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Medicine 3 > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

Hepatitis

A
  • Inflammatory disease localized to the liver or part of a generalized systemic process leading to hepatocellular destruction
  • ACUTE: <6 mo; self limited - Etiology: viruses, drugs, alcohol
  • CHRONIC: >6 mo; unresolving; often leads to cirrhosis
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2
Q

Acute viral hepatitis

A
  • Viral: systemic infection whose primary manifestations are hepatic.
  • Serotypes: A, B, C, E, G (D (Delta) subtype of B: infection with the delta particle is dependant on concomitant infection with type B)
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3
Q

Characteristics of Acute viral hepatitis

A
  • The one thing to know about Hep E is that it primarily affects pregnant women
  • Hep A wont make you sick on your vacation, but it will make you very sick when you get back because it has such a long incubation time
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4
Q

Clinical findings of acute viral hepatitis

A
  • Initial symptoms: Flu-like syndrome (fatigue, nausea, myalgias), Abdominal pain
  • Clinical presentations similar for all serotypes; B & C usually more severe, higher incidence of morbidity and mortality
  • 70% pts will have: Tender, palpable liver, Posterior cervical lymphadenopathy, Splenomegaly, Jaundice usually disappears 2-8 weeks after onset
  • Jaundice & Icterus; Hepatomegaly
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5
Q

hepatitis labs

A
  • Transient anemia, lymphocytosis with atypical lymphs, increased reticulocyte count (young RBCs d/t anemia)
  • Increased direct and total serum bilirubin (if the bilirubin is 10, 12, 15, 20, that person has a severe hepatitis) – you usually see jaundice with bilirubin around 10 (Level indicates severity)
  • Increased serum aminotransferase: ALT/AST – the ratio will tell you if this is a viral infection (ALT typically higher than AST (if AST is higher, think alcohol), provides a rough estimate of hepatocellular injury but no prognostic value)
  • Alk Phos rises early (due to liver damage) and often remains elevated after clinical recovery
  • Prothrombin time: usually normal; if elevated suspect fulminant hepatitis (You always want to check, If it is elevated or prolonged, that means that the liver is so inflamed that it can’t make the clotting factors)
  • *Rapid fall in serum aminotransferase from high to normal in < 1 week may be an indication of fulminant hepatitis with massive necrosis / destruction of liver parenchyma
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6
Q

general managment of hepatitis

A
  • Acute viral hepatitis usually resolves completely in 1-3 mo.
  • Treat nausea, vomiting, anorexia (Compazine or other antiemetics)
  • Benadryl, Atarax (Sedatives may precipitate hepatic encephalopathy – get ammonia buildup in the brain and they get really confused)
  • Avoid ETOH and tobacco use, hepatic cleared meds until 1 month after all labs return to normal
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7
Q

hepatitis A

A
  • Most common type of acute hepatitis
  • Epidemic outbreaks: Poor hygienic conditions, Contaminated water supply, Infected food handlers, Ingestion of contaminated shellfish, Institutions/daycare
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8
Q

hepatitis A vaccine

A
  • Children – Incorporated into routine childhood vaccination schedule in 2006 (2 doses starting at 12 mos, 6-12 mos apart)
  • Adults – recommended for high risk individuals: Chronic liver disease, Clotting disorders, Occupational or travel exposure)
  • Due to peds vaccination prevalence of disease shifting to adults
  • The Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control and Prevention (CDC) has recommended hepatitis A vaccination of adults who have any of the following medical, occupational, or lifestyle risk factors (Persons with clotting-factor disorders or chronic liver disease, Men who have sex with men, IV drug users, Persons working with hepatitis A virus infected primates or HAV in a research laboratory, Persons traveling to countries with high or intermediate endemicity recommended in HIV-infected patients)
  • vaccine efficacy is decreased in the setting of advanced immunosuppression
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9
Q

Hep A diagnosis

A
  • Serum anti-HAV IgM antibodies gold standard detecting acute illness
  • Anti-HAV positive at onset of sx, peaks during convalescent phase, remains positive 4-6 mos
  • Serum ALT > AST
  • Bilirubin > 10 common
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10
Q

Hep A treatment and prognosis

A
  • Tx is supportive
  • 85% have full recovery w/in 3 months and nearly all have complete recovery by 6 months
  • Acute infection confers immunity
  • Fatalities most common in elderly or those with chronic Hep C
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11
Q

Hep B

A
  • Usual transmission is blood borne
  • Less common: sexual transmission
  • Delta agent (Hep D): defective virus particle, same route of transmission assoc with Hep B (Causes clinical exacerbation for Hep B carriers, Implicated in fulminant hepatitis, Rapid progression to cirrhosis)
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12
Q

Hep B vaccine

A

-Recommended for everyone: Given at birth, 3 doses at 0, 2, 6 months (varying schedules), Post-exposure prophylaxis, High risk individuals

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13
Q

Hep B diagnosis

A
  • HBsAg present 1-10 wks after acute exposure (Usually undetectable after 6 months, Persistence of HBsAg after 6 months implies chronic infection/carrier state, < 1% of immunocompetent pts will progress to chronic infection)
  • Anti-HBs indicates long term immunity
  • HBeAg present early and is a marker for HBV replication and degree of infectivity
  • Post vaccine testing should be 1-2 months after third vaccine dose for meaningful results
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14
Q

Hep B LFTs

A
  • ALT & AST elevated up to 2000 in acute phase with ALT higher than AST
  • PTT or PT/INR is the best predictor of prognosis
  • Recovery = normalization of LFT’s in 1-4 months
  • Persistent elevation of ALT > 6 months = progression to chronic hepatitis
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15
Q

Chronic Hep B

A
  • Persistence of Hep BsAg > 6mo after acute infection
  • Incidence of progression to chronic by age: 90% perinatal, 20-50% for age 1-5 years, < 5% for adults – if you acquire hep B as an adult, about 95% will clear the infection without becoming chronic
  • Symptoms: nonspecific; fatigue; acute exacerbations of infection that mimic acute hepatitis; hepatic failure
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16
Q

Carrier State Hep B

A
  • Patients in low or nonreplicating phase / inactive carrier state are HBeAg negative (Their envelope is negative – they are not carrying active virus)
  • Persistent Positive HBsAg > 6 mo following acute infection (Carries risk of infectivity)
  • Liver disease in remission as evidenced by normal serum ALT concentrations (But may progress to chronic Hep B, cirrhosis, HCC)
  • HBeAg is a marker for HBV replication and degree of infectivity
17
Q

Hep B treatment

A
  • Goal: suppression of viral replication
  • Indications for treatment: acute liver failure, clinical complications of cirrhosis, advanced fibrosis with high serum HBV DNA, or reactivation of chronic HBV after chemotherapy or immunosuppression, INR >1.5, fulminant hepatitis)
  • Antivirals: Interferon (avoid in pts w/ cirrhosis due to risk of hepatic inflammation) many serious side effects, Lamivudine, entecavir, telbivudine; negligible side effects, Adefovir, Tenofovir: nephrotoxicity
18
Q

Chronic Hep B prognosis

A
  • 5 year prognosis for progression to: Cirrhosis 12 - 20%, Hepatic failure 20%, Hepatocellular Carcinoma 15%
  • Lifetime mortality from liver disease = 50%
  • Complete eradication rarely occurs after acute infection
  • Immunocompromised pts more likely to have reactivation, progression
19
Q

Hep C

A
  • Most common chronic liver disease, accounts for 8,000 to 13,000 deaths each year
  • Majority of liver transplants in the US
  • Acute infection often asymptomatic
  • Slowly progresses; rarely causes fulminant hepatic failure
  • Up to 80% progress to chronic infection leading to fibrosis and cirrhosis (3% of these develop hepatocellular CA, accounts for 30% of HCC cases in US)
20
Q

HCV screening guidelines

A
  • Anyone born in the United States between 1945 and 1965
  • Those with h/o illicit IVDU or intranasal cocaine use, even if only used once
  • Those who received clotting factors made before 1987
  • Those who received blood/organs before July 1992
  • Those who have been informed that they received blood from a donor who later tested positive for HCV
  • Those who were ever on chronic hemodialysis
  • Those with evidence of liver disease (persistently elevated ALT level)
  • Those infected with HIV
  • Children born to HCV-infected mothers
  • Those with a needle stick injury or mucosal exposure to HCV-positive blood
  • Those who are a current sexual partner of an HCV-infected person
  • Incarcerated individuals
21
Q

Hep C diagnosis

A
  • Anti HCV ELISA allows detection in about 95% of pts 2 weeks after exposure
  • More sensitive: HCV RNA by PCR
  • LFT’s elevated 6-12wks after exposure
  • Acute illness typically lasts 2-12 wks
  • Difficult to distinguish acute vs chronic dz unless there is previous neg HCV RNA serology
  • there is suggestive circumstantial evidence for new infection such as a history of a recent high risk exposure, new clinical features of acute hepatitis, previous absence of elevated aminotransferase levels, and absence of a prior risk for HCV infection. Although the presence of symptoms compatible with acute hepatitis can also be informative, most patients are asymptomatic during acute infection with HCV.
  • A new positive HCV PCR usually followed by a positive anti-HCV within 12 weeks is generally considered definitive proof of acute HCV infection. However, this requires availability of a recent serum sample with a negative HCV PCR and anti-HCV. In the absence of such documentation, the distinction between acute hepatitis C virus infection and newly discovered chronic infection is not straightforward since in both settings patients may have detectable HCV RNA, antibodies against HCV, and elevated serum aminotransferases.
  • The pattern and timing of serologic markers, including HCV RNA (usually positive within two weeks after inoculation), serum aminotransferases (usually preceding anti-HCV seropositivity), and antibodies (usually several weeks after exposure) can be helpful
22
Q

hep C diagnosis and evaluation

A
  • Determination of HCV genotype is essential to making decisions about treatment
  • Assessment for liver fibrosis through biopsy or noninvasive measures is helpful in guiding decisions regarding treatment and surveillance
  • Testing for HIV, hepatitis B, and hepatitis A (Vaccination should be administered to those without immunity to Hep A & B)
23
Q

HCV: general mangement

A
  • Antiviral therapy
  • Psychologic counseling
  • Alcohol avoidance
  • Symptom control
  • Dose adjustment of medications
  • Assessment of fibrosis
  • Screening for complications of cirrhosis if present
24
Q

HCV treatment

A
  • The goal of treatment in patients with chronic HCV is to eradicate HCV RNA, which is associated with decreases in all-cause mortality, liver-related death, need for liver transplantation, hepatocellular carcinoma rates, and liver-related complications
  • All patients with detectable viral load >6 mos should consider treatment
  • Treatment selection varies by genotype and other patient factors
25
Q

HCV: cirrhosis treatment

A
  • Cirrhosis: late stage of progressive hepatic fibrosis; distortion of the hepatic architecture and the formation of regenerative nodules
  • Generally irreversible in advanced stages
  • In earlier stages, specific treatments aimed at the underlying cause of liver disease may improve or even reverse cirrhosis
26
Q

HCV: treatment for treatment-naive pts

A

-Harvoni has 95% cure rate (no detectable virus by PCR at 6 mos post-treatment) in genotype 1; once daily dosing, ease of use, very expensive.

27
Q

HCV prognosis

A
  • Recheck viral loads at 12 & 24 wks (SVR defined as undetectable viral load after 24 wks)
  • Survival linked to development of cirrhosis
  • Cirrhosis in about 50% of pts with chronic Hep C
  • Cirrhosis = 3% per year chance developing HCC
  • Host factors predictive of dz progression: Genetic, Acquisition of HCV > age 40, Acquisition of CV by blood transfusion, Coinfection with B, *Children and AA less likely to progress, ETOH abuse, W / cirrhosis, 3 yr survival = 96%, 5 yr survival = 91%, 10 yr survival = 79%
28
Q

cirrhosis

A
  • Widespread hepatic fibrosis
  • Extensive hepatocellular destruction
  • Insidious onset with nonspecific: fatigue, anorexia, weight loss, nausea, abdominal pain
  • Labs: Anemia, Thrombocytopenia, Elevated bilirubin, Decreased albumin, Increased bleeding time, Elevated ammonia
29
Q

cirrhosis disease progression

A
  • Hepatocellular failure
  • Jaundice
  • Edema
  • Ascites
  • Electrolyte abnormalities
  • Bleeding disorders
  • Hepatomegaly
  • Portal hypertension
30
Q

cirrhosis complications

A
  • Hepatic encephalopathy – can see asterixis
  • Bleeding from varices
  • Ascites
  • Spontaneous bacterial peritonitis
  • Hepatocellular CA
31
Q

management of cirrhosis

A
  • Diuretics
  • Paracentesis
  • Vitamin K
  • Multivitamins
  • Lactulose (reduces ammonia level)
  • Avoid ETOH
  • Liver transplant
  • Vitamin K is essential for activity of several carboxylase enzymes within the hepatic cells, and therefore is necessary for the activation of coagulation factors VII, IX, X, and prothrombin.
32
Q

fulminant hepatitis

A
  • Rare Subtype of acute Hepatitis
  • Prevalence varies; hep A least common
  • Presents with massive necrosis and liver failure
  • Hepatic encephalopathy
  • Onset within 8 weeks of disease
  • High mortality
  • Tx = Liver transplant
  • Association with alcohol, tylenol use, methamphetamine use, hx of weight loss
33
Q

summary of serologic markers

A
  • Hep A: Surface antigen/ antibody (Acute infection confirmed by + IgM Anti HAV)
  • Hep B: surface antigen/ core antibody (Acute infection confirmed by + HBsAg or Anti-HBc; delta agent: Anti HDV, Anti-HBs= long term immunity to Hep B infection)
  • Hep C: HCV RNA by PCR
  • Hep E : HEV RNA by PCR
  • 30% in US have anti-Hep A
  • 90% in developing countries
34
Q

drug induced hepatitis

A
  • Direct hepatotoxicity: dose dependent and reproducible (Anabolic steroids, IV tetracyline, acetaminophen)
  • Idiosyncratic reaction (most common form)
  • Host hypersensitivity (Phenothiazines, antibiotics, thyroid, cytotoxic, oral hypoglycemics)
  • Fever
  • RUQ pain
  • Pruritis
  • Skin rash
  • Eosinophilia
  • Increased transaminases
35
Q

alcoholic hepatitis

A
  • Occurs after prolonged (10 yrs) heavy intake
  • Anorexia, fatigue, jaundice
  • Tender hepatosplenomegaly
  • Fever, leukocytosis
  • Elevated AST > ALT
  • Definitive DX by liver biopsy
  • 33% progress to cirrhosis
  • Risk of hepatic encephalopathy

Medicine 3 (11 decks)

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