Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Pathophysiology > Liver Disorders > Flashcards

Liver Disorders Flashcards

Exam II

1
Q

Hepatitis pathophysiology

A

Inflammation triggers a fibrogenesis process, where hepatic stellate cells become activated and cause scarring, which leads to fibrosis

Fibrosis progresses through standardized stages and can lead to cirrhosis (advanced, irreversible fibrosis)

Regenerative nodules can produce dysplastic cells, causing hepatocellular carcinoma (HCC)

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

Two types of liver injury

A
  1. Hepatocellular injury
  2. Cholestatic injury (biliary tree)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Transaminases

A

AST and ALT

ALT is more specific for liver damage

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

IgM

A

Indicates an acute infection

M for “miserable”

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

IgG

A

Indicates a past exposure

G for “gone”

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

PCR testing

A

Looks for viral load

Always choose quantitative testing, not qualitative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Antibody testing

A

looking for immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Antigen testing

A

looking for virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hepatitis A presentation

A

Acute infectious hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hepatitis A transmission

A

Fecal-oral

HAV bile excretion with shedding in stool occurring 2 weeks prior to and 1 week after onset of sx/clinical illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hepatitis A pathophysiology

A

Viruses replicate and proliferate within the liver cells

  1. Hepatocyte viral uptake via a receptor on plasma cell membrane
  2. Viral replication within hepatocytes
  3. RNA is uncoated and ribosomes bind to form polysomes
  4. Viral proteins are synthesized
  5. Genome is copied by polymerase
  6. Assembled virus particles are shed into the biliary tree and excreted into feces

Hepatocellular injury leading to diffuse liver necrosis and portal triad membrane changes

Prominent centrilobular damage, increased portal cellularity, and regional lymph node enlargement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Impaired synthetic liver function

A

Decreased albumin
Prolonged PT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cholestasis

A

Injury to bile ducts causing leaking of bile into the blood stream

Causes jaundice and hyperbilirubinemia in more severe case

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

Hepatitis A vaccinations

A

Mandatory pediatric vaccinations and given for at risk populations (military, international travelers, people moving to endemic areas, illicit drug users, male homosexuals, institutionalized individuals)

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

Serum (HAV) immunoglobulin

A

Given to those exposed

Pre-exposure prophylaxis: ex. leaving too soon for travel for standard vaccine
( <2 week trip, >2 yo)

=Post-exposure prophylaxis:
(Up to 2 weeks post-exposure)

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

Hepatitis A incubation period

A

Incubation period of 28 days (15-50 range)

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

Hepatitis A symptoms

A

70% of infections in children <6 yo are asymptomatic

Most cases are symptomatic in adults and older children, with individuals normally only having flu-like symptoms and seeking care following jaundice presentation

		§ Fever
		§ Fatigue
		§ Loss of appetite
		§ N/V
		§ Abdominal px
		§ Dark urine
		§ Diarrhea
		§ Clay-colored stools
		§ Joint pain 
                    § Jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

HAV treatment

A

supportive measures

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

HAV Ab IgG

A

Chronic marker (past infection)

20
Q

HAV Ab IgM

A

acute marker (current infection)

21
Q

HAV Ab total

A

Assessing immune status, no concern for acute infection

(+) means previous exposure or vaccination (immunity)

22
Q

Hepatitis B presentation and natural hx

A

Acute and chronic infectious hepatitis

Adult infections: 95% of individuals clear the infection and develop lifelong immunity
Neonate: 90% chronicity
Children <6 yo: 25-50% chronicity

Acute HBV is a “common” form of acute hepatic failure

Can progress to Cirrhosis and HCC

23
Q

HBV pathophysiology

A

Following exposure to HBV, a cell-mediated immune response is triggered

HBV replicates in the cell nucleus (cccDNA), and virus is constantly being shed into the blood

  1. Attachment–virus binds to receptor
  2. Cytotoxic T cells and NKC are sent to the
    virus and release inflammatory cytokines
  3. Hepatocytes are attacked by the cytokines and infiltrated by HBV
  4. Penetration–viral membrane merges with the host cell membrane, then sends DNA and other proteins into the cell cytoplasm
  5. Uncoating–HBV uses RNA to replicate
  6. Assembly–virions are formed and returned to the nucleus where they are recycled and make additional virions
  7. Release–DNA is synthesized via reverse transcription and new virus is sent into the cytoplasm, then towards the cell membrane where it is released

Ground glass appearance under microscope

24
Q

HBV transmission

A

Blood-to-blood transmission

Mucosal contact with infected blood or body fluid (aka semen, saliva [contains some blood])

Perinatal infection is also common (maternal-fetal/vertical transmission)

Virus can survive for 7 days outside the body and still cause infection

25
Q

HBV risk factors

A

○ Hemodialysis (HD)
○ Blood transfusions (ask about hx of transfusions outside of the US)
○ Perinatal
○ Sexual
○ Household
○ Occupational
○ IV drug use
○ Nosocomial
○ UNK

26
Q

HBV vaccination

A

routine childhood vaccinations since 1982
( 95% effective at preventing infection and the development of chronic disease)

Vaccinate those at exposure risk and families of those with chronic disease

ex. Hemodialysis patients are at risk and will get “double dosed” with vaccine–different than the standard childhood vaccination

27
Q

HBV factors increasing cirrhosis risk

A

Host: >40 yo, Male sex, Immunocompromised

Viral: High serum HBV DNA (>2,000 IU/mL), Elevated ALT, Prolonged time to HBeAg serocoversion, Development of HBeAg neg CHB, Genotype C

Environmental: Concurrent viral infections (HIV, HCV, HDV), Heavy alcohol use, Metabolic syndrome

28
Q

HBV factors increasing HCC risk

A

Host: cirrhosis risks PLUS familial hx and born in sub-saharan africa

Viral: Cirrhosis risks PLUS presence of cirrhosis

Environmental: Cirrhosis risks PLUS aflatoxin and smoking

29
Q

Acute HBV symptoms

A

□ General illness
□ Loss of appetite
□ N/V
□ Body aches
□ Mild fever

□ Dark urine
□ Jaundice

30
Q

Acute HBV relevant history

A

Exposure to infected fluids/blood in the past few months

31
Q

Chronic HBV s/sx

A

Can be asymptomatic

Prodromal period (1-4 months):
Serum sickness
RUQ abdominal px 2/2 hepatomegaly
Fatigue
Joint px

Hepatosplenomegaly
Spider telangiectasias
Jaundice
Ascites
Peripheral edema

32
Q

Chronic HBV relevant history

A

Risk factor &/or serological testing + for 6 months

Tattoos, military vaccinations, etc.

33
Q

Acute HBV tx

A

Watch and wait

Oral meds are controversial as they are mostly used for chronic and there is not much data
(Treating viral replication; can develop resistance)

Transplantation

34
Q

Chronic HBV tx

A

When to treat:
Viremia (+ viral load >2,000 or 20,000 IU/mL)
FHx of HCC
>40 yo
ALT elevation >2x upper limit of normal (ULN)
Liver biopsy/non-invasive fibrosis measure showing advanced fibrosis or cirrhosis (F3 or F4)

Who not to treat:

Contradictions to interferon therapy:
SI, severe depression
Previous significant side effects (IFN retinopathy, etc.)
Autoimmune disease
Cytopenias
Severe cardiac disease
Uncontrolled seizures
Decompensated cirrhosis

Immune tolerant HBV (need close f/u q6 mo for reassessment)

Carriers (have low level of virus)

Pediatric and CKD oral med restrictions
(though some can be renally dose)

35
Q

Transplantation considerations

A

Suppress the virus if going to be transplanted

The new liver will be infected

Post transplantation immunosuppression

36
Q

HBsAg

A

First detectable viral antigen (protein on the surface of the HBV)

Marker of active (infectious) acute or chronic disease

Window period–may be (-)

37
Q

HBcAb Total

A

Core protein (from the nucleus)

Indicates ongoing or past infection
**NOT a marker for active disease

Remains (+) for life

38
Q

IgM anti-HBc

A

Acute infection marker

Helps r/o acute vs. chronic disease

Indicator of recent infection (<6 mo)

39
Q

HBsAb

A

Marker of immunity—the body has mounted an antibody to HBV

(+) following vaccination

Window period–may be negative

40
Q

HBeAg

A

Advanced testing during tx

A secreted product of the nucleocapsid gene of HBV that is chronic hepatitis B

Marker of active viral replication

Infectivity state?
Non-mutant strains?

41
Q

HBeAb

A

Advanced testing during tx

marker of seroconversion

42
Q

HBV DNA PCR quantitative

A

viral load testing

43
Q

Hepatitis C presentation

A

Primarily a chronic disease (one of the most common forms of chronic liver disease)

85% of cases result in chronic infection
15% of cases occur as acute hepatitis, with individuals mounting an immune response and clearing the virus (rare)

Acute disease is not often detected

44
Q

HCV transmission

A

Blood to blood

45
Q

HCV risk factors

A

HD
Transfusions
Perinatal
Nasal cocaine
Sexual?? Non-monogamy
Unregulated tattoos (non-single use only dye)
Nosocomial
IVDU

46
Q

HCV disease progression

A

2-22 week incubation period

Advanced Pathophysiology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions