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Liver disease Flashcards

0
Q

Increased alk phos and bilirubin signify what kind of injury?

A

Cholestasis

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1
Q

Increased AST and ALT signify what kind of injury?

A

Hepatocellular injury

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2
Q

Progression of alcoholic liver disease

A

Fatty liver -> hepatitis -> cirrhosis
Fatty liver is asymptomatic
Hepatitis has an increased AST/ALT/alk phos/GGT/bilirubin
Cirrhosis has all the signs of ESLD

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3
Q

Workup of isolated hyperbilirubinemia

A

Direct (conjugated) hyperbilirubinemia: Dubin-Johnson and Rotor
Unconjugated hyperbilirubinemia: hemolytic anemia, Criggler-Najjar, and Gilberts

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4
Q

Gilberts disease

A

Unconjugated hyperbilirubinemia
Asymptomatic most of the time
May present with mild jaundice when stressed, sick, etc.
2/2 decreased activity of glucuronyl transferase

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5
Q

Crigler-Najjar

A

The only form of hyperbilirubinemia which can be dangerous
Unconjugated hyperbilirubinemia
Type I: severe, often p/w permanent neuro damage
Type II: less severe
Tx: phototherapy or plasmapharesis

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6
Q

Phototherapy helps which kind of bilirubinemia?

A

Unconjugated

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7
Q

Dubin-Johnson disease

A

Conjugated hyperbilirubinemia
Asymptomatic, can p/w icterus. Triggered by URI, OCPs, pregnancy
Black liver pigmentation on biopsy
Labs: normal urine coproporphyrin level but the breakdown is very altered (normally, 80% is coproporphyin III, in this dz 80% is coproporphyin I)

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8
Q

Rotor syndrome

A

Asymptomatic conjugated hyperbilirubinemia
Defect of hepatic storage leads to leakage into plasma
Elevated direct and indirect bili w/ nl LFTs
No pigmented granules

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9
Q

Ddx of increased alk phos and bilirubin

A

Cholestasis:

  • Ductal dilation present: biliary obstruction (stone, stricture, cancer)
  • No ductal dilation: intrahepatic cholestasis (postop, sepsis, medications)
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10
Q

Metabolic syndromes that can cause chronic hepatitis

A

Hemochromatosis
Wilson’s dz
Alpha 1 antitrypsin deficiency

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11
Q

Clinical presentation of acute hepatitis

A

Viral prodrome (fever, nausea, vomiting, malaise) followed by jaundice and RUQ tenderness

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12
Q

Lab differences between acute and chronic hepatitis

A

Acute: markedly elevated AST, ALT and elevated bili/alk phos

Chronic: persistently elevated ALT and AST for 3-6 months

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13
Q

Timeline of HBV serologies

A

Acute infection: HBsAg +
As infection progresses: HBeAg starts to appear
Then a large titer of Anti-HBc (anti-core antigen) presents (2 months)
HBsAg and HBeAg start to decrease and disappear at 5 months
Anti-HBe starts to present around this time also
Window period: between disappearance of HBsAg and appearance of Anti-HBs

You are not immune unless you have Anti-HBs

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14
Q

Viral serology for HAV infection

A

Look for IgM antibody to HAV

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15
Q

Autoimmune hepatitis serologies

A

Anti-smooth muscle antibodies

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16
Q

Labs for hemochromatosis

A

High ferritin, high transferrin saturation (>50%)

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17
Q

Labs for Wilson’s disease

A

Low ceruloplasmin, high urine copper

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18
Q

Treatment of chronic HBV infection

A

Interferon and lamivudine (3TC) or adefovir

19
Q

Treatment of chronic HCV infection

A

Interferon and ribavirin

20
Q

Definition of cirrhosis

A

Fibrosis and nodular regeneration 2/2 chronic hepatic injury

21
Q

Budd-Chiari syndrome

A

Hepatic vein thrombosis 2/2 hypercoaguable state

22
Q

Non-hepatitis causes of cirrhosis

A

Right sided heart failure, biliary disease (primary sclerosing cholangitis or primary biliary cirrhosis), Budd-Chiari syndrome, constrictive pericarditis

23
Q

Effects of portal HTN

A 
Varices (esophageal, hemorrhoids)
Melena (2/2 variceal bleeding)
Splenomegaly
Caput medusae (blood vessels near the umbilicus)
Ascites
24
Effects of liver cell failure
Neuro: AMS and asterixis Synthetic: gynecomastia, loss of sexual hair, and testicular atrophy, hypercoagulation, anemia, edema Others: spider nevi, scleral icterus, jaundice
25
Serum-ascites-albumin-gradient
Serum albumin - ascites albumin If > 1.1: 2/2 portal HTN If < 1.1: 2/2 nephrotic syndrome, Tb, malignancy with peritoneal carcinomatosis
26
Causes of portal HTN
Pre-sinusoidal: splenic or portal vein thrombosis, schistosomiasis Sinusoidal: cirrhosis Post-sinusoidal: RHF, Budd-Chiari, constrictive pericarditis
27
MOA of lactulose
Lactulose is digested by gut bacteria | This acidifies the gut and converts NH3 -> NH4+, which is not absorbed
28
MOA and use for neomycin
Antibiotic that destroys ammonia producing gut bacteria Short term use for hepatic encephalopathy and liver failure SE: ototoxicity and nephrotoxicity
29
Complications of cirrhosis
``` Variceal bleeding Coagulopathy Hepatic encephalopathy Hepatorenal syndrome Spontaneous bacterial peritonitis Ascites ```
30
Diagnosis of SBP
PMNs > 250/mL and a + Gram stain
31
Tx of SBP
IV antibiotics ie 3rd generation cephalosporin IV albumin PPx w/ fluoroquinolone to prevent future infections
32
How to treat coagulopathy in liver disease
FFP. Vitamin K will not help
33
Primary biliary cirrhosis: what is it
An autoimmune disorder characterized by destruction of intrahepatic bile ducts
34
Presentation of primary biliary cirrhosis
Jaundice, pruritis, and fat-soluble vitamin deficiency (A, D, E, K)
35
Lab findings of primary biliary cirrhosis
Increased alk phos, increase bilirubin + antimitochondrial antibody Increased cholesterol
36
Treatment of primary biliary cirrhosis
Ursodeoxycholic acid slows progression | Liver transplant
37
Biopsy findings of primary biliary cirrhosis
Ductopenia which can be caused by failing liver transplant, Hodhkins, CMV, sarcoid, HIV
38
Lab values in hepatocellular carcinoma
Abnormal LFTs | Significantly elevated AFP levels
39
Presentation of hemochromatosis
Diabetes, abdominal pain, hypogonadism, arthropathy of the MCP joints, heart failure, restrictive cardiomyopathy, cirrhosis Bronze skin pigmentation, hepatomegaly, and testicular atrophy
40
Labs in hemochromatosis
``` Elevated serum iron, elevated ferritin, decreased transferrin Transferrin saturation (serum Fe/TIBC) > 45% is highly indicative ```
41
Tx of hemochromatosis
Weekly phlebotomy until iron levels normalize, phlebotomy every 2-4 months Deferoxamine (iron chelator) can be used as maint therapy
42
Presentation of Wilson's disease
Hepatitis/cirrhosis Neurologic dysfunction: ataxia and tremor Psychiatric abnormalities: psychosis, anxiety, mania, depression PE: Kayser-Fleischer rings, jaundice, hsm, asterixis, rigidity
43
Wilson's disease labs
Decreased serum ceruloplasmin, increased urinary Cu excretion
44
How to treat Wilson's disease?
Penicillamine: copper chelator that increases urinary excretion Zinc: increases fecal excretion

GI (8 decks)

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