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Adult Clinical Medicine > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

Liver accomplishes many things such as

A
  • the synthesis and metabolism of proteins, carbs, and fats
  • Production and secretion of bile and vitamin storage.
  • dextoxification of metabolic wastes (urea), drugs, and toxins (ammonia, ethanol)
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2
Q

describe the portal vein

A

-delivers blood from organs of digestion and functions similarly to an artery as it empties into a terminal capillary bed in the liver

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3
Q

while the portal vein delievers __, __, and __ to the liver, the hepatic artery functions to support hepatocytes with __ and ___.

A

nutrients, drugs, and toxins

oxygen and nutrients

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4
Q

what does the bile duct do?

A

drains bile from the liver to the gallbladder.

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5
Q

what makes up the portal triad?

A

portal vein, hepatic artery, bile duct

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6
Q

what is jaundice? and when is it typically visible

A
  • yellow staining of tissue due to deposition of bilirubin
  • Typically not visible until serum bilirubin levels exceed 3-4 mg/dL
  • first noticed in sclera (also skin, mucous membranes)
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7
Q

causes of hyperbilirubinemia

A
  1. conjugated
  2. unconjugated
  3. mixed
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8
Q

how is bilirubin produced

A
  • Bilirubin is produced from heme when RBCS are broken down primarily in the spleen= unconjugated or indirect bilirubin
  • In the liver, unconjugated bilirubin is conjugated with a glucuronide molecule to form conjugated or direct bilirubin.
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9
Q

Conjugated bilirubin is delivered to the GI tract via the __

A

biliary duct

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10
Q

what is the difference between indirect and direct hyperbilirubinemia?

A
  • defect causing Hyperbilirubinemia occur before conjugation the patient will manifested with an indirect hyperbilirubinemia.
  • if the defect occurs after conjugation, a direct hyperbilirubinemia will result
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11
Q

3 phases of bilirubin metabolism to consider when evaluating jaundice

A
  1. Pre-hepatic cause
  2. hepatic cause
  3. extra-hepatic causes (aka obstructive or cholestatic jaundice)
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12
Q

what are pre-hepatic causes of jaundice

A

ex. Excessive hemolysis (e.g. hemolytic anemias), large hematoma
- leads to a pure indirect, unconjugated hyperbilirubinemia

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13
Q

what does hepatic causes of jaundice lead to?

A
  • unconjugated or mixed hyperbilirubinemia: disorders of enzymatic conjugation pathway
    ex. Gilbert’s Syndrome

-predominantly conjugated*

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14
Q

what is Gilbert’s syndrome?

A

-hepatic cause of hyperbilirubinemia

  • hereditary, decreased activity of glucuronosyltransferase, an enzyme in the conjugation pathway
  • benign, often found incidentally

*most patients have a persistently slightly elevated indirect bilirubin but may increase due to illness, stress, and fasting

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15
Q

hepatic causes of jaundice that lead lead to conjugated hyperbilirubinemia

A
  1. Hepatocellular disease (hepatitis):
  2. Viral infection (HAV, HBV, HCV, others), chronic alcohol use, autoimmune
  3. Drugs, pregnancy, sepsis, sarcoidosis, others
  4. Primary biliary cirrhosis
  5. Primary sclerosing cholangitis
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16
Q

Extra-hepatic (or obstructive or cholestatic jaundice)

causes of jaundice?

A
  1. Mechanical obstruction: Gallstones, surgical stricture
  2. Infection: Often seen in secondary infections with HIV
  3. Malignancy: Hepatic, metastatic, cholangiocarcinoma, pancreatic
  4. Pancreatitis
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17
Q

what does extra-hepatic jaundice result in?

A

conjugated or direct hyperbilirubinemia

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18
Q

associated findings of conjugated hyperbilirubinemia

A
  1. Pale stool and dark urine

2. Bilirubin in the urine

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19
Q

associated findings of unconjugated hyperbilirubinemia

A
  1. Normal stool and urine color

2. No bilirubin in the urine

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20
Q

what are the aminotransferase (transaminase) and what do they measure

A

AST, ALT

-they are released into circulation following hepatocellular injurty so they are a measure of liver injury NOT function

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21
Q

ratio of AST: ALT less than 1=

ratio of AST: ALT greater than 2=

A

Less than 1= viral hepatitis

Greater than 2= alcoholic hepatitis

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22
Q

what is alkaline phosphatase (AP or ALP)?

A
  • present in Kupffer cells, lining the biliary tract

- also present in bone: isoenzymes can be ordered to distinguish source of AP

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23
Q

what can elevated AP or ALP suggest?

A
  1. in obstructive biliary disease* 2. may see slight elevations in hepatocellular disease
  2. Normal in childhood and pregnancy
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24
Q

what is included in a bilirubin panel?

A
  1. total
  2. direct
  3. indirect
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25
Q

Bilirubin in ___ is ALWAYS a pathologic finding

A

urine

*Urobilinogen in urine is usually normal, depending on levels

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26
Q

what is Gamma-glutamyl transpeptidase (GGT or GGTP)

A
  • The most sensitive liver enzyme for detecting biliary obstruction
  • also very sensitive for cholangitis, cholecystitis

-highest concentrations are found in liver and biliary tract

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27
Q

Elevated GGT and AP = ___

Normal GGT and elevated AP = ____

A

very likely hepatobiliary disease

skeletal disease, childhood, pregnancy

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28
Q

what is albumin?

A
  • Large protein Synthesized in the liver, thus a true measure of hepatic function
  • Long serum half life (12-18 days) so not very useful for acute processes
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29
Q

Hepatocellular disease causes ____ albumin synthesis

A

decreased

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30
Q

what is prothrombin time (PT or Pro-Time) used for?

A
  • Used to evaluate clotting function

- Since most clotting factors are synthesized in the liver, PT allows indirect assessment of liver function

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31
Q

PT prolongation can suggest ___

A

hepatocellular or obstructive biliary disease

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32
Q

what lab value can be used to monitor acute changes in liver function

A

prothrombin time (PT or Pro-Time bc it has a short half-life

-albumin has a long serum half life (12-18 days) so not very useful for acute processes

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33
Q

what are the 3 forms of hepatitis

A
  1. viral
  2. toxic
  3. autoimmune
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34
Q

describe HepA and its route of transmission

A
  • Highly-contagious, generally sporadic (non-epidemic) caused by a virus
  • Fecal-oral transmission
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35
Q

describe the incidence of HepA

A
  1. Highly endemic in developing countries
    - Contaminated shellfish common source for tourists
  2. In US, infection often linked to: Outbreaks
    - Infected food handlers at point of sale
    - Certain fresh produce (onions, strawberries)

*Incidence decreasing since targeted use of vaccine in 1995

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36
Q

describe the clinical corse of HepA

A
  1. Incubation: LONG (Average: ~25 days)
  2. Preicteric phase (5-7 days): (sx of viral illness) Abrupt onset fever, malaise, nausea, vomiting, anorexia, abdominal pain, headache. Signs include: hepatomegaly, splenomegaly, bradycardia
  3. Icteric phase (4-30 days): Conjugated bilirubinuria, followed by pale stools and jaundice (70% of adults)
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37
Q

what is the prognosis of HepA

A
  • in a healthy host: Self-limited, no chronic form of disease
  • Rarely associated with fulminant hepatitis, usually only with HCV co-infection
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38
Q

evaluation of HepA

A
  1. Evaluation should include: LFTs and hepatitis A,B, and C serology. ALT levels can be very high but do not correlate with disease severity
  2. Anti HAV IgM: Detectable 5-10 days before symptoms, remains elevated for 4-6 months
  3. Anti HAV IgG: Present for life, confers immunity
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39
Q

describe why HepA highly contagious

A

-Viremia and viral shedding proceeds clinical illness thus patients are quite capable of transmitting infection before they are aware of their illness

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40
Q

how is HepB spread?

A
  • Transmitted through blood and other bodily fluids, e.g. semen, saliva
  • 100 times more infectious than HIV (HIGHLY CONTAGIOUS)
  • Can live in dried blood for up to 1 week
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41
Q

what is the prognosis of viral HepB

A

90% of infected children progress to chronic disease

-less than 5% of infected adults progress to chronic disease

  • Incidence of new infection has declined significantly since vaccine introduced in the early 1980s
  • There are still over 1 million cases of chronic HBV infection in the US
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42
Q

risk factors for HepB

A
  1. IV drug use
  2. History of STD
  3. Health care workers
  4. Infants of HBV-positive mothers
  5. Household contacts of HBV-infected persons
    - Most commonly child-to-child
  6. Men who have sex with men
  7. More than one sex partner in a six-month period
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43
Q

First evidence of HBV infection, implies infectivity

A

HBs-Ag (surface Ag)

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44
Q

Appears after clearance of HBs-Ag or after immunization, implies immunity

A

Anti-HBs (Ab to HBs-Ag)

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45
Q

antibody to HB core antigen

A

Anti-HBc

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46
Q

Appears shortly after HBs-Ag, eventually disappears (up to 6 months), implies acute hepatitis B

A

IgM

47
Q

Persists indefinitely, implies chronic infection or recovery from previous infection, but NOT immunization

A

IgG

48
Q

correlates with high levels of (HBV) viral replication, a “marker of infectivity”

A

HBe-Ag (HepB e antigen)

49
Q

correlates with low rates of viral replication of HBV

A

Anti-HBe (antibody to HBe-Ag)

50
Q

what type of antigens do vaccines have?

A

ONLY have surface Ag

*therefore if there are Ab to the core antigen the patient has been exposed to HBV

51
Q

if one suspect HBV what initial screen tests should be done?

A
  1. HBs-Ag
  2. Anti-HBs
  3. Anti-HBc
  • If HBV positive, evaluation should include:
    1. CBC,
    2. LFTs,
    3. hepatitis A, C and D serology,
    4. HIV,
    5. STDs.
52
Q

acute HBV infection is supported by what labs?

A

(HBs-Ag (+), Anti-HBs (-), Anti-HBc IgM (+)): WBC normal or low, ALT and AST elevated, alk phos and bilirubin elevated.

53
Q

chronic HBV infection is supported by what labs?

A

(HBs-Ag (+ > 6 mos), Anti-HBs (-), Anti-HBc IgG (+)): ALT and AST elevated, alk phos and bilirubin elevated, serum albumin decreased, PT prolonged

54
Q

acute HBV infection is Subclinical in ___% of adults, ___% of children under 5

A

60-70%

over 90%

55
Q

what is the incubation period for acute HBV infection

A

1-4 months

56
Q

sx of acute HBV infection

A
  1. low-grade fever
  2. malaise
  3. myalgia
  4. N/V
  5. anorexia
  6. abdominal pain
  7. jaundice. Usually resolve in 1-3 months.
57
Q

describe the difference between chronic ACTIVE HBV and chronic PERSISTENT HBV

A

Chronic active hepatitis:

  • Symptoms range from asymptomatic to severe
  • LFTs significantly elevated

Chronic persistent hepatitis:

  • Symptoms range from asymptomatic to mild
  • LFTs mildly elevated
58
Q

__% of adults with HBV will full recovery or be healthy carries

A

95%

59
Q

Most common chronic liver disease in the US

A

Hep C

*Accounts for 8,000 to 13,000 deaths each year

60
Q

HepC is most commonly transmitted by

A

sharing of IV needles

61
Q

The majority of liver transplants performed in the US are for ___

A

chronic hepatitis C

62
Q

__% of all acute hep c infections will lead to chronic hep

-20% of those will end with ____

A

85%

cirrhosis or hepatocellular carcinoma

63
Q

risk factors for HepC

A
  1. IV-drug use
  2. Sexual transmission (most from sex with IV-drug users or multiple sex partners)
  3. Sexual transmission is very rare between monogamous heterosexual partners
  4. Health care workers at slightly higher risk than the general population but only if there is a history of needle stick
  5. born between 1945-1965 (baby boomers)
64
Q

CDC recommends testing all adults once who were born from ___ - ___ for Hep C

A

1945-1965 (Baby Boomers)

65
Q

how do you evaluate for HepC

A
  1. screen: Ab tests– dect anti-HCV Ab
    if +
  2. Confirmatory test: RNA assay
    - PCR based, able to detect small amounts of viral RNA
    - Quantitative: Estimates viral load, used to monitor treatment.
    - Genotype testing: Useful for determining choice of medication, length of treatment and likelihood of response to therapy.
66
Q

treatment of acute hepA

A
  1. suppportive
  2. Hospitalization for severe dehydration (rare), coagulopathy, encephalopathy
  3. Avoidance of hepatotoxins (EtOH, acetaminophen)
  4. Immune globulin (IgG): prevents transmission and attenuates symptoms, also used for post-exposure prophylaxis for household and intimate contacts
  5. Adults are usually non-infectious 2 weeks after symptom onset
67
Q

treatment for chronic hepB

A

*involve a hepatologist!

  1. meds: Nucleoside analogs: Entecavir (Baraclude) or tenofovir (Viread)
  2. avoid hepatotoxins
  3. hepA immunization
  4. Yearly U/S and AFP levels if high risk (Asian male over 40, Asian female over 50, African over 20, family hx of HCC)
68
Q

treatment for chronic hepC

A
  1. Involve a hepatologist!
  2. Avoidance of hepatotoxins
  3. Hep A and B immunization
  4. Meds:
    - Depends on genotype (1,2,3 or 4)
    - Involves the use of ribavirin in combination with one or more of several nucleoside analogues, such as sofosbuvir and ledipasvir.
    - New drugs are in the pipeline.
69
Q

why should alcohol be avoided in HCV?

A

alcohol:

  1. Accelerates fibrosis and progression to cirrhosis in a dose dependent manner
  2. Increases risk of HCC
  3. Decreases the efficacy of HCV therapy
70
Q

how can you prevent HepA

A
  1. Immunization: Now recommended (CDC) for all children in high risk states, also travelers, IV drug users, men who have sex with men, chronic liver disease
  2. Post-exposure immune globulin
  3. Hygiene
  4. Report cases to health department
71
Q

how can you prevent HepB

A
  1. Immunization: Now recommended for all persons (CDC)
  2. Safe sex practices
  3. “Safe” IV drug practices
72
Q

how can you prevent HepC

A
  1. No immunization available

2. Avoidance or modification of high-risk behaviors

73
Q

there are vaccines for what hepatitises

A

hep A and B

74
Q

3 causes of autoimmune liver disease

A
  1. Autoimmune hepatitis
  2. Primary biliary cirrhosis
  3. Primary sclerosing cholangitis
75
Q

autoimmune hepatitis is most commonly seen in who

A

Classically seen in young, caucasian, female patients

76
Q

characteristics of autoimmune hepatitis

A
  1. May present as acute hepatitis or more insidiously
  2. Hepatomegaly, jaundice, spider angiomata are very common physical findings
  3. Hypergammaglobulinemia usually present
  4. Associated with other autoimmune diseases (Grave’s, type 1 DM, RA, others)
77
Q

labs associated w/ autoimmune hepatitis and what is its tx

A

-Usually antinuclear antigen (ANA) positive, aminotransferases are always elevated

tx: prednisone
- fatal in 10 yrs if untreated

78
Q

what is primary biliary cirrhosis (PBC) and who is it most commonly seen in?

A
  • Autoimmune-mediated destruction of intrahepatic bile ducts and resultant cholestasis
  • females, 40-60y/o (10:1 F:M)
79
Q

presentation of PBC

A
  1. often asymptomatic
  2. may present with insidious-onset generalized pruritis
  3. fatigue
80
Q

lab findings of PBC

A
  • Elevated alkaline phosphatase,
  • antimitochondrial antibodies (95%),
  • elevated IgM
  • elevated cholesterol (HDL)

*biopsy helpful for dx, necessary for staging

81
Q

what is the tx and prognosis of PBC

A

tx:
Early stages – Ursodiol (a bile acid) – palliative while waiting liver transplant
Late stages – Liver transplantation

Prognosis: Without liver transplantation, 7-10 year survival after symptoms develop

82
Q

what is primary sclerosing cholangitis (PSC)? and who is it most seen in?

A
  • (Probably) Autoimmune-mediated inflammation and sclerosis of bile ducts and resultant cholestasis
  • Male preponderance ~3:1, usually between ages 20-40

-Very strong association with inflammatory bowel disease (70-80%)

83
Q

how does PSC present

A

Typically presents as progressive obstructive jaundice

84
Q

what labs are associated w/ PSC

A
  • Elevated alkaline phosphatase,
  • GGT,
  • elevated bilirubin,
  • negative antimitochondrial antibodies

*biopsy and cholangiogram necesssary for diagnosis

85
Q

what is the tx and prognosis of PSC

A

tx:
Various pharmacologic strategies, none affect survival or need for liver transplantation.

Prognosis: Without liver transplantation, ~10 year survival after symptoms develop

86
Q

describe what alcoholic liver disease is

A

Severe exposure to alcohol can lead to alcoholic hepatitis and eventually cirrhosis, which is fibrosis of liver tissue. In the absence of multiple bouts of alcoholic hepatitis, fatty change (AKA steatosis) can occur and lead to cirrhosis.

  • Changes from hepatitis and steatosis are potentially reversible with abstinence.
  • Changes resulting in cirrhosis are typically not reversible.
87
Q

what is cirrhosis

A

Chronic injury to the liver parenchyma leading to a progressive, generally irreversible, diffuse fibrosis

88
Q

sources of liver injury that lead to cirrhosis

A
  1. Alcohol (60-70%)
  2. Chronic Hep B or C (10%)
  3. NAFLD (10%)
  4. Hemochromatosis (5-10%)
  5. Biliary obstruction (5-10%)
  6. Many less common causes
89
Q

Typically, ____% of the liver parenchyma must be destroyed before cirrhotic liver failure manifests clinically

A

80-90%

90
Q

how does cirrhosis typically present?

A
  • often asymptomatic for years
  • Early, well-compensated disease can present with fatigue, anorexia and weight loss, weakness
  • Decompensated disease can result in numerous complications stemming from:
    1. Loss of hepatocyte function
    2. Consequences of portal hypertension
    3. Hepatocellular carcinoma
91
Q

complications of cirrhosis

A

*loss of hepatocyte function

  1. Hypoalbuminemia
  2. Jaundice
  3. Coagulapathy
  4. Protein-calorie malnutrition
  5. Renal dysfunction
  6. Osteoporosis
  7. Pruritis
  8. Susceptibility to infection
  9. Gonadal failure
  10. Altered drug metabolism
92
Q

consequences of portal hypertension (caused by cirrhosis)

A
  1. Splenomegaly
  2. GI bleeding, varices
  3. Ascites
    - Spontaneous bacterial peritonitis
  4. Hernias
  5. Hepatic encephalopathy
  6. Hepatorenal syndrome
  7. Hepatopulmonary syndrome
93
Q
  • scleral icterus
  • jaundice
  • spider angioma
  • caput medusae
  • umbilical hernia
  • white nails/clubbing
  • edema
  • muscle wasting
  • gynecomastia
  • splenomegaly
  • ascites
  • testicular atrophy
  • palmar erythema
  • purpura/petechia
A

cirrhosis

94
Q

how do you diagnosis cirrhosis

A
  1. labs- can be misleading,
    - a liver panel (AST, ALT, bilirubin panel, alkaline phosphatase, serum albumin, GGT),
    - CBC
    - prothrombin time
    - a platelet count
  2. Doppler US- 1st line imaging modality
  3. biopsy is GOLD standard for dx
95
Q

tx of cirrhosis

A
  1. Get a hepatologist involved!
  2. Complete abstinence from EtOH
  3. Immunize for Hep A and B
  4. Treat complications
    - e.g. Evaluate for varices and treat, if indicated
  5. Consider wait list for transplant
  6. Annual screening for HCC with US/CT/MRI
96
Q

what is nonalcoholic fatty liver disease (NAFLD)

A

a spectrum of disease including steatosis (fatty liver), nonalcoholic steatohepatitis (NASH) and cirrhosis

97
Q

what is the most common cause of elevated transaminases in US adults

A

nonalcoholic fatty liver disease (NAFLD)

*may affect 30% of population

98
Q

nonalcoholic fatty liver disease (NAFLD) is strongly associated with:

A
  1. obesity
  2. DM2
  3. hypertriglyceridemia
99
Q

how can you dx nonalcoholic fatty liver disease (NAFLD)?

A

To make the diagnosis of NAFLD other causes (EtOH, viral, etc.) must be ruled out

100
Q

For evaluation of suspected NAFLD, AGA recommends:

A
  1. Thorough history of alcohol use
  2. Labs: ALT, AST, Alk Phos, bilirubin, viral hepatitis screen, PT, albumin
  3. US or CT – often confirmatory
  4. Biopsy is definitive but controversial, should be made on a case-by-case basis
101
Q

management of NAFLD

A
  1. Focused on treating underlying conditions: obesity, dyslipidemia, DM
  2. Steatosis: expectant management
  3. NASH: No consensus on medical treatment. Metformin (Glucophage) TZDs, and statins lower AST and ALT and decrease degree of steatosis BUT NO demonstrable effect on morbidity/mortality
  4. Rapid weight loss (e.g. following bariatric surgery) may actually worsen NASH.
    * ***Target is 1-2 lb/week
102
Q

what is hereditary hemochromatosis and who is it most commonly seen in?

A
  • Increased intestinal absorption of iron and deposition in the liver, pancreas, other organs
  • Slow build-up of iron - usually does not present until 3rd or 4th decade

-common: (1:250 caucasians, 1:10 carriers)

103
Q

how does herediatry hemochromatosis typically present?

A
  1. Symptoms are generally non-specific (weakness, fatigue, lethargy) until cirrhosis manifests
  2. If unrecognized or untreated will lead to cirrhosis and/or other complications (e.g. diabetes mellitus)

*often dx based on known fhx or discovery following routine screening labs

104
Q

dx of herediatry hemochromatosis

A

Serum iron, ferritin, transferrin are elevated, total iron-binding capacity (TIBC) is low or normal

105
Q

tx and prognosis of herediatry hemochromatosis

A

Serial phlebotomy weekly until serum ferritin normalizes, then every 3 months for life

*if diagnosed before the irreversible end organ damage has occured- the prognosis is excellent

106
Q

what are examples of benign liver neoplasms

A
  • Hemangioma(2-7%of the population), adenoma, cysts

* Benign lesions are very common and often picked up incidentally during imaging

107
Q

___ are the most common malignant neoplasms of the liver

A

Metastatic tumors

*most common: GI tract, lung, breast

108
Q

Most common primary liver malignancy (1-2 per 100,000)

A

hepatocellular carcinoma (HCC)

109
Q
  • Usually arises in cirrhotic livers, secondary to EtOH, HBV, HCV, hemochromatosis, others
  • Generally associated with poor prognosis
A

hepatocellular carcinoma (HCC)

110
Q

how do you evaluate a patient w/ mildly elevated aminotransferases in an asymptomatic person

A

Approach to mildly elevated ALT/AST–> thorough H and P and discontinuation of EtOH and hepatotoxins–> recheck ALT/AST–> if still elevated get labs: bilirubin, GGT, PT, albumin, CBC, hep A, B, C serologies, serum ion, TIBC, ferritin

111
Q

if AST and ALTare elevated in an asymptomatic person what should you consider?

A
  1. AST and ALT are markers of hepatocellular injury
  2. ALT is considered more specific for hepatic injury since AST is found in other tissues
  3. Ratio of AST/ALT can be useful: if over 2, usually related to alcoholic hepatitis
112
Q

examples of hepatotoxins

A
  1. EtOH
  2. acetaminophen
  3. NSAIDS
  4. statins
  5. Antiepileptics
  6. Anti-TB
  7. Herbals
113
Q

what autoimmune hepatitis is strong associated with IBD?

A

PSC

Adult Clinical Medicine (26 decks)

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