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GI- Week 3 > Alcoholic Liver Disease > Flashcards

Alcoholic Liver Disease Flashcards

1
Q

INR was about 1.8

A

Note how the bilirubin is almost 12x elevated and alk phos is normal in this alcoholic pt.

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2
Q

What are the classic trends of ALT and AST with alcohol?

A

Both are not that elevated and AST is typically at least double what the ALT is

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3
Q

Alcoholic liver disease is especially prevelant in what demographic?

A

Native Americans, especially in women

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4
Q
A
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5
Q

What are the major causes of chronic liver disease in the US?

A

Hep C

Alcohol

Nonalcoholic Fatty Liver Disease

Hep B

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6
Q

Most inflammation assoicated with liver disease is primarily _____, except ______ which is neutrophilic

A

lymphocytic, except alcoholic liver disease

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7
Q

What are some of the components/sequelae of alcoholic liver disease?

A
  • steatosis
  • alcoholic hepatitis
  • alcoholic cirrhosis, HCC, and rarely cholangiocarcinoma
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8
Q

How much alcohol is usually enough to induce alcoholic liver disease?

A

It usually requires more than 40-80g/day (aka 6+ drinks/day) over a 5 yr duration

for reference, a 12 gm= 12 oz beer, 4 ozwine, 1 oz liquor

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9
Q
A
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10
Q

Compared to men who typically require up to 6 drinks/day + to develop alcoholic liver disease, women can develop it with only 3 drinks/day. What account for this difference?

A
  • Women tend to be smaller (less volume of distribution)
  • women have decreased gastric alcohol dehydrogenase activity, particularly in younger women
  • there are differences in first pass metabolism of alcohol
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11
Q

What is the standard alcoholic hepatitis pt?

A
  • typically 40-60 yo
  • 80+ gm/dy of EtOH over 5 yrs
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12
Q

How does alcoholic hepatitis present intitially?

A

usually this is a slow developing process but pts will present with acute symptoms that can come on rapidly (after a ‘tipping’ pt) like rapid onset of jaundice, fever, ascites, and/or muscle wasting

and tend to have signs of hepato/splenomegaly with tenderness on physical exam

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13
Q

How does alcoholic hepatitis present in labs?

A
  • AST/ALT rarely over 300 (300+ think alcohol plus something else- tylenol, cocaine, etc.)
  • AST 2+x ALT
  • leukocytosis
  • Elevated INR
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14
Q

Why is the liver enlarged in alcoholic hepatitis?

A

fatty infiltration

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15
Q

What is the risk of alcoholic cirrhosis in pts. drinking 30-60 gm EtOH/day? 120+ gm/day?

A

30-60: 1%

120+: 5%

Even if you drink heavily, you are unlikely to get cirrhosis!

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16
Q

Genetics has been proposed as one of the reasons why some people who drink heavily (or maybe not so heavily) get ALD and others do not. What genetic groups are particularly at risk?

A
  • monozygotic twins regardless of environment
  • East Asians, with polymorphisms of ADH2*1 gene
  • TNFa-238 polymorphism in causasians
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17
Q

How does EtOH cause liver injury?

A

Ethanol and acetylaldehyde cause intestinal injury and increase permeability resulting in endotoxemia resulting in an inflammatory response by Kupffer cells

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18
Q

What is the two-hit theory of ALD development?

A

1) Hit 1: Fatty liver induction
2) Hit 2: Inflammation/necrosis/ hypoxia etc.

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19
Q

What are some things that can induce the first Hit of the 2 Hit theory of ALD?

A
  • oxidative stress related to alcohol
  • increased NADH/NAD ratio
  • obesity and/or DM

fat sensitives the liver to the 2nd hit

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20
Q

What are some predictive scores used for prognosis of ALD?

A

-Maddrey Score

0Glasgow Alcoholic Hepatitis Score

-MELD

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21
Q
A
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22
Q
A
23
Q

high MELD= high mortality rate

A
24
Q

In addition to genetics, most/many people who get ALD and its sequelae have acquired co-morbiites that harm the liver. Name some common ones

A
  • Hep C
  • Cocaine Use/IVDU
  • hemochromatosis
  • A1-antitryspin deficiency
25
Q

T or F. Alcohol + HCV, or HCV are more common causes of chronic liver disease than just chronic alcohol use

A

T. So again drinking a lot of alcohol may or may cause liver disease, but you are far more likely if you have Hep C

26
Q

What is this?

A

Prussian blue stain for hemochromatosis. Hemochromatosis + alcohol make it more likely to get chronic liver disease

27
Q

What are some trends with liver disease in pts that have both hemochromatosis and alcoholism?

A

These pts are more like to get advanced fibrosis and short durations of survival

28
Q

What mutations lead to a hereditary risk of hemochromatosis?

A

homo (or hetero)zygous C282Y, these pts have increased hepatic iron scores and higher rates of HCC

29
Q

What is this showing?

A

A1-antirpysin globules in the liver seen in A1AT deficiency

30
Q

What genotypes of anti-trypsin have an increased lieklyhood of getting cirrhosis?

A

MZ (M is normal; Z is mutated) or ZZ

Note that typically MZ pts require a history of extensive alcoholism to develop liver cirrhosis, and ZZ pts require less

31
Q

What are the most important environmental factors of acquiring ALD?

A
  • ethanol patterns
  • obesity
  • hyperglycemia
32
Q

What is the tx of ALD?

A
  • Alcohol abstinence and optimize nutrition
  • Pentoxifylline (TNFa inhibitor) and corticosteroids to reduce inflammation
33
Q
A
34
Q
A
35
Q

All alcoholic related liver changes (inflammation, fibrosis, etc.) start where?

A

perivenular or aka centrilolublar ZONE 3 of the acinus and then extend outward toward the portl tracts

36
Q

Classically, on a microscopic level, alcohol induced fatty steatosis is ______

A

macrovesicular

37
Q
A
38
Q

What likelihood of a chronic alcohol user getting steatosis?

A

90-95%

39
Q

What likelihood of a pt with steatosis from alcohol turning into fibrosis?

A

10-20%

40
Q

What likelihood of a pt with fibrosis from alcohol turning into cirrhosis?

A

8-20%

41
Q
A
42
Q

How does fatty liver appear macroscopically/grossly?

A

large, heavy, and soft that is yellow and greasy

43
Q

What are some of the general effects of alcohol on the liver?

A
  • steatosis
  • dysfunction of mitochondrial and cellular membranes,

hypoxia

oxidative stress

44
Q

How does hepatocellular steatosis arise from alcohol?

A

1) Shunting of normal substrates away from catabolism and toward lipid biosynthesis, as a result of increased generation of NADH by alcohol dehydrogenase and acetaldyhyde dehydrogenase
2) impaired assembly and secretion of lipoproteins
3) increased peripheral catabolism of fat, thus releasting free FAs into circulation

45
Q

What are the main histological features of ALD aka steatohepatitis?

A
  • hepatocyte swelling (ballooning) and necrosis with overlying inflammation (below)
  • Mallory-Denk bodies
46
Q

What are Mallory-Denk bodies?

A

tangled skeins of intermediate filaments with other proteins

not specific

47
Q

What is this showing?

A

Perivenular fibrosis, the EARLIEST pattern of hepatic fibrosis in ALD, stained purple via a trichrome stain

48
Q

What causes fibrosis in ALD?

A

steatosis leads to activation of sinusoidal stellate cells and portal fibroblasts

49
Q

What is this showing?

A

Cirrhosis from ALD induced fibrosis- notice the almost branching quality of the fibrosis

50
Q
A
51
Q

T or F. Liver cirrhosis is reversible

A

T. Stop drinking!!

52
Q

What is this showing?

A

Left shows extensive liver cirrhosis and the right shows the reversible nature of cirrhosis and regeneraiton of hepatocytes

53
Q

How does hepatic steatosis present in labs?

A

Hepatic steatosis may cause hepatomegaly, with mild elevation of serum bilirubin and alkaline phosphatase levels. Severe hepatic dysfunction is unusual.

54
Q

The risk of developing hepatocellular carcinoma in alcoholic cirrhosis is _____ annually

A

1% to 6%

GI- Week 3 (15 decks)

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