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CSP - Exam 4 > Hepatitis - Ornelles > Flashcards

Hepatitis - Ornelles Flashcards

1
Q

Hep. A does not have the ability to go ___. It is acquired by eating ___ foods

A

Hep. A does not have the ability to go chronic. It is acquired by eating contaminated foods.

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2
Q

What are the symptoms of viral hepatitis?

Trans Heppy Rock Fan listens to Jams in his Dark Urine Pale interior Family Van.

A 
Increase trans aminase
RUQ pain
Fever
Jaundice
Dark Urine
Pale feces
Fatique
Vomiting
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3
Q

___ fever, __ and __ can cause hepatitis

A

Yellow fever, EBV, CMV can cause hepatitis

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4
Q

HBV is huge in ___ and western ___

A

Uganda and western Africa

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5
Q

HCV is largely ____ but there is an increased incidence in ___ and N. ____.

A

HCV is largely worldwide, but there is an increased incidence in Asia and N. Africa

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6
Q

HCE is highly endemic in __, __ and __

A

India, Asia, Africa

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7
Q

Heb B’s prevalence is decreasing due to blood screening. Hep B has a higher mortality rate than Hep A and has the potential to go ___

A

Heb B’s prevalence is decreasing due to blood screening. Hep B has a higher mortality rate than Hep A and has the potential to go chronic

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8
Q

Hep C is a ___ virus with an ___ and is a _RNA virus. It can go ___.

A

Hep C is a flavi-virus with an envelope and is a +RNA virus. It can go chronic.

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9
Q

HepD is a -_ virus and has ___, ___ RNA. Almost like a virulence factor for Hep __. When presented WITH ___, it causes a more severe infection, especially if Hep D is acquired AFTER.

A

HepD is a delta virus and has a small, circular, -RNA. Almost like a virulence factor for Hep B. When presented WITH Hep B, it causes a more severe infection, especially if Hep D is acquired AFTER.

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10
Q

T/F: HepE is non-enveloped.

A

True

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11
Q

Mortality rates of Hep, A, B, C. Put in order

__ < ___ < ___

A

Hep A < Hep B < Hep C

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12
Q

Prevalence of Hep A, B and C

__

A

Hep A < Hep B < Hep C

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13
Q

HAV is a ___ virus, __ssRNA, naked and icosohedral. It directs synthesis of polyprotein that requires proteolysis by proteases.

A

HAV is a picorna virus, +ssRNA, naked and icosohedral. It directs synthesis of polyprotein that requires proteolysis by proteases.

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14
Q

HAV is an __-stabile virus.
Transmission?
Control?

A

HAV is an acid stabile virus
It is transmitted fecal-orally
Control is by having good hygeine and vaccination

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15
Q

How is an acute infection of HAV diagnosed?

A

Through anti-HAV IgM.

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16
Q

T/F: HAV is usually self limiting

A

True

17
Q

In HAV, anti-HAV IgG’s are eventually replaced by anti-HAV Ig_

A

M’s

18
Q

“Serum” Hep __ virus is part of the ___ virus family.
DNA is ___
It is enveloped/nonenveloped
icosahedral/non icosohedral?
Encodes for ____ ____
Produces large amounts of ___ particles in the serum.
Virus goes from ___ to ___ back to ___ (very weird)

Infectious virus serum is the ___ particle, a spherical particle.

Acute: if cell mediated response is sufficient, infected hepatocytes are cleared, resulting in acute disease, and lasting immunity.

Chronic: inadequate cell mediated response will trigger mild, chronic disease. Chronic disease leads to ___ or ___ carcinoma. Co-infection with ___ can exacerbate fulminate hepatitis.

A

“Serum” Hep __ virus is part of the ___ virus family.
DNA is ___
It is enveloped/nonenveloped
icosahedral/non icosohedral?
Encodes for ____ ____
Produces large amounts of ___ particles in the serum.
Virus goes from ___ to ___ back to ___ (very weird)

Infectious virus serum is the ___ particle, a spherical particle.

Acute: if cell mediated response is sufficient, infected hepatocytes are cleared, resulting in acute disease, and lasting immunity.

Chronic: inadequate cell mediated response will trigger mild, chronic disease. Chronic disease leads to ___ or ___ carcinoma. Co-infection with ___ can exacerbate fulminate hepatitis.

19
Q

Early effects of Hep B:
__ (joint pains), ___ and ___ (hives).
Chronic effects
___, ___, ___

A

Early effects of Hep B:
Arthalgia (joint pains), arthritis and urticaria (hives).
Chronic effects
glomerulonephritis, cryoglobulinemia, vasculitis

20
Q

“Post-transfusion” - Hep C:
It is part of the __ virus family
Enveloped?
dna/rna?
Synthesis of polyprotein requires ___. Relies on __ cell protease + __ ___ proteins.
Exceptionally __ __ RdRP. It has poor __ to __ exonuclease reading activity.

Transmission?
Body fluids, parenterally, needles

Control?
Blood and body fluid safeguards

Hep-C virus is a ____particle. It exists within a ___ ___ and binds to the __ uptake receptors on the ___. It can promote ___ and disrupt normal __ homeostasis.

The Hep C genome is translated into a polyprotein in the ____. The polyprotein is then cleaved by ___ ___. There is no ___ ___ tail.

The envelop is derived from the __ __.

Vaccination?

Outcomes of an acute HCV infection:
15% –>
15%–>
70% –>

From a persistent infection, 
40% --> 
6% --> 
4% -->
2% -->
A

“Post-transfusion” - Hep C:
It is part of the flavivirus family
Enveloped? Yes, enveloped
dna/rna? +ssRNA
Synthesis of polyprotein requires proease. Relies on host cell protease + 2 viral proteins.
Exceptionally error prone RdRP. It has poor 3’ to 5’ exonuclease proof reading activity.

Transmission?
Body fluids, parenteral, needles

Control?
Blood and body fluid safeguards

Hep-C virus is a lipoviro particle. It exists within a lipid droplet and binds to the lipid uptake receptors on the liver. It can promote steatosis and disrupt normal cholesterol homeostasis.

The Hep C genome is translated into a polyprotein in the ER. The polyprotein is then cleaved by host proteases. There is no poly A tail.

The envelop is derived from the cell membrane
Vaccination? None available

Outcomes of an acute HCV infection:
15% –> recovery and clearance
15%–> cirrhosis rapid onset
70% –> persistent infection

From a persistent infection, 
40% --> asymptomatic
6% --> liver failure
4% --> hepatocellular carcinoma
2% --> cirrhosis
21
Q

HCV:
Treatments:
No __ available
but IFN given with ___, a guanosine analog targets __ __. Direct-acting antivirals target ___ encoded proteins.

A

HCV:
Treatments:
No __ available
but IFN given with ribavirin, a guanosine analog targets RNA synthesis. Direct-acting antivirals target HCV-encoded proteins.

22
Q

Delta Agent Hep-D
__-like agent
circular, _ssRNA, and enveloped/nonenveloped
Envelope contains __ antigens.
Depends entirely on ___ virus.
Has ___ cellular RNA polymerases which contributes to the replication and expression of its ONE gene.
It has __ activity.

A 
Delta Agent Hep-D
virioid-like agent
circular, -ssRNA, and enveloped
Envelope contains Hep-B antigens. 
Depends entirely on Hep B virus. 
Has THREE cellular RNA polymerases which contributes to the replication and expression of its ONE gene. 
It has RdRP activity.
23
Q 
Hep E is part of the \_\_ viral family. 
Is it enveloped?
Where is it found?
Who is at risk?
How is it transmitted?
What type of genome?
It is self limiting?
A 
Hep E is part of the Hepe viral family. 
Is it enveloped? No
Where is it found? S. and E. Asia
Who is at risk? Women, who are pregnant in the third trimester. 20% die who get it.
How is it transmitted? fecal-orally
What type of genome? +ssRNA.
It is self limiting
24
Q

Which two Hep viruses cause chronic infection? Which two viruses can promote hepatocellular carcinoma?

A

B and C

25
Q
  • Induces by herpes viruses ABCDE + EBV, CMV, and yellow fever virus
  • Hep C is more common than Hep B which is more common than Hep A in US; Hep A and E are the only ones transmitted fecal-orally (vowels through the bowels)
  • Hep A (picornavirus): exceptionally stable, oral-fecal transmission through water or shellfish, food handlers and child workers at risk, HAV IgM in serum during acute infection
  • Hep B (Hepadnavirus): small partially dsDNA encoding RT, transmitted parenterally, through birth (chronic) or sex
  • HBsAg and HBV Abs cause early (joint pain and inflammation, uticaria) and late (GN, membranoproliferative GN, vasculitis, cryoglobulinemia) disease effects
  • 3 types of HBV in serum: infectious Dane particles (virions), filaments and spheres of HbsAg
  • “SPECIES” Ag and Ab for diagnostics: HbsAg first (acute and chronic), HbeAg next (high infectivity, replication), anti-HbcAg Ab is first Ab (Ags will be negative, window zone), followed by Ab response starting with anti-HbeAg Ab (low infectivity), anti-HbsAg Ab (recovered, immune)
  • Anti-core Abs against HBV can help distinguish acute (IgM) from chronic/recovered (IgG)
  • The release of large quantities of viral antigen into the serum is associated with active hep B infection, the apparent absence of serum Ab (b/c it’s bound to Ag), and immune complex deposition in tissue
  • Hep C (flavivirus): has 2 viral proteases and use 1 host protease, every error prone RNA pol, transmitted through body fluids and moves in/out of liver cells as lipid causing fatty liver & disrupting cholesterol, 70% will have persistent infection with most having chronic hepatitis leading to cirrhosis
  • HCV antiviral tx target NS3-protease w/ NS4 co-factor proteinase (-previr), NS5A replication and assembly cofactor (-asvir) or NS5B RNA pol (-buvir), but tx remains as IFN with Ribavirin
  • HCV is identified by the CDC as the most common blood-borne pathogen in the US
  • Hep D: responsible for 40% of fulimant hepatitis and uses HBsAg as envelope (co-infection leading to cirrhosis or more serious superinfection on top of existing HBV)
  • Hep E (): can be passed to fetus, 20% fatality in pregnant mothers
A
  • Induces by herpes viruses ABCDE + EBV, CMV, and yellow fever virus
  • Hep C is more common than Hep B which is more common than Hep A in US; Hep A and E are the only ones transmitted fecal-orally (vowels through the bowels)
  • Hep A (picornavirus): exceptionally stable, oral-fecal transmission through water or shellfish, food handlers and child workers at risk, HAV IgM in serum during acute infection
  • Hep B (Hepadnavirus): small partially dsDNA encoding RT, transmitted parenterally, through birth (chronic) or sex
  • HBsAg and HBV Abs cause early (joint pain and inflammation, uticaria) and late (GN, membranoproliferative GN, vasculitis, cryoglobulinemia) disease effects
  • 3 types of HBV in serum: infectious Dane particles (virions), filaments and spheres of HbsAg
  • “SPECIES” Ag and Ab for diagnostics: HbsAg first (acute and chronic), HbeAg next (high infectivity, replication), anti-HbcAg Ab is first Ab (Ags will be negative, window zone), followed by Ab response starting with anti-HbeAg Ab (low infectivity), anti-HbsAg Ab (recovered, immune)
  • Anti-core Abs against HBV can help distinguish acute (IgM) from chronic/recovered (IgG)
  • The release of large quantities of viral antigen into the serum is associated with active hep B infection, the apparent absence of serum Ab (b/c it’s bound to Ag), and immune complex deposition in tissue
  • Hep C (flavivirus): has 2 viral proteases and use 1 host protease, every error prone RNA pol, transmitted through body fluids and moves in/out of liver cells as lipid causing fatty liver & disrupting cholesterol, 70% will have persistent infection with most having chronic hepatitis leading to cirrhosis
  • HCV antiviral tx target NS3-protease w/ NS4 co-factor proteinase (-previr), NS5A replication and assembly cofactor (-asvir) or NS5B RNA pol (-buvir), but tx remains as IFN with Ribavirin
  • HCV is identified by the CDC as the most common blood-borne pathogen in the US
  • Hep D: responsible for 40% of fulimant hepatitis and uses HBsAg as envelope (co-infection leading to cirrhosis or more serious superinfection on top of existing HBV)
  • Hep E (calicivirus): can be passed to fetus, 20% fatality in pregnant mothers

CSP - Exam 4 (22 decks)

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