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CMS200 > Week 1- Fatty liver disease > Flashcards

Week 1- Fatty liver disease Flashcards

1
Q

Criteria for NAFLD

A

hepatic steatosis (fat) and exclusion of secondary causes (i.e. alcohol, medication, hereditary disorders)

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2
Q

steatosis

A

abnormal retention of fat (lipids) within an organ

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3
Q

hepatic steatosis

A

fat accumulation in the liver

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4
Q

hepatitis

A

inflammation of the liver

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5
Q

steatohepatitis

A

fat accumulation and inflammation of the liver (steatosis + hepatitis)

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6
Q

fibrosis

A

scarring

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7
Q

progression of NAFLD

A

simple steatosis/ NAFL –> non-alcoholic steatohepatitis (NASH) –> NASH with fibrosis or NASH with cirrhosis –> NASH with hepatocellular carcinoma

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7
Q

cirrhosis

A

permanent liver damage (scar tissue replaces liver cells)

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8
Q

what % of hepatic steatosis is need for NAFLD and NASH

A

> 5%

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9
Q

prevalence of NAFLD

A

20% CAD, 37% USA

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10
Q

prevalence of NASH

A

5%

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11
Q

average age of NAFLD diagnosis

A

50 yrs (childhood rate is rising bc of obesity)

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12
Q

race effected by NAFLD most

A
  • Hispanics > Caucasians > African Americans
  • In Caucasians, men > women (but no sex difference in Hispanics and African-Americans)
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13
Q

3 risk factors of NAFLD

A
  1. obesity
  2. diabetes mellitus
  3. dyslipidemia/hypertriglyceridemia

AKA insulin resistance and metabolic syndrome

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14
Q

metabolic syndrome criteria

A

3/5
-blood pressure elevated
-fasting glucose level
-HDL cholesterol
-triglyceride level
-waist circumference >

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15
Q

MAFLD

A

metabolic associated fatty liver disease

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16
Q

maternal risk factors of NAFLD

A

maternal obesity and high maternal early pregnancy glucose concentrations

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17
Q

maternal protective factors for NAFLD

A

breastfeeding >6 months (reduces risk in mom and offspring)

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18
Q

risk factors and causes of NAFLD

A

-drugs (i.e. corticosteroids)
-toxins (i.e. vinyl chloride)
-diet (fructose, malnutrition, starvation and referring, total parenteral nutrition ie IV feeding)
-genetic factors

19
Q

genetic polymorphisms at risk for NAFLD

A
  • Polymorphisms of the gene encoding apolipoprotein C3
  • Polymorphisms of the patatin-like phospholipase domain- containing 3 (PNPLA3) gene
  • Polymorphism of TM6SF2
  • Variants of MBOAT1 and GCKR
  • Polymorphism of HSD17B13 is protective
20
Q

associated conditions with NAFLD

A
  • Cushing syndrome
  • Hypopituitarism
  • Polycystic ovarian syndrome
  • Hypothyroidism
  • Hypobetalipoproteinemia (low apolipoprotein B and LDL cholesterol)
  • Obstructive sleep apnea
  • Gut dysbiosis
  • Altered bile acid metabolism
  • Cholecystectomy
  • Psoriasis
21
Q

NAFLD clinical course

A

slow progression (i.e. 10 years), reversible (when NAFLD, not NASH if cirrhosis present, NASH with fibrosis is reversible)

NAFL –> 20% NASH –> 20% cirrhosis –> liver failure or cancer

22
Q

symptoms of NAFLD

A

asymptomatic
fatigue, malaise, mild RUQ pain

23
Q

advanced stages of NAFLD symptoms

A

nausea, vomit, jaundice, pruritis, memory impaired, easy bleeding, loss of appetite, hepatomegaly,

spider angiomas (blood vessels on skin), portal hypertension (edema, ascites, caput medusae - network of veins of abdomen), palmar erythema, gynecomastia (man boobs from excess estrogen), petechiae

24
Q

physical exam for hepatomegaly

A

palpable liver edge better LR than liver span

25
Q

hepatocellular disease with jaundice physical findings

A

dilated abdominal veins, palmar erythema, spider angiomas, ascites

palpable gallbladder is good to rule out

26
Q

cirrhosis physical findings

A

LR+ dilated ab wall veins, gynecomastia, jaundice, reduced body or pubic hair

27
Q

cirrhosis in chronic liver disease findings

A

LR+ encephalopathy (disordered consciousness and asterixis- tremor), ascites, liver edge firm on palpation

28
Q

where is palmar erythema in chronic liver disease and due to what

A

thenar and hypothenar eminences and fingertips

due to high estrogen levels

29
Q

capute medusae is? and cause?

A

veins on abdomen from portal hypertension

30
Q

gynecomastia is and cause

A

man boobs from estrogen

31
Q

Liver enzymes in NAFLD

A

Alanine aminotransferase (ALT) and aspartate aminotransferase (AST)

Alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT)

32
Q

ALT and AST ratios in NAFLD vs alcoholic liver

A

AST/ALT ratio < 0.8 (ALT/AST ratio > 1) in early NAFLD (in contrast to alcohol associated liver disease where AST/ALT ratio > 1.5); but AST may be > ALT (i.e., AST/ALT ratio increases) as advanced fibrosis and cirrhosis develop

33
Q

what will ALT and AST do in NAFLD (and ALP and GGT)

A

maybe elevated mildly, but normal in 80%

ALP and GGT are maybe elevated

34
Q

other testing for NAFLD

A

lipid levels, fasting glucose, HbA1C, fasting insulin

35
Q

testing to exclude other causes of liver disease

A

i.e. antinuclear antibody test to exclude autoimmune hepatitis,

copper measurement for Wilson disease

CBC and ferritin for hereditary hemochromatosis

hep B and C tests

36
Q

imaging tests for NAFLD, which is preferred?

A

Ultrasonography is best

CT
MRI

37
Q

what is the fatty liver index based on

A

BMI, waist circumference, GGT and triglycerides

38
Q

NAFLD in metabolic syndrome score

A

high BMI, high AST/ALT ratio, high ALT, type 2 diabetes, central obesity (waist to hip)

calculate and add up points

39
Q

what is needed to diagnose NASH and what are the findings

A

liver biopsy

fat accumulation, ballooning degeneration (and possible mallory hyaline or fibrosis)

40
Q

do all NAFLD patients need a liver biopsy?

A

no, only if high risk of developing fibrosis

41
Q

what is ultrasound elastrography for

A

measure liver stiffness and stage of liver fibrosis

42
Q

what to encourage in NAFLD for patients

A

weight loss, diet (fructose), fibre increase, exercise, no alcohol, stop hepatotoxic drugs, treat diabetes and hyperlipidemia

43
Q

treatment of NASH

A

specialist needed

maybe liver transplant if cirrhosis

44
Q

what AST/ALT ratio should you refer to a specialist for

A

> 1

45
Q
A

CMS200 (18 decks)

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