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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
physical exam for hepatomegaly
palpable liver edge better LR than liver span
25
hepatocellular disease with jaundice physical findings
dilated abdominal veins, palmar erythema, spider angiomas, ascites palpable gallbladder is good to rule out
26
cirrhosis physical findings
LR+ dilated ab wall veins, gynecomastia, jaundice, reduced body or pubic hair
27
cirrhosis in chronic liver disease findings
LR+ encephalopathy (disordered consciousness and asterixis- tremor), ascites, liver edge firm on palpation
28
where is palmar erythema in chronic liver disease and due to what
thenar and hypothenar eminences and fingertips due to high estrogen levels
29
capute medusae is? and cause?
veins on abdomen from portal hypertension
30
gynecomastia is and cause
man boobs from estrogen
31
Liver enzymes in NAFLD
Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) Alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT)
32
ALT and AST ratios in NAFLD vs alcoholic liver
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
what will ALT and AST do in NAFLD (and ALP and GGT)
maybe elevated mildly, but normal in 80% ALP and GGT are maybe elevated
34
other testing for NAFLD
lipid levels, fasting glucose, HbA1C, fasting insulin
35
testing to exclude other causes of liver disease
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
imaging tests for NAFLD, which is preferred?
Ultrasonography is best CT MRI
37
what is the fatty liver index based on
BMI, waist circumference, GGT and triglycerides
38
NAFLD in metabolic syndrome score
high BMI, high AST/ALT ratio, high ALT, type 2 diabetes, central obesity (waist to hip) calculate and add up points
39
what is needed to diagnose NASH and what are the findings
liver biopsy fat accumulation, ballooning degeneration (and possible mallory hyaline or fibrosis)
40
do all NAFLD patients need a liver biopsy?
no, only if high risk of developing fibrosis
41
what is ultrasound elastrography for
measure liver stiffness and stage of liver fibrosis
42
what to encourage in NAFLD for patients
weight loss, diet (fructose), fibre increase, exercise, no alcohol, stop hepatotoxic drugs, treat diabetes and hyperlipidemia
43
treatment of NASH
specialist needed maybe liver transplant if cirrhosis
44
what AST/ALT ratio should you refer to a specialist for
>1
45

CMS200 (22 decks)

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