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Gen Med: GI > Hepatic Disease > Flashcards

Hepatic Disease Flashcards

1
Q

What are the general characteristics of hepatitis?

A
  1. Inflammation of the liver
    A. Acute or chronic
  2. Both types cause hepatocellular damage
    A. Acute – initial signs & sx’s of infection
    B. Chronic – chronic inflammation > 6 mo duration
    -Persistently elevated AST & ALT
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2
Q

What are the possible etiologies of hepatitis?

A
  1. Acute viral (Hep A, B, C, D, E, HSV, EBV, CMV)
  2. Acetaminophen toxicity
  3. Drug-induced liver disease
  4. Alpha-1 antitrypsin deficiency (A1AD)
  5. Autoimmune hepatitis
  6. HELLP syndrome
  7. Acute fatty liver of pregnancy
  8. Cholestasis
  9. Infections
    A. Bacterial, parasitic, fungal, mycobacterial & protozoal
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3
Q

What are the most common viral etiologies of acute hepatitis?

A

Hep A, B, C, D, E

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4
Q

What are the most common viral etiologies of chronic hepatitis?

A

Hep B, C, D

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5
Q

What are the most common toxic etiologies of acute hepatitis?

A
  1. Alcohol
  2. Meds
  3. Solvents
  4. Plants/herbal remedies
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6
Q

What systemic disease can have hepatic effects?

A

Autoimmune disease

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7
Q

What inherited diseases can cause hepatitis?

A

Alpha-1antitrypsin def. (A1AD)

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8
Q

What is the pathophys of viral hepatitis?

A
  1. Virus enters liver cells → immune system attacks liver → inflammation & impaired function
  2. Can be self-limiting or progress tofibrosis(scarring) & cirrhosis
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9
Q

What are the general characteristics of acute viral hepatitis?

A
  1. Lasts < 6 mo
  2. Usually asymptomaticin children
  3. Incubation period ≈ 7-10 days (or >), w/ total illness lasting weeks
  4. Small proportion progress toacute liver failure
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10
Q

What are the general characteristics of chronic viral hepatitis?

A

Lasts > 6 mo

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11
Q

What is the most common type of hepatitis worldwide? US?

A
  1. World: Hep B

2. US: hep C

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12
Q

How is hep B transmitted?

A
  1. Most often transmitted vertically in areas of high incidence (perinataly from mother to baby during birth)
  2. Transmitted via exposure to infected blood, blood products, or mucus membranes
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13
Q

True/false: there is a vaccine for Hep B

A

Vaccine routinely given in developed world

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14
Q

What are the initial sxs of acute viral hepatitis?

A
  1. Flu-like
  2. Malaise
  3. Muscle&joint aches
  4. Fever
    5 N/V
  5. Diarrhea
  6. Headache
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15
Q

What are the acute sxs of acute viral hepatitis?

A
  1. Profoundloss of appetite
  2. Smokers w/ aversion to smoking
  3. Choluria(dark urine)
  4. Jaundice
  5. Abdominal discomfort
  6. Clay colored stools
  7. Jaundice
  8. Tenderenlarged liver
  9. Lymphadenopathyin 5%
  10. Splenomegaly
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16
Q

What labs and dx studies are performed for hepatitis?

A
  1. Bilirubin
  2. Hepatitis Panel
  3. Acute vs Chronic abnormalities of LFT
  4. +/- USN
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17
Q

What are the screening tools for acute viral hepatitis?

A
  1. IgM anti-HAV
  2. HBsAg
  3. Anti- HBs, IgM anti-HBc
  4. HBeAg
  5. Anti-HCV, HCV RNA
  6. Biliary obstruction or Budd-Chiari syndrome using Transabdominal USN w/ Doppler
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18
Q

What is the rx for acute viral hepatitis?

A
  1. Treatment for acute viral hepatitis is supportive
  2. Pts w/ HAV must be cautious regarding transmission:
    A. No sharing food or dishes
    B. Frequent hand-washing
  3. All pts w/ hepatitis should avoid alcohol & other hepatotoxins
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19
Q

Define hep A

A
  1. Hepatitis A virus (HAV) infection usually results in an acute, self-limited illness & rarely leads to fulminant hepatic failure
  2. Incubation period avg 30 days
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20
Q

How is hep A spread?

A
  1. Spread via fecal-oral route
  2. ↑ in low socioeconomic areas
  3. ↑ Risk w/ international travel to Mexico, C. & S. Americas
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21
Q

True/false: there is a vaccine for Hep A

A

In US, Hep A vaccine has decreased Dz by 92% since 1999 (high risk) & 2006 in all infants

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22
Q

True/false: Hep A is a reportable dz

A

True

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23
Q

How is Hep A tested for?

A
  1. IgM anti HAV

2. IgG anti-HAV

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24
Q

What is IgM anti-HAV?

A
  1. Occurs as primary immune response
  2. Peaks during 1st week of clinical Dz
  3. Remains ↑ 4-6 months
  4. ↑ IgM anti-HAV w/ (-) IgG anti-HAV, acute infection is suspected
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25
Q

What is IgG anti-HAV?

A
  1. ↑ after 1 month of Dz onset
  2. May persist for years
  3. ↑ IgG anti-HAV w/ (-) IgM anti-HAV, convalescent stage of HAV is suspected
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26
Q

How can hep A be prevented?

A
  1. Safe water supply
  2. Proper environmental hygiene
  3. Hand-washing
  4. Gloves when preparing food or cannot prepare food until hep A is gone
  5. IgG given for pre-exposure & post-exposure prophylaxis
  6. Vaccine
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27
Q

What are the HAV vaccine recommendations?

A
  1. Immunization schedule for infants > 1 yr
    A. Repeat dose 6-12 mo after 1st dose
  2. Adults 2 wk prior to travel to endemic areas & booster 6-12 mo later
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28
Q

What are the post exposure prophylaxis recommendations for Hep A?

A
  1. Single dose HAV vaccine or IgG ASAP
    A. HAV vaccine: 1 yr - 40 yr
    B. IgG: < 1 yr and > 40 yr
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29
Q

What are the characteristics of hep B?

A
  1. Incubation period 1-10 weeks
  2. Acute illness
  3. Can cause chronic & severe hepatitis leading to liver failure & death
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30
Q

Who is at risk for hep B?

A
  1. Blood transfusion recipients
  2. IV drug abusers
  3. Transplant patients
  4. Dialysis patients
  5. Homosexual male
  6. (+)Leukemia or lymphoma
  7. Hospital personnel
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31
Q

Who needs Hep B screening?

A
  1. Individuals w/ signs & sx’s of acute hepatitis
  2. Individuals w/ chronic liver Dz (chronically ↑ ALT or AST)
  3. Individuals born in countries w/ HBV prevalence ≥ 2 %
  4. Pregnant women
  5. Person born in US but parents born in regions w/ HBV prevalence ≥ 8 %
  6. (+) HIV or HCV
  7. IV drug users
  8. (+) multiple sexual partners&/or (+) STD
  9. Hemodialysis
  10. (+) contacts of HBV infected persons
  11. Prison inmates
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32
Q

How is Hep B screened?

A
  1. Hep B surface antigen (HBsAg)
  2. Hepatitis B core antibody (anti-HBc)
  3. Hepatitis B surface antibody (anti-HBs)
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33
Q

What is Hep B surface antigen (HBsAg)?

A
  1. Hallmark of acute HBV infection
  2. Serum (+) 1-10 wk post exposure
  3. Reacts before sx’s or 4. ALT rises
  4. Undetectable after 4-6 mo
  5. (+) > 6 mo → chronic infection
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34
Q

What is Hepatitis B surface antibody (anti-HBs)?

A
  1. (+) after HBsAG becomes (-)
  2. Usually (+)
    A. Long-term immunity
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35
Q

What is IgM anti-HBc?

A
  1. HBV infection marker during window between disappearance of HBsAg appearance of anti-HBs
  2. Indicates acute HBV infection
  3. Can remain (+) up to 2 yr after acute infection
  4. IgM anti-HBc titer may ↑ to detectable levels during exacerbations of chronic Hep B
    A. False (+) for acute HBV
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36
Q

What test is performed if HBsAg and anti-HBs are both negative?

A
  1. Occ. HBsAg & anti-HBs not detectable
    A. Dx by detection of IgM Ab against Hep B core Ag
    B. ↑ IgM anti-HBc = acute Hep B: fall back test
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37
Q

What is the dx when IgG anti HBc and abti-HBs are present?

A

IgG anti-HBc remains ↑ w/ anti-HBs after recovery from acute Hep B

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38
Q

What are the markers for chronic Hep B?

A

IgG anti-HBc remains ↑ w/ HBsAg in chronic Hep B

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39
Q

What is the usefulness of Hep B core antigen?

A
  1. Hepatitis B core antigen (HBcAg) Intracellular Ag in infected hepatocytes during infection
  2. NOT detectable in serum
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40
Q

What marker is present in the contagious state of Hep B?

A
  1. Hepatitis B-e antigen (HBeAg)
    A. Circulates in infected blood when virus is actively replicating
    B. Contageous state
    C. Used as index of infectivity
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41
Q

What marker indicates the acute phase of HBV is over?

A

Hepatitis B-e antibody (Anti-HBe)

42
Q

When is PCR used in the context of hep B infection?

A
  1. Direct determination of HEP B virus DNA (HBV DNA)
  2. Low detection ability
  3. Used to determine if candidate for antiviral therapy in chronic Hep B
43
Q

What happens to AST and ALT in hep B? Hep A?

A

↑ in Hep B > Hep A

44
Q

How is acute HAV and HBV treated?

A
  1. If symptoms are marked:
    A. Bed rest
    B. If N/V persists, IV 10% glucose
    C. Avoid ETOH & other hepatotoxic drugs
45
Q

What is the prognosis of HAV and HBV?

A

Prognosis: Clinical recovery is generally complete w/in 3 mo (HAV) & up to 6 mo (HBV)

46
Q

How can hep B be prevented?

A
  1. Thorough hand-washing after contact w/ contaminated bedding, utensils, clothing
  2. Needle safety
  3. Condoms
  4. Post-exposure prophylaxis
    A. Hep B Immune globulin (HBIG) + begin HBV series
  5. Prevention
    A. HBV series
47
Q

What is the prognosis for HBV? How do we know when chronic HBV is occuring?

A
  1. In most pts, clinical recovery is complete at 3-6 months
  2. Abn LFT’s may persist longer
    A. Elevated ALT levels > 6 months
  3. Chronic hepatitis develops in 1-2 % pts
  4. Risk of cirrhosis, liver failure & hepatocellular CA w/ chronic Hep B
    A. Correlates w/ serum HBV DNA levels
48
Q

What are the sxs of chronic hep B?

A 
1. Nonspecific symptoms
A. Malaise 
B. Weakness 
C. Often asymptomatic
D. Jaundice = advanced liver damage 
E. +/- hepatomegaly
49
Q

What are the drug classes used to treat Hep B?

A
  1. Nucleoside or nucleotide analog
  2. continued for 6-12 months after sero-conversion
  3. Interferon
50
Q

What are the goals of Hep B treatment?

A

Seroconversion to anti-HBe

51
Q

What are the preferred firs tline oral agents for hep B?

A
  1. Entecavir

2. Tenofivir

52
Q

What is the class and moa of entecavir?

A
  1. Nucleoside analog
  2. Infrequent resistance
  3. Suppresses HBV DNA & histologic improvement
53
Q

What is the class and moa of Tenofovir?

A
  1. Nucleotide analog
  2. Used if resistance to nucleoside analog develops
  3. Infrequent resistance
54
Q

What are the alternative meds for hep B?

A

1 Nucleoside analogs
A. Lamivudine (oldest)
2. Nucleotide analog
A. Adefovir dipivoxil (least potent

55
Q

What isLamivudine?

A
  1. Suppresses HBV DNA
  2. 15-30% resistance rate after 1 year
  3. 70% resistance rate by 5 yrs
56
Q

What is Adefovir dipivoxil?

A
  1. Used w/ lamivudine
  2. Resistance rate 29% after 5 yrs
    3 Nephrotoxicity potential S/E
57
Q

What drug can be used SQ for chronic hep B?

A 
1. Peginterferon (PEG IFN α)
A. SQ weekly x 48 wks
B. Normalization of AST levels
C. Histologic improvement
D. Disappearance HBeAg & HBV DNA from serum
58
Q

What are the general characteristics of acute Hep C?

A
  1. Self-limited
  2. Rarely causes hepatic failure
  3. Usually leads to chronic infection
59
Q

What are the general characteristics of chronic Hep C?

A
  1. Progressive course over many years
  2. Can result in
    A. cirrhosis
    B. hepatocellular carcinoma
    C. need for liver transplantation
60
Q

How is hep C tested?

A
  1. EIA (Enzyme immunoassay) detects HCV Ab

2. Antibodies develop w/in 4 weeks of onset of infection

61
Q

How is hep C treated?

A

Peginterferon (PEG IFN-α) + Ribavirin

62
Q

What is the function of peginterferon?

A
  1. Normalizes ALT levels
  2. Histologic improvement
  3. Disappearance HCV DNA from serum
63
Q

What is the function of Ribaviron?

A
  1. Nucleoside analog

2. Inhibits viral RNA & protein synthesis

64
Q

What is the prognosis of acute hep C?

A
  1. 80% of persons w/ acute HCV, chronic infection develops

2. In approx 20% of pts w/ chronic HCV, cirrhosis develops over 20 yrs of infection

65
Q

How is the level of liver injury in hep C determiend?

A

Liver Bx done to determine level of liver injury

66
Q

What can hep C lead to?

A
  1. Cirrhosis w/ chronic HCV ↑ the risk of Liver CA dramatically
  2. ↑ risk of nonHodgkin’s lymphoma
67
Q

What is Hep D seen with?

A

HDV only in assoc. w/ HBV, presence of HBsAg

68
Q

Who is at risk for hep D?

A
  1. Especially prevalent in drug users & dialysis patients since same mode of transmission as HBV
  2. In U.S., new cases of HDV are infrequent 2°to ↓ HBV incidence
69
Q

What can hep D lead to?

A

> 60% develop cirrhosis

70
Q

How is HDV tested?

A
  1. HDAg
  2. IgM Anti-HDV
  3. HDV – Ab total
71
Q

When does HDAg rise and what does it mean?

A

Rises in 1-3 days

Indicates active HDV infection

72
Q

When does IgM anti-HDV rise and what does it mean?

A

Rises ≈ 10 days

Indicates active HDV infection

73
Q

When does HDV-ab total rise and what does it mean?

A

Rises in 2-3 months

Indicates chronic infection

74
Q

What are the characteristics of hep E?

A
  1. Uncommon in U.S. unless pt traveled to endemic areas
    A. Waterborne HEV outbreaks
  2. Self limiting
  3. No chronic carrier state
75
Q

What is toxic hepatitis?

A
  1. Chemical-driven liver damage: Hepatocellular necrosis assoc. w/ infiltration of inflammatory cells
  2. Toxic hepatitis caused by numerous agents
    A. > 900 drugs have been implicated in causing liver injury
  3. Most common reason for a drug to be withdrawn from market
  4. Drug-induced liver injury responsible for
    5% of all hospital admissions
    50% of allacute liver failures
76
Q

How is liver injury defined?

A
  1. Rise in any of the following
    A. ALTlevel > 3x of upper limit of normal (ULN)
    B. ALPlevel > 2x twice ULN
    C. Total bilirubin level > 2x ULN when assoc. w/ ↑ ALT or ALP
77
Q

What are the 3 types of drug-induced hepatitis?

A 
1. Viral 
A. INH, Phenytoin
2. Focal 
A. ASA
3. Chronic
A. Methyldopa, diclofenac
78
Q

What is cholestatic hepatitis? what are the sxs?

A
  1. Liver injury leads to impairment of bile flow

2. Sx’s - itching & jaundice

79
Q

What can cause cholestatic hepatitis?

A

OCP’s, anabolic steroids, androgens, allopurinol, carbamazepine, chlorpromazine,
flucloxacillin

80
Q

What is steatosis hepatitis? What can cause it?

A
  1. Hepatotoxicity may manifest as triglyceride accumulation

A. ASA (Reye’s Syndrome), ketoprofen,TCN, APAP, MTX, amiodarone

81
Q

What is granulomatous hepatitis? What can cause it?

A
  1. Usually assoc. w/ granulomas in other tissues w/ features of systemic vasculitis & hypersensitivity

A. > 50 drugs have been implicated
INH, phenytoin, allopurinol, PCN, quinine, quinidine

82
Q

What is vascular hepatitis? What can cause it?

A
  1. Injury to the vascular endothelium

A. ChemoTx agents, anabolic steroids, Bush tea, OCP’s

83
Q

What is neoplastic hepatitis? What can cause it?

A
  1. Hepatocellular carcinoma, angiosarcoma, & liver adenomas

A. Vinyl chloride, arsenic, combined OCP’s, anabolic steroids

84
Q

What is herbal toxicity hepatitis? What can cause it?

A
  1. Camphor,Copaltra,Cycasin,Garcinia,
    Kavaleaves,pyrrolizidine alkaloids,horse chestnut leaves, Valerean, Comfrey
  2. Chinese herbal remedies:Jin Bu Huan,Ma- huang,Shou Wu Pian,Bai Xian Pi
85
Q

What are the criteria for alcoholic hepatitis?

A
  1. Often 40-50 yr, most present before 60
  2. Hx of daily heavy ETOH use
    A. > 100g/day for > 20 yrs
  3. Obtaining accurate Hx can be difficult
86
Q

What are the manifestations of alcoholic hepatitis?

A
  1. Jaundice
  2. Anorexia
  3. Fever
  4. Tender hepatomegaly
  5. RUQ/epigastric pain
87
Q

What are lab results in alcoholic hepatitis?

A

↑ AST/ALT
↑ GGT
↑ Bilirubin
↑ INR (impaired production of coag factors)

88
Q

What is the treatment for toxic hepatitis?

A
  1. Stop offending agent
  2. Supportive care
  3. Acetylcysteine (Mucomyst)
    A. Used for acetaminophen toxicity
  4. Fulminant hepatic failure may require liver transplantation
89
Q

What is the prognosis for toxic hepatitis?

A
  1. If pt survives acute episode, prognosis good
  2. Toxic hepatitis may be reversible
    A. Depends on amount of toxin
    B. In most cases, liver function returns to normal if offending drug is stopped early
  3. Serum bilirubin level > 2x ULN & ↑ ALT → ominous sign
90
Q

What are the general characteristics of liver neoplasms?

A
  1. Liver neoplasms may be malignant or benign

2. Malignant neoplasms may be primary or metastatic

91
Q

What are the malignant neoplasms?

A
  1. Primary hepatocellular carcinoma (HCC)
    A. aka malignant hepatoma
    B. 80% cases asst w/ cirrhosis
92
Q

What cancers metastasize to the liver?

A

Lung, breast, colon

93
Q

What are the risk factors for HCC?

A 
1. Cirrhosis
A. Primary risk factor
2. Other include:
A. Male gender
B. Age > 55 yr
C. Asian or Hispanic ethnicity
D. (+) FH
E. Overweight / obesity
F. DM
G. HCV or HBV infection
94
Q

What are the presenting sxs of HCC?

A
  1. Malaise
  2. Weight loss
  3. Abd swelling
  4. Weakness
  5. Jaundice
  6. Abd pain
  7. Hepatomegaly
  8. Splenomegaly
  9. Ascites
  10. Jaundice
  11. Muscle wasting
95
Q

What labs are used to dx HCC?

A

LFT’s, Coag studies, CBC, AFP

96
Q

What imaging is used to dx HCC?

A
  1. USN
  2. CT or MRI
  3. Location & vascularity of tumor
97
Q

When can bx of liver be avoided?

A
  1. Bx can be avoided if below studies are diagnostic:
    A. Alpha fetoprotein > 200 ng/mL
    B. Hypervascular mass > 2 cm in cirrhotic liver
98
Q

How is HCC staged?

A
  1. Size
  2. Spread
  3. Involvement of liver vessels
  4. Presence of a tumor capsule
  5. Presence of extrahepatic metastases
  6. Presence of daughter nodules
  7. Vascularity of the tumor
  8. MRI is the best imaging method to detect the presence of a tumor capsule
99
Q

How is HCC treated?

A
  1. Surgical resection of solitary hepatocellular carcinoma may result in cure
    A. If liver function preserved
  2. Adjuvant chemotherapy
  3. Liver transplant
    A. Small unresectable tumor w/ advanced cirrhosis
  4. Benign lesions should be treated if tumor size indicates danger of hepatic capsule rupture
  5. Treatment of metastatic disease involves treating primary lesion
  6. Surgical resection
    A. If HCC is confined to one lobe
  7. Liver transplant can be considered
  8. High intensity focused ultrasound(HIFU)
  9. Cryosurgery-destruction of abnormal tissue using sub-zero temperatures
  10. Selective internal radiation Tx(SIRT)
    A. Interventional radiologist injects artery supplying tumor w/ a chemo agent
  11. Palliative
100
Q

What is the prognosis for HCC?

A
  1. 5 yr survival rates rise to 56% for pts w/ localized resectable disease
  2. The usual outcome is poor
    10–20% of hepatocellular carcinomas can be completely resected
  3. If the CA cannot be completely removed, the Dz is usually deadly w/in 3 - 6 months
  4. Prognosis for metastatic or unresectable hepatocellular carcinoma has recently improved due to the approval ofsorafenib(Nexavar) for advanced hepatocellular carcinoma

Gen Med: GI (16 decks)

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