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DEMS Exam 1 > Functional Liver Tests and Treatment of Chronic Hepatitis > Flashcards

Functional Liver Tests and Treatment of Chronic Hepatitis Flashcards

1
Q

what can cause Prolongation of PT (INR)

A

Significant hepatocellular dysfunction

Vitamin K deficiency

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2
Q

how can you differentiate liver Dysfunction vs. Vit K deficiency?

A

Administer subcutaneous vitamin K and assess response
No correction = liver dysfunction
Normalization = vitamin K deficiency

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3
Q

predominately elevated AST and ALT would indicate what pattern of disease?

A

Hepatocellular Injury or Necrosis

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4
Q

predominately elevated alk phos would indicate what pattern of disease?

A

Cholestatic Pattern

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5
Q

where in AST located in the hepatocyte?

A

Cytosol and mitochondria

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6
Q

where is ALT located in the hepatocyte?

A

Cytosol

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7
Q

what organs express AST?

A

liver, heart, muscle, blood

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8
Q

what organs express ALT

A

Liver only

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9
Q

what is a Typical AST:ALT ratio

A

<1

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10
Q

AST:ALT Ratio >1 is seen in _____

A

cirrhosis

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11
Q

AST:ALT Ratio >2 is suggestive of ________

A

alcoholic liver disease

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12
Q

what is alkaline phosphatase

A

Hydrolase enzyme responsible for removing phosphate groups from nucleotides, proteins and alkaloids

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13
Q

alkaline phosphatase can be elavated in

A

Cholestatic or infiltrative diseases of liver
Obstruction of biliary system
Bone disease
Pregnancy

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14
Q

what do glutamyltransferase (GGT) lab values represent

A

GGT is Not present in bone
so if GGT is elevated and alk phos is elevated then you know the origin is the liver

Is Elevated after alcohol consumption and almost all types of liver disease

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15
Q

what are 7 hepatobiliary causes of increased alk phos?

A 
Bile duct obstruction
Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)
Medications
Hepatitis
Cirrhosis
Infiltrating disease
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16
Q

what are 6 non-hepatic causes of elevated alk phos?

A 
Bone disease
Pregnancy
Chronic renal failure
Lymphoma and other malignancies
Congestive heart failure
Infection and inflammation
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17
Q

what are 3 things that can cause Unconjugated (indirect) hyperbilirubinemia

A

Gilbert’s syndrome
Hemolysis (increased heme breakdown)
Crigler-Najjar syndrome

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18
Q

what 4 things can cause conjugated hyperbilirubinemia

A

Extrahepatic obstruction of bile flow
Intrahepatic cholestasis
Hepatitis
Cirrhosis

19
Q

what is HBsAg and what does it indicate?

A

Hepatitis B surface antigen
Marker of active infection
Presence for >6 months defines chronic hepatitis B infection

20
Q

what is HBsAb (or anti-HBs) and what does it indicate?

A

Antibody to HBsAg

Marker of immunity to hepatitis B

21
Q

what is HBcAb and what does it indicate?

A

Hepatitis B core antibody

Marker of active or prior infection

22
Q

what is HBeAg and what does it indicate?

A

Hepatitis B “e” antigen

Surrogate marker of high viral load

23
Q

what is HBeAb (or anti-Hbe) and what does it indicate

A

Antibody to hepatitis B “e” antigen

Associated with lower viral load

24
Q

what does HBV DNA indicate on lab tests

A

Presence means active viral replication

25
Q

what are the goals of HBV treatment?

A

HBeAg seroconversion -> Loss of HBeAg and development of HBeAb associated with negative HBV DNA when treatment stopped.

Prevention of decompensated cirrhosis in those with advanced fibrosis

26
Q

what are the 3 indications for treatment of chronic HBV

A

1) HBsAg(+) > 6 months*
2) Serum HBV DNA >105 copies/mL
3) Persistent or intermittent elevation in ALT and AST levels

Likelihood of HBeAg seroconversion with normal ALT is very low

27
Q

what are 2 treatment options for HBV

A

1) Interferon
Finite duration of therapy (1 year)
Absence of resistant mutations
More durable response

2) Nucleoside/tide analogues
Fewer side effects
Resistant mutations

28
Q

Chronic HCV defined as presence of HCV RNA in blood ____ months after infection

A

> 6

29
Q

Goal of antiviral therapy is to clear HCV RNA such that they remain HCV RNA negative ______ after stopping therapy.

A

12 weeks

30
Q

what is a current Tx option For HCV

A

NS5B polymerase inhibitor (SOFOSBUVIR)
+
NS5A inhibitor (LEDIPASVIR)

For 12 weeks

31
Q

what is hereditary hemochromatosis

A

Inherited disorder resulting in increased intestinal iron absorption

32
Q

what is the treatment of hereditary hemochromatosis

A

Therapeutic phlebotomy
500 mL of whole blood = 200-250 mg iron
Endpoint is serum ferritin 50 ng/mL
Maintenance phlebotomy to keep ferritin 50-100
ng/mL

33
Q

what is the tx for hereditary hemochromatosis in anemic patients not able to tolerate phlebotomy?

A

chelation therapy with desfuroxamine

34
Q

for diagnosis of hereditary hemochromatosis, Initial iron studies are ordered; what results would make you proceed with a gene test?

A

% iron saturation is >45% OR

ferritin (>500 ng/mL)

35
Q

what is the mutation seen in hereditary hemochromatosis

A

HFE Gene mutation -> C282Y, H63D, S65C

36
Q

If gene testing comes back positive for hereditary hemochromatosis, what should be the next step?

A

Evaluate for end organ involvement
Liver -> MRI
Heart -> Cardiac MRI
Pancreas, gonads, thyroid, joints

37
Q

Primary Biliary Cholangitis

A

Immune mediated disease causing damage to small intrahepatic bile ducts

38
Q

what is the treatment for Primary Biliary Cholangitis

A 
ursodeoxycolic acid (UDCA)
-> Improves bile acid transport, “detoxifies” bile and providing cytoprotection
39
Q

what is Primary Sclerosing Cholangitis

A

Inflammatory disease of the intra- and EXTRAHEPATIC large bile ducts -> Leads to strictures and obstruction of bile ducts and can ultimately result in cirrhosis

40
Q

what is the Tx of Primary Sclerosing Cholangitis

A

Treatment focused on management of complications of bile duct obstruction

1) Stenting strictures
2) Antibiotics for cholangitis

41
Q

what is wilsons disease?

A

Autosomal recessive disorder

Decreased hepatocullar copper excretion resulting in hepatic copper accumulation and injury

42
Q

what is the Tx of wilson’s disease

A

copper chelation -> D-penicillamine, Trientine

Maintenance therapy with zinc

43
Q

what is Non-Alcoholic Steatohepatitis (NASH)

A

NASH is presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning with or without fibrosis

44
Q

what is the Tx of Non-Alcoholic Steatohepatitis (NASH)

A

Treatment focused on modifying risk factors
Obesity
Diabetes mellitus type 2
Dyslipidemia

DEMS Exam 1 (28 decks)

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