Limjoco - Hepatitis Flashcards

1
Q

Hepatotropic viruses (A, B, C, D, E, G) have an affinity for the liver.

Name 5 other viruses (systemic) that can cause Viral Hepatitis?

A
  1. EBV (infectious mononucleosis)
  2. CMV
  3. HSV
  4. Adenovirus (neonates, immunosuppressed)
  5. Yellow Fever
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2
Q

Mnemonics for Viral Hepatitis

AcutE Hepatitis: A and E (never chronic)
*Note: HEV is bad in immunocompromised hosts, pregnant women

Consonants B, C, D: can cause Chronic Disease

Hepatitis B can be transmitted by Blood, Birthing and Bonking.

A
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3
Q

Which Hepatitis?

80% or more develop chronic hepatitis and 20% of these people develop cirrhosis

A

Hep C (Chronic and Cirrhosis)

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4
Q

Typical Course for What Condition?

Incubation period: asymptomatic

Symptomatic Pre-icteric period: malaise, fatigue, anorexia, nausea, fever
*2 weeks post-exposure

A

Acute Viral Hepatitis

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5
Q

Typical Course for What Condition?

Icteric Phase (1-2 weeks after prodrome, last up to 6 weeks)

jaundice, dark urine, clay-colored stools, hepatomegaly

Convalescence (6-8 weeks post-exposure): dinminishing jaundice

A

Acute Hepatitis

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6
Q

When is an individual with Viral Hepatitis most infectious?

A

Last asymptomatic days of Incubation Period

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7
Q

What do lab results look like for Viral Hepatitis?

  1. Liver Enzymes?
  2. ________bilirubinemia (hyper/hypo)
  3. Viral Serology; also RNA or DNA detection by PCR
A

High Levels of ALT, AST (>1000 U/L)

Hyperbilirubinemia

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8
Q

After how many months of infection, do you have chronic hepatitis?

A

6 months

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9
Q

Definition (Viral Hepatitis).

  • harbors orgs without signs & symptoms
  • either no liver damage or with liver damage –> reservoirs for future infection
A

Carrier State

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10
Q

During a Viral Hepatitis Infection, hepatocellular damage is due to the host’s ________ immune response to viral protein expressed by infected cells.

It is not due to direct viral cytopathic effect.

What immune cells are activated and what damage ensues?

A

adaptive

T Cells

  • ->Necroinflammatory activity
  • ->Apoptosis (“cell suicide” - elimination of infected/damaged cell)
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11
Q

Which Hepatitis?

  • Family: Picornavirus
  • Genus: Hepatovirus
  • Small, naked +SS RNA
  • Benign, self-limited course, rare relapse
  • NO chronic or carrier state
  • history of travel to endemic areas*
A

Hep A

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12
Q

Which Hepatitis?

  • fecal-oral route
  • ingested through contaminated water and food
  • contaminated undercooked shellfish concentrates virus
  • endemic in countries with poor sanitation
  • in developed countries, better hygience but NO herd immunity
  • older age group will be more symptomatic an severe
A

Hepatitis A

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13
Q

Serology for Hepatitis A.

_____ (what Ab): rises with onset of symptoms; marker of ACUTE infection

_____ (what Ab): rises on decline of IgM after months, persists
confers LIFELONG IMMUNITY AGAINST REINFECTIONS WITH
ALL STRAINS

NOTE: there is no direct detection for IgG. It is derived from [Total Ig - IgM]

A

IgM

IgG

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14
Q

Total Anti-HAV Antibody = Ig____ + Ig_____

A

IgM + IgG

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15
Q

How is HAV spread rapidly?

Fecal shedding of HAV Virus occurs _____ weeks before and ____ week after the start of jaundice.

A

2-3 weeks before

1 week after

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16
Q

Which Hepatitis?

  • more sporadic than HAV
  • **India, Asia, Africa, ME, China, mexico
  • Developed world: pig farms
  • High mortality rate in Pregnant Women
A

Hep E

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17
Q

Which Hepatitis?

Genus: Hepevirus

  • naked +SS RNA
  • virions shed during acute illness
  • RNA and Virions detectable in stool/serum prior to symptoms appearing

CLINICAL: Inc. AST/ALT
Inc. IgM

-self-limited, resolves in 4-6 weeks

A

Hep E

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18
Q

Which Hepatitis?

Family: Flavivirus

  • small +SS RNA virus
  • RNA codes only for 1 polyprotein, processed into functional proteins
  • RNA polymerase, poor fidelity in copying (Antigenic variation)
A

Hep C

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19
Q

Hepatitis C

_____ envelope glycoprotein (target of anti-HCV antibodies) is the MOST VARIABLE region of the genome.

New virus strains can escape neutralizing antibodies.

A

E2

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20
Q

Why no vaccine for Hep C?

Anti-HCV Ig____ produced after infection does NOT confer immunity –> HIGH RATE OF CHRONICITY

A

genomic instability, antigenic variation (Exonuclease lacks proofreading capacity in the 3’-5’ so the RNA is prone to frequent mutations)

IgG

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21
Q

What are the top 3 Risk factors for contracting Hep C?

A
  1. IV Drug use
  2. Multiple sex partners
  3. Undergoing surgery in the last 6 months

Others: Needle Sticks, Multiple contacts w/HCV-infected person, Work in medical/dental field, perinatal infections

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22
Q

True or False.

There is a higher risk for HCV than HIV by needle stick.

A

True!

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23
Q

Which Hepatitis?

Incubation period: 4-26 weeks (1-6 months)

Majority Asymptomatic

Best Diagnostic method: PCR to detect RNA in blood together with elevated AST, ALT levels

-milder clinical course than HBV

A

Hep C

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24
Q

Fact. Hepatitis C - Acute and Chronic Infection Serum HCV RNA Levels

A
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25
Hepatitis C - **majority develop chronic hepatitis** --\> up to **20% develop \_\_\_\_\_\_\_\_\_\_.** - despite Ab production, **HCV _____ remains in the blood** - **\_\_\_\_\_\_\_\_\_\_\_\_\_ remain elevated** (inc or dec but never normalize) * \*Need close follow-up*
cirrhosis RNA Transaminases
26
FACT: **Drugs for Hep C** **Pegylated INF-alpha, Ribavirin** **Newer Drugs** with Better Response: **ABT-450 Ombitavir Dasabuvir** (+/- Ribavirin) Response Depends on: HCV Genotype: 2,3 best response Host Genotype: IL28B gene (encodes IF-lambda)
27
\_\_\_\_\_\_\_\_\_\_\_\_ is the primary reason for liver transplantation.
HCV-related Cirrhosis
28
True or False. **HCV infection recurs** in transplants. **Cirrhosis recurs** in 20-30% of transplants.
TRUE!!
29
Which Hepatitis? -Family: Hepadnavirus **-Circular,** Double-Shelled (**enveloped**) **-partially DS DNA virus** **-resistant** to **extreme temps**/humidity -it's **own Polymerase Complex** (Reverse transcriptase, DNA polymerase) so **replication DNA --\> RNA --\> DNA**
Hep B
30
Name the Antigen for Hepatitis B Virus (HBV) Nucleocapsid CORE: \_\_\_\_\_\_ Envelope Glycoprotein: \_\_\_\_\_\_\_ Lipid envelope glycoproteins (surface): \_\_\_\_\_\_\_\_\_\_
HB**_c_**Ag HB**_e_**Ag HB**_s_**Ag
31
What is the name of the particle that is the **complete virion for Hepatitis B** and is **infectious**?
Dane Particle
32
What **antigen of the Hepatitis B Virus aggregates** to form **subviral particles** that are **non-infectious** small spheres and filaments?
HBsAg
33
What Serological markers are present during the **Acute Stage of Hep B** Infection?
HBsAg HBeAG HBV DNA HBcAB: IgM
34
IgM is replaced by **\_\_\_\_\_\_ anti-HGcAb** after several months of Hep B Infection.
IgG
35
What Serological markers are present during **the Chronic Stage of Hepatitis B Infection?**
HBsAg HBeAg HBV DNA HBcAb: IgG
36
Summary of Hepatitis B Antigens and Antibodies.
37
Modes of Tranmission for Hepatitis B? 1. \_\_\_\_\_\_\_\_\_\_\_\_: high prevalence regions 2. \_\_\_\_\_\_\_\_\_\_\_\_: intermediate prevalence regions 3. \_\_\_\_\_\_\_\_\_\_\_\_: low prevalence regions
1. Childbirth/vertical 2. Horizontal 3. Sexual/IV Drug
38
Fact: Potentital Outcomes of Hep B Infection
39
Fact: Hepatitis B - Most Self-Limited - Small % may progress to cirrhosis and/or develop HCC - **AGE at time of infection predicts chronicity** - -\> **Younger:** more likely becomes chronic - -\> **Vertical Transmission** (mom-to-baby)
40
Why is it **hard to achieve complete cure** in **chronic cases of Hepatitis B**?
**Virus inserts itself in to the host DNA**. Thus, **host cannot mount effective response** via production of HBsAb and virus persists.
41
What is the treatment for Hepatitis B?
Slow down progress of disease and Limit damage to liver (prevent cirrhosis or HCC).
42
**The outcome of Hepatitis B Infection depends on Host Immune Response.** **Early Stage**: ______________ (natural killer T cells, interferon) **protects the individual** **If CD4+ and CD8+** produce INF-y, etc. and clear infected cells --\> _____________ (result?) **If weak immune response**, some infected cells not killed/cleared --\> ____________ (result?)
Innate Immune Response resolution chronicity
43
What **antigen of the Hep B virus** is **incorporated in to the HDV envelope**, needed for **assembly of HDV virion.**
HBsAg
44
Which Hepatitis? - very **small** molecule - **Circular, -RNA, enveloped** - **uses host's RNA polymerase to replicate** through RNA-directed RNA synthesis - delta antigen (HDAg) protein produced by virus
Hep D
45
Hepatitis D Absolute requirement for ________ (which hepatitis?) for replication --\> needs HBsAg in envelope. Delta agent, defective virus, is directly cytopathic to cells.
HBV
46
Self-limited infection for Hep B & D **EXCEPT FOR ___________ --\> leads to acute liver failure.**
IV Drug abusers
47
Two possible scenarios of Infection by Hepatitis D Virus 1. \_\_\_\_\_\_\_\_\_\_\_\_: simulataneous infection with HBV, HDV --\> Acute, self-limited; rarely chronic 2. \_\_\_\_\_\_\_\_\_\_\_\_: when HBV carrier gets HDV 30-50 days later --\> Severe acute hepatitis. Worsens the Hep B Infection (likely bc of direct viral toxicity of HDV)
1. Coinfection 2. Superinfection
48
Fact: Histopathologic changes in hepatitis are essentially similar in all viral, autoimmune and drug-induced hepatitides.
49
Fact: Liver Biopsy - Why Do It? - Confirm the clinical diagnosis - Exclude simultaneous conditions - Grade extent of inflammation and injury - Stage the degree of fibrosis - Monitor treatment effectiveness
50
Interpret the Lab Results: HBsAg: negative anti-HBc: negative anti-HBs: negative
Susceptible (no protective immunity exists - HBsAB: IgG)
51
Interpret the Lab Results: HBsAg: negative anti-HBc: positive anti-HBs: positive
Immune due to natural infection (protective IgG - HBsAB)
52
Interpret the Lab Results: HBsAg: negative anti-HBc: negative anti-HBs: positive
Immune due to Hep B Vaccination (no antibodies against the core antigen, only antibodies against surface antigen - protective IgG)
53
Interpret the Lab Results: HBsAg: positive anti-HBc: positive IgM anti-HBc: positive anti-HBs: negative
Acutely Infected (no IgG antibody - HBsAg)
54
Interpret the Lab Results: HBsAg: positive anti-HBc: positive IgM anti-HBc: negative anti-HBs: negative
Chronically Infected (HBcAB = IgG)
55
Interpret the Lab Results: HBsAg: negative anti-HBc: positive anti-HBs: negative
Interpretation unclear; 4 possibilities: 1. Resolved infection (MOST COMMON) 2. False-positive anti-HBc; thus susceptible 3. "Low level" chronic infection 4. Resolving acute infection
56
What do you see?
Spotty/Lytic Necrosis
57
What do you see?
Interface hepatitis (AKA “piecemeal necrosis” in older literature)
58
What do you see?
Hallmark of Hepatitis B-infected cells: “ground-glass” cells Large cells with pale, finely granular cytoplasm with peripheral halo = surface antigens in endoplasmic reticulum
59
What do you see?
Inflamed portal tract (bile ductule at arrow) with lymphoid follicle = typical of Hepatitis C infection
60
What do you see?
See picture.
61
What do you see?
Systemic infection with herpes simplex virus (HSV) (non-hepatotropic virus): infected hepatocytes with Cowdry bodies Apoptotic or acidophil bodies seen in various hepatitides