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Flashcards in Hepatitis and Liver Disease Deck (96)
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1

AST/ALT levels leading to differentials

Toxic or ischemic injury when >1000
Acute Hep C, A, C >300-3000
EtOH
Chronic Hep B and C about 100

2

Liver disease with highest prevalence in US

Nonalcoholic fatty liver disease

3

Abnormal labs seen in hepatitis

Liver tests/LFTs: hepatocellular pattern (<10xULN)
Predominantly increased ALT and AST (liver transaminases)
Maybe elevated ALP (sometimes see in NASH)

4

What is hepatitis?

Inflammation of the liver

5

General guidelines to interpret increased AST/ALT

AST:ALT >2 (alcoholic liver disease)
ALT>AST (NASH and usually ratio is less than 1 and acute/chronic viral hepatitis)

6

What is a fatty liver?

Hepatic steatosis

7

What is non-alcoholic steatoheatitis (NASH)?

Fatty liver with inflammation of liver with hepatocyte injury (higher risk in developing fibrosis and cirrhosis)
Biopsy may show fibrosis (scarring of liver)

8

What is a non-alcoholic?

<20g ETOH/day (<2-3 drinks/day)

9

Subtypes of nonalcoholic fatty liver disease

Isolated steatosis (NAFL)
Non alcoholic steatohepatitis (NASH)

10

What is isolated steatosis?

Fatty liver without injury or fibrosis of hepatocytes on bx
Minimal risk of progression to cirrhosis

11

What should be considered in all pts with NAFLD?

Aggressive modification of CVD risk factors (also DM)

12

Risk factors of NAFLD

Abd obesity
DM2 (insulin resistance)
Hyperlipidemia (high TG and low HDL)
Metabolic syndrome
Genetic factors-PNPLA3, TM6SF2 and age (less common)

13

Strongest predictor for NASH

Metabolic syndrome

14

What is seen on biopsy for NAFLD/NASH?

Steatosis (fat accumulation)
Inflammation and maybe fibrosis
(will see fatty infiltration on imaging)
*gold standard but not necessary for dx

15

Lab features of NASH

Hepatocellular pattern (mild elevation ALT/AST rarely above 300)
Normal bilirubin, albumin, INR
Ferritin elevated (marker for inflammation)
Hyperlipidemia
Glucose (elevated)
ALP elevated in 1/3 and maybe GGT

16

Cornerstone of management for NASH

Exercise and weight loss

17

How can weight loss help NASH?

>3% improves steatosis
7-10% NASH resolution
>10% fibrosis regression seen

18

Other management for NASH

Minimize alcohol, modify CVD risk factors, control DM and HLD, monitor LFTs, vaccinate Hep A and B (check for IgG Ab etc)

19

What is hereditary hemochromatosis?

Hereditary disorder of iron metabolism (genetic mutation results in increased GI absorption of iron and leads to accumulation in liver/pancreas/heart/other organs)

20

Clinical findings of hereditary hemochromatosis

FHx or incidental note increase AST/ALT
Caucasians or northern european origin
Fatigue, malaise, RUQ discomfort

21

Late manifestations of hereditary hemochromatosis

(generally seen in 4th-5th decade)
Hepatomegaly, hepatic insufficiency, cirrhosis, DM, impotence, arthralgia (2nd and 3rd MCPs), bronze pigmentation of skin, cardiomegaly with/without CHF

22

Bronze diabetes

Triad of DM, bronze pigmentation of skin and cirrhosis

23

Labs in hereditary hemochromatosis

Elevated LFTs (AST, ALT, alk phos)
Screen with serum Fe and TIBC and ferritin (Fe/TIBC equals transferrin saturation)

24

What to do if transferrin sat >45 and/or ferritin >200 ng/mL in men or >150 ng/mL in women?

Proceed to GI (HFE mutation and analysis)
Tx is therapeutic phlebotomy

25

How to diagnose hereditary hemochromatosis

Genetic testing and maybe liver biopsy

26

Tx for hereditary hemochromatosis

Prevent cirrhosis from iron overload
Avoid vit C and iron supplements, uncooked shellfish and EToH
Do regular phlebotomy (therapeutic)
Cirrhosis screen q 6 mos (US and AFP)

27

What to do for all 1st degree relatives in hereditary hemochromatosis?

Genetic screening (HFE genotype) and iron testing

28

Who do you screen for hereditary hemochromatosis in (AASLD)?

Elevated liver tests (AST/ALT)
Abnormal iron studies
First degree relative dx with HH
Evidence of liver disease
Suggestive sxs of HH

29

What is Wilson's disease?

Very rare hereditary disorder of copper metabolism
Autosomal recessive
Genetic defect results in decreased excretion of copper into bile and accumulation of copper in liver (when exceeds that it builds up everywhere else)

30

Findings of Wilsons disease

Predominantly hepatic, neuro or psychiatric findings
Neuro/psych sxs (tremor, dysarthria, incoordination, ataxia, parkinsonism, personality changes)