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GI- Week 3 > Non-Alcoholic Liver Disease > Flashcards

Non-Alcoholic Liver Disease Flashcards

1
Q

T or F. Non-Alcoholic Fatty Liver Disease is becoming the most common liver disease

A

T. Due to obesity, diet, being pieces of shit basically

TEST QUESTION!!!

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2
Q

Describe Nonalcohlic fatty liver disease

A

This is an acquired liver disease in both children and adults that has arise primarily in correlation with obesity in the US over the past 30-40 yrs

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3
Q

What EtOH consumption rates would be defined as NAFLD?

A

less than 20g/day (probably closer to 10g/day in women)

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4
Q

What is the classic histo of NAFLD?

A

Macrovesicular hepatic steatosis

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5
Q

What are the two main categories under the diagnosis of NAFLD?

A

1) ISolated steatosis
2) Non-alcoholic steatohepatitis (NASH) which is marked by significant inflammation, and more likely to progress to fibrosis and cirrhosis

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6
Q

What is the main player in the development of such prevelant NAFLD?

A

BMI over 30

others: Type 2 Diabetes, Sleep Apnea, Hyperlipidemia, and Metabolic Syndrome

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7
Q

NAFLD is the most common!!

A
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8
Q

Can NAFLD steatosis only occur in obese pts?

A

No, while up to 70% of obese pts have signs of steatosis, 10-15% of normal BMI pts do as well

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9
Q

Can NAFLD-related NASH only occur in obese pts?

A

No, this is obivously worse than steatosis and thus less common, being seen in 15-20% of obese pts but still 3% in normal BMI pts

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10
Q

Why do some people with elevated BMIs show NAFLD and others do not?

A

It is highly correlated to the distribution of fat. Those with central obesity (in the stomach) and much more liekly to get it than those with peripheral obesity (i.e. arms, legs, back)

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11
Q

What races commonly get NAFLD?

A

Mexicans are the most common and AA are the least likely to get it

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12
Q

Which gender is most likely to get NAFLD?

A

Women

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13
Q

Does NAFLD occur in children?

A

Yes, 10% of children have NAFLD making it the leading cause of Pediatric liver disease

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14
Q

When does NAFLD most commonly occur in children?

A

Mean age at 12

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15
Q

What is the prognosis of progression on NAFLD in children? Will it go to fibrosis or cirrhosis?

A

In 100 children with NASH, 8% had advanced fibrosis and 3% had cirrhosis

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16
Q

What are some other causes of Nonalcoholic Fatty Liver Disease?

A

•Nutritional Abnormalities

-Total Parenteral Nutrition, Starvation, Refeeding

•Metabolic Diseases: Abetalipoproteinemia, Hypobetalipoproteinemia

  • Occupational Chemical Exposure
  • Drugs like Tamoxifen, Corticosteroids, Methotrexate
17
Q

How could starvation lead to NAFLD?

A

Starvation leads to peripheral fat being shifted to the liver!! Not just the fatties

18
Q

What kinds of surgeries have been assoicated with NAFLD?

A

Those promoting rapid weight loss such as:

Jejunoileal bypass (causes fat deposition in the liver)

Gastric bypass – less common

19
Q

Are pts with NAFLD-related fatty liver likely to progress to NASH?

A

No, limited

20
Q

Are pts with NAFLD-related NASH likely to progress to advanced fibrosis? cirrhosis?

A

•30-40% with advanced fibrosis

10-15% will advance to cirrhosis

21
Q

T or F. NASH caused cirrhosis can lead to HCC

A

T.

22
Q

How are TAGs from the GI normally handled?

A

•Normally triglycerides incorporated into chylomicrons

–Travel via lymphatics for storage in peripheral fat

23
Q

What happens to peripheral fat in NAFLD?

A

Peripheral fat is hydrolyzed to free FAs and transported to the liver where they are oxidized by mitochondria promoting free radical formation and damage, thus:

steatosis is a result of disturbed balance between periphery and liver fat

24
Q

What is another significant aspect about the pathology of NAFLD?

A

Insulin resistance leads to increased peripheral lipolysis leading to increased levels of FFAs that are depositied in the liver and subjected to mitochondrial fatty acid oxidation promoting free radical formation and liver damage.

Increased free FAs in the liver also promoted increased gucose output, increasing insulin levels which promote increased hepatic lipogenesis

25
Q
A
26
Q

What is the two hit hypothesis of NAFLD?

A
  1. Hepatic fat accumulation
  2. Oxidative Stress via lipid peroxidation and free radical formation
27
Q

T or F. Mallory bodies can be seen in NASH too! Not specific to ALD

A

T.

28
Q

Normally NAFLD is not going to cause significant damage to the liver, and when it does these pts often have co-morbidities that precipitate the damage. What are some common co-morbidities?

A
  • Hepatitis C + NASH
  • Hemochromatosis + NASH
  • Alpha 1 Antitrypsin Deficiency + NASH
  • Alcohol + NASH
29
Q

How does isolated NAFLD typically present?

A

Mostly asymptomatic with some signs of fatigue

30
Q

How might NAFLD present upon physical exam?

A
  • Obesity – 30-100% of patients
  • Hepatomegaly – up to 50%
  • Spider angiomata
  • Palmer erythema
31
Q

How does NASH present in labs?

A
  • 50-90% have elevated liver enzymes
  • AST and ALT: moderately elevated (up to 4 times normal)
  • Unlike Alcohol, AST is rare 2x ALT (usually evenly elevated if they are)
  • Alkaline Phosphotase: up to 2x normal but not significantly elevated
32
Q
A

Can try to estimate fat. Fat in the liver is making it darker here (they should be the same density)

33
Q

T or F. A “fatty” appearance on Ultrasound or CT does not make a diagnosis of NAFLD

A

T.

34
Q

What is the gold standard for NAFLD diagnosis?

A

Liver biopsy is the only definitive way to diagnose NASH

35
Q
A
36
Q

How is NAFLD tx?

A
  • Weight reduction of 10% helpful
  • If diabetic, optimize control
  • If hyperlipidemic, treat this – particularly due to the increased cardiac risks
37
Q

Can surgery help to tx NAFLD?

A
  • Surgery may have a role in properly selected patients
  • Bariatric surgery may help people with NASH whose BMI is >35
  • Gastric banding associated with improvement in inflammation and even fibrosis
38
Q
A

GI- Week 3 (15 decks)

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