DERS 03 - GIT Infections 1 Flashcards

1
Q

When is hepatitis considered acute or chronic?

A

Acute - <6 months

Chronic - >6 months

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2
Q

List and describe the different symptom phases for viral hepatitis.

A
  • Prodromal (pre-icteric) phase - fever, nausea, vomiting, loss of appetite, chronic fatigue, abdominal pain/swelling, leg/ankle swelling, easy bruising, itchy skin
  • Icteric (jaundice) phase - jaundice, bilirubinemia (dark urine color), and pale, bloody, or tar-colored stools
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3
Q

What are the key plasma levels to check for when determining the extent of liver injury or malfunction?

A
  • Liver injury
    • High aspartate amino transferase (AST)
    • High alanine amino transferase (ALT)
    • High LDH
    • High alkaline phosphatase (AP)
  • Liver Malfunction
    • Increased bilirubin (total, diret and indirect)
    • Decreased albumin
    • Increased prothrombin time (PT)
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4
Q

List the hepatitis viruses and routes in which they are usually transmitted.

A
  • Hep A & E - Enterically Transmitted (fecal-oral)
  • Hep B, C, D, & G - Parenterically Transmitted (needle sticks, sex, etc.)
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5
Q

Answer the following about Hepatitis A Virus (HAV):

  • Is it enveloped?
  • What shape is it?
  • What type of genome does it have?
  • How can it be inactivated?
A
  • Non-enveloped
  • Icosahedral
  • +ve ssRNA
  • Very stable, requires extended boiling or formaldehyde/chlorine treatment to be inactivated
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6
Q

Describe the life cycle of HAV from transmission to the end of replication.

A
  1. Binds receptors on hepatocytes and kupffer cells for entry
  2. Genome is uncoated in cytoplasm
  3. Host ribosomes translate viral RNA into a single polyprotein
  4. Polyprotein is cleaved by host proteases into several polypeptides, including RNA dependent RNA polymerase
  5. The viral RNA dependent RNA polymerase then synthesizes both +ve and -ve RNA strands
  6. The +ve strands are packaged and the virus exits the cell by lysis
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7
Q

Facts to know about HAV transmission

A
  • Transmitted via fecal-oral route
    • Often through consumption of contaminated food. Especially fish because of filter feeder concentration of the viral particles
  • Spreads very efficiently because:
    • the virus is often present in a persons stool (aka - viral shedding) before or in the absence of symptoms.
    • it is shed in high concentrations
    • It is extermely stable
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8
Q

Describe the basic pathogenesis of HAV

A
  1. Ingestion
  2. Replication in oropharynx/GIT
  3. Transportation to liver
  4. Shed in bile, which ends up in feces
  5. Cellular immune response leads to clinical symptoms
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9
Q

What are the usual clinical manifestations of HAV infections?

A
  • Typical hepatitis pre-icteric symptoms will abruptly appear 3-4 weeks (the incubation period) after initial exposure, and will intensify for 4-6 days before the icteric phase begins
  • The symptoms will gnerally lessen during the icteric phase with complete recovery in 99% of cases
  • Very rarely, fulminant hepatitis can develop
  • Chronic cases of HAV are practically never seen
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10
Q

How are lab diagnostics for HAV done?

A

Specific serologic tests:

  • anti-HAV IgM indicated acute infection
  • anti-HAV igG indicates previous infection
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11
Q

What treatment and prevention meds are available for HAV?

A
  • Prevention
    • inactivated vaccine
    • Sanitation/personal hygiene
  • Treatmetn
    • Immune serium globulin from previously infected people can be used in preventing clinical illness if given before or <2 wks after initial exposure
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12
Q

Facts to know about Hepatitis E Virus (HEV)

A

HEV is identical to HAV except:

  • Family, genus, and species
  • HEV has a higher mortality rate in pregnant women
  • Not really any treatment or vaccine. Ig prepared from donors has unknown efficacy.
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13
Q

Answer the following about Hepatitis C Virus (HCV):

  • Is it enveloped?
  • What shape is it?
  • What type of genome does it have?
A
  • Enveloped
  • Icosahedral
  • +ve ssRNA
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14
Q

Describe the HCV life cycle

A
  1. HCV particle circulate through blood by binding to LDLs and VLDLs
  2. Viral membrane proteins, particularly E1 and E2, bind to liver cell receptors and are endocytosed
  3. The endosome bursts in the cytoplasm
  4. Ribsomes translate one large polyprotein which is then cleaved into several polypeptides, including RNA dependent RNApol
  5. -ve and +ve sense RNA strands are synthesized and the +ve sense strands are packaged into a virus
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15
Q

Facts to know about HCV transmission and epidemiology

A
  • Humans are the reservoir and transmission is via blood
  • High occurrence in HIV patients with history of IV drug use
  • High incidence of chronic, asymptomatic infections
  • There are several different genotypes of HCV which are usually localized to different parts of the world. Treatment varies amongst the genotypes
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16
Q

Describe the pathogenesis of an HCV infection

A
  1. HCV replicates in hepatocytes, but is not cytotoxic
  2. Humoral and cellular immune responses kill infected hepatocytes and cause inflammation
  3. If the HCV becomes chronic, there is a high incidence of hepatocellular carcinoma (HCC) development
17
Q

Describe the symptom progression of an HCV infection

A

The percentages aren’t important

18
Q

Facts to know about HCV lab diagnostics

A
  • ELISA or RIBA (recombinant immunoblot assay) are used to detect anti-HCV antibodies
  • Seroconversion is 7-31 weeks after infection
  • RT-PCR used to detect viral genome

Chronic infection is established when liver enzymes, anti-HCV Abs, and HCV RNA are present for at least 6 months

19
Q

How is HCV infection prevented and treated?

A
  • Prevention
    • NO vaccine
    • Prophylactic Igs are not effective
    • Screen blood supply
    • Eliminate risky behavior
  • Treatment
    • Interferon
    • Antivirals-polymerase inhibitors (nucleoside/nucleotide analogs)
20
Q

Answer the following about Hepatitis G Virus (HAV):

  • What is it AKA?
  • Is it enveloped?
  • What type of genome does it have?
  • How is it transmitted?
A
  • GV virus
  • Enveloped
  • +ve ssRNA
  • Transmitted via blood and sexual contact
21
Q
A

E