Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Advanced Pathophysiology > Liver Disorders > Flashcards

Liver Disorders Flashcards

Exam II (46 cards)

Start Studying
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

Study These Flashcards
A

Chronic marker (past infection)

20
Q

HAV Ab IgM

Study These Flashcards
A

acute marker (current infection)

21
Q

HAV Ab total

Study These Flashcards
A

Assessing immune status, no concern for acute infection

(+) means previous exposure or vaccination (immunity)

22
Q

Hepatitis B presentation and natural hx

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
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
HBV risk factors
○ Hemodialysis (HD) ○ Blood transfusions (ask about hx of transfusions outside of the US) ○ Perinatal ○ Sexual ○ Household ○ Occupational ○ IV drug use ○ Nosocomial ○ UNK
26
HBV vaccination
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
HBV factors increasing cirrhosis risk
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
HBV factors increasing HCC risk
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
Acute HBV symptoms
□ General illness □ Loss of appetite □ N/V □ Body aches □ Mild fever □ Dark urine □ Jaundice
30
Acute HBV relevant history
Exposure to infected fluids/blood in the past few months
31
Chronic HBV s/sx
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
Chronic HBV relevant history
Risk factor &/or serological testing + for 6 months Tattoos, military vaccinations, etc.
33
Acute HBV tx
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
Chronic HBV tx
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
Transplantation considerations
Suppress the virus if going to be transplanted The new liver will be infected Post transplantation immunosuppression
36
HBsAg
First detectable viral antigen (protein on the surface of the HBV) Marker of active (infectious) acute or chronic disease Window period--may be (-)
37
HBcAb Total
Core protein (from the nucleus) Indicates ongoing or past infection **NOT a marker for active disease Remains (+) for life
38
IgM anti-HBc
Acute infection marker Helps r/o acute vs. chronic disease Indicator of recent infection (<6 mo)
39
HBsAb
Marker of immunity---the body has mounted an antibody to HBV (+) following vaccination Window period--may be negative
40
HBeAg
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
HBeAb
Advanced testing during tx marker of seroconversion
42
HBV DNA PCR quantitative
viral load testing
43
Hepatitis C presentation
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
HCV transmission
Blood to blood
45
HCV risk factors
HD Transfusions Perinatal Nasal cocaine Sexual?? Non-monogamy Unregulated tattoos (non-single use only dye) Nosocomial IVDU
46
HCV disease progression
2-22 week incubation period

Advanced Pathophysiology (6 decks)

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