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Clin Med II > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

What are some functions of the liver?

A

Synthetic functions (coagulation factors, cholesterol and triglycerides, amino acids, bile, glucose, glycogen, albumin, angiotensinogen)

Detoxification/catabolism

Drug metabolism and detoxification

Hormone degradation

Ammonia degradation

Storage (iron, copper, vitamin A, D and B12)

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2
Q

What are a few ways to classify liver disease?

A

Hepatocellular - liver injury, inflammation, and necrosis

Cholestatic (obstructive) – problem with bile flow

Mixed pattern - features of both hepatocellular and cholestatic injury

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3
Q

Staging or timing of liver diseases

A

Acute liver disease
Chronic liver disease
Cirrhosis –> final end point of most liver diseases

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4
Q

Liver disease common symptoms

A 
Many are asymptomatic
Fatigue 
Nausea
Anorexia
RUQ discomfort
Abdominal distention
Pruritus
Jaundice
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5
Q

Risk factors for liver disease

A 
Alcohol
IDU
Medications
Sexual activity (Hep B)
Travel
Occupational exposure (e.g., needlesticks)
Transfusions
Family history of liver disease
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6
Q

What are some possible exam findings for liver disease?

A

Often normal

May reveal risk factors

Icterus, hepatomegaly, hepatic tenderness, splenomegaly, spider angiomata, palmar erythema, and excoriations

More signs as liver disease advances – muscle wasting, bruising, ascites, edema, dilated abdominal veins, asterixis, AMS

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7
Q

Lab testing for liver disease

A

Liver enzymes: ALT, AST
ALP
GGT

Synthetic function: Serum albumin, Prothrombin time (PT), INR

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8
Q

Acute liver failure (fulminant hepatic failure) characteristics

A
  1. Acute liver injury: LFTs typically > 15 times upper limit of normal
  2. Hepatic encephalopathy: Delirium, changes in personality, irritability, aggressive behavior, declining LOC –> coma
  3. Elevated PR/INR > 1.5
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9
Q

Which hepatitis viruses can go on to cause chronic liver disease?

A

HBV, HCV, and HDV

HDV require HBV

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10
Q

Acute viral hepatitis clinical features

A

A large number of infections are asymptomatic

May have jaundice and elevated liver enzymes.

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11
Q

Acute viral hepatitis initial phase

A

Incubation (inoculation) phase

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12
Q

Acute viral hepatitis prodromal phase

A

Constitutional symptoms – fever, anorexia, nausea, vomiting, diarrhea, fatigue, malaise, myalgia -
and dull RUQ pain

Precedes jaundice by 1-2 weeks

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13
Q

Acute viral hepatitis icteric (jaundice) phase

A

Heralded by onset of clinical jaundice and lasts 1-3 weeks.

The constitutional symptoms diminish.

Liver becomes enlarged and tender (RUQ pain/discomfort).

Many pts never become icteric

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14
Q

Acute viral hepatitis: recovery phase

A

Lasts from 2-12 weeks

Symptoms continue to resolve but can still have some liver enlargement and LFT abnormalities.

Complete clinical and biochemical recovery usually within 6 months

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15
Q

Acute viral hepatitis: Aminotransferases

A

AST/ALT increase during prodromal phase and precede rise of bilirubin

ALT/AST acute levels do not correlate to degree of liver cell damage or risk of developing liver failure

Typically >25 times the upper limit of normal

Peak levels of ALT/AST vary from 400-4000+ IU/L and are usually reached at time pt is icteric. If patient has markedly elevated transaminases then hepatitis should be on the list of concerns.

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16
Q

Acute viral hepatitis: bilirubin

A

With jaundice, serum bilirubin from 5-20 mg/dL

Can rise and persist after decrease in AST/ALT

Persistently elevated bilirubin associated with poorer prognosis

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17
Q

Acute viral hepatitis: PT

A

PT prolongation may indicate severe liver damage/extensive hepatocellular necrosis and poorer prognosis

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18
Q

Acute viral hepatitis: ALP

A

ALP may be normal or mildly elevated

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19
Q

Acute viral hepatitis: Albumin

A

Alb usually normal with acute, uncomplicated illness

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20
Q

Acute viral hepatitis: LDH

A

May also be elevated (1-3 times normal) but not specific

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21
Q

Other infectious causes of increased transaminases

A

EBV, CMV, VZV, rubella, measles, mumps, coxsackie B

Disseminated HSV (in immunocompromised pts)

Rickettsial infections, bacterial sepsis, Legionella, syphilis, disseminated mycobacterial, fungal infections

Yellow fever (Central and South America)

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22
Q

Acute viral hepatitis: Treatment

A

Supportive: bed rest, avoidance of hepatotoxic meds, no alcohol

Most pts do not require hospitalization and recover within 3-6 months

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23
Q

When should a patient be hospitalized for acute viral hepatitis

A

Severe dehydration
Hepatic failure
Bilirubin >15-20 mg/dL
If PT is prolonged

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24
Q

Acute hepatitis follow up

A

Transaminases, ALP, bilirubin, PT - monitored 1-2 times per week for 2 weeks initially

Then, every other week until they return to normal

Pts with fulminant hepatic failure are considered for liver transplant

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25
Q

Viral hepatitis immunizations

A

Vaccines available for hepatitis A and B

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26
Q

Hepatitis A epidemiology

A

Only leads to acute hepatitis – no chronic form of the disease

You can only get it once

Spread via oral-fecal route. Usually through contaminated food.

Rare in industrialized countries.

Incidence in US has declined drastically since vaccination.

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27
Q

Risk factors for hepatitis A

A

Most common risk factor is international travel (up to 50% of cases)

Lower SES, food and water contamination, sexual and household contact, MSM, IDU, childcare

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28
Q

When is hepatitis A most infectious?

A

Most infectious during the first 2 weeks before onset of clinical illness. Fecal shedding continues 2-3 weeks after onset of symptoms.

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29
Q

Hepatitis A clinical features

A

Malaise, fatigue, flu-like symptoms (coryza, photophobia, headache, and cough) myalgia, arthalgia, abdominal pain, N/V, anorexia, fever and jaundice

Can be silent or subclinical particularly in children (>80%)

Patients present with acute illness typically several weeks after infection.

Rarely, patients can go on to develop fulminant hepatic failure requiring liver transplant for survival

Risk of liver failure in HAV infection increases with age and other liver disease

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30
Q

What are the two clinical features of hepatitis A?

A
  1. Pts can have long period of jaundice after HAV infection (prolonged cholestasis)

These pts can have months of jaundice during recovery from HAV infection. These pts can also have elevated ALP levels as well

Treatment is supportive and the jaundice slowly fades over time

  1. Pts can have a relapse of the disease weeks or months after the initial infection

Treatment is supportive unless the pt develops fulminant hepatic failure

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31
Q

Hepatitis A diagnosis

A

Anti-HAV IgM antibodies in the serum + typical clinical presentation is diagnostic
May be positive in 5-10 days prior to onset of sxs
Detectable up to 6 months after exposure

Aminotransferases are elevated (10-100 times the upper limit of reference range) – usually >1,000 IU/dL.

Resolution of the illness is associated with emergence of anti-HAV IgG antibodies

Change from detection of IgM antibodies to IgG antibodies distinguishes acute from convalescent infection

IgG confers life-long immunity

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32
Q

Hepatitis A treatment

A

Supportive

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33
Q

Hepatitis A prevention

A

HAV vaccine

Good hygiene

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34
Q

Who should receive routine vaccination for Hep A?

A

All children at one year of age (12-23 months)
MSM
Chronic liver disease
Illicit drug users (injection and non-injection
Household contacts of child adopted from endemic country
Homeless

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35
Q

Vaccination for international travel to high risk areas

A

< 40= I dose HAV and booster within 6-12 months
>40 or immunocompromised, chronic disease: 2 full dose schedule before departure

If not enough time before travel give initial vaccine dosage with immune globulin.

36
Q

Post exposure prophylaxis- within 2 weeks of exposure

A
  1. 1- 40 years and healthy: HAV vaccine
  2. > 40 years: HAV vaccine +/- immune globulin
  3. <1 year, immunocompromised, chronic liver disease: HAV vaccine + immune globulin
  4. <1 year or allergic to vaccine: immune globulin
37
Q

Prevaccination testing for anti-HAV antibodies

A

Consider cost, delay of vaccination:
Can test populations expected to have high rates of previous HAV infection and natural immunity:
1. Adults >40 years of age
2. Adults in certain populations – American Indian, Alaska Native, Hispanic
3. Adults born in or lived in endemic regions
4. Risk groups with high HAV seroprevalence, (eg, IDU, MSM, or HIV-infected)

38
Q

Hepatitis A prognosis

A

Usually self-limited infection

Most symptoms and labs resolve by 3-6 months

Prolonged or relapsing symptoms possible

Acute liver failure is rare but risk increases with age and other comorbid chronic liver disease

No chronic disease or cirrhosis

39
Q

Acute hepatitis B epidemiology

A

Major cause of acute viral hepatitis and most common cause of chronic viral hepatitis worldwide

Rare in Western, developed countries – 2% of population

In U.S., <2% prevalence

Sexual transmission

40
Q

High risk individuals for acute hepatitis B

A 
H/o multiple transfusions
IDU
Hemodialysis
Risky sexual behavior
MSM
Household and heterosexual contacts of hepatitis B carriers
Residents and employees of residential care facilities
Travelers to endemic areas
41
Q

Acute hepatitis B clinical presentation

A

Incubation period 60-160 days. Symptoms developing months after infection - varies from mild to acute liver failure

Subclinical disease possible, especially in children but most should be vaccinated.

More insidious onset and more prolonged course than HAV

Malaise, fatigue, jaundice, pruritus, headache, RUQ abdominal pain, N/V, anorexia, dark urine.

These symptoms all decrease rapidly after the onset of jaundice

Most acute HBV infections are self-limited in adults

42
Q

Hepatitis B serum sickness-like illness

A

~10% of pts with acute HBV can present with a serum sickness-like illness (fever, maculopapular rash or urticarial, migratory arthritis)

43
Q

Hepatitis B diagnosis

A

Liver chemistries- AST, ALT, Alkaline phosphatase, total bilirubin are typically elevated.
ALT and AST - typically up to 1000-2000 units/L.

44
Q

Hepatitis B surface antigen: HBsAg

A

HBsAg appears in serum 1-10 weeks after exposure, prior to onset of symptoms or elevation of serum ALT

In pts who recover, HBsAg becomes undetectable in 4-6 months

Persistence of HBsAg for >6 months implies chronic infection

45
Q

Hepatitis B e antigen; HBeAg

A

Hepatitis B envelope antigen

Serves as a marker for hepatitis B replication and infectivity

The presence of HBeAg indicates high HBV DNA and high rates of transmission

46
Q

Hepatitis B surface antibody: HBsAb

A

Appears when HBsAg declines in pts who mount a protective immune response. A person who clears the virus through having it or by having vaccine.

It confers immunity in patients with recovered hepatitis B or with previous vaccination. No one with HBsAb will actively have the disease.

47
Q

Hepatitis B core antibory: HBcAb

A

Suggests HBV infection

IgM HBcAb could be the only positive antibody in the “window period”

Period of acute HBV infection when both HBsAg and HBsAb may be negative

Transient presence of IgM anti-HBc forms an important basis for diagnosis of acute infection

48
Q

Hepatitis B e antibody: HBeAb

A

Development is a marker for low HBV DNA and lower rates of transmission in pts without protective immunity

49
Q

HBV viral DNA

A

The most accurate marker of viral replication. Risk of transmission during acute infection is very high during the incubation period because of high viral load.

50
Q

Treatment of acute HBV

A

Supportive watching to liver failure (rare) and progression of the disease.

51
Q

HBV preexposure prophylaxis

A

HBV vaccine for everyone

52
Q

HBV postexposure prophylaxis

A

Infants for HBsAg positive should receive HBV vaccine and hepatitis B immune globulin within 12 hours.

Susceptible sexual partners of individuals with HBV and needle-stick injury should receive immune globulin within 24 hours.

53
Q

HBV prognosis

A

Can have spontaneous resolutions or progression to chronic disease.
5-10% of adults with develop chronic HBV. Should take about 4 months for aminotransferases to go down but it greater than 6 months then assume chronic hepatitis.

54
Q

Hepatitis C epidemiology

A

Usually presents as a chronic infection
Primary route of transmission is blood exposure (eg, transfusion or IDU)
80% of pts infected with HCV has no signs or symptoms of the infection.

55
Q

Risk factors for hepatitis C

A

IDU, HIV, hemodialysis, incarceration, blood transfusion (rare)

56
Q

Acute hepatitis C clinical presentation

A

20% with acute infection have jaundice; if sxs, may have nausea, malaise

Most patients who are acutely infected with HCV are asymptomatic.

Symptomatic patients may experience jaundice, nausea, dark urine, and right upper quadrant pain, with a mean onset of symptoms at seven to eight weeks after infection.

57
Q

HCV diagnosis

A

HCV RNA by PCR and anti-HCV antibody testing by enzyme-linked immunosorbent assay (ELISA)

Screening test is the HCV antibody. The presence of HCV antibody suggests prior exposure to HCV but does not convey immunity so you would have to do further testing if it was positive to confirm.

HCV RNA positive and HCV antibody positive confirms HCV infection.

Can also check LFTs, HIV, and tests to exclude other disorders.

58
Q

Hepatitis prevention and screening

A

No vaccine or postexposure prophylaxis

CDC testing guidelines recommend a 1-time test for HVC in baby boomers without assessing HCV risk.

59
Q

Hepatitis C treatment

A

Some patients are able to clear acute hepatitis C virus spontaneously. Tratment can be delayed to 6 months or more to allow for spontaneous resolution.

  1. Interferon based regimens
  2. Direct-acting antivirals (DAA)

DAAs are highly effective in treating chronic infection and can lead to higher cure rates.

Recheck HCV RNA & anti-HCV antibody in 12 weeks.

All patients with virologic evidence of chronic HCV infection for over 6 month period should be considered for treatment.

Goal of treatment is sustained virologic response (SVR)

60
Q

Hepatitis D epidemiology

A

Requires HBsAg to enable replication and infection so HDV always occurs in associated with HBV infection.

Endemic in Mediterranean, Middle East, and parts of south america

61
Q

Hepatitis D “superinfection”

A

Superinfection results in chronic HDV infection along with chronic HBV infection
HDV tends to be a severe illness with high mortality (2-20%)

Often a protracted course that leads to cirrhosis

62
Q

Hepatitis D clinical features

A

Typical hepatitis sxs: jaundice, abdominal pain, anorexia, fatigue, N/V, arthralgia

63
Q

Hepatitis D diagnosis

A

Test include HDV RNA and Anti-HDV antibody

Testing done only when evidence of HBV infection (HBsAg+).

64
Q

Hepatitis D treatment

A

Mostly supportive care

No evidence of benefit of interferon Rx for coinfection or superinfection in acute phase

65
Q

Hepatitis E epidemiology

A

HEV resembles HAV – fecal-oral transmission

Most occur in developing countries (India, Southeast Asia, Africa, Mexico)

US cases typically with history of travel to endemic area

66
Q

Hepatitis E diagnosis

A

Anti-HEV

PCR and serologic testing through CDC

67
Q

Chronic viral hepatitis

A

Defined as the presence of liver inflammation persisting for ≥6 months and associated with HBV, HCV, or HDV infection

68
Q

Chronic viral hepatitis physical exam

A

Findings occur late in the disease process and are due to cirrhosis:

spider angiomata, hepatomegaly, splenomegaly, ascites, jaundice, gynecomastia, testicular atrophy, asterixis, loss of body hair

69
Q

Chronic hepatitis diagnosis

A
  1. Serology testing for HBV and HCV:
    HBsAg, anti-HBsAb, anti-HBcAb, HBeAg, anti-HBeAb and Anti-HCVAb
  2. Transaminases, bilirubin, alkaline phosphatase, PT, albumin. AST/ALT usually 2-5 times normal (ALT>AST)
    ALP usually minimally elevated unless cirrhosis
  3. Liver biopsy may be done for diagnosis confirmation and to determine the severity of disease. Liver fibrosis historically the gold standard for assessing the liver stage and predicting the prognosis.
70
Q

HBV acute infection leads to chronic HBV in:

A

90% of newborns of HBeAg positive mother
25% of infants/children
5-10% of adults

71
Q

Resolved hepatitis B

A

Infection controlled evidenced by resolution of symptoms, normalization of liver enzymes and clearance of HBsAg - with associated antibodies to hepatitis B surface antigen (anti-HBs)

The presence of anti-HBs following acute infection generally indicates recovery and protective immunity against re-infection

In addition, patients with resolution of infection have disappearance of HBeAg and development of antibodies to hepatitis B e antigen (anti-HBe).

72
Q

Chronic hepatitis B e antigen

A

HBsAg and anti-HBc (IgG antibodies) generally persist for life and HBV DNA can usually be detected. But e antigen can either be positive or negative:

The continued presence of HBeAg generally reflects higher HBV DNA levels and greater infectiousness (chronic hepatitis B e antigen positive)

Some patients with chronic HBV infection may have resolution of their HBeAg along with appearance of anti-Hbe (chronic hepatitis B e antigen negative)

73
Q

Inactive hepatitis B (HBsAg carrier)

A

Persistent HBsAg >6 months after acute infection without any necroinflammation

Normal liver enzymes

Nondetectable HBV DNA levels (< 2000)

Transmission to others still possible

Much less incidence of cirrhosis, ESLD, liver cancer than with chronic hepatitis B e antigen positive or e antigen negative.

74
Q

Chronic hepatitis B giagnosis

A

HBV – ALT (made only by hepatocytes) and HBV DNA (via PCR) are also important markers of severity and prognosis.

75
Q

Chronic hepatitis B risk factors for progression to cirrhosis

A 
Older age
HBV genotype C
High levels of HBV DNA
Alcohol consumption
Concurrent infection with HCV, HDV, or HIV
76
Q

Chronic liver disease lab testing

A

CBC, LFTs (AST, ALT, total bilirubin, alkaline phosphatase, albumin), PT, and tests for HBV replication (HBeAg, anti-HBe, HBV DNA).

Want to check for immunity to Hep A, evaluation for other causes of liver disease.

77
Q

Chronic hepatitis B treatment

A

Refer!
Complex and depends on multiple factors including:
Clinical variables (eg, the presence or absence of liver inflammation and/or cirrhosis)
Patient’s immunologic response to infection (eg, hepatitis B e antigen status)
HBV viral load and genotype
Risk factors for disease progression (eg, age >40; FHx of hepatocellular carcinoma)

Interferon alpha, Nucleoside and nucleotide analogs –> both aimed at inhibiting HBV replication.

78
Q

Chronic hep B goals of treatment

A

Reduced risk of end stage liver disease (ESLD) and cancer
Sustained suppression of HBV DNA
HBsAg and HBeAg seroconversion (transition to resolution)
Decreased ALT/AST
Decreased necroinflammation (transition to inactive hepatitis B)
Reduce transmission

79
Q

Treatment response measure by:

A
  1. loss of HBeAg
  2. development of HBeAb and
  3. cessation of viral replication in HBeAg positive patients or
  4. viral suppression in HBeAg negative patients
80
Q

Hepatitis C is a ____ disease based on genotype

A

Curable in up to 82% of patients with treatment

81
Q

Hepatitis C predictors of poor response to treatment:

A 
Cirrhosis
Male
Advanced age
HIV
HCV genotype 1 or 4
82
Q

Chronic Hep C diagnosis

A

Screening: HCV Ab (hepatitis C antibody)

> 90% sensitivity
Confirm with HCV RNA (also used to determine more acute infection when HCV Ab negative early on; also used to assess Rx response)

HCV RNA genotype/subtype (and HCV viral load) help predict response to treatment

83
Q

Hep C treatment goals

A

HCV RNA eradication (cure)

sustained virologic response (SVR), defined as an undetectable RNA level 12 weeks following the completion of treatment.

84
Q

Hep C treatment

A

Refer!
Antiviral therapy of HCV has been rapidly evolving
Choice of medication depends on patient factors and genotype. Genotype 1 most common in US.

Direct-acting antivirals (DAAs)
Interferon alfaq

85
Q

Chronic Hepatitis D

A

Occurs only in presence of chronic HBV

Limited therapy options with limited efficacy.

Clin Med II (7 decks)

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