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Block 10 week 4 > Liver II-Usera > Flashcards

Liver II-Usera Flashcards

1
Q 
What is this:
idiopathic, chronic progressive hepatitis.
What gender is it more common in?
What is the defect?
What can trigger it?
A

Autoimmune hepatitis
females
defective T-Cell regulation
Infection, acute illness, drugs

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2
Q

Autoimmune hepatitis is associated with other (blank) disease

A

autoimmune

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3
Q

In autoimmune hepatitis, what will the cell infiltrate look like?
What will the labs look like?

A

portal plasma

Elevated serum IGG and T-globulin levels

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4
Q

What are the drugs that can cause autoimmune hepatitis?

A 
Minocycline
Statins
Methyldopa
Interferons
Nitrofurantoin
Herbal products
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5
Q

What antibodies will be present in autoimmune hepatitis?

A
  • anti-nuclear antibodies (ANA)
  • anti-smooth muscle antibodies (SMA)
  • anti-actin antibodies (AAA)
  • anti-soluble liver antigen/liver pancreas antigen antbodies (SLA/LP)
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6
Q

What is type 1 autoimmune hepatitis associated with?

A

HLA-DR3 serotype

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7
Q

What are the antibodies to type 2 autoimmune hepatitis?

A

anti-liver kidney microsome-1
antibodies (ALKM-1) (directed against CYP2D6)
anti-liver cytosol-1 antibodies (ACL-1)

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8
Q

What is the most common cause of fulminant hepatitis?

(blank) percent of adverse drug reaxns result in toxicity

A

toxicity

10%

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9
Q

Hepatic injury because of toxicity is due to one of three mechanisms, what are they?

A
  • direct injury
  • injury due to toxic metabolites
  • immunogenic
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10
Q

Why is acetaminophen the worst?

A

it binds to liver and idney causing toxicity

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11
Q

How long does it take for hepatic toxicity to occur?

A

weeks to motnhs

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12
Q

What injury is associated with this:

contraceptives, anabolic steroids, estrogen replacement therapy

A

cholestatic

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13
Q

What injury is this associated with:

antibiotics and phenothiazines

A

cholestatic hepatitis

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14
Q

What injury is this associated with:

methyldopa, phenytoin, acetaminophen, halothane, isoniazid, phenytoin.

A

Hepatocellular necrosis

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15
Q

What inury is this associated with:

ethanol, methotrexacte, corticosteroids, total parental nutrition

A

Steatosis

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16
Q

What injury is associated with this:

amiodarone, ethanol

A

steatohepatitis

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17
Q

What injury is associated with this:

methotrexate, isoniazid, enalapril

A

Fibrosis and cirrhosis

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18
Q

What injury is associated with this:

sulfonamides

A

granulomas

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19
Q 
What injury is associated with this:
High-dose chemotherapy, bush teas
Oral contraceptives
Oral contraceptives
Anabolic steroids, tamoxifen
A

Veno-occlusive disease, obliteration of central veins
Budd-Chiari syndrome
Sinusoidal dilation
Peliosis hepatis

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20
Q 
What injury is associated with this:
Oral contraceptives, anabolic steroids
Thorotrast
Thorotrast
Thorotrast, vinyl chloride
A

Hepatic adenoma
HCC
Cholangiocarcinoma
Angiosarcoma

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21
Q

What kind of necrosis occurs with acetaminophen toxicity?

A

perivenular necrosis

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22
Q

What kind of fibrosis do you get with ethanol toxicity?

A

perivenular fibrosis with perisinusoidal extension

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23
Q

What are the histological findings of drug and toxins on hepatocytes?

A

cholestasis
cholestatic hepatitis
ballooning degeneration
hepatocyte necrosis

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24
Q

What is this:
Rare and potentially fatal syndrome of mitochondrial dysfunction in liver and brain

What is it characterized?

What is it associated with?

A

Reye syndrome

extensive microvesicular stetosis

Administration of aspirin (acetylsalicyclic acid) i.e you should avoid use of aspirin in children

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25
Q

What are the clinical features of alcoholic liver disease?

A

appears acutely after heavy drinking episode

  • anorexia
  • weight loss
  • upper abdominal discomfort
  • tender hepatomegaly
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26
Q

(blank) is a type of liver disease, characterized by inflammation of the liver with concurrent fat accumulation in liver.

A

Steatohepatitis (also known as fatty liver disease)

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27
Q

What is the final stage of alcoholic liver disease?
Is this reversible?
What percent of patients develop cirrhosis?

A

alcoholic cirrhosis
no
10-15%

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28
Q

What is hepatic steatosis?

Is it reversible?

A

microvesicular and macrovesicular steatosis

Fatty change is reversible with abstention from alcohol

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29
Q

What are the clinical features of hepatic steatosis?

A
  • mild elevation of serum bilirubin and alkaline phosphatase

- severe hepatic dysfunction is unusual

30
Q

What is indicative of alcoholic steatohepatitis?

A 
hepatocyte swelling (ballooning degeneration)
mallory bodies
31
Q

What does hepatocyte swelling look like?

A

swollen cells, feathery cytoplasm, reactive, not pathological

32
Q

(bank) fibrosis is specific for alcoholic fibrosis/ethanol toxicity, Where does the fibrosis start? What does the necrosis look like in fatty liver disease? What is it characterized by?

A

perisinusoidal, central vein
spotty necrosis throughout the lobular
pain, anorexia, lethargy

33
Q

What kind of inflammation do you have in alcoholic hepatitis?
What kind of inflammation do you have in viral and autoimmune hepatitis?

A

lobular inflammation

Periportal inflammation

34
Q

What are the 2 types of metabolic liver disease?

A

Inherited or acquired disorders of metabolism

35
Q

What is the acquired metabolic liver disease?

A

non-alcoholic fatty liver disease

36
Q

What is the inherited metabolic liver disease?

A
  • hemochromatosis
  • wilson disease (build up of copper)
  • A1-anti-trypsin deficiency
37
Q

What is the most common cause of chronic liver disease in the US? What type of person does this typically present in?

A

Nonalcoholic fatty liver disease

70% of obese people

38
Q

What are the group of conditions associated with nonalcoholic fatty liver disease?

A
  • hepatic steatosis
  • steatosis with minor inflammation
  • non-alcoholic steatohepatitis (NASH)
39
Q

What are the clinical findings of nonalcoholic fatty liver disease?

A 
Asymptomatic (steatosis)
Elevated AST/ ALT
Fatigue 
Malaise
Right sided abdominal pain
40
Q

In nonalcoholic fatty liver disease, you will get hepatic steatosis (with/without) inflammation and is a (unstable/stable) condition without significant clinical problems

A

with or without

stable

41
Q

In non alcoholic fatty liver disease (NASH), there will be hepatocyte injury with progression to (Blank) in 10-20% of cases. It is strongly asociated with (blank) and (Blank).

A

cirrhosis

Obesity and metabolic syndrome

42
Q

NASH (nonalcoholic fatty liver disease) is the most common cause of (Blank)

A

cryptogenic cirrhosis

43
Q

What is this:

primary and secondary disorder of excessive body iron accumulation

A

Hemochromatosis

44
Q

(blank) is a homozygous recessive inherited disorder of excessive body iron absorption

A

Primary hemochromatosis

45
Q

Secondary iron accumulation (hemosiderosis) is due to (blank)

A

acquired causes

46
Q

In hereditary hemochromatosis what are the mutations?

A
  • HFE
  • Transferrin receptor 2
  • Hepcidine genes
  • HJV gene
47
Q

What causes hemosiderosis?

A 
Parenteral iron overload
Ineffective erythropoiesis with increased erythroid activity
Increased oral iron intake
Congenital atransferrinemia
Chronic liver disease
Neonatal hemochromatosis
48
Q

In hemochromatosis, normal total body iron is (blank) GM. Regulation of intestinal absorption of dietary iron is (blank).
Iron accumulates at a rate of (blank) /year
The disease will manifest after (blank) GM have accumulated.
Iron levels may reach (blank) with >30% accumulated in the liver

A 
2-6 GM
abnormal
0.5-1.0 GM/year
20 GM
50 GM
49
Q

Hemochromatosis presents early in life or late in life? If you suspect this, what are the first things you should look at? When should you send for genetics?

A

late
transferrin and iron sat (first thing that goes up)
-When iron sat gets greater than 50%

50
Q

(blank) is directly toxic to tissues

Why?

A

Iron

  • lipid peroxidation through Fe-catalyzed free radical production
  • stimulation of collagen formation through activation of hepatic stellate cells
  • interaxn of ROS and Fe w/ DNA leading to lethal cell injury
51
Q

The effects of Fe are (reversible/irreversible) in cells that are not fatally injured

A

reversible

52
Q

What is the main regulator of Fe absorption by lowering plasma Fe levels?
How does it work?

A

Hepcidin

an efflux channel ferroportin that prevents release of Fe from intestinal cells and macrophages

53
Q

What does a deficiency in hepcidin result in?

A

iron overload

54
Q

What does HJV do?

What can mutations in this cause?

A

regulates hepcidin levels

severe juvenile hemochromatosis

55
Q

What does transferrin receptor 2 do?

What will mutations in this cause?

A

regulates hepcidin levels

classic adult hemochromatosis

56
Q

What does HFE do?

What would a mutation in this cause?

A

Regulates hepcidin leels

calssic adult hemochromatosis

57
Q

What regulates hepcidin?
What will cause classic adut hemochromatosis if there is a mutation in it?
What will cause severe juvenile hemochromatosis?

A

HFE
Transferrin receptor 2
HJV

Classic Adult: transferrin receptor 2 and JFE
-HJV

58
Q

What all does hemochromatosis affect?

A
  • liver
  • pancreas
  • myocardium
  • pituitary
  • adrenal
  • thyroid
  • parathyroid
  • joints
  • skin
59
Q

What gender is hemochromatosis more common in?
What age do symptoms appear?
What are physical signs you will see?
What are other diseases that result form this?

A

men
50-60s

hepatosplenomegaly
skin pigmentation
abdominal pain

DM
Arthritis
hypogonadism
cardiac dysfunction

60
Q

Where is iron located in hemosiderosis?

A

in the macrophages (kupffer cells) and if prolonged, goes to hepatocytes

61
Q

What is this:
Disease of unknown origin manifested by severe liver disease and extrahepatic hemosiderin deposition
Not an inherited disease

What do people speculate this is due to?

A

Neonatal Hemochromatosis

liver damage happens in utero due to maternal alloimmune injury to fetal liver

62
Q

Wilison disease is a (blank) disorder caused by a mutation in the (Blank) gene.

A

AR

ATP7B

63
Q

What is the pathology of Wilsons diseae?

A
  • Impaired copper excretion into bile
  • failure to incorporate copper into ceruloplasmin
  • inhibition of ceruloplasmin secretion into blood
64
Q

How will Wilson’s disease clinically manifest?

A

Liver-steatosis, hepatitis, cirrhosis

Brain-atrophy of the basal ganglia and putamen

Eye- Kayser-Fleischer Rings

65
Q

What is the most common way to get Wilson disease and what is the gene that is mutated?

A

Compound heterozygotes

ATP7B

66
Q

What are the really sad consequences of Wilson disease?

A

Chronic liver disease

Neuropsychiatric manifestations

67
Q

How do you diagnose Wilson disease?

WHAT LEVELS SHOULD YOU NOT GET!!?!?!?

A
  • Serum ceruloplasmin levels
  • Increase in hepatic copper content
  • Increased urinary excretion of copper

-Do not use SERUM copper levels

68
Q

Alpha 1 antitrypsin is an (blank) disorder that is characterized by decreased inhibition of (blank).

A

proteases (i.e increased proteases)

69
Q

A1 antitrypsin deficiency manifests as (blank) and (blank)

A

pulmonary emphysema

Liver disease

70
Q 
Where is A1 antitrypsin synthesized? What kind of protease inhibitor is it?
It is (blank)morphic with at least (bank) forms identified
A

liver
Serine protease inhibitor
poly
75

71
Q

What are the common genotypes for a1 antitrypsin deficiency?

A

PiMM (90% of people)
PiZZ (clinically significant mutation)
PiMZ

Block 10 week 4 (10 decks)

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