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GI > Hepatic Inflammation and Fibrosis > Flashcards

Hepatic Inflammation and Fibrosis Flashcards

1
Q

What are the 5 stage of fibrosis?

A 
0 - No fibrosis
1 - Portal fibrosis
2 - Periportal fibrosis
3 - Septal fibrosis 
4 - Cirrhosis
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2
Q

Acute liver failure complicated by coagulopathy and encephalopathy

A

Fulminant liver failure

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3
Q

What is the most common cause of acute and fulminant liver failure?

A

Medications (acetaminophen)

Viral hepatitis

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4
Q

What constitutes heavy drinking for women and men?

A 
Women = more than 1 drink per day on average
Men = more than 2 drinks per day on average
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5
Q

What enzyme takes ethanol to acetaldehyde? How much is metabolized by this?

A

Alcohol dehydrogenase – 75-80%

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6
Q

What is another mechanism by which ethanol is metabolized?

A

Microsomal Ethanol Oxidizing System (MEOS) – 20-25%

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7
Q

What is the enzyme that many asians have a mutation in?

A

Aldehyde dehydrogenase

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8
Q

What are some consequences of alcohol metabolism?

A

Increased NADH – inhibits TCA cycle, reduces gluconeogenesis; reduced fatty acid oxidation

Increased acetaldehyde – activates stellate cells to form collagen, microfilaments are sheared, Kupffer cells produce TNFa

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9
Q

What does the histology of alcoholic hepatitis look like?

A

Fat cells and inflammatory cells

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10
Q

What are some risk factors for ALD?

A

Quantity of alcohol (>30g/day in men or >20g/day in women)
Drinking on an empty stomach
Binge drinking
Hep C

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11
Q

What lab abnormalities can be found with ALD?

A 
AST/ALT ration >2-3
ALT usually <300 
Rarely raised alk phase 
Low albumin
Prolonged INR (advanced) 
Macrocytosis/anemia 
Thrombocytopenia (advanced)
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12
Q

Treatments for alcoholic hepatitis

A

Abstinence and lifestyle modifications

Anti-inflammatory drugs = Glucocorticoids, Pentoxifylline–inhibits TNFa

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13
Q

What is the equation to determine when to treat alcoholic hepatitis?

A

4.6 (PT - PT control) + T BILI

If >32 have 1 month mortality from 30-50%

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14
Q

Why is pentoxifylline preferred in a patient that has an active infection?

A

Steroids will make it worse!

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15
Q

Most common cause of elevated transaminases in the US.

A

Non-alcoholic fatty liver disease

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16
Q

What are the two histological classes of NAFLD?

A
  1. Non-alcoholic fatty liver (NAFL) = presence of hepatic steatosis without inflammation or hepatocellular injury
  2. Non-alcoholic steatohepatitis (NASH) = presence of hepatic steatosis and inflammation with hepatocellular injury with or without fibrosis
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17
Q

What are the stages in progression of NAFLD?

A

Fatty liver (Hepatosteatosis) –> Steatohepatitis (NASH) –> Steatohepatitis with fibrosis –> Cirrhosis

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18
Q

What is NAFL associated with?

A

Metabolic syndrome

  1. Obesity
  2. Diabetes
  3. Hypertriglyceridemia - 3 fold greater risk with triglycerides > 200
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19
Q

Who is particular susceptible to NAFLD?

A

Increased age
Males > Females
Hispanics > Caucasians > African Americans

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20
Q

What is the most common liver disease in children in the US?

A

NAFLD

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21
Q

Some common causes of steatosis and steatohepatitis to be aware of.

A

Alcohol
Medications = amiodarone, steroids, HAART, tamoxifen, diltizem
Nutritional: TPN, weight changes - gastric bypass

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22
Q

How can a fatty liver be diagnosed on ultrasound?

A

Fat comes out bright and if nodules are observed = NASH

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23
Q

What are some treatments for NAFLD?

A

Diet/exercise
Gastric band
Orlistat

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24
Q

How much of your body weight must you lost to improve steatosis? How much to improve inflammation?

A

3-5% to improve steatosis

10% to improve inflammation

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25
Q

What are some treatment options for non-diabetic NAFLD?

A

Vitamin E

Pioglitazone

26
Q

What is the genetic alteration that accounts for 82-90% of cases of hemochromatosis?

A

HFE gene on chromosome 6

C282Y/C282Y

27
Q

What is the compound heterozygote in hemochromatosis?

A

C282Y/H63D

28
Q

What is the role of the HFE gene?

A

HFE regulates the absorption of iron from the small intestine. When we need iron, it is absorbed and mobilized by transferrin. HFE will down regulate transferrin when iron supplies are adequate. With mutation, iron continues to be absorbed from the small intestine.

29
Q

What might be some causes of secondary iron overload?

A

Anemia caused by ineffective erythropoiesis
Liver Disease
Parenteral Iron Overload

30
Q

Where does Fe deposit in primary vs secondary hemochromatosis?

A 
Primary = hepatocytes
Secondary = Kupffer cells
31
Q

How does hereditary hemochromatosis present?

A 
Liver function abnormalities
Weakness and lethargy 
Skin hyper pigmentation (bronze diabetes) 
Diabetes
Arthralgia
Impotence in males
EKG abnormalities
32
Q

What test is used as a work up for hereditary hemochromatosis?

A 
Fasting transferrin saturation 
If elevated (>45%) then check with genetic testing
33
Q

When do you biopsy for hereditary hemochromatosis?

A

You consider it is genetic testing shows C282/H63D

If C282Y/C282Y you biopsy if the patient is over 40 or if they have an elevated ALT/AST
Then do phlebotomy for treatment

34
Q

What is the goal serum ferritin in hemochromatosis?

A

<50

Initially do weekly phlebotomy, then once quarterly after

35
Q

What are some dietary sources of copper?

A 
Seafood
Organ meats
Nuts and nut butters
Legumes
Chocolate
Enriched cereals
Fruits and veggies
36
Q

What parts of copper metabolism are reduced Wilson’s Disease?

A

Excretion in the bile

Binding to ceruloplasmin

37
Q

Where does Cu start to deposit in Wilson’s Disease?

A

Extrahepatic in kidney, brain and cornea

38
Q

How is Wilson’s Disease diagnosed?

A

No one single finding is adequate - combination of clinical biochemical and pathological analysis
Consider the diagnosis in patients 3-40 years old with unexplained liver disease, acute liver failure, cirrhosis, near symptoms, psychiatric symptoms

39
Q

How is Wilson’s Disease characterized?

A

Autosomal recessive

Defect in ATP7B gene

40
Q

How does ceruloplasmin contribute to a diagnosis of Wilson’s disease?

A

95% of homozygotes have level <20mg/dL

But high CP can occur in inflammation so there may be some false negatives

41
Q

What might the urinary excretion of copper be in a patient with symptomatic Wilson’s Disease?

A

May exceed 100 micrograms/24 hours

42
Q

What are some treatments for Wilson’s Disease?

A

D-penicillimine (lots of SE)
Trientine
Zinc

43
Q

Where is alpha-1 antitrypsin made?

A

In the liver

44
Q

How does alpha-1 antitrypsin deficiency differ between children and adults?

A

It is the most common genetic liver disease in children, leading to liver transplant
In adults it can cause hepatitis, cirrhosis, liver cancer; most common cause of emphysema in adults

45
Q

What are the possible inherited genes in alpha-1 antitrypsin deficiency?

A

M (main)
S
Z (most common mutant)

*Most healthy individuals with normal A1-AT are PiMM

46
Q

What is the pathogenesis of lung and liver disease in A1-AT deficiency?

A

Lung = loss of function mechanism, lack of A1AT allows uninhibited PMN mediated damage to CT of lung

Liver = gain of function mechanism, retention of inefficiently secreted A1AT Z molecule in ER triggers serious of hepatotoxic events

47
Q

Which A1-AT deficiencies lead to disease?

A

PiSZ - 30-40% activity, causes lung disease only
Pi null-null - 0% activity, causes lung disease only
PiZZ - 10-15% activity, can cause both lung and liver disease

48
Q

What do the labs of someone with autoimmune hepatitis look like?

A

ALT, AST elevation, occ. > 1000
Elevated gamma-globulin or elevated IgG
Autoantibodies

49
Q

What are some differentials to think of with really high AST, ALT?

A

Hepatitis B
Autoimmune Hepatitis
Medications
Ischemic Liver Disease

50
Q

What is visible on histology of an individual with autoimmune hepatitis?

A

Interface hepatitis

Plasma cell infiltrate

51
Q

What are the two subclassifications of AIH?

A

Type 1 = Classic (80-90%), adults; in nucleus, ANA, ASMA

Type 2 = anti-LKM 1 hepatitis, children; in microsome, anti-liver-kidney microsomal antibody

52
Q

What is present in approximately 50% of AIH cases?

A

Other associated autoimmune conditions

53
Q

What is the treatment for AIH?

A

Prednisone only

Prednison + Azathioprine

54
Q

When do you stop treatment for AIH?

A

With normal ALT, AST, IgG, gamma-globulin, and resolution of inflammation on biopsy

55
Q

Chronic, progressive, cholestatic liver disease

Destruction of intrahepetatic bile ducts

A

Primary biliary cirrhosis

56
Q

What is the probably pathogenesis for PBC?

A

Autoimmune
90-95% women, caucasian, mean age of 52 at presentation (range 30-65)
High prevalence of serum autoantibodies (Antimitochondiral antibodies, AMA)
Elevated IgM
Increased familial incidence of disease

57
Q

What is the major target antigen in PBC?

A

PDC-E2 on the membrane of biliary epithelial cells

58
Q

How do patients with PBC present?

A

Elevated alk phos (3-4x normal)
AMA +
Investigation for other autoimmune diseases
Bilirubin usually rises
Cholesterol elevated – but not associated with heart disease
Fatigue and Itching!

59
Q

What is a common complication with PBC?

A

Fat soluble vitamin deficiency
Vitamin D deficiency –> osteomalacia, fractures, regular bone densitometry
Vitamin K deficiency –> prolonged PT

60
Q

What is the most common autoimmune disorder associated with PBC?

A

Sjogren’s/Sicca syndrome

61
Q

What is a histological finding of PBC?

A

Florid-duct lesion = lymphocytes and mononuclear cells causing inflammatory changes around bile ducts

62
Q

Treatment for PBC.

A 
Ursodeoxycholic acid (UDCA) -- decreases inflammation around bile ducts to lead to less fibrosis 
For itching -- cholestyramine or benedryl at night

GI (34 decks)

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