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GI: Clin Med IIA > Disorders of the liver part 2 > Flashcards

Disorders of the liver part 2 Flashcards

1
Q

how is viral hepatitis spread?

A
  • Hepatitis A - Fecal-oral route; Crowding and poor sanitation favor spreading
  • Hepatitis B - Bloodborne, sexually transmitted
  • Hepatitis C - Bloodborne, sexually transmitted
  • Hepatitis D - Only associated with Hepatitis B co-infection
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2
Q

incbuation period for hep A

A

30 d

fecally excreted 2 wks before clinical illness and up to a week after clinical illness

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3
Q

clinical findings of hep A

A
  1. More severe in adults than children
  2. Onset can be abrupt or insidious
    - Malaise, Arthralgia, Fatigability, URI sx, Anorexia
  3. Distaste for smoking
  4. N/V frequent
  5. +/- diarrhea/constipation
  6. Low grade fever
  7. Mild, constant abdominal pain in RUQ aggravated by exertion/jarring
  8. Jaundice after 5-10 d
    - With onset of jaundice, symptoms often worsen or peak
    - Followed by progressive clinical improvement
  9. Acholic Stools
  10. Hepatomegaly

subsides >2-3 wks with complete clinical and laboratory recovery by 9 wks - May relapse during this time, but not common

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4
Q

The diagnosis of acute HAV infection should be suspected in patients with:

A
  • Abrupt onset of prodromal symptoms (nausea, anorexia, fever, malaise, or abdominal pain) and
  • Jaundice or
  • Elevated serum aminotransferase levels, particularly in the setting of known risk factors for hepatitis A transmission
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5
Q

The dx of acute hep A is established by ?

A

detection of serum IgM anti-HAV antibodies

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6
Q

T/F: IgM and IgG levels detectable soon after onset

A

T

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7
Q

which antibody level peaks during first wk of sx for acute hep A

A

IgM - Best indicator of active infection

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8
Q

which antibody is the best indicator of previous exposure, non-infectivity, and immunity in acute hep A

A

IgG
continues to rise and peaks several months after onset, persists for years.

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9
Q

Other labs for acute hep A

A
  • ALT > AST
  • Elevations in bilirubin
  • WBC - normal to mildly elevated
  • Atypical large lymphocytes on blood smear
  • Imaging is not usually indicated
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10
Q

tx for acute hep A

A
  • Sx - rest, fluids
  • Avoidance of physical exertion, alcohol, and hepatotoxic drugs
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11
Q

prevention of acute hep A

A
  • Hand washing after BM to prevent spread in patients with active disease
  • If exposed - single dose vax or immune globulin
  • Vaccination
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12
Q

hep A vax recommendations

A
  1. 2 wks before travel to countries with high or imtermediate endemicity of infection (africa, SE asia, mediterranean basin, eastern europe, middle east, mexico, central and south america, parts of carribean
  2. household members and other close contacts of adopted children arriving from regions of moderate and high hep A endemicity
  3. all children (12-23 mo) as part of routine vax
  4. men who have sex with men with others with high-risk sexual behaviors
  5. users of injection and noninjecting drug of abuse
  6. persons with occuptional risk for infection (foodhandlers, child-care, lab, people wokring with primates)
  7. susceptible persons who receive clotting factor concentrates, esp solvent deterent treated preparations
  8. military
  9. populations iwht cyclic outbreaks of hep A
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13
Q

which hepatitis is a RNA virus

A

hep A

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14
Q

which hep is a partially double stranded DNA

A

hep B

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15
Q

what are the antigens that make up hep B

A
  1. Inner core protein
    - Hepatitis B core antigen (HBcAg)
    - Secretes Hepatitis B e antigen (HBeAg)
  2. Outer surface coat
    - Hepatitis B surface antigen (HBsAg)
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16
Q

Etiology/Risk Factors of hep B

A
  1. Transmitted bloodborne through inoculated infect blood/blood products
  2. Sexual contact/risky sexual behavior
  3. Present in semen, and vaginal secretions
  4. Mother can transmit to baby - Risk of chronic infection in the infant up to 90%
  5. men who have sex with men
  6. Patients and staff at hemodialysis centers
  7. Personnel working in clinical and pathology laboratories and blood banks
  8. Half of pt with acute hepatitis B in the US have previously been incarcerated or treated for a STD
  9. At risk populations:
    - IV drug users
    - Prison inmates
    - Healthcare workers

Since 1990, incidence decreased from 8.5 to 1.5 cases per 100k; almost universally because of vaccination

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17
Q

presentation of hep B

A
  1. Incubation period: 6 wks-6 mo - Avg - 12-14 weeks
  2. Can be insidious or abrupt onset
  3. Sx similar to HAV
    - Malaise, myalgia, easy fatigability, anorexia
    - Low grade fever
    - Recurrent infections (URI’s), enlarged lymph nodes
    - Distaste for smoking
    - Mild RUQ pain and hepatomegaly
    - Jaundice
  4. May present with severe fulminant disease with liver failure in a few days and death
  5. Acute illness usually subsides in 2-3 weeks
    1% will have fulminant disease
  6. Can become chronic
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18
Q

serologic markers of hep B

A
  • HBsAg - Hepatitis B surface antigen
  • Anti-HBs - Hepatitis B surface antibody
  • Anti-HBc - Antibody to hepatitis B core antigen
  • HBeAg - Hepatitis B envelope antigen
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19
Q

which HBV is first to elevate - first sign of infection

A

Hepatitis B surface antigen (HBsAG)

Persists throughout clinical illness
Persistence beyond 6 months indicates chronic disease

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20
Q

Appearance of anti-HBs and decline in HBsAG indicates what?

A

recovery of acute infection and non-infectivity.

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21
Q

Persistence of anti-HBs without elevated HBsAG indicates ?

A

immunity with previous vaccination.

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22
Q

which HBV marker
appears 1 mo after HBsAg is detected
indicates a dx of declining acute Hepatitis B
Can persist for 3-6< mo
Can appear with acute flares of chronic

A

IgM anti-HBc

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23
Q

which HBV serologic markers
appears during acute hepatitis B, but persists indefinitely

A

IgG anti-HBc
With recovery → IgG occurs with Anti-HBs
With chronic ds → IgG occurs with HBsAG

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24
Q

which HBV serologic marker

  • Appears shortly after HBsAG in the serum in the incubation period
  • Indicates viral replication and infectivity (when patient is most infectious)
  • Disappearance is often followed by appearance of anti-HBe - Signifying diminished viral replication and decreased infectivity
A

Hepatitis B core secretory antigen (HBeAG)

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25
Q

which HBV serologic marker

  • Follows the disappearance of HBeAg
  • Acute phase over, chance of infectivity low
A

Hepatitis B e-antibody (HBeAb)

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26
Q

which HBV serologic marker

  • Parallels the presence of HBeAg
  • More sensitive and precise marker of viral replication and infectivity
  • Very low levels may persist in serum and liver long after patient has recovered from acute hepatitis B, but is bound to IgG and is rarely infective
A

HBV DNA

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27
Q

other labs for hep B besides serologic markers

A
  • Marked elevation of ALT/AST (ALT > AST), greater than HAV
  • Elevated bilirubin
  • Prolongation of PT associated with fulminant hepatitis
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28
Q

tx for acute hep B

A
  • Rest, increase fluids, adequate nutrition
  • Avoid strenuous activity, alcohol and hepatotoxic agents
  • Antiviral therapy not indicated in acute hep B
  • Clinical recovery typical in 3-6 mo
  • Fulminant attacks with associated liver manifestations requires hospitalization
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29
Q

tx/prophylaxis for acute hep B

A

Hepatitis B immune globulin (HBIG)
* Contains large amount of Hepatitis B antibodies
* Can shorten duration and reduce severity
* Give w/n 7 d of exposure
* Followed by the initiation of the vaccine series
* Indicated in newborns with HBV + mothers: HBIG and initiation of vaccine series within 12 hours of birth to infant

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30
Q

prevention of acute hep B

A
  1. Universal Precautions
  2. Safe sex education
  3. Needle sharing education
  4. All pregnant women should undergo testing
  5. Vaccination
    - Now required for children
    - Healthcare workers
    - 3 dose series: Initial, 1 month later, 6 months after initial

Overall, rates of HBV infection have drastically decreased in the US!

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31
Q

Elevated ALT/AST for > than 6 months and presence of HBsAg is what condition?

A

chronic hep B

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32
Q

40% of Chronic Hepatitis B will develop what condition?

A

cirrhosis
Higher if co-infection with HCV or HDV

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33
Q

chronic hep B is at increased risk of what 3 conditions?

A

hepatocellular carcinoma, cirrhosis, and liver failure

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34
Q

tx for chronic hep B

A

Tx pts with active viral replication, acute on chronic (HBeAG and the presence of HBV DNA) or with s/sx liver failure or cirrhosis
1. Nucleoside and nucleotide analog (1st line) - Entecavir, Tenofovir
- incorporates into viral DNA and inhibits reverse transcriptase = mutations of virus rendering ineffective
- Lowest cost
2. Interferon (2nd line)
- Inhibits viral replication
- Many SE - BBW for infections

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35
Q

which hep virus is a single stranded RNA virus

A

hep C

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36
Q

at risk populations for hep C

A
  • IV drug users (reinfection common)
  • Prison inmates (26% of inmates in US)
  • Healthcare workers
  • Body piercing, tattoos, hemodialysis
  • Sexual contact/risky sexual behavior (MSM while high on methamphetamine, multiple sexual partners)
  • Bloodborne

Risk of maternal-neonatal and sexual transmission low

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37
Q

MC bloodborne infection in the US

A

acute hep C

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38
Q

acute hep C leads to increased risk of ?

A

acute liver failure
more rapid progression of chronic hepatitis C to cirrhosis

39
Q

presentation of acute hep C

A
  1. Average 6-7 week incubation period
  2. Clinical presentation varies
    - Can be and is often mild
    - fatigue, myalgias, jaundice wax and wane
  3. High incidence develop chronic hepatitis (up to 85%)
  4. At least 7 major genotypes
    - Can determine the severity of the disease
    - Can see spontaneous resolution with specific genotype (CC)
40
Q

labs for acute hep C

A

Dx:Enzyme Immunoassay

  1. ALT/AST levels also rise and decline
  2. HCV antibodies = presence of Anti-HCV
    - Presence of Anti-HCV signifies HCV as cause of hepatitis (whether acute or chronic) - Associated elevation of ALP and ALT/AST and HCV RNA help determine if acute
  3. HCV RNA
    - Presence indicates current infection
    - Presence of Anti-HCV without HCV RNA indicates prior exposure with recovery
41
Q

complications with acute hep C

A
  1. High incidence of becoming chronic (85%) - Chronic Hepatitis C commonly leads to cirrhosis
  2. Increases risk for:
    - Non-Hodgkin’s lymphoma
    - Glomerulonephritis, idiopathic pulmonary fibrosis, and thyroiditis
42
Q

prevention of acute hep C

A
  • Testing donated blood for HCV
  • CDC recommends HCV screening for all persons over age 18 and all pregnant women
  • HCV infected persons should practice safe sex, but fortunately there is little evidence that HCV is spread easily by sexual contact or perinatally
  • Because most are acquired by injection drug use, public officials have recommended avoidance of shared needles and access to needle exchange programs for IV drug users
  • No vaccine
43
Q

tx for acute hep C

A
  1. ledipasvir/sofosbuvir x 6 wks - prevent chronic hepatitis in acute genotype 1
    - Inhibit viral replication
44
Q

prognosis for chronic hepatitis

A
  1. Progression to cirrhosis occurs in 20% of affected patients after 20 years
    - Increased risk in men
    - Those who drink more than 50g alcohol daily
    - Those who acquire HCV infection after age 40 years
  2. Tobacco and cannabis smoking and hepatic steatosis promotes progression of fibrosis
    - Coffee consumption slows progression
45
Q

chronic hep C tx

A
  1. HCV protease inhibitors
  2. HCV polymerase inhibitors
46
Q

MOA of HCV protease inhibitors

A

Inhibits a protease essential for replication

glecaprevir/pibrentasvir (Mavyret)
8 weeks
Genotypes 1-6

47
Q

MOA of HCV polymerase inhibitors

A

Inhibits viral replication

Sofosbuvir + velpatasvir (Epclusa)
12 weeks
Genotypes 1,2,4,5,6

48
Q

Only associated with Hepatitis B - coinfection; specifically only in presence of HBsAg

which hepatitis?

A

hep D

49
Q

who is at risk for hep D

A

Mainly among people who inject drugs

  • Coinfection with acute hep b, similar in severity to symptoms of hep b
  • Coinfection with chronic hep b carries worse prognosis, increase risk for fulminant hepatitis B
50
Q

dx for hep D

A

detection of serum antibodies - anti-HDV

51
Q

tx for hep D

A

Self care, supportive, avoid ETOH

52
Q

RNA virus that is a major cause of acute hepatitis throughout Central and Southeast Asia, the Middle East, and North Africa, where it is responsible for waterborne hepatitis outbreaks

which hep?

A

hep E

53
Q

who is at risk for hep E

A
  • young adults, a subpopulation that ordinarily would be immune to enterically transmitted endemic agents, and hepatitis can be particularly severe among pregnant women.
  • In industrialized countries, it may be spread by swine, and consuming undercooked organ meats
  • Illness is self-limited (no carrier state), but instances of chronic hepatitis with rapid progression to cirrhosis attributed to HEV possible
54
Q

incubation period and dx for hep E

A
  • Incubation period: 2-10 weeks
  • Dx: testing for IgM anti-HEV in serum
55
Q

presentation of hep E

A
  1. Prodromal phase of “flu-like symptoms”
  2. Followed by “icteric phase” of frank jaundice
    - pronounced elevation of aminotransaminase and bilirubin levels
  3. Extrahepatic manifestations include: arthritis; pancreatitis; thrombocytopenia; and a variety of neurologic complications, including Guillain-Barré syndrome and peripheral neuropathy
56
Q

tx and prevention of hepE

A

Treatment: oral ribavirin x 3 mo
Prevention: Recombinant vaccines against HEV have shown promise in clinical trials, and one (Hecolin) is approved in China

Acute hepatitis E can be very severe in PREGNANT WOMEN, in whom the mortality rate can reach 15–25%.

57
Q

cause of hemochromatosis

A
  1. Autosomal recessive - HFE gene mutation (HFE: homeostatic iron regulator gene)
  2. Increased iron absorption from duodenum and stored in liver
    - Iron stored in liver as hemosiderin
    - Increased Hemosiderin deposits found in liver, pancreas, adrenals, heart, kidneys, testes
  3. Cirrhosis is more likely to develop in affected persons who drink alcohol excessively or who have obesity-related hepatic steatosis
    - Risk factors: advanced age and DM
  4. MC in Northern European and North American Caucasians
58
Q

presentation of hemochromatosis

A
  • Sx do not typically present until age 50+
  • Commonly diagnosed d/t routine lab screenings much earlier
  • Early Sx nonspecific: fatigue, arthralgias
  • Late Sx: symmetric arthropathy, hepatomegaly, hepatic dysfunction, bronze skin pigmentation (melanin deposition), cardiac enlargement (can progress to heart failure), DM.
  • ED
  • 15-20% chance of developing cirrhosis
59
Q

labs for hemochromatosis

A
  1. Elevated serum iron levels and serum ferritin - Low TIBC
  2. Mildly elevated liver enzymes (AST/ALT)
  3. Iron studies and HFE testing recommended for all 1st-degree family members
    - Genetic testing for HFE mutations can be conducted to confirm dx
    - Liver bx - determine extent of liver damage = extensive iron deposition in hepatocytes
60
Q

tx for hemochromatosis

A
  1. Low iron diet - Such as red meat
  2. Decrease alcohol
  3. Weekly phlebotomy of 1 / 2 U blood
    - Monitoring of serum iron and HCT
    - Often continued for 2-3 years to deplete iron stores then PRN
  4. Deferoxamine IV or Deferasirox PO
  5. chelating agents
  6. can be used if patient unable to tolerate phlebotomy (anemia)
  7. tx associated complications
61
Q

prognosis of hemochromatosis

A
  1. Frequent phlebotomy improves course and limits liver damage
  2. Risk of advancing to cirrhosis increases without phlebotomy - If cirrhosis develops - liver transplant curative
62
Q

what is wilson dz

A
  1. Rare autosomal recessive disorder
  2. Presents before age 40
  3. Genetic defect on chromosome 13
    - Affects a copper transporting enzyme
    - Excessive absorption of copper from intestines
    - Decreased excretion by the liver - Low ceruloplasmin (copper carrying protein)
  4. Leads to excessive deposition of copper in liver and brain
63
Q

presentation of wilson dz

A
  1. Components of liver disease and neuropsychiatric disease
  2. Often presents in childhood or young adult: Hepatitis with hepatomegaly; Splenomegaly
  3. Can range from elevated liver tests, or can progress to fulminant hepatitis or cirrhosis
  4. Neurologic manifestations: Parkinsonian like sx, migraines, insomnia, seizures, ataxia, dysphagia, incoordination
    - Psychiatric features such as behavioral/personality changes may precede neurologic features
  5. Pathognomonic sign: Kayser-Fleischer ring
    - copper deposits in cornea
64
Q

labs for wilson dz

A
  1. Can be challenging
  2. Should be considered in any child or young adult with hepatitis and or neurologic/psychiatric abnormalities
    - Increased urinary copper excretion
    - Low serum ceruloplasmin levels
    - Liver bx to assess chronic hepatitis and cirrhosis
65
Q

tx for wilson dz

A
  1. Restriction of dietary copper (shellfish, nuts, mushrooms, chocolate)
  2. Oral penicillamine - Drug of choice
    - Chelating agent
    - Binds copper and increases urinary excretion of bound copper
    - Vitamin B6 (pyridoxine) added b/c penicillamine is an antimetabolite of B6
  3. Oral zinc promotes fecal excretion of copper
  4. Treatment required indefinitely
66
Q

if a pt has a poor prognosis with wilson dz and develop fulminant hepatitis or cirrhosis, what is the next step in tx?

A

liver transplant

67
Q

Screen 1st degree family members for wilson dz with what finding

A

serum ceruloplasmin

68
Q

Characterized by mild unconjugated bilirubinemia
Most common - often familial - presents in adolescents
Non-hemolytic unconjugated hyperbilirubinemia
Recurrent episodes of jaundice
Triggered by dehydration, fasting, infection, menstruation, over-exertion, alcohol

what is this condition

A

Gilbert syndrome

69
Q

Gilbert syndrome has reduce activity of what enzyme

A

glucuronyl transferase

Liver enzyme that gives glucuronic acid and changes bilirubin into a form that can be removed from body in bile - Impaired conjugation
Benign - no intrinsic liver damage

70
Q

dx for Gilbert syndrome

A

Unconjugated hyperbilirubinemia ( < 3mg/dL)
Normal range unconjugated .2-.8mg/dl
Normal CBC, blood smear and reticulocyte count
Normal AST and ALT

71
Q

tx for gilbert syndrome

A

Benign course - no treatment necessary
Patient education regarding triggers - Flares resolve on own

72
Q

what is Crigler Najjar Syndrome

A
  • Congenital nonhemolytic jaundice
  • Glucuronyl transferase deficiency - Complete or partial
  • Rare autosomal recessive disorder
  • Occur in infancy
  • Rapidly severe, High levels of unconjugated hyperbilirubinemia
73
Q

High levels of bilirubin can lead to neurological damage called ?

A

Kernicterus

74
Q

types/levels of Crigler Najjar Syndrome

A

Type I levels 20-50 mg/dL
Type II levels < 20mg/dL
High levels definitive for diagnosis

75
Q

tx for Crigler Najjar Syndrome

A
  1. Phototherapy
    - Fluorescent light over baby
    - Lowers bilirubin levels through photo-oxidation: Adds oxygen to bilirubin so it easily dissolves; Body can excrete through urine/feces
  2. Plasmapheresis

Can lead to death if not treated
Liver transplant is curative

76
Q

Type II Crigler Najjar Syndrome can also treated with ?, which will induce the enzyme

A

phenobarbital

77
Q

what is Dubin Johnson Syndrome

A
  1. Genetic mutation affecting transport proteins of bilirubin
    - Bilirubin conjugated in the hepatocyte, but does not get transported to bile ducts
    - Elevations in Conjugated serum bilirubin
78
Q

presentation of Dubin Johnson Syndrome

A

Intermittent Jaundice, fatigue

79
Q

dx for Dubin Johnson Syndrome

A

Conjugated hyperbilirubinemia in the absence of other abnormalities
May see darkly pigmented liver on gross inspection

80
Q

tx for Dubin Johnson Syndrome

A

Benign condition = no treatment needed
Can be exacerbated by illness, OCPs, and pregnancy

81
Q

what is rotor syndrome

A
  1. Rare genetic disorder
  2. Hepatic defect in storage of conjugated bilirubin - Leaks back into bloodstream
  3. identical to Dubin Johnson
  4. Benign condition - no tx needed
82
Q

how to differentiate rotor vs Dubin Johnson

A
  • Can inject dye and do “transport study” to determine if Rotor or Dubin Johnson
  • Liver bx can also differentiate
83
Q

what is Budd-Chiari syndrome

A

Hepatic venous outflow obstruction

  1. Hereditary and acquired hypercoagulable states can be defined in 75% of pts
  2. 50% of cases are associated with polycythemia vera or myeloproliferative disorders
  3. May see associated RHF or constrictive pericarditis
    - Also with neoplasms that cause vein obstruction
    - pregnancy
84
Q

presentation of Budd-Chiari Syndrome

A
  1. Insidious onset MC - Can be sudden acute, or chronic illness
  2. Clinical manifestations generally include:
    - tender, painful hepatic enlargement (RUQ pain)
    - Jaundice
    - Splenomegaly
    - Ascites
  3. With chronic disease, bleeding varices and hepatic encephalopathy may be evident
84
Q

imaging for Budd-Chiari Syndrome

A
  1. Doppler US
    - sensitivity of 85% for detecting evidence of hepatic venous or inferior vena caval thrombosis
    - occlusion/absence blood flow in hepatic veins/IVC
    - May show a prominent caudate lobe, since its venous drainage may be occluded
    — Caudate portion (small independent portion of liver) supplied by L/R hepatic veins
    — May see “spider web” pattern of occluded hepatic veins
  2. MRI w/ contrast - visualization of obstructed veins and collateral vessels
85
Q

tx for budd-chiari syndrome

A
  1. Treat complications - ascites
  2. Prompt recognition of underlying hematologic disorder- LMWH (Lovenox)
  3. Infusion of a thrombolytic agent into recently occluded veins has been attempted with success
  4. TIPS placement
  5. Balloon Angioplasty
  6. Liver transplantation can be considered in patients with hepatic failure, and cirrhosis
  7. Patients often require lifelong anticoagulation and treatment of the underlying disease
86
Q

Hepatocellular Carcinoma
arise from ?

A

liver parenchymal cells

80% of Hepatocellular Carcinoma d/t Cirrhosis

87
Q

RF in pts with cirrhosis to develop Hepatocellular Carcinoma

A

Obesity
Male gender
Age > 55
Family History
DM
HCV or HBV infection
Alcohol

88
Q

presentation of Hepatocellular Carcinoma

A
  1. Deterioration in patient with cirrhosis
  2. Cachexia, severe weight loss, anorexia, weakness, muscle wasting
  3. Bloody ascites - Bleeding from necrotic tumor tissue or tumor invading vessels
  4. Tender Hepatomegaly
89
Q

labs for Hepatocellular Carcinoma

A
  1. Spike in ALP
  2. Alpha fetoprotein in 70% of pts
  3. CT and MRI - 1st line imaging to identify masses
  4. Liver Biopsy confirms - Can be deferred if mass on CT + alpha fetoprotein
90
Q

staging for Hepatocellular Carcinoma

A

TNM

T0 - No tumor
T1 - Solitary tumor without vascular invasion
T2 - Solitary tumor with vascular invasion or multiple tumors < 5cm
T3 - Multiple tumors > 5cm or tumor involving major branch of the portal or hepatic vein
T4 - Tumor/s with direct invasion into adjacent organs (other than the gallbladder).

91
Q

screening for Hepatocellular Carcinoma

A

Pts with Cirrhosis or Chronic HBV/HCV should begin screening for Hepatocellular Carcinoma

  1. Standard approach - Liver US + alpha fetoprotein q 6mo
    - Problem: US only detects 60%
    - CT better - but too expensive for screening
92
Q

tx for Hepatocellular Carcinoma

A
  1. Resection if solitary tumor not invading vasculature and preserved liver function
  2. Liver transplant
    - A MELD score > 20 is associated with poor post-transplant survival rates.

GI: Clin Med IIA (12 decks)

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