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MHD2 > Block 11 - L10-L11 > Flashcards

Block 11 - L10-L11 Flashcards

1
Q

Compare Hepatitis A and E (Structure, transmission, onset, incubation period, severity, mortality, chronicity/carrier state, disease associations, lab diagnosis).

A

A: picornavirus; capsid, RNA
E: calcivirus-like capsid, RNA

Transmission: fecal-oral
Onset: abrupt
Incubation period: 15-50 days
Severity: mild (E severe in pregnant women)
Mortality: A <0.5%, E 1-2% (normal), 20% (pregnant)
Chronicity/carrier state: no
Disease associations: none
Laboratory diagnosis - A: symptoms + anti-HAV IgM

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2
Q

Compare Hepatitis B, C, and D (Structure, transmission, onset, incubation period, severity, mortality, chronicity/carrier state, disease associations, lab diagnosis).

A

B: hepadnavirus; envelope, DNA
C: flavivirus; envelope, RNA
D: viroid-like; envelope, circular RNA

Transmission: parenteral, sexual
Chronicity/carrier state: yes
Disease associations: primary HCC, cirrhosis, + fulminant hepatitis (D only)
Lab diagnosis:
B - symptoms + serum levels of HBsAg, HBcAg, and anti-HBc IgM
C - symptoms + anti-HCV ELISA
D - anti-HDV ELISA

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3
Q

Describe the structure of HBV.

A

Partially double-stranded DNA virus in a capsid that is made up of self-assembling surface antigens

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4
Q

How does HBV replicate?

A

Virus enters the cytoplasm and completes the double-stranded DNA genome. This enters the nucleus and is transcribed. mRNA moves back to the cytoplasm, is translated, then reverse transcribed

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5
Q

How is HBV transmitted?

A

Blood products, mother to child

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6
Q

What are the outcomes of acute HBV infection?

A
  1. Resolution (90%)
  2. Infection continues for 6+ months (9%)
  3. Fulminant hepatitis (1%)
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7
Q

What are the outcomes if acute hepatitis B infection persists?

A
  1. Resolution (50%)
  2. Asymptomatic carrier state
  3. Chronic persistent hepatitis
  4. Chronic active hepatitis
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8
Q

What are the outcomes of chronic persistent hepatitis due to HBV infection?

A

Extrahepatic disease (polyarteritis nodosum and glomerulonephritis)

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9
Q

What are the outcomes of chronic active hepatitis due to HBV infection?

A

Cirrhosis
Hepatic cell carcinoma
Extrahepatic disease (polyarteritis nodosum and glomerulonephritis)

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10
Q

What are the stages of HBV infection?

A
  1. Incubation period
  2. Pre-icteric
  3. Icteric
  4. Convalescent period
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11
Q

What are the symptoms of acute HBV?

A 
Fever, rash, arthritis
Jaundice
Dark urine
Malaise
Anorexia
Nausea
RUQ pain
Itching (10%)
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12
Q

Discuss the Ag and Ab seen in acute self-limiting HBV infection.

A
  1. Incubation (4-12 weeks) - nothing
  2. Acute viremia (4-12 weeks) - Increase and decrease of HBsAg and HBeAg + increase in anti-HBc
  3. Convalescence (2-16 weeks) - anti-HBc, anti-HBe, anti-HBs
  4. Healthy (years) - anti-HBc remains elevated, anti-HBe and anti-HBs slowly decline
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13
Q

Discuss the Ag and Ab seen in chronic active HBV infection.

A
  1. Incubation (4-12 weeks) - nothing
  2. Acute viremia (6 months) - increase in HBsAg and HBeAg + anti-HBc
  3. Chronic viremia (years) - #2 levels maintained
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14
Q

What is the window period of HBV infection?

A

The period of time when HBsAg is negative and anti-HBs has yet to appear

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15
Q

Interpret the serologic assay for HBV:

HBsAg: negative
HBeAg: negative
anti-HBc: negative
anti-HBe: negative
anti-HBs: negative
A

No evidence of present or past HBV infection

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16
Q

Interpret the serologic assay for HBV:

HBsAg: positive
HBeAg: negative
anti-HBc: negative
anti-HBe: negative
anti-HBs: negative
A

Incubation period of HBV

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17
Q

Interpret the serologic assay for HBV:

HBsAg: positive
HBeAg: positive
anti-HBc: positive
anti-HBe: negative
anti-HBs: negative
A

Early in acute infection with HBV or chronic HBV infection with high infectivity

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18
Q

Interpret the serologic assay for HBV:

HBsAg: positive
HBeAg: negative
anti-HBc: positive
anti-HBe: positive
anti-HBs: negative
A

Later in acute infection, or chronic HBV infection with lower infectivity

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19
Q

Interpret the serologic assay for HBV:

HBsAg: negative
HBeAg: negative
anti-HBc: positive
anti-HBe: positive/negative
anti-HBs: negative
A

Window period late in acute HBV infection

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20
Q

Interpret the serologic assay for HBV:

HBsAg: negative
HBeAg: negative
anti-HBc: positive
anti-HBe: positive
anti-HBs: positive
A

Convalescent from HBV

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21
Q

Interpret the serologic assay for HBV:

HBsAg: negative
HBeAg: negative
anti-HBc: positive
anti-HBe: negative
anti-HBs: positive
A

Later in convalescence (anti-HBe has waned)

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22
Q

Interpret the serologic assay for HBV:

HBsAg: negative
HBeAg: negative
anti-HBc: negative
anti-HBe: negative
anti-HBs: positive
A

Response to HBV vaccine or recent administration of hyperimmune anti-HB’s immunoglobulin

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23
Q

How is HBV infection treated?

A
  1. Lamivudine

2. Hepsera (adefovir)

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24
Q

What are the MOAs of lamivudine and hepsera (adefovir)?

A

Nucleoside analogues that inhibit reverse transcription and reduce HBV DNA

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25
Q

What is a unique indication of adefovir?

A

Works against laminvudine resistant HBV

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26
Q

How does the HBV vaccine work?

A

Sub-unit vaccine using HBsAg

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27
Q

What is unique about HDV?

A

Must co-infect with HBV, as it is a circular single-stranded RNA virus that encodes one protein (delta Ag) - surrounds itself with HBsAg to make the virus particle

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28
Q

What is a ribozyme?

A

Enzyme that cleaves and ligates RNA; found in the hepatitis D virus

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29
Q

True or false - vaccination with HBV protects from HDV.

A

True

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30
Q

Describe the structure of HCV.

A

Positive strand RNA virus of the flavivirus family

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31
Q

How is HCV treated?

A

Direct acting anti-virals (DAAs) -

Protease inhibitors (NS3)
Phsophoprotein inhibitors (NS5A)
Polymerase inhibitors (NS5B)

Multiple drug regimen most effective

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32
Q

What are the outcomes of acute HCV infection?

A
  1. Recovery and clearance (15%)
  2. Cirrhosis - rapid onset (15%)
  3. Persistent infection (70%)
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33
Q

What are the outcomes of persistent infection with HCV?

A

Chronic hepatitis

40% are asymptomatic

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34
Q

What are the outcomes of chronic hepatitis due to HCV?

A
  1. Liver failure (6%)
  2. Cirrhosis (20%)
  3. HCC (4%)
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35
Q

What factors influence HCV disease progression?

A
  1. Females who are young at infection - slower progression

2. Alcohol use, coinfection - faster progression

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36
Q

How is HCV diagnosed?

A

Serologic assays (screen for anti-HCV, supplemental Ab test)

Molecular assays (qualitative test for HVC RNA, quantitative tests for viral RNA, HCV genotype tests)

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37
Q

What was the original treatment for HCV, and what was the typical outcome?

A

Interferon - worked for a few weeks, then relapsed

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38
Q

Where is HEV primarily seen?

A

SE Asia (India, Nepal)

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39
Q

What is the family and genome of Hepatitis A virus?

A

Single stranded positive RNA Enterovirus

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40
Q

How is HAV most commonly transmitted?

A

Fecal-oral

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41
Q

What is the recommended current method of detection for Hepatitis A infection?

A

Serology by antibody capture for HAV specific IgM

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42
Q

What is the mechanism of pathogenesis for HAV?

A

Viremia resulting in targeting of the liver

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43
Q

Are there anti-viral therapies available against HAV?

A

Vaccine can be administered during the prodrome period of infection

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44
Q

Is there a vaccine available for protection against HAV?

A

Killed-virus injected vaccine

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45
Q

Are there long term consequences of a HAV infection?

A

Long-lived protective immunity

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46
Q

What is the family and genome of Hepatitis B virus?

A

Partly Single stranded DNA Hepadnavirus

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47
Q

How can HBV be transmitted?

A
  1. Sexual
  2. Transfusion/sharing needles
  3. Mother to newborn
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48
Q

What is the recommended current method of detection for Hepatitis B virus infection?

A

Serology by antibody capture for HBV specific antibodies

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49
Q

What is the mechanism of pathogenesis for HBV?

A

Viremia resulting in targeting of the liver

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50
Q

Are there anti-viral therapies available against HBV?

A

Nucleoside reverse transcriptase inhibitors (NRTIs) such as Lamivudine or Adefovir Dipivoxil

51
Q

Is there a vaccine available for protection against HBV?

A

Subunit vaccine

52
Q

What is the most clinically significant long term consequence of HBV infection?

A

Hepatocellular carcinoma

53
Q

What is the family and genome of Hepatitis C virus?

A

Single stranded positive RNA Enveloped Flavivirus

54
Q

How is HCV most commonly transmitted?

A

Transfusion, needle sharing, contact with blood

55
Q

What is the recommended current method of detection for Hepatitis C infection?

A

RT-PCR and sequencing for genotype

56
Q

What is the mechanism of pathogenesis for HCV?

A

Viremia resulting in targeting of the liver and persistent infection in the majority of patients

57
Q

Are there anti-viral therapies available against HCV?

A

Direct acting anti-virals (DAAs) including protease inhibitors and polymerase inhibitors

58
Q

Is there a vaccine available for protection against HCV?

A

No

59
Q

What is the most clinically significant long term consequence of HCV infection?

A

Hepatocellular carcinoma

60
Q

What is the genome of Hepatitis D virus?

A

Single-stranded RNA viroid

61
Q

How is HDV most commonly transmitted?

A

Sexual, transfusion/sharing needles, mother to newborn

62
Q

What is the recommended current method of detection for Hepatitis D infection?

A

Serology by antibody capture for HDV specific IgM

63
Q

What is the mechanism of pathogenesis for HDV?

A

Co-infection with HBV, viremia resulting in targeting of the liver and fulminant disease

64
Q

Are there anti-viral therapies available against HDV?

A

Nucleoside reverse transcriptase inhibitors (NRTIs) such as Lamivudine or Adefovir Dipivoxil

65
Q

Is there a vaccine available for protection against HDV?

A

Subunit vaccine to HBV

66
Q

Are there long term consequences of a HDV infection?

A

Reinfection is common with lesser severity

67
Q

What is the family and genome of Hepatitis E virus?

A

Single stranded positive RNA Calicivirus

68
Q

How is HEV most commonly transmitted?

A

Fecal-oral

69
Q

What is the recommended current method of detection for Hepatitis E infection?

A

Serology or RT-PCR by the public health department

70
Q

What is the mechanism of pathogenesis for HEV?

A

Viremia resulting in targeting of the liver

71
Q

Are there anti-viral therapies available against HEV?

A

No

72
Q

Is there a vaccine available for protection against HEV?

A

No

73
Q

Are there long term consequences of a HEV infection?

A

Long-lived protective immunity in healthy individuals; higher chance of mortality in pregnant women

74
Q

Discuss the global localization of HIV infections.

A

Africa - 70%
Asia - 14%
US - 3%

75
Q

What percent of people with HIV infections are getting antiretroviral treatment?

A

57%

76
Q

Which groups have experienced increased rates of new HIV infections in the US since 2011?

A

Black and Latino MSM

MSM category comprises the majority of infections in the US - 67%

77
Q

What is the average life span of a 20 y/o diagonosed with HIV today and treated with ART?

A

53-56 years (normal would be 66 years)

78
Q

Why is the prevalence of HIV infection increasing in the US?

A

People are living longer

79
Q

How does acute/primary HIV infection present?

A 
Fever, fatigue (90%)
Pharyngitis, weight loss (75%)
Myalgias (60%)
Lymphadenopathy (50%)
Thrombocytopenia, leukopenia (40-45%)
Maculopapular rash (35%)
Oral ulcers, headache , diarrhea, nausea, aseptic meningitis

50-90% have a least some symptoms
Onset: 1-4 weeks after exposure
Non-specific symptoms with many mimics

80
Q

What are the characteristics of acute/primary HIV infection (labs)?

A

High viral load and below normal CD4 count (normal = 500-1200 cells/mm3)

81
Q

When is risk of transmission of HIV highest?

A

Acute/primary HIV infection

82
Q

What are the CDC recommendations regarding HIV testing?

A
  1. All people 13-64 (opt-out rather than opt-in)
  2. People at high risk annually (IVDU, HIV-infected partner, multiple partners, exchanging sex for drugs)
  3. People with STI, TB, illnesses compatible with HIV
  4. All pregnant women
83
Q

Which age group in the US are most likely to be unaware of their HIV infection?

A

Young people ages 13-24, especially high school students

84
Q

Until recently, HIV diagnosis was made using what tests?

A

HIV ELISA and a confirmatory Western blot (antibody testing)

85
Q

What is the current recommendation to test for HIV?

A

Combined antibody/antigen assay

86
Q

What is involved in a 4th generation HIV test?

A

Detects HIV Ab as well as circulating virus (p24 Ag)

87
Q

Why is Western blot testing no longer recommended for detecting HIV infection?

A

False negatives or indeterminate results

88
Q

What should be done if a test is p24 Ag positive but HIV Ab negative?

A

HIV nucleic acid testing (NAT)

89
Q

What else is HIV RNA PCR used for?

A

Follow response to ART

90
Q

What are important components of the history and physical when evaluating a new case of HIV?

A

Complete history, including other STIs, immunization status, travel history, sexual history, substance use, depression, ROS directed at possible opportunistic complications

Look for evidence of more advanced HIV/opportunistic complications and STIs on exam

91
Q

What labs should be done as part of a baseline evaluation of HIV?

A
  1. HIV RNA PCR (viral load) and CD4 count
  2. HIV resistance testing (mutations to HIV meds)
  3. Chemistries, CBC, lipids, UA
  4. STI screening (gonorrhea/chlamydia screening, RPR)
  5. TB screening
  6. Hepatitis screening
  7. Cervical pap smear
  8. Toxoplasma IgG
  9. Labs for medication side effects (e.g., HLA B5701)
92
Q

When should ART be started?

A

When HIV is diagnosed, regardless of CD4 and VL

93
Q

What is the rate of HIV transmission from an HIV-infected person on ART to his/her partner if the viral load in the person with HIV is < 200 copies/ml?

A

0% - when ART results in viral suppression (<200 copies/mL = undetectable), it prevents sexual transmission

94
Q

How is HIV monitored?

A
  1. CD4 and VL - baseline, check every 3-6 months
  2. Check VL 2-8 weeks after starting/changing ART
  3. Regular chemistries and CBC to monitor side effects
  4. Yearly screenings for TB/STIs
95
Q

What are the complications of HIV seen at >500 CD4 count?

A

Neuropathy
Bell’s palsy
Low platelets

96
Q

What are the complications of HIV seen at 200-500CD4 count?

A

Herpes zoster
TB
Pneumonia (bacterial)
Non-CNS lymphoma

97
Q

What are the complications of HIV seen at <200 CD4 count?

A 
Thrush
PJP
KS
Cryptococcus
MAC
CMV
PML
CNS lymphoma
Toxoplasma
98
Q

What is the indication for prophylactic treatment of pneumocystis carinii in HIV?

A

CD4 <200 OR
Oral candida OR
Cd4% <14% OR
AIDS-defining illness

99
Q

What is the prophylactic treatment of pneumocystis carinii in HIV?

A

TMP-SMX

100
Q

What is the indication for prophylactic treatment of toxoplasma in HIV?

A

CD4 <100 AND positive Toxo IgG

101
Q

What is the prophylactic treatment of toxoplasma in HIV?

A

TMP-SMX

102
Q

What is the indication for prophylactic treatment of mycobacterium TB in HIV?

A

Positive screening test for LTBI

103
Q

What is the prophylactic treatment of mycobacterium TB in HIV?

A

INH 300 mg daily x 9 months + pyridoxine

104
Q

What is the indication for prophylactic treatment of Mycobacterium avium complex (MAC) in HIV?

A

CD4 <50

105
Q

What is the prophylactic treatment of MAC in HIV?

A

Azithromycin 1200 mg weekly OR
600 mg 2x weekly OR
Clarithromycin

106
Q

What are some early physical HIV manifestations?

A

Seborrheic dermatitis
Oral hairy leukoplakia
Herpes zoster (dewdrops on a rose petal)

107
Q

What are common lung diseases in HIV?

A 
PJP
Bacterial pneumonia (S. pneumo)
TB
Histoplasmosis
Blastomycosis
Coccidioidomycosis (in SW US)
Cryptococcus
Respiratory viruses (influenza)
Tumors - lymphoma, Kaposi's sarcoma
108
Q

How does pneumocystis pneumonia present?

A

Insidious symptoms present for weeks; exam is often normal, may desaturate on walking

Elevated LDH
CXR - bilateral reticulonodular interstitial infiltrates, perihilar (may be normal)
CT

109
Q

What are 3 common ring-enhancing brain lesions in HIV?

A
  1. CNS lymphoma
  2. Bacterial abscess (IVDU)
  3. Chagoma
110
Q

What are less common ring-enhancing brain lesions in HIV?

A

Tuberculoma
Cryptococcoma
Histoplasoma
Metastatic cancer

111
Q

How does one get toxoplasmosis?

A

Eating undercooked meat with tissue cysts or ingesting cysts that have been shed in cat feces

112
Q

How does toxoplasmosis manifest?

A

Encephalitis with multiple brain lesions (often ring-enhancing)

113
Q

How is toxoplasmosis treated?

A

Sulfadiazine + pyrimethamine

Clindamycin + pyrimethamine

TMP-SMX

114
Q

What is the usual cause of CNS lymphoma in HIV?

A

EBV reactivation

115
Q

How does CNS lymphoma appear on MRI?

A

Single lesion with contrast enhancement and edema/mass effect

116
Q

How is CNS lymphoma treated in HIV?

A

Chemo, radiation, ART

117
Q

How does cryptococcus present?

A

Fever, HA, altered mentation, pneumonia, skin lesions

118
Q

How is cryptococcus treated?

A

Amphotericin B + 5-flucytosine then fluconazole

119
Q

What retinal disease is common in HIV?

A

CMV retinitis

120
Q

How does CMV retinitis appear on PE and what is an initial symptom?

A

Scrambled eggs and ketchup; floaters

121
Q

How is CMV retinitis treated?

A

Ganciclovir

122
Q

What is immune reconstitution inflammatory syndrome (IRIS)?

A

Systemic infalmmatory syndrome with signs and symptoms identical to the infection; occurs after ART initiation/increase in CD4

Not related to uncontrolled infection, but to the improved immune response from ART - leads to a paradoxical worsening of infection

123
Q

What is PrEP?

A

Tenofovir-emitricitabine, approved for use in high-risk HIV-negative persons to prevent transmission

MHD2 (34 decks)

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