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Flashcards in Liver Dz Deck (65):
1

liver damage Pathophysiology:

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

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Tests of Hepatic Synthesis:

Serum Albumin (14-21 days)

PT/PTT (hours) - better for acute

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Tests of Hepatic Cellular Damage:

AST/SGOT/aspartate

ALT/SGPT/alanine

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hepatocellular injury panel pattern


Increased ALT/AST +/- Bilirubin

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cholestatic injury panel pattern

Increased Alk Phos +/- Bilirubin:

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causes of hepatocellular injury (5)

Viral hepatitis

Drug/alcohol induced

Fatty Liver dz

Autoimmune

Metabolic causes (hemochromatosis, Wilson’s dz)

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causes of cholestatic injury (6)

Drugs/Medications
Liver Congestion
PSC
PBC
Sarcoidosis
Infiltrative Liver dz

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in-depth way to study liver fibrosis

liver biopsy

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disadvantages of liver biopsy

Invasive

Complications (serious bleeding)

Susceptible to sampling error

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

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non invasive liver studies

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

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advantages of non invasive liver evals

non invasive

allows you to determine if fibrosis is present

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ddx of jaundice

ESRD
Addison's

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causes of Unconjugated Hyperbilirubinemia

(BEFORE liver)
1.Over production of bilirubin

2.Decreased Hepatic uptake/conjugation

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over production of bilirubin MC caused by + labs

hemolysis

INCREASED LDH, DECREASED HAPTOGLOBIN, INCREASED BILIRUBIN

unconjugated hyper

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causes of decreased hepatic uptake/conjugation

drugs
hepatocellular disease
Gilbert's syndrome

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drugs that cause decreased hepatic uptake/conjugation

rifampin
radiocontrast agents
chloramphenicol

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gilbert's syndrome

genetic defect, male predominance

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

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lab results of gilbert's syndrome

elevated unconjugated bilirubin but normal AST/ALT and no hemolysis

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conjugated hyperbilirubinemia causes

1. impaired excretion
2. extra-hepatic billiard obstruction

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causes of impaired bilirubin excretion (4)

hepatocellular disease
hepatitis
drug or pregnancy induced cholestasis
sepsis

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causes of extra hepatic biliary obstruction

gallstones
tumors
biliary structures

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what do we use to determine severity of liver disease?

child Pugh
MELD

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child Pugh measures

measures encephalopathy, ascites, serum bilirubin, albumin PTT

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MELD measures

bilirubin, CR, INR

score >25 = increased mortality

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Hepatitis phases

1. prodromal phase
2. icteric phase
3. convalescent phase

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prodromal phase time length

abrupt in HAV

insidious in HBV or HCV

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s.s of prodromal phase

Pain

GI symptoms (anorexia, nausea)

Skin (pruritus)

Fever

Systemic (fatigue, weakness)

URI symptoms (flu like)

Myalgia

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pain of hepatitis

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

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icteric phase

5-10 days after prodrome

jaundice + worsening of prodromal symptoms

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convalescent phase

gradual return of appetite, disappearance of jaundice

abdominal pain and fatigue

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3 main signs of hepatitis

hepatomegaly
liver tenderness (RUQ)
jaundice

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lab values of hepatitis

Normal-Low WBC
Mild proteinuria and hyperbilirubinemia

Striking AST/ALT elevations, elevated bilirubin and alk phos

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hepatitis DDX:

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

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hepatitis General Tx:

small meals

IV hydration

avoidance of strenuous exertion, EtOH and hepatotoxic agents

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Chronic Viral Hepatitis:

inflammation of the liver for 3-6 months

persistently elevated transaminases

gradually progressive damage

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toxins to AVOID in chronic hepatitis

NSAIDs, Alcohol, herbal medicine

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hepatitis A transmission

fecal oral, spread is facilitated by crowding and poor sanitation

* contaminated water or food (undercooked shellfish)

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HAV incubation

30 days

excreted in feces for 2 weeks before clinical illness is apparent

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symptoms HAV

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

SPIKING FEVERS

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

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HAV Testing

Anti-HAV IgG and IgM Abs

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

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Prevention HAV

immun globulin w/in 30 days

vaccination

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HBV transmission

Infected blood or blood products, sexual contact or vertical transmission

Present in semen, saliva, vaginal fluid

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HBV high risk

IV drug users

health care workers

blood transfusions (esp. older pts)

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infants and HBV spreading

vertical (@ or before birth)

No prevention benefit via C-Section, started vax series

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HBV incubation

insidious onset (6 weeks-6 months)

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Chronic Hep B risk if you have HBV

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

Persists in 5% of immunocompetent adults and more immunocompromised pts

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HBV testing

HBsAg - first serum marker for acute infection

HBeAg present for life of patient

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Chronic HBV

detectable HBV Ig in serum for 3 months

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chronic HBV tx candidates

Decompensated, compensated cirrhosis

High viral load and sustained ALT > 2x ULN

Prior immunosuppressive therapy

Prior to tx of HCV co-infection

Hepatocellular carcinoma

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tx of HBV

pegylated interferon SQ injection

seroconversion still common in 30-40% of patients

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

Asian men > 40

Asian women >50

Pts with HBV and cirrhosis

African and North American Blacks

Pts with family history of HCC

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Hep D infection

Only causes infection in presence of HBsAg present

53

Hep D Prognosis:

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

Hep C associated conditions

Glomerulonephritis
autoimmune thyroiditis
monoclonal gammopathies
pulmonary fibrosis
T2DM

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Transmission of HCV

MC due to drug use

Infected blood, contaminated medical equipment

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

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clinical course of Acute Hep C

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

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chronic hep C (how many people and definition)

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

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

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who gets chronic HCV tx

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

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tx HCV goal

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

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hep E

- Waterborne hepatitis, rare in US
- High mortality rate in pregnant women, worsening of chronic liver disease

61

mechanisms drugs cause liver injury

Directly hepatotoxic

Idiosyncratic reactions

Non-inflammatory cholestatic reactions

Inflammatory cholestatic reactions

Acute or chronic hepatitis

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how does estrogen cause liver damage?

non inflammatory cholestatic rxn

neoplasm

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how does augmentin cause liver damage?

Inflammatory cholestatic reactions

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how do glucocorticoids cause liver damage?

fatty liver

65

how does methotrexate cause liver damage?

fibrosis and cirrhosis