Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

2H SystemicPatho Liver/ BILIARY TRACT > Chapter 18 –Liver: Infectious Disorders > Flashcards

Chapter 18 –Liver: Infectious Disorders Flashcards

1
Q

Inflammatory disorders of the liver dominate the clinical practice of hepatology.

Why?

A

This is partly
because virtually any insult to the liver can kill hepatocytes and recruit inflammatory cells, but
also because inflammatory diseases are frequently long-term chronic conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Among
inflammatory disordersof the liver, what is by far most frequent?

A

viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Systemic viral infections can involve the liver as in

A
  • (1) infectious mononucleosis (Epstein-Barr virus), which may cause a mild hepatitis during the acute phase;
  • (2) cytomegalovirus infection, particularly in the newborn or immunosuppressed patient; and
  • (3) yellow fever (yellow fever virus), which has been a major and serious cause of hepatitis in tropical countries.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Infrequently, in children and immunosuppressed patients, the liver is affected in the course of what?

A
  • rubella,
  • adenovirus,
  • herpesvirus, or
  • enterovirus infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is hepatitis?

A

However, unless otherwise specified, the

term viral hepatitis is applied for hepatic infections caused by a group of viruses known as
hepatotropic virus(hepatitis viruses A, B, C, D, and E) that have a particular affinity for the liver
( Table 18-4 ).

We first present the main features of each hepatotropic virus, followed by a
discussion of the clinicopathologic characteristics of acute and chronic viral hepatitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

TABLE 18-4 – The Hepatitis Viruses

Virus

A
  • Hepatitis A
  • Hepatitis B
  • Hepatitis C
  • Hepatitis D
  • Hepatitis E
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

TABLE 18-4 – The Hepatitis Viruses

Type of
virus

A
  • Hepatitis A:ssRNA
  • Hepatitis B:partially dsDNA
  • Hepatitis C: ssRNA
  • Hepatitis D: Circular defective ssRNA
  • Hepatitis E: ssRNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TABLE 18-4 – The Hepatitis Viruses

Viral family

A
  • Hepatitis A:Hepatovirus; related to picornavirus
  • Hepatitis B:Hepadnavirus
  • Hepatitis C: Flaviridae
  • Hepatitis D: Subviral particle in Deltaviridae family
  • Hepatitis E: Calicivirus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TABLE 18-4 – The Hepatitis Viruses

Route of
transmission

A
  • Hepatitis A:Fecal-oral (contaminated food or water)
  • Hepatitis B:Parenteral, sexual contract, perinatal
  • Hepatitis C:Parenteral; intranasal cocaine use is a risk factor
  • Hepatitis D: Parenteral
  • Hepatitis E: Fecal-oral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

TABLE 18-4 – The Hepatitis Viruses

Mean
incubation
period

A
  • Hepatitis A:2–4 weeks
  • Hepatitis B:1–4 months
  • Hepatitis C:7–8 weeks
  • Hepatitis D: Same as HBV
  • Hepatitis E: 4–5 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TABLE 18-4 – The Hepatitis Viruses

Frequency of chronic liver disease

A
  • Hepatitis A:Never
  • Hepatitis B:10%
  • Hepatitis C:∼80%
  • Hepatitis D: 5% (coinfection); ≤70% for superinfection
  • Hepatitis E: Never
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

TABLE 18-4 – The Hepatitis Viruses

Diagnosis

A
  • Hepatitis A:Detection of serum IgM antibodies
  • Hepatitis B:Detection of HBsAg or antibody to HBcAg
  • Hepatitis C:PCR for HCV RNA; 3rdgeneration ELISA for antibody detection
  • Hepatitis D: Detection of IgM and IgG antibodies; HDV RNA serum; HDAg in liver
  • Hepatitis E: PCR for HEV RNA; detection of serum IgM and IgG antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Hepatitis A?

A

Hepatitis A virus (HAV), the scourge of military campaigns since antiquity, is a benign, selflimited
disease with an incubation period of 3 to 6 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the clinical course of HAV?

A

HAV does not cause chronic hepatitis
or a carrier state and only rarely causes fulminant hepatitis, so the fatality rate associated with
HAV is about 0.1%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the epidemiology of HAV?

A

HAV occurs throughout the world and is endemic in countries with substandard hygiene and sanitation, where populations may have detectable antibodies to HAV by the age of 10 years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the clinical symptoms of

A

Clinical disease tends to be mild or asymptomatic, and is rare after childhood.

In developed countries, the prevalence of seropositivity (indicative of previous exposure) increases gradually with age, reaching 50% by age 50 years in the United States.

In this population acute HAV tends to be a sporadic febrile illness. Affected individuals have
nonspecific symptoms such as fatigue and loss of appetite, and often develop jaundice.

Overall, HAV accounts for about 25% of clinically evident acute hepatitis worldwide and an estimated
30,000 to 50,000 new cases per year in the United States.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the biology of HAV?

A
  • discovered in 1973, is a
  • small,
  • nonenveloped,
  • positive-strand RNA picornavirus that occupies its own genus, Hepatovirus.
  • icosahedral capsid
  • 27 nm in diameter and can be cultured in vitro.
  • The receptor for HAV is HAVcr-1, a 451–amino acid class I integralmembrane mucin-like glycoprotein of unknown normal function. [21]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

WHat is the MOT of HAV?

A

HAV is spread by ingestion of contaminated water and foods and is shed in the stool for 2 to 3 weeks before and 1 week after the onset of jaundice.

Thus, close personal contact with an infected individual or fecal-oral contamination during this period accounts for most cases and explains the outbreaks in institutional settings such as schools and nurseries, and the water-borne epidemics in places
where people live in overcrowded, unsanitary conditions.

HAV can also be detected in serum
and saliva.

Because HAV viremia is transient, blood-borne transmission of HAV occurs only rarely; therefore, donated blood is not specifically screened for this virus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In developed countries, sporadic infections of HAV is contracted by what?

A

may be contracted by the consumption of raw or steamed shellfish (oysters, mussels, clams), which concentrate the virus from seawater contaminated
with human sewage.

20
Q

What explains the result of outbreaks of HAV infections?

A

HAV is spread by
ingestion of contaminated water and foods and is shed in the stool for 2 to 3 weeks before and
1 week after the onset of jaundice.

Thus, _close personal contact with an infected individual or fecal-oral contamination during this period accounts for most cases and explains the outbreaks
in institutional settings such as schools and nurseries,_and the water-borne epidemics in places
where people live in overcrowded, unsanitary conditions.

Infected workers in the food industry may also be the source of outbreaks.

21
Q

What plays a key role in hepatocellular injury during HAV infection?

A

HAV itself does not seem to be cytopathic.

_Cellular immunity, particularly CD8+ T cells, plays a
key role in hepatocellular injury during HAV infection_

22
Q

When does specific Igm antibody against HAV appears in blood?

A
  • *at the onset of symptoms,** constituting a
  • *reliable marker of acute infection** ( Fig. 18-8 ).
23
Q

When does fecal shedding of the virus ends?

A
  • *IgM titer
    rises. **

The IgM response usually begins to decline in a few months and is followed by the appearance of IgG anti-HAV.

The latter persists for years, perhaps conferring lifelong immunity against reinfection by all strains of HAV.

However, there are no routinely available tests for IgG
anti-HAV. The presence of this antibody is inferred from the difference between total and IgM
anti-HAV. HAV vaccine, available since 1992, is effective in preventing infection

24
Q
A

FIGURE 18-8 The sequence of serologic markers in acute hepatitis A infection. HAV,
hepatitis A virus.

25
What can HBV produce?
* (1) **acute hepatitis** with **recovery and clearance of the virus,** * (2) **nonprogressive chronic hepatitis,** * (3) **progressive chronic disease** ending in **cirrhosis,** * (4) **fulminant hepatitis** with **massive liver necro**sis, and * (5) an **asymptomatic carrier state.**
26
HBVinduced chronic liver disease is an important precursor for the development of hepatocellular carcinoma. [24] T or F
True
27
FIGURE 18-9 Potential outcomes of hepatitis B infection in adults, with their approximate frequencies in the United States. * \*Recovery from acute hepatitis refers to complete recovery as well as latent infections with maintenance of T cell response. * \*\*Recovery from chronic hepatitis is indicated by negative test for HBsAg. * \*\*\*Healthy carrier state is indicated by positive HBsAg \>6 months; * HBeAg negative; serum HBV DNA \<10 5 copies/mL; persistently normal AST and ALT levels; absence of significant inflammation and necrosis on liver biopsy.
28
What is the epidemiology of HBV?
Liver disease due to HBV is an enormous global health problem. One third of the worldpopulation (2 billion people) have been infected with HBV, and 400 million people have chronicinfection. Seventy-five percent of all chronic carriers live in Asia and the Western Pacific rim. The global prevalence of chronic hepatitis B infection varies widely, from high (\>8%) in Africa, Asia, and the Western Pacific to intermediate (2% to 7%) in southern and eastern Europe to low (\<2%) in western Europe, North America, and Australia. As will be discussed later, the carrier rate is largely dictated by the age at infection, being the highest when infection occurs in children perinatally and the lowest when adults are infected. In the United States, incidence of HBV infection has dramatically decreased; there are now an estimated 46,000 new infections per year with about 5,000 acute symptomatic cases.
29
The carrier rate of HBV is largely dictated by what?
As will be discussed later, the carrier rate is **largely dictated by the age at infection,** being the **highest when infection occurs in children perinatally**and the**lowest when adults are infected.** In the United States, incidence of HBV infection has dramatically decreased; there are now an estimated 46,000 new infections per year with about 5,000 acute symptomatic cases.
30
What is the MOT of HBV?
The mode of transmission of HBV **varies with geographical areas**. * In**high prevalence regions of** **the world**, ***_perinatal transmission during childbirth_*** accounts for **90% of cases**. * In areas with **intermediate prevalence**, ***_horizontal transmission,_*** especially in early childhood, is the dominant mode of transmission. Such spread occurs through minor cuts and breaks in the skin or mucous membranes among children with close bodily contact. * In **low prevalenc**e areas such as the United States, **unprotected heterosexual or homosexual intercourse** and * *intravenous drug** **abuse** (sharing of needles and syringes) are the chief modes of spread. * The **incidence of transfusion-related spread** has dwindled greatly in recent years due to screening of donated blood and HBsAg and exclusion of paid blood donors.
31
What is the MOT of HBV in high prevalence regions?
**perinatal transmissio**n during childbirth accounts for 90% of cases.
32
What is the MOT of HBV in intermediate prevalence?
***_horizontal transmission_***, especially in early childhood, is the dominant mode of transmission. Such spread **occurs through minor cuts and breaks in the skin or mucous membranes among children with close bodily contact.**
33
What is the MOT of HBV in low prevalence areas such as the United States, ?
1. **unprotected heterosexual or homosexual intercourse** and 2. **intravenous drug abuse (sharing of needles and** syringes) are the chief modes of spread.
34
The incidence of transfusion-related spread has dwindled greatly in recent years due what?
to screening of donated blood and HBsAg and exclusion of paid blood donors.
35
What is the incubation period of HBV?
HBV has a prolonged incubation period **(4–26 weeks).** Unlike HAV, **HBV remains in the blood until and during active episodes of acute and chronic hepatitis.**
36
Which is mostly affected by acute HBV infection?
In the United States acute HBV infection mostly affects **adults.** Approximately 70% have mild or no symptoms and do not develop jaundice. The remaining 30% have nonspecific constitutional symptoms such as anorexia, fever, jaundice, and upper right quadrant pain. **In almost all cases the infection is selflimited and resolves without treatment.** Chronic disease rarely occurs in adults in non-endemic areas. Fulminant hepatitis is also rare, occurring in approximately 0.1 to 0.5% of cases.
37
HBV was first linked to hepatitis in the 1960s when Australia antigen (later known as HBV surface antigen) was identified. [25] What is the biology of HBV?
* Hepa**dn**aviridae, a family of DNA viruses that cause hepatitis in multiple animal species. * There are eight HBV genotypes with geographic distribution around the globe. * The mature HBV virion is a 42-nm, spherical **double-layered “Dane particle**” that has an outer surface envelope of protein, lipid, and carbohydrate enclosing an electron-dense, 28-nm, slightly hexagonal core. * The genome of HBV is a **partially double-stranded circular DNA** molecule having 3200 nucleotides ( Fig. 18-10 ). Mnemonics: HBV: **D**eadly! Hepa**D**na **D**ane particle **D**ouble standed **D**na
38
The HBV genome contains four open reading frames coding for:
* **• A nucleocapsid “core” protein** * • **Envelope glycoproteins (HBsAg, hepatitis B surface antigen)** * • **A polymerase (Pol)** * • **HBx protein**
39
What are the nucleocapsid "core" protein of HBV?
A nucleocapsid “core” protein **(HBcAg, hepatitis B core antigen) .**
40
HBV longer polypeptide transcript with a precore and core region, designated as what?
HBeAg (hepatitis B “e” antigen).
41
What directs the HBeAg polypeptide toward secretion into blood?
Th**e precore region** directs the HBeAg polypeptide toward secretion into blood, whereas *_HBcAg remains in hepatocytes_* for the assembly of complete virions.
42
``` Envelope glycoproteins (HBsAg, hepatitis B surface antigen), which consist of three related proteins: ```
1. large HBsAg (containing Pre-S1, Pre-S2, and S), 2. middle HBsAg (containing Pre-S2 and S), and 3. small HBsAg (containing S only). Infected hepatocytes are capable of synthesizing and secreting massive quantities of noninfective surface protein (mainly small HBsAg).
43
What is the function of A polymerase (Pol) in HBV genome?
exhibits **both DNA polymerase activity** and **reverse transcriptase activity.** Genomic replication occurs via an intermediate RNA template, through a unique replication cycle: **DNA ➙ RNA ➙ DNA.**
44
Wha is the uniqiue genomic replication of HBV?
Genomic replication occurs via an intermediate RNA template, through a unique replication cycle: ## Footnote **DNA ➙ RNA ➙ DNA.**
45
What is the importance of the HBx protein in the HBV genome?
HBx protein, which is **necessary for virus replication** and may **act as a transcriptional transactivator** of the viral genes and a wide variety of host genes. It ha**s been implicated in the pathogenesis of liver cancer in HBV infection.**
46
What genonme has been implicated in the **pathogenesis of liver cancer in HBV infection.**
HBxI

2H SystemicPatho Liver/ BILIARY TRACT (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions