What is mutation in Wilsons disease?

A

mutation in ATP7B copper transporter

53
Q

Progression of wilsons disease?

A

steatosis –> hepatitis –> cirrhosis

  • degeneration of basal ganglia
  • aminoaciduria
  • hemolytic anemia
  • cardiomyopathy
54
Q

Adults with wilsons disease usually present with?

A

neurologic and psychiatric issues –> deposits in the brain

55
Q

What are Kaiser-Fleisher rings?

What disease

A
  • Wilsons disease

- eyes have brown ring on outside rim of iris

56
Q

Alpha1 antitrypsin deficiency

  • hereditary inh?
  • gene involved?
  • what happens?
A
  • auto recessive
  • normal gene is PiMM - PiZZ genotype (PiZ protein made)
  • misfolded protein –> accumulation of PiZ in hepatocytes–>reduced intracellular protein degredation and increased autophagocytosis
57
Q

Diagnosis/LABS for alpha1 antitrypsin def:

A
  • low serum alpha1-antitrypsin
  • abnormal electrophoresis of the protein
  • liver biopsy (PAS+ = pink/magenta color)
58
Q
  • tumor like conditions:

- feature of each?

A
  • nodular regenerative hyperplasia = NO FIBROUS TISSUES MAKING MULTIPLE NODULES
  • focal nodular hyperplasia = single lesion
59
Q

focal nodular hyperplasia

  • what is it?
  • sex prevalence?
A
  • benign liver tumor

- women - usually associated with estrogen

60
Q

Features of focal nodular hyperplasia:

A
  • Solitary mass with central scarring

- fibrous septa

61
Q

nodular regenerative hyperplasia

  • definition/characteristics:
  • -causes what main issue?
A
  • nodules without fibrous septa

* *-cause of non-cirrhotic portal hypertension

62
Q

What is the TIPS procedure?

A

bypass of liver from portal vein to hepatic vein - for nodular regenerative hyperplasia

63
Q

hemangioma

  • prevalent sex?
  • symptoms?
  • risk?
A
  • most common benign hepatic tumor
  • more common in women - associated with oral contraceptives
  • asymptomatic or abd pain
  • risk of rupture and hemorrhage – no biopsy bc itll bleed!
64
Q

most common benign hepatic tumor?

A

hemangioma

65
Q

liver cell adenoma

  • benign/malig?
  • prevalent sex?
  • predisposing factors?
  • risk?
A

BENIGN

  • women
  • oral contraceptives; glycogen storage disease
  • may rupture in pregnancy; may harbor HCC (if more than 10 lesions)
66
Q

HCC

  • predominant sex?
  • common where?
A
  • males, african amerincas
  • Asia and africa
  • associated with HepB transmission at birth
67
Q

Most common primary malignant liver tumor?

A

HCC

68
Q

Main risk factor for HCC/

A 
cirrhosis
alcoholism
HBV HCV
hereditary hemochromatosis
-alpha1 antitrypsin
-alflatoxin from aspergillus
-tyrosinemia
69
Q

How does HCV cause HCC?

A

genomic instability - inflammation drive toward cancer

-no particular proteins involved

70
Q

How does HBV cause HCC?

A
  • has viral DNA integration damage AND LHBS mutant protein –> genomic instability

PROTEINS IN HBV contribute to HCC while HCV is only genomic.

71
Q

HCC diagnosis/LABS

A
  • ultrasound
  • angiography
  • CT
  • MRI
  • INC AFP>1000*****
72
Q

What is the only “good” variant of HCC? What age patients get this?

A

fibrolamellar HCC - better prognisosis - broad bands of fibrosis

young patients

73
Q

Cholangiocarcinoma - what is proliferating tissue?

A

GLANDS

74
Q

Cholangiocarcinoma

  • what is it?
  • risk factors:
A
  • malignant primary tumor of the bile duct epithelium
  • primary sclerosing cholangitis
  • thorotrast (come contrast agent we dont use anymore)
  • caroli disease (dilation of biliary system)
  • liver flukes - clonorchis opistorchis**
75
Q

hepatoblastoma

  • age?
  • associated conditions?
  • markers?
A
  • <3 yo
  • congenital
  • AFP is very high!
76
Q

most common primary malignant hepatic tumor in children?

A

heptoblastoma

77
Q

Angiosarcoma

  • what population? age?
  • exposure to what inc risk?
A

-men 50s-60s
-exposure to thorotrast, vinyl chloride, arsenic, androgenic steroids
POOR PROGNOSIS

78
Q

*most common tumor of the liver?

A

cancer that has spread to the liver

79
Q

What are the common primary sites for metastatic tumors in liver?

A

-GI, breast, lung, pancreas, melanoma

GI Exam 2 (11 decks)

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