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Clinical Nutrition 1 > NAFLD and NASH Part II > Flashcards

NAFLD and NASH Part II Flashcards

1
Q

Wha may excess fat and fructose within the diet lead to?

A

Intestinal dysbiosis

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2
Q

Describe intestinal dysbiosis and how it relates to NAFLD

A

Microbes slip through the intestinal epithelium, as there is increased intestinal permeability, and will contribute to fatty and apoptotic hepatocytes and fibrosis

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3
Q

The severity of nonalcoholic fatty-liver disease is associated with what? (2)

A
  • Gut dysbiosis

- Shift in the metabolic function of the gut microbiota

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4
Q

What is diagnostic of NASH?

A

Inflammation and steatosis

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5
Q

What indicates that NASH has progressed?

A

Liver fibrosis, staging, cirrhosis

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6
Q

NAFLD can sometimes be ____

A

a slient disease

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7
Q

How is NAFLD usually discovered?

A

Incidental LFT, bright liver on imaging or hepatomegaly during routine check ups

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8
Q

NAFLD is _____ and frequently ___

A

frequent

aysmptomatic

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9
Q

79% with NAFLD have normal/abnormal ALT

A

NORMAL

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10
Q

What is the be considered about ALT and NAFLD?

A

That both high and normal ALT levels can be associated with the progression of the disease, and no cut-off designated for predicting NASH or advanced fibrosis

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11
Q

We know that ALT is inaccurate is assessing NAFLD, what are other ways to asses? (3)

A
  • Biopsy
  • Imaging
  • Biomarkers
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12
Q

How does transient elastrography (fibroscan) work?

A

The stiffer the liver, the FASTER the shear wave propagate the underlying tissue, measuring CAP (Controlled Attenuation Paramete)

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13
Q

_____ is the single most important predictor of mortality

A

Fibrosis

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14
Q

Describe the increasing prognostic value

A

Ballooning –> NASH –> Portal inflammation –> Fibrosis –>Advanced fibrosis

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15
Q

What increases with fibrotic stage?

A

Liver-related and all-cause mortality

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16
Q

What is the essential test for diagnosing NASH?

A

Liver biopsy showing steatosis, hepatocyte ballooning and lobular inflammation

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17
Q

Why is it unadvised to use clinical, biochemical or imaging measures when diagnosing NASH?

A

Cannot distinguish NASH from steatosis

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18
Q

NAFLD can progress to ___

A

NASH

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19
Q

Clinical predictors of NASH in patients with NAFLD?

A
  • Advanced Age
  • Sex
  • Race
  • HTN, central obesity, dyslipidemia, insulin resistance/diabetes
  • AST/ALT ration >1, low platelets
  • Persistently elevated ALT
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20
Q

Advanced age?

A

Greater duration of disease

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21
Q

Sex?

A

Post-menopausal women experience accelerated disease

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22
Q

Race?

A

Incr. in hispanic, asian and decr. in blacks

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23
Q

HTN, central obesity, dyslipidemia, insulin resistance/diabetes?

A

Increase risk wih MetS

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24
Q

60% prevalence of fibrosis if older that 50 y/o AND obese or diabetic?

A

If pt initially presents with NAFLD

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25
Q

Persistently elevated ALT?

A

Greater risk of disease progression

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26
Q

Gold standard of NAFLD diagnosis?

A

Liver biopsy

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27
Q

Discuss the importance of lifestyle in NAFLD

A

Unhealthy lifestyle will play a role in the development and progression of NAFLD. Assessment of dietary and PA habits is part of comprehensive NAFLD screening.

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28
Q

____ is needed for NASH improvement

A

Weight-loss

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29
Q

Weight loss >/= 10?

A

Reduces fibrosis in 45% of cases

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30
Q

Weight-loss >/= 7% ?

A

NASH resolution in 64-90%

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31
Q

Weight loss >/= 5% ?

A

Reduces ballooning/inflammation in 41-100%

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32
Q

Weight loss >/= 3%?

A

Steatosis improves in 35-100%

33
Q

______ can improve NASH and fibrosis

A

Bariatric surgery

34
Q

Macronutrient recommendations?

A
  • Low-to-mod fat and mod-to-high CHO intake
  • Low-CHO keto diet or high-protein
  • Med diet
35
Q

Fructose recommendations?

A

Avoid, contributes to intestinal dysbiota

36
Q

PA recommendations?

A

150200 min/week of mod intensity PA

-Resistance training

37
Q

What should be considered about PA?

A

Patient may be experiencing fatigue, and reduce compliance with PA

38
Q

Energy restriction recommendations?

A

500-1000 kcal res./week

  • 7-10% weight loss
  • Long-term maintenance
39
Q

Bottom line on coffee

A

Protective in NAFLD in reducing histological severity and liver-related outcomes

40
Q

Alcohol in NAFLD?

A

Recall that NAFLD is CV risk factor, and alcohol can red. CV risk –> recommended 1 drink/day

41
Q

Bottom line on alcohol?

A

Moderate alcohol consumption (wine) below the risk threshold is associated with lower prevalence of NAFLD, NASH and lower fibrosis and histology.

42
Q

What are recommendations below the risk threshold for alcohol consumption?

A

30 g men

20 g women

43
Q

When is total abstinence of alcohol mandatory?

A

NAHS-cirrhosis, reduce the risk of HCC risk

44
Q

Paradox with alcohol?

A

Major risk factor for the global disease burden and results in significant loss of health

45
Q

Alcohol and cancer risk?

A

Risk of death from all causes, and cancers in particular, increase as consumption is increased.

46
Q

What else may be recommended in liver disease?

A

Vit E supplements (Not an official recommendation)

Pioglitazone (T2DM medication)

47
Q

Why is Vit E not an official recommendation?

A
  • Not recommended without a liver biopsy
  • Not recommended in mild NAFL with no evidence of NASH
  • Not recommended in diabetes or cirrhosis
48
Q

When should caution be exerted with Vit E supplementation?

A

Older men, uncontrolled HTN, Hx of prostate cancer, PMx of stroke/prostate cancer

49
Q

When is pioglitazone recommended?

A

For biopsy-proven NASH with diabetes or pre-diabetes

50
Q

What should be monitored when on pioglitazone?

A
  • Body weight
  • ALT and AST
  • DEXA scan
51
Q

When should pharmacological agents be used?

A

Reserved with patients with biopsy-proven NASH, and with significant fibrosis.

52
Q

Who else are candidates for pharmacological agents?

A

Less severe disease but at risk fo progression (diabetes, metS, ALT, inflammation)

53
Q

What is recommended for pts with steatosis alone?

A

Focus on CVD risk factor modification in primary care, no need for liver clinic

54
Q

How is fibrosis screened?

A

Surveillance for HCC/varices

55
Q

Treatments for fibrosis?

A
  • Life style intervention/co-morbidities treatment
  • Bariatric surgery
  • Pharmacotherapy
56
Q

Most likely cause of death in NAFL/NASH stage 0?

A

CVD event or extrahepatic cancer

57
Q

Most likely cause of death in NASH stage 1-2?

A
  • CVD event/extahepatic cancer

- Liver-related disease q

58
Q

Most likely cause of death in NASH stage 3-4?

A

Liver-related diseases

59
Q

Which drug is mostly administered in end-stage NASH?

A

Selonsertib

60
Q

What is recommended for diabetics with NAFLD?

A

Glycemic control, pioglitazone

61
Q

When may 800 UI of Vit E be recommended?

A

Non-diabetics

62
Q

Surgical options for NAFLD?

A

Bariatric surgery, liver transplantation

63
Q

When a patient has fibrosis/cirrhosis, what next?

A

treatment and screning for cirrhosis/esophageal varices

64
Q

What is occult cirrhosis?

A

No sign indicating such diagnosis to clinical

65
Q

What are clinical signs of cirrhosis?

A
  • Thrombocytopenia
  • Ultrasound signs of liver disease
  • Splenomegaly
  • Varices
  • Ascites
66
Q

When should Hepatocellular Carcinoma (HCC) be screened for pt with NASH cirrhosis?

A

Every 6 months, where HCC in NAFLD have worse survival

67
Q

HCC in NAFLD are less likely to have ____

A

curative Tx

68
Q

Should we screen “at-risk” patients for NAFLD/fibrosis?

A

In Europe, Yes
In the US, no
But we should

69
Q

What may indicate a high-risk patient who may benefit from screening?

A
  • Age >50 y/o
  • T2DM
  • Obesity, dyslipidemia
  • HIV +
  • NAFLD at 50-90%
70
Q

What does the MUHC conclude about liver screening?

A

Diabetic patients have a high prevalence of NAFLD and advanced fibrosis, where those with obesity and dyslipidemia are at high risk –> SCREEN!

71
Q

What other group may be at increased risk for NAFLD, liver fibrosis and cirrhosis?

A

Inflammatory bowel disease

72
Q

Metabolic risk factors —> Ultrasound/fibroscan screening —> steatosis present —> Normal liver enzymes —> Serum fibrosis markers Low risk?

A

continue to follow-up with liver enzymes in 2 yrs.

73
Q

Metabolic risk factors —> Ultrasound/fibroscan screening —> steatosis present —> Normal liver enzymes —> Serum fibrosis markers med/high risk?

A

Refer to specialist, and identify other chronic liver diseases, assess severity, may perform biopsy

74
Q

Metabolic risk factors —> Ultrasound/fibroscan screening —> steatosis present —> Abnormal liver enzymes?

A

Refer to specialist, and identify other chronic liver diseases, assess severity, may perform biopsy

75
Q

Metabolic risk factors —> Ultrasound/fibroscan screening —> steatosis ABSENT —> Normal liver enzymes ?

A

Follow-up 3/5 yrs with ultrasound/liver enzymes

76
Q

Metabolic risk factors —> Ultrasound/fibroscan screening —> steatosis ABSENT —> Abnormal liver enzymes?

A

Refer to specialist, and identify other chronic liver diseases, assess severity, may perform biopsy

77
Q

NAFLD is the most _____ in western countries

A

frequent

78
Q

NADLT is ______ disease which requires a multi-disciplinary approach

A

multi-system

79
Q

What is the strongest prognostic predictor?

A

Liver fibrosis stage, where 3-4 has the worst prognosis

Clinical Nutrition 1 (30 decks)

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