Brainscape's Knowledge GenomeTM

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


See full index

GI2 > Liver Dz > Flashcards

Liver Dz Flashcards

1
Q

liver damage Pathophysiology:

A

chronic injury damages liver lobules (collapse + lose function), causes formation of fibrous septa and hepatocyte regeneration w/nodule formation

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

Tests of Hepatic Synthesis:

A

Serum Albumin (14-21 days)

PT/PTT (hours) - better for acute

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

Tests of Hepatic Cellular Damage:

A

AST/SGOT/aspartate

ALT/SGPT/alanine

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

hepatocellular injury panel pattern

A

Increased ALT/AST +/- Bilirubin

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

cholestatic injury panel pattern

A

Increased Alk Phos +/- Bilirubin:

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

causes of hepatocellular injury (5)

A

Viral hepatitis

Drug/alcohol induced

Fatty Liver dz

Autoimmune

Metabolic causes (hemochromatosis, Wilson’s dz)

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

causes of cholestatic injury (6)

A 
Drugs/Medications
Liver Congestion
PSC
PBC
Sarcoidosis 
Infiltrative Liver dz
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

in-depth way to study liver fibrosis

A

liver biopsy

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

disadvantages of liver biopsy

A

Invasive

Complications (serious bleeding)

Susceptible to sampling error

Common that pts who need bx would have contraindications (INR >1.5, thrombocytopenia <50k)

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

non invasive liver studies

A

Used to stage fibrosis in chronic liver disease, used to determine if advanced fibrosis is present

Determines liver stiffness (elasticity and viscosity) via MRI or U/S

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

advantages of non invasive liver evals

A

non invasive

allows you to determine if fibrosis is present

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

ddx of jaundice

A

ESRD

Addison’s

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

causes of Unconjugated Hyperbilirubinemia

A

(BEFORE liver)
1.Over production of bilirubin

2.Decreased Hepatic uptake/conjugation

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

over production of bilirubin MC caused by + labs

A

hemolysis

INCREASED LDH, DECREASED HAPTOGLOBIN, INCREASED BILIRUBIN

unconjugated hyper

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

causes of decreased hepatic uptake/conjugation

A

drugs
hepatocellular disease
Gilbert’s syndrome

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

drugs that cause decreased hepatic uptake/conjugation

A

rifampin
radiocontrast agents
chloramphenicol

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

gilbert’s syndrome

A

genetic defect, male predominance

recurrent episodes of jaundice, worsened by over exertion/febrile illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

lab results of gilbert’s syndrome

A

elevated unconjugated bilirubin but normal AST/ALT and no hemolysis

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

conjugated hyperbilirubinemia causes

A
  1. impaired excretion

2. extra-hepatic billiard obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

causes of impaired bilirubin excretion (4)

A

hepatocellular disease
hepatitis
drug or pregnancy induced cholestasis
sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

causes of extra hepatic biliary obstruction

A

gallstones
tumors
biliary structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what do we use to determine severity of liver disease?

A

child Pugh

MELD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

child Pugh measures

A

measures encephalopathy, ascites, serum bilirubin, albumin PTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

MELD measures

A

bilirubin, CR, INR

score >25 = increased mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Hepatitis phases

A
  1. prodromal phase
  2. icteric phase
  3. convalescent phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

prodromal phase time length

A

abrupt in HAV

insidious in HBV or HCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

s.s of prodromal phase

A

Pain

GI symptoms (anorexia, nausea)

Skin (pruritus)

Fever

Systemic (fatigue, weakness)

URI symptoms (flu like)

Myalgia

28
Q

pain of hepatitis

A

(RUQ pain, severe to mild, radiate to back of epigastrium)

29
Q

icteric phase

A

5-10 days after prodrome

jaundice + worsening of prodromal symptoms

30
Q

convalescent phase

A

gradual return of appetite, disappearance of jaundice

abdominal pain and fatigue

31
Q

3 main signs of hepatitis

A

hepatomegaly
liver tenderness (RUQ)
jaundice

32
Q

lab values of hepatitis

A

Normal-Low WBC
Mild proteinuria and hyperbilirubinemia

Striking AST/ALT elevations, elevated bilirubin and alk phos

33
Q

hepatitis DDX:

A

other infectious disease, drug induced liver dz, ischemic hepatitis, autoimmune hepatitis, metastatic CA of liver

34
Q

hepatitis General Tx:

A

small meals

IV hydration

avoidance of strenuous exertion, EtOH and hepatotoxic agents

35
Q

Chronic Viral Hepatitis:

A

inflammation of the liver for 3-6 months

persistently elevated transaminases

gradually progressive damage

36
Q

toxins to AVOID in chronic hepatitis

A

NSAIDs, Alcohol, herbal medicine

37
Q

hepatitis A transmission

A

fecal oral, spread is facilitated by crowding and poor sanitation

  • contaminated water or food (undercooked shellfish)
38
Q

HAV incubation

A

30 days

excreted in feces for 2 weeks before clinical illness is apparent

39
Q

symptoms HAV

A

Illness is more severe in adults (children are typically asymptomatic)

SPIKING FEVERS

Fulminant hepatitis is rare, no carrier state and no chronic hepatitis A

40
Q

HAV Testing

A

Anti-HAV IgG and IgM Abs

-IgM persists for 3-6 months only, IgG persists for decades

41
Q

Prevention HAV

A

immun globulin w/in 30 days

vaccination

42
Q

HBV transmission

A

Infected blood or blood products, sexual contact or vertical transmission

Present in semen, saliva, vaginal fluid

43
Q

HBV high risk

A

IV drug users

health care workers

blood transfusions (esp. older pts)

44
Q

infants and HBV spreading

A

vertical (@ or before birth)

No prevention benefit via C-Section, started vax series

45
Q

HBV incubation

A

insidious onset (6 weeks-6 months)

46
Q

Chronic Hep B risk if you have HBV

A

Age at time of infection, inversely related to likelihood of developing chronic HBV

Persists in 5% of immunocompetent adults and more immunocompromised pts

47
Q

HBV testing

A

HBsAg - first serum marker for acute infection

HBeAg present for life of patient

48
Q

Chronic HBV

A

detectable HBV Ig in serum for 3 months

49
Q

chronic HBV tx candidates

A

Decompensated, compensated cirrhosis

High viral load and sustained ALT > 2x ULN

Prior immunosuppressive therapy

Prior to tx of HCV co-infection

Hepatocellular carcinoma

50
Q

tx of HBV

A

pegylated interferon SQ injection

seroconversion still common in 30-40% of patients

51
Q

Pts with HBV that gets serial ultrasounds to screen for HCC:

A

Asian men > 40

Asian women >50

Pts with HBV and cirrhosis

African and North American Blacks

Pts with family history of HCC

52
Q

Hep D infection

A

Only causes infection in presence of HBsAg present

53
Q

Hep D Prognosis:

A

Worse short-term prognosis if superinfection bc it is development of fulminant hepatitis

Chronic HDV has 3x higher risk of hepatocellular CA than chronic Hep B alone

54
Q

Hep C associated conditions

A 
Glomerulonephritis
autoimmune thyroiditis
monoclonal gammopathies
pulmonary fibrosis
T2DM
55
Q

Transmission of HCV

A

MC due to drug use

Infected blood, contaminated medical equipment

Transmitted via tattooing, sharing razors and acupuncture, common HIB co-infections

56
Q

clinical course of Acute Hep C

A

mild or asymptomatic w/waxing and waning ALT levels

70-85% of acute HCV in immunocompetent pts will become chronic, higher rate in immunocompromised

No immunity provided by antibodies

57
Q

chronic hep C (how many people and definition)

A

70-85% of acute HCV in immunocompetent pts become chronic

Detectable levels of HCV RNA in blood > 6 months after acute infection

58
Q

who gets chronic HCV tx

A

All patients with chronic HCV who are able to adhere to treatment protocol should be offered tx

59
Q

tx HCV goal

A

SVR: negative PCR test for HCV RNA 3 months after conclusion of therapy

60
Q

hep E

A
  • Waterborne hepatitis, rare in US

- High mortality rate in pregnant women, worsening of chronic liver disease

61
Q

mechanisms drugs cause liver injury

A

Directly hepatotoxic

Idiosyncratic reactions

Non-inflammatory cholestatic reactions

Inflammatory cholestatic reactions

Acute or chronic hepatitis

62
Q

how does estrogen cause liver damage?

A

non inflammatory cholestatic rxn

neoplasm

63
Q

how does augmentin cause liver damage?

A

Inflammatory cholestatic reactions

64
Q

how do glucocorticoids cause liver damage?

A

fatty liver

65
Q

how does methotrexate cause liver damage?

A

fibrosis and cirrhosis

GI2 (6 decks)

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