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M2 GI > 34. Alcoholic Liver Dz, Non-alc Fatty Liver > Flashcards

34. Alcoholic Liver Dz, Non-alc Fatty Liver Flashcards

1
Q

Histologically, can we distinguish between alcoholic liver disease and non-alcoholic fatty liver disease?

A

Nope, histologically they look the same. have to rely on history and other tests.

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2
Q

What is the evidence that alcohol usage causes liver disease?

A

We don’t have biochemical or clinical studies on this - our evidence is epidemiological.

Liver dz declined during Prohibition, and is lower in countries that don’t allow alcohol.

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3
Q

Once you have alcoholic cirrhosis, what determines your prognosis?

A

Cirrhosis is the most advanced form of liver disease.

Prognosis determined by continued EtOH use, and complications from liver dz (ascites, hyper-bili, bleeding)

Can improve your prognosis if you stop drinking.

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4
Q

What are the general risk factors for alcoholic liver injury?

A

amount of alcohol

type of alcohol

drinking behavior

gender

ethnicity

Obesity

Hep C

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5
Q

How does the amount of alcohol consumed affect your risk of getting liver injury?

What % of heavy drinkers get liver injury?

A

If you drink more than 80g/day of alcohol, your risk increases (approx 1 L wine, 8 beers, 1/2 pint of liquor)

Duration makes a difference (how many years you have been drinking)

Most heavy drinkers do not get liver injury - probably only 7%

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6
Q

If you’re going to be an alcoholic, what type of alcohol should you choose?

A

Go for the wine.

Wine drinkers may be less likely to dev alcoholic liver disease than beer or spirits.

(Evid not that strong though: could be that wine drinkers tend to have better nutrition or drink with meals)

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7
Q

How does drinking behavior influence your risk of gettign alcoholic liver disease?

A

Binge drinking is worse than intermittent drinking. Binge drinking increases risk of alcoholic hepatitis 5x.

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8
Q

Effect of gender of alcoholic liver injury?

A

Women are more likely to dev alcoholic liver disease for the same amount of alcohol (less intake is required to produce damage)

could be due to lower body mass, or reduced gastric alcohol metabolism.

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9
Q

Ethinicity/gender most at risk for developing alcoholic liver disease?

A

Hispanic males

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10
Q

If you have Hep C, what is your relative risk for developing alcoholic liver injury? (age of onset of liver dz, risk for developing cirrhosis, risk of hepatocellular carcinoma)

A

If you have comorbid conditions (Hep C, obesity, hemochromatosis) your risk for alcoholic liver disease is higher.

Alcoholics who are HCV+ will dev liver disease at earlier age, they have higher risk of dev cirrhosis, and higher risk of HCC.

There is no amount of alcohol that is safe to drink if you have HCV.

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11
Q

If you are an alcoholic who is also obese, or who has insulin resistance, what is your relative risk of dev alcoholic liver disease?

A

Obesity is associated with a 2 to 5 fold increased risk of alcoholic liver injury.

Insulin resistance also increases this risk.

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12
Q

How have genetics been associated with increased risk of alcoholic liver injury?

A

Polymorphisms in the genes encoding enzymes involved in alcohol metabolism are associated with incr risk of alcohol-related liver injury.

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13
Q

Describe the pathway of alcohol metabolism: oxidative metabolism.

A
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14
Q

In chronic alcoholics, what metabolic pathway is used to metabolize alcohol? What is the problem with using this pathway?

A

Chronic alcoholics use the Microsomal enzyme oxidative system (MEOS) – MEOS predominates at higher concentrations of alcohol. Cytochrome P450 enzyme is involved, and yields a more toxic product. Also leads to metabolism of Tylenol into a more toxic product than normal (–> increased tylenol hepatotoxicity in alcoholics)

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15
Q

Where are the 2 places where alcohol is metabolized? how does this lead to the differing metabolism of alcohol between men and women?

A

metabolized by ADH in both liver and in stomach.

Women have less gastric ADH –> they metabolize alcohol less readily than men

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16
Q

Theories of how alcohol causes liver disease?

A

-Centrilobular hypoxia: causes a zone of hypoxia around the CV as ethanol consumes the oxytem

-Neutrophil infiltration: leading to release of ROS, which are pro-inflammatory and pro-fibrinogenic

-Acetaldehyde effects: (product of alcohol metabolism) - stimulating collagen symthesis

-Cytokines: TNF, IL-6 may lead to necrosis, inflammation

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17
Q

Alcoholic fatty liver (aka alcoholic steatosis): what are symptoms? what are lab findings?

Prognosis?

A

-Rarely clinically diagnosed as pt’s are usually asymptomatic

-Tender hepatomegaly may be presen

-LFT’s may be normal or somewhat elevated

-GGT may be the only abnormal liver test

-Can develop after a single binge

-Generally reversible

-Does not predict progression to cirrhosis

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18
Q

Alcoholic hepatitis: what do we see on biopsy?

A

Hepatocytes are dying/ballooning around the central veins.

Neutrophils are invading, lots of inflammation

Mallory bodies (not specific to this dz, but commonly seen)

19
Q

Alcoholic hepatitis: symptoms?

A
  • Heavy alcohol use history
  • Fever (usually less than 101° F)
  • Hepatomegaly
  • Jaundice
  • Anorexia
  • Ascites (in approx 30% of pt’s)
20
Q

Alcoholic Hepatitis: Lab test results?

A

-AST usually 2x ALT

-incr GGT, incr Alk Phos, incr Bili, incr INR, decr albumin

  • leukocytosis
  • thrombocytopenia (suggests underlying cirrhosis)
  • mild anemia (EtOH is directly toxic to RBC membranes)
21
Q

Alcoholic Hepatitis: Prognosis? what are 2 calculations/scores that can assess prognosis?

A

Prognosis is poor overall.

  • Modified Discrimant Function (mDF) = calculation to predict mortality using PT and bili levels. Value > 32 predicts high 30 day mortality.
  • MELD score > 18 also predictive of higher 30 day mortality (uses creatinine, bili, INR). Used to determine need for transplant.
22
Q

Alcoholic hepatitis: treatment?

A

Supportive care (fluids, nutrients, etc)

Nutrition (> 3000 cal/day)

Corticosteroids (if severe: may use mDF calculation to determine need)

Some investigational meds…..

23
Q

What are the recommendations for steroid use in Alcoholic Hepatitis?

A

-Make sure diagnosis is correct

-Severe alcoholic hepatitis: mDF of 32 or higher or hepatic encephalopathy

  • Infections, GI bleeding, renal failure should exclude patients
  • Prednisolone 40mg/d for 4 weeks then tapered over 2-4 weeks
24
Q

What is Pentoxifylline (PTX) - how could it be helpful in treating Alcoholic Hepatitis?

A

TNF-alpha inhibitor. May modify inflammatory response by decreasing the effects of TNF-alpha

25
Q

What is treatment for Alcoholic Cirrhosis?

A

Abstinence!

Treat cirrhosis-related complications

Transplant

26
Q

Non Alcoholic Fatty Liver Disease (NAFLD): what is this?

Is there a blood test? how is it diagnosed?

A

Alcohol-like liver disease in people who do not consume excessive alcohol.

(Describes the histologic spectrum of liver damage (non-alcoholic fatty liver, non-alcoholic steatohepatitis, cirrhosis).)

Diagnosis of exclusion - no blood tests, no imaging

27
Q

Some individuals who become cirrhotic from NAFLD can develop what?

A

Hepatocellular Carcinoma (HCC)

28
Q

NAFLD: prevalence?

A

Somewhere between 5-31%, depending on whether you are considering people with normal or abnormal liver function tests.

29
Q

In patients who are found to have non-alcoholic hepatitis that is unexplained, what do we think may be the cause?

A

Metabolic Syndrome: incr BMI, incr waist circumference, high triglycerides, elevated insulin levels, decr HDL cholesterol

30
Q

what are risk factors for NAFLD progressing to cirrhosis?

A

Age > 45 yrs

Obesity

Diabetes

31
Q

Non-Alcoholic Fatty Liver vs. Non-Alcoholic Steatohepatitis + fibrosis: which is more likely to advance to cirrhosis?

A

NASH with fibrosis progresses to cirrhosis both more consistently and more rapidly than simple NAFL.

32
Q

How do fat-derived factors and metabolic syndrome contribute to hepatic inflammation?

A

fat-derived factors regulate hepatic inflammatory response via hormones: specifically Adiponectin (anti-inflammatory) and TNF-alpha (pro-inflammatory).

Metabolic syndrome increases levels of TNF and decreases levels of adiponectin.

33
Q

TNF-alpha: what are its pro-inflammatory actions?

A
  • Pro-apoptotic
  • recruits WBCs
  • Promotes insulin resistance
34
Q

Adiponectin: what are its anti-inflammatory actions?

A
  • inhibits FA uptake
  • stimulates FA oxidation and lipid export
  • enhances insulin sensitivity
35
Q

Since NAFLD is a diagnosis of exclusion, what are the diseases we need to exclude before making a diagnosis?

What patient symptoms should alert you to possible NAFLD?

A

Exclude as hepatitis B (HBV), hepatitis C (HCV), autoimme hepatitis (AIH), primary biliary cirrhosis (PBC), hereditary hemochromatosis (HH), Wilsons disease & alpha-1-antitrypsin deficiency (a1-AT).

If the patient has metabolic syndrome, definitely need to consider NAFLD. So, labs that suggest metabolic syndrome also suggest NAFLD

36
Q

How can we establish the severity of liver damage?

A

Clinical prognosis depends on histology:

  • Steatosis generally benign
  • Steatohepatitis increases risk for cirrhosis
  • Cirrhosis is associated with significant morbidity and mortality

Severity can be determined by lab tests:

  • Aminotransferase level not useful
  • AST/ALT ratio can indicate progression to cirrhosis
  • Thrombocytopenia suggests cirrhosis
37
Q

What is the role of imaging in establishing severity of NAFLD?

A
  • Can’t distinguish fatty liver from steatohepatitis or “early” cirrhosis
  • Stigmata of portal HTN suggest cirrhosis
  • May detect unsuspected HCC

SO: not useful for early stages, more useful for later stages

38
Q

What is the role of biopsy in establishing severity of NAFLD?

A

Liver biopsy = gold standard!

But there are limitations: may have sampling error, there is risk to the patient, and it is expensive

39
Q

NAFLD: standard recommended treatment?

A

At present, there is no standard recommended treatment for NAFLD/NASH

-Mainly due to lack of large randomized studies:

Large trials are difficult to carry out

Disease is slowly progressive requiring long follow up to assess therapeutic advantage (>2 yrs)

Histology is required to assess improvement

40
Q

Since there is no standard recommended treatment for NAFLD, what do we recommend to patients?

A

Weight loss and exercise: weight loss of 10% seems to improve outcomes

Low carb, low cal diet (but any diet that leads to weight loss is fine). Especially avoid high fructose corn syrup &trans-fatty acids.

Bariatric surgery has caused regression of steatosis, inflammation and fibrosis

Meanwhile, we treat the metabolic syndrome (statins, beta blockers, T2DM drugs, etc)

41
Q

What is the best med combo that has been shown to treat NASH?

A

Pioglitazone + Vitamin E

Showed improved liver histology (steatosis, inflammation)

Still, there’s not enough data to recommend this treatment.

42
Q

Can we give Vit E to any patients with NASH?

A

As long as they don’t have heart disease, we can give Vit E.

Especially given to patients with NASH of at least stage 2 seen via biopsy.

43
Q

Patients with NASH/cirrhosis: what should we be screening for?

A
  • portal hypertension
  • hepatocellular carcinoma
44
Q

What characteristic histology is shown here?

A

Classic for NASH:

  • inflammation around the central vein
  • Neutrophils
  • Balloon degeneration of hepatocytes

M2 GI (41 decks)

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