Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > Liver disease > Flashcards

Liver disease Flashcards

0
Q

Increased alk phos and bilirubin signify what kind of injury?

A

Cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Increased AST and ALT signify what kind of injury?

A

Hepatocellular injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Workup of isolated hyperbilirubinemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Phototherapy helps which kind of bilirubinemia?

A

Unconjugated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Metabolic syndromes that can cause chronic hepatitis

A

Hemochromatosis
Wilson’s dz
Alpha 1 antitrypsin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical presentation of acute hepatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Viral serology for HAV infection

A

Look for IgM antibody to HAV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Autoimmune hepatitis serologies

A

Anti-smooth muscle antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Labs for hemochromatosis

A

High ferritin, high transferrin saturation (>50%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Labs for Wilson’s disease

A

Low ceruloplasmin, high urine copper

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Effects of liver cell failure

A

Neuro: AMS and asterixis
Synthetic: gynecomastia, loss of sexual hair, and testicular atrophy, hypercoagulation, anemia, edema
Others: spider nevi, scleral icterus, jaundice

25
Q

Serum-ascites-albumin-gradient

A

Serum albumin - ascites albumin
If > 1.1: 2/2 portal HTN
If < 1.1: 2/2 nephrotic syndrome, Tb, malignancy with peritoneal carcinomatosis

26
Q

Causes of portal HTN

A

Pre-sinusoidal: splenic or portal vein thrombosis, schistosomiasis
Sinusoidal: cirrhosis
Post-sinusoidal: RHF, Budd-Chiari, constrictive pericarditis

27
Q

MOA of lactulose

A

Lactulose is digested by gut bacteria

This acidifies the gut and converts NH3 -> NH4+, which is not absorbed

28
Q

MOA and use for neomycin

A

Antibiotic that destroys ammonia producing gut bacteria
Short term use for hepatic encephalopathy and liver failure

SE: ototoxicity and nephrotoxicity

29
Q

Complications of cirrhosis

A 
Variceal bleeding
Coagulopathy
Hepatic encephalopathy
Hepatorenal syndrome
Spontaneous bacterial peritonitis
Ascites
30
Q

Diagnosis of SBP

A

PMNs > 250/mL and a + Gram stain

31
Q

Tx of SBP

A

IV antibiotics ie 3rd generation cephalosporin
IV albumin
PPx w/ fluoroquinolone to prevent future infections

32
Q

How to treat coagulopathy in liver disease

A

FFP. Vitamin K will not help

33
Q

Primary biliary cirrhosis: what is it

A

An autoimmune disorder characterized by destruction of intrahepatic bile ducts

34
Q

Presentation of primary biliary cirrhosis

A

Jaundice, pruritis, and fat-soluble vitamin deficiency (A, D, E, K)

35
Q

Lab findings of primary biliary cirrhosis

A

Increased alk phos, increase bilirubin
+ antimitochondrial antibody
Increased cholesterol

36
Q

Treatment of primary biliary cirrhosis

A

Ursodeoxycholic acid slows progression

Liver transplant

37
Q

Biopsy findings of primary biliary cirrhosis

A

Ductopenia which can be caused by failing liver transplant, Hodhkins, CMV, sarcoid, HIV

38
Q

Lab values in hepatocellular carcinoma

A

Abnormal LFTs

Significantly elevated AFP levels

39
Q

Presentation of hemochromatosis

A

Diabetes, abdominal pain, hypogonadism, arthropathy of the MCP joints, heart failure, restrictive cardiomyopathy, cirrhosis
Bronze skin pigmentation, hepatomegaly, and testicular atrophy

40
Q

Labs in hemochromatosis

A 
Elevated serum iron, elevated ferritin, decreased transferrin
Transferrin saturation (serum Fe/TIBC) > 45% is highly indicative
41
Q

Tx of hemochromatosis

A

Weekly phlebotomy until iron levels normalize, phlebotomy every 2-4 months

Deferoxamine (iron chelator) can be used as maint therapy

42
Q

Presentation of Wilson’s disease

A

Hepatitis/cirrhosis
Neurologic dysfunction: ataxia and tremor
Psychiatric abnormalities: psychosis, anxiety, mania, depression

PE: Kayser-Fleischer rings, jaundice, hsm, asterixis, rigidity

43
Q

Wilson’s disease labs

A

Decreased serum ceruloplasmin, increased urinary Cu excretion

44
Q

How to treat Wilson’s disease?

A

Penicillamine: copper chelator that increases urinary excretion
Zinc: increases fecal excretion

GI (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions