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Clinical nutrition 1 > NAFLD & NASH > Flashcards

NAFLD & NASH Flashcards

1
Q

malnutrition can’t cause chronic liver disease. True or false

A

true, malnutrition alone can cause severe fatty liver but it isn’t known to cause chronic liver disease

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2
Q

which tool is used for screening of malnutrition in patients with NAFLD/NASH

A

NRS 2002

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3
Q

what do the questions of the NRS screening tool address?

A
  • BMI
  • weight loss
  • nutritional intake
  • comorbidities (illness)
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4
Q

what are the 2 main screening sections of the NRS 2002

A
  • nutritional disorder

- illness severity

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5
Q

how can sarcopenia be assessed?

A

using Dual energy X-ray absorptiometry (DXA) or CT imaging

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6
Q

which patients will be screened for sarcopenia?

A

mostly patients with cirrhosis, liver cancer, planned for liver transplant

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7
Q

patients with NAFLD or NASH are screened for sarcopenia. True or false

A

False, only those with severe cirrhosis, liver cancer, need for livre transplant

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8
Q

what is the first line treatment for overweight/obese NAFL/NASH patients

A

lifestyle interventions leading to weight loss in conjunction with physical activity

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9
Q

what are the benefits of losing 7-10% of the weight in overweight/obese NAFL/NASH patients

A

it will improve steatosis and liver biochemistry [irrespective of how weight loss is achieved]

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10
Q

what are the benefits of losing >10% of the weight in overweight/obese NAFL/NASH patients

A

improve fibrosis

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11
Q

what does the ESPEN guideline regarding weight loss suggest

A

a hypocaloric diet should be followed according to current obesity guidelines irrespective of the macronutrient composition [large range of CHO and fat during weight loss as long as diet provides high content of protein] => people have to adhere to diet to then continue with it and maintain weight loss

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12
Q

what kind of evidence is there for the diet and exercise, lifestyle intervention recommendation

A

STRONG evidence coming from observational and experimental studies showing positive effects on liver outcomes

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13
Q

to see significant effect on NASH resolution and fibrosis regression, how much weight loss should be achieved?

A

7-10%

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14
Q

what are the 4 As in the Canadian adult obesity clinical practice guideline that must be followed

A
  • ask
  • assess
  • agree
  • assist
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15
Q

when dealing with patients that have NAFL and NASH which type of diet or dietary pattern do we usually recommend?

A

mediterranean diet

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16
Q

when dealing with patients that have NAFL and NASH what type of intervention do we implement

A

INTENSIVE lifestyle intervention with a MULTIDISCIPLINARY TEAM

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17
Q

what are the key messages regarding the obesity guidelines for NAFL/NASH

A
  • weight should NOT be the endpoint, we want to focus on health improvement => liver enzymes and other cardio metabolic markers, steatosis, fibrosis
  • education
  • best diet is one that is SUSTAINABLE
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18
Q

what are the benefits of a high protein diet during weight loss

A
  • greater reduction in body weight, fat mass, and serum TG

- less reduction in lean mass and REE

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19
Q

what is the best diet for weight maintenant after weight loss

A

high protein + low GI foods

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20
Q

what are the Canadian physical activity guidelines

A

general, not specific to NASH/NAFL

  • 150min of moderate-vigorous aerobic PA per week
  • muscle and bone strengthening 2days/week
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21
Q

what are the benefits of aerobic PA (30-60min of moderate-vigorous intensity on most days)

A
  • achieve reduction in abdominal visceral fat and ectopic fat such as LIVEr and heart fat
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22
Q

the Mediterranean diet is high in which nutrients? and low in which nutrients?

A
  • high in: MUFA, omega-3/6, polyphenols, dietary fibre, plant proteins
  • low in: saturated/trans fats, animal protein, simple sugars
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23
Q

what is one food in the mediterranean diet that could not be dissociated from whole diet? why?

A

olive oil, because it provides oleic/MUFA and antioxidants that are beneficial in NAFL and NASH

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24
Q

is a low CHO diet recommended for NASH/NAFL? why or why not?

A

No because there is much less evidence, with much smaller sample size, alot of neutral evidence

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25
Q

Vitamin E supplementation is recommended for which population

A

to non-diabetic adults with histologically confirmed NASH

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26
Q

what is the recommended supplement content of vitamin E

A

800 IU of alpha-tocopherol daily

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27
Q

although omega-3 FA supplementation seems to have a positive effect on liver outcomes, why isn’t it a strong recommendation?

A

no optimal dose was determined

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28
Q

what source of omega-3 FA is recommended for NASH/NAFL

A

dietary omega-3

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29
Q

what are the observed positive effects of 3-4cups of coffee per day

A

positive outcome on fibrosis, steatosis, liver dimension, bright liver

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30
Q

how does fructose affect NAFLD

A

excess fructose will lead to de novo lipogenesis in liver + alter the gut microbiome increasing permeability of intestine and causing more inflammation leading to aggravation of NAFL to NASH

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31
Q

recommendation of alcohol in NASH/NAFL

A

ABSTAIN

-> strong robust recommendation

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32
Q

is taking pre/probiotics recommended by ESPEN?

A

yes, although there is no strong evidence as there are no side effects and some positive benefits have been observed (decrease in liver enzymes, decrease in intrahepatic TG, decreased inflammation)

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33
Q

is taking antioxidants recommended by ESPEN?

A

No due to lack of data

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34
Q

what treatment has the strongest benefits in NASH patients

A

weight loss

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35
Q

a _____ treatment strategy is necessary for treating NAFL and NASH

A

multimodal

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36
Q

what are the major liver functions (8)

A
  • bile formation
  • metabolism of drugs
  • CHO metabolism
  • lipids and lipoproteins production
  • amino acids metabolism
  • protein production and secretion
  • metabolism of iron, copper, and trace elements
  • haem biosynthesis
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37
Q

what is the functional unit of the liver

A

acinus

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38
Q

what makes up the portal triad

A

the portal vein, arteriole and bile ductule

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39
Q

what are the 4 different liver function tests

A
  • aspartate aminotransferase AST
  • alanine aminotransferase ALT
  • AST/ALT ration
  • alkaline phosphatase ALP
40
Q

what is AST and what is it used for

A

AST is an enzyme found throughout the body but predominantly in the heart and liver cells. its useful in detecting liver damage due to hepatitis, drugs toxic to the liver, cirrhosis and alcoholism

41
Q

what is ALT and how is it used in liver function tests

A

enzyme found mostly in the cells of the liver and kidney ->when the liver is damaged, ALT is released into the blood stream, it is useful to detect liver damage due to hepatitis and drugs or other substances toxic to the liver

42
Q

significance of ALP

A

it can indicate blockage of one or more bile ducts, liver cancer, hepatitis, cirrhosis, or when hepatotoxic drugs are taken

43
Q

in alcoholic liver disease ____ is higher than ____

A

AST > ALT => ratio >1

44
Q

In viral hepatitis ____ is higher than ____

A

ALT is higher than AST => ratio <1

45
Q

which liver function test is more specific to the liver

A

ALT

46
Q

elevations in hepatocellular enzymes (AST and ALT) indicate _______

A

parenchymal injury

47
Q

cholestatic enzymes (ALP, GGT, bilirubin) indicate _____

A

disease to biliary system

48
Q

what is the difference in ALT elevation between acute hepatitis and chronic hepatitis

A

acute: >10 fold increase
chronic: 1.5-10 fool increase

49
Q

what is the difference in treatment between acute hepatitis and chronic hepatitis

A

acute: supportive treatment
chronic: address aetiology, what caused chronic hepatitis [treat virus]

50
Q

what are the common causes of acute hepatitis

A
  • drug-induced [no tests available, exclusion diagnosis]
  • Hepatitis A
  • Hepatitis B
51
Q

what are the common causes of chronic hepatitis

A
  • NAFL or NASH
  • hepatitis C
  • hepatitis B
  • Alcoholic liver disease
52
Q

what are the common causes of cholestasis

A
  • PBC/PSK

- Large duct obstruction

53
Q

patients dealing with cholestatis are quite ____ in last stages of disease -> need of ____

A

wasted

need of nutritional support

54
Q

conjugated hyperbilirubinemia indicates _____

A

pure obstruction

55
Q

definition of cirrhosis

A

a diffuse process characterized by liver necrosis and fibrosis and conversion of normal liver architecture into structurally abnormal nodules that lack normal lobular organization

56
Q

what is the pathology of cirrhosis

A
  • nodularity
  • fibrosis (deposition of dense fibrous septa, deposition of collagen)
  • abnormal liver architecture
  • hepatocyte abnormalities
  • irregular surface, yellowish color, small, firm
57
Q

the portal vein brings blood to _____ from _____

A

to the liver from intestine and bowel

58
Q

what are the consequences of nodularity in liver cirrhosis

A

portal hypertension: there is increased resistance to blood flow coming in through the portal vein into the liver causing increase in pressure and backflow into all small vessels that originate from portal vein

59
Q

what is the most important event when there is liver cirrhosis

A

portal hypertension

60
Q

what are the consequences of liver cirrhosis

A

portal hypertension and liver insufficiency

61
Q

what are the complications of portal hypertension

A
  • variceal hemorrhage
  • ascites [spontaneous bacterial peritonitis and hepatorenal syndrome]
  • hepatic encephalopathy
  • congestive splenomegaly
62
Q

what are the complications of liver insufficiency

A
  • encephalopathy

- jaundice

63
Q

definition of portal hypertension and cutoff

A

an increase in portal venous pressure, >12mmHg

64
Q

what are the three different aetiology of portal hypertension

A
  • intrahepatic - 80%, cirrhosis [scar tissue blocks blood flow and slows liver functions]
  • prehepatic - portal vein thrombosis
  • post hepatic [rare]
65
Q

what are the mechanisms of ascites in cirrhosis

A
  • portal hypertension
  • hypoalbuminemia [albumin keeps fluid inside vessels]
  • arterial vasodialtion
  • hyperaldosteronism; ADH
66
Q

what causes hepatic encephalopathy

A

the ammonia, glutamine methionine, nitrogen, GABA go to the diseased liver from gut which fails to metabolize ammonia NH3 and enters blood stream and crosses blood Brian barrier

67
Q

to avoid hepatic encephalopathy it is recommended to decrease protein intake to reduce ammonia accumulation. true or false

A

false, it was recommended but now we don’t because these patients are at high risk of malnutrition

68
Q

what is the driver of mortality in patients with liver disease

A

sarcopenia

69
Q

which classification method is used to assess severity of cirrhosis and what are the factors taken into account

A

Child-Turcotte-Pugh classification

  • encephalopathy
  • ascites
  • bilirubin
  • albumin
  • prothrombin time
70
Q

why are liver function tests done/useful

A

to orient towards aetiology of liver disease (hepatocellular or cholestatic enzymes)

71
Q

what is the relationship between NAFLD and NASH

A

they both have a fatty overload => hepatic steatosis, with no significant alcohol intake
however NASH also have inflammation in addition to fat accumulation

72
Q

what are the established risk factors of NASH

A
  • obesity
  • T2DM
  • dyslipidemia
  • metabolic syndrome
  • hypertension
73
Q

why is there an urge to transition from NAFLD to Metabolic Associated Fatty liver disease MAFLD

A

NAFLD is a diagnosis of exclusion where as MAFLD is a positive diagnosis caused by overweight/obesity, diabetes or >2 metabolic risk abnormalities
=> accent is put on metabolic abnormalities

74
Q

what is the most frequent factor of NAFLD

A

obesity

75
Q

what are the different stages from NAFL to hepatocellular carcinoma

A
  • NAFL: fat accumulation in liver
  • NASH: fat + inflammation, scarring
  • fibrosis
  • Cirrhosis: scar tissue replaces liver cells
  • Hepatocellular carcinoma
76
Q

NAFLD is not just about the liver, it is a ______ disease

A

multi-system disease [causes chronic inflammation in the body - CVD, osteoporosis, cancer]

77
Q

Most commonly, patients with NAFLD die from liver. true or flase

A

false, they die from heart attack usually

78
Q

what are the 2 main drivers of NASH

A

INSULIN resistance AND OXIDATIVE stress

79
Q

what does the perfect storm refer to in the case of NASH

A

presence of T2DM [independent risk factor for development of NASH] presence of NASH [independent risk factor for development of T2DM]

80
Q

which is the most important genetic contributor in NASH development

A

PNPLA3 (encodes adiponutrin)

81
Q

how does the gut dysbiosis/ microbiome play a role in NASH

A

it causes intestinal permeability and absorption of some nutrients that are deleterious for NASH such as fructose and fat

82
Q

what are the factors used to diagnose NASH

A

inflammation and steatosis

83
Q

what factor is looked at to give a prognosis of NASH

A

liver fibrosis staging and cirrhosis

84
Q

there are not many visible symptoms associated with NAFLD thus it is referred to as a silent killer. true or false

A

true, NAFLD is frequent and frequently asymptomatic

=> 79% with NAFLD have normal ALT levels

85
Q

if a patient has normal transaminases, can I exclude NASH?

A

no

86
Q

how do you evaluate NAFLD/NASH/fibrosis

A
  • biopsy [showing steatosis, hepatocyte ballooning and lobular inflammation]
  • imaging
  • biomarkers
87
Q

what is taken into account in the FIB-4 score and what is it used for

A

FIB-4 score includes age, AST, ALT, platelets

it is used to rule out advanced fibrosis if <1.3

88
Q

which patients should receive pharmacotherapy

A
  • NASH
  • NASH with fibrosis
  • advanced fibrosis
  • NASH-related cirrhosis
89
Q

which are the recommended pharmacotherapies for NASH

A
  • vitamin E

- pioglitazone

90
Q

which pharmacotherapies are not recommended to treat NASH but can be used to treat risk factors of NASH

A
  • metformin [treat T2D]
  • statin [treat dyslipidemia and reduce CV risk ]
  • omega-3 FA [treat hyperTG]
91
Q

____ lower risk of portal hypertension in cirrhosis

A

statins

92
Q

in adults with need to minimize weight gain or promote wight loss, guidelines recommend ____ and _____

A

GLP-1 RAs (semaglutide) and SGLT2

93
Q

what are the 2 end points of clinical trial for NASH

A
  • reduction of inflmmaiton

- reduction in fibrosis

94
Q

which patients should be screened for NSH/NAFLD/fibrosis

A
  • T2D/ prediabetes
  • obese
  • HIV +
  • elevated ALT or fatty liver
  • person at high CVD risk
  • polycystic ovary syndrome PCOS
  • inflammatory bowel disease
95
Q

____ is the most frequent liver disease in western countries

A

NAFLD

96
Q

what is the strongest prognostic predictor of NAFLD/NASH

A

liver fibrosis stage

97
Q

what are the general treatment recommendations

A
  • diet + exercise

- pharmacologic therapy in those with ASH/lier fibrosis

Clinical nutrition 1 (7 decks)

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