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Foundations III-GI > Liver > Flashcards

Liver Flashcards

1
Q

What is acute liver failure?

A

onset of liver injury, hepatic encephalopathy, & coagulopathy (INR > 1.5) in patients with no prior hx of liver disease

rapid decline of liver func.

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2
Q

MCC of liver acute liver failure?

A

Tylenol OF

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3
Q

s/s of acute liver failure?

A

AMS (early: personality change > lethargy> coma)

Cerebral Edema

Coagulopathy

Multiple Organ Failure

Ascites and anasarca

Serial Physical Exams: shrinking liver

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4
Q

Clinical features of acute v. subacute hepatic failure?

A

Encephalopathy develops within 1- 4 weeks of onset of liver injury

Encephalopathy develops 12- 24 weeks after onset of liver injury

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5
Q

lab findings in acute liver failure?

A

Severe coagulopathy ( increased PT/INR)

CBC: leukocytosis

BMP: hyponatremia, hypokalemia, hypoglycemia

LFTs: marked elevation of bilirubin, ALT, AST

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6
Q

Tx of acute liver failure?

A

Admit: transfer to a liver transplant center

Continuous monitoring and supportive care

Await spontaneous resolution

If recovery seems unlikely: prepare for liver transplantation

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7
Q

What is hepatitis? MCC?

A

Acute or chronic hepatocellular damage

lots of causes

MCC acute &chronic: viral

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8
Q

How are Hepatitis A& E transmitted?

A

by fecal-oral route, do not cause chronic infection

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9
Q

How are viral Hep B,C & D transmitted?

A

transmitted parenterally or via mucous membrane contact, can progress to chronic infection

hx: IVDA, tattoos, infx mother, blood transfusion

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10
Q

What are the dif. categories of acute hepatitis?

A

self limited (HAV, HEV)

acute liver failure

cholestatic hep (HAV)

Relapsing hep (HAV)

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11
Q

patho of acute viral hep?

A

Cell-mediated immune mechanisms hepatocyte injury (degeneration and apoptosis)

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12
Q

s/s of self limited acute viral hep?

A

asxs-> lots

prodromal: GI sxs, flu like sxs, abrupt onset in HAV & HEV

Then: jaundice, pruritis

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13
Q

PE findings in acute self limited hep?

A

Mild enlargement/slight tenderness of liver

Mild splenomegaly and posterior cervical lymphadenopathy

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14
Q

s/s of acute cholestatic viral hep?

A

Severe jaundice for several months

Prominent pruritis

Persistent anorexia and diarrhea (small percentage of patients)

Excellent px for complete recovery

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15
Q

s/s of relapsing acute hepatitis?

A

Sxs recur weeks – months after improvement/apparent recovery

Arthritis, vasculitis, and cryoglobulinemia (excess proteins/cryglobulins in the blood) may be seen

Px is excellent for eventual complete recovery ( may have multiple relapses)

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16
Q

lab findings in self limited acute viral hepatitis?

A

ALT & AST > 500 units/L, ALT>AST

Total bilirubin: norm

Alkaline phos: normal to mild elevation

Prolonged PT/INR: normal to mild elevation

Albumin: normal to mild decrease

CBC: +/- mild leukopenia
Possible lymphocytosis

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17
Q

Labs seen in cholestatic viral hep?

A

Bilirubin ≥20 mg/dL

Elevation of alkaline phos

Initial elevation of ALT/AST may decrease despite persistent cholestasis

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18
Q

labs seen in relapsing viral hepatitis?

A

Elevation of ALT, AST, Bilirubin recurs after normalization

Usually relapses do not exceed previous levels

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19
Q

Tx for self limited and relapsing acute hepatitis?

A

Outpt unless severe dehydration

Adequate POs

No etoh

Rest

DC non-essential drugs

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20
Q

Pharm tx for self limited and relapsing acute hepatitis

A

HAV, HEV, HDV – no specific drug treatment

HCV – if spontaneous resolution does not occur in 3 months use oral antiviral as per chronic HCV tx guidelines

HBV – tenofovir or entecavir only indicated in severe cases

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21
Q

25

A

25

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22
Q

Risk factors for Hep A?

A

living in endemic region
High prevalence areas = Africa and parts of Asia and Latin America

close personal contact with an infx person

men who have sex with men

known foodborne outbreak

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23
Q

s/s of Hep A?

A

Incubation: ~28 days

preicteric phase 5-7 d > Fever likely to occur with HAV

icteric phase Jaundice peaks typically at 2 weeks

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24
Q

Dx tests for Hep A?

A

IgM Antibody to HAV (Anti-HAV)
-detected 5-10 days before sxs onset and stay for 3-6mo

IgM is replaced with IgG anti-HAV
-stays helpful for life

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25
Q

Tx for Hep A?

A

supportive

nearly all recovered in 6 months

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26
Q

Pt Ed for Hep A?

A

good handwashing, disposal of wastes

careful food handling

Immunizations: HAV vaccination

Avoid Tylenol and ETOH

children should stay home for 1 wk

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27
Q

Hep A post-exposure prophylaxis?

A

for anyone recently exposed?

give ASAP, within 2 wks

Healthy persons 12mos – 40 yo: HAV vaccine

> 40yo, <12 mos., chronic liver disease, immunocompromised: Immune globulin

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28
Q

Epidemiology of Hep E?

A

Highly endemic in Mexico, Cuba, Asia, Africa, and the Middle East

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29
Q

How is Hep E transmitted?

A

Can be spread by animals, most commonly swine

Contaminated drinking water is common source of infection

Consumption of undercooked pork, deer meat, shellfish

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30
Q

Clinical features of Hep E?

A

Abrupt onset of prodromal sxs

Acute liver failure occurs in high frequency (10-20%) in pregnant women with HEV (especially in 3rd trimester)

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31
Q

Dx of Hep E?

A

IgM Anti-HEV detectable for at least 6 wks (usu. first few months)

IgM is replaced with IgG Anti-HEV which is usually only detectable for 12 – 20 mos

HEV RNA test confirms and quantifies presence of HEV

  • stool sample
  • good for immunocompromised
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32
Q

Prevention of Hep E?

A

NO vaccine in US, no immune globulin

  • good sanitation
  • avoid unpurified water
  • avoid raw pork and venison
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33
Q

What are the blood-borne hepatits?

A

HBV, HDV, HCV

Linked to chronic liver disease

Associated with persistent viremia

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34
Q

What is HBV?

A

DNA virus transmitted by percutaneous and permucosal routes
sexually transmitted disease

may result in a self-limited disease requiring no treatment

may also result in chronically infx state

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35
Q

Characteristics of HBV infx?

A

neonates: asxs, most chronic carries
adult: asxs, some have sxs icteric hepatitis

10-30% risk of developing cirrhosis

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36
Q

Patho of HBV?

A

Most of the liver injury occurs due to the host immune response to HBV, a cell-mediated response against HBcAg

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37
Q

What are some sig. risk factors for Hep B?

A

infant born to an HBV-infected mother

Multiple sexual partners

MSM

IVDA

Asian, eastern European, or African ancestry

FHx of HBV and/or chronic liver disease

FHx HCC

Household contact with HBV

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38
Q

Dx of HBV?

A

70% have norm PE

Acute:

  • elevated ALT
  • HBsAg and Anti-HBc

Prior HBV:
-Anti-HBs, IgG anti-HBc, Anti HBe

Chronic:

  • HBsAg >6 mo
  • Persistence of HBeAg & HBV DNA

Inactive carries:
asxs, normal ALT, low level HBV DNA, anti-HBe, negligible infectivity

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39
Q

acute s/s of HBV?

A 
Fever/chills 
Malaise
Maculopapular or urticarial rash 
Nausea/vomiting 
Arthralgia/arthritis
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40
Q

Tx of HBV?

A

Acute – self-limiting

Fulminant – liver transplant

Chronic – anti-viral therapy, liver bx, refer to hepatology

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41
Q

Tx options for chronic Hep B?

A

Peginterferon alfa-2a– anti-viral, weekly SQ injections for 48 wks
-For: young, non-cirrhotic, low HBV DNA level

Nuceloside analogues– inhibit HBV replication, daily po, may require indefinite therapy

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42
Q

Goals for anti-viral HBV therapy?

A

Primary: sustained low or undetectable HBV DNA

Secondary: seroconvert HBeAg and HBsAg and normalize ALT

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43
Q

When dx-ing Hep B, what else should you r/o?

A

HIV

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44
Q

What types of Hepatitis vaccinations for we have?

A

A and B

Hep B: recombinant inactive HBsAg at birth and 6 mo

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45
Q

What other prevention options are there?

A

Hep B immune globulin (post exposure prophylaxis, new borns of + moms)

those with HBV: avoid heavy ETOH, barrier protection during sex, cover open cuts/scratches, no blood/organ/semen donations

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46
Q

Presentation of Hep B?

A

Most asxs, although some will present with complications such as cirrhosis, hepatocellular carcinoma, or liver failure.

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47
Q

What is HDV?

A

A defective RNA virus that requires presence of HBV, specifically only in the presence of HBsAg

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48
Q

When should you suspect HDV?

A

Fulminant HBV infection

Acute HBV infection that improves and then relapses

Progressive chronic HBV without active HBV replication

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49
Q

Labs for HDV?

A

anti-HDV, HDV RNA

Acute vs chronic: IgM and IgG anti-HBc

IgM Anti-HBc = co-infection

IgG Anti-HBc = HDV superinfection

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50
Q

Tx for HDV?

A

High dose interferon alpha and PEG IFN only approved treatments for chronic disease

Therapy is not optimal (high risk of relapse), better regimes are under investigation

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51
Q

What is HepC?

A

An infectious, hepatotropic virus belonging to the Flavivirus family

ss-enveloped RNA virus

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52
Q

USPSTF screening recommendations for Hep C?

A

high risk groups

all people born between the years of 1945 and 1965, regardless of perceived risk

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53
Q

Presentation of HCV?

A

Acute infection (self-limited in 15-45% of cases): Almost all patients develop a vigorous antibody and cell-mediated immune response

Persistent viremia: accompanied by variable degrees of hepatic inflammation and fibrosis over time

chronic infections

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54
Q

What can accelerate liver cirrhosis in HCV?

A

chronic alcohol consumption

coincidental viral infections

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55
Q

What is the main HCV genotype seen in the US, Western Europe and Japan?

A

Genotype 1

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56
Q

How is Hep C transmitted?

A

transmitted by any percutaneous blood exposure

MCly around IVDA

less freq: sexual activity, perinatally, after accidental blood contact

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57
Q

RF for HCV?

A

IVDA, blood transfusion (before 1992), HIV

58
Q

Presentation of HCV?

A

most asxs

Prodromal/jaudice sxs

young women: many clr virus

majority will dvelop chronic infx

African Americans: less likely to spontaneously clear

59
Q

Acute HCV infx tests?

A

hepatitis C antibody (Anti- HCV)- several wks after exposure

HCV RNA testing is needed to diagnose acute infection

Others:
Human interleukin-28B (IL28B) genotype CC: more frequent spontaneous resolution

IL28B genotypes CT and TT: less frequent spontaneous resolution

60
Q

Time period for acute HCV testing?

A

HCV RNA detectable days from exposure – 8 wks after

ALT and AST elevated 6 -12 weeks from exposure

Anti-HCV detectable 8 weeks – several months

61
Q

Dx of chronic Hep C?

A

detection of HCV RNA in the blood for at least 6 mos

usually asxs

62
Q

What are some factors that influence the development of chronic/ progressive liver disease?

A

older

male

Concurrent chronic hepatitis B

HIV infection

high alcohol intake

63
Q

Tests for chronic HCV?

A

EIA detects antibodies against the virus

(+) = presence of active infx

Qualitative studies used to confirm viremia, generally low limits of detection

Quantitative tests give wide dynamic range of viral loads

64
Q

Work up for HCV?

A

Confirm HCV viremia (Quantitative)

Eval for co-existent liver disease and HIV

Vaccinate for HAV / HBV

Obtain viral genotype

Consider co-existent cirrhosis

Eval for ongoing substance use

Discuss transmission to spouse/sexual partners

65
Q

Why do you care about genotype for HCV?

A

helps to determine tx type

66
Q

Goal of Hep C antiviral tx?

A

clr virus

stabilize

sxs control

prevent comps of progressive liver disease

if already cirrhotic: clr virus before transplant

67
Q

Pharm tx for Hep C?

A

antiviral therapy

1st Line: Sofosbuvir (new)
-NS5B polymerase inhibitors

usually Sofosbuvir + some other antiviral

68
Q

What information determines tx regimen for Hep C?

A

HCV genotype

Has the patient been treated before?

Does the patient have cirrhosis?

69
Q

HCV chronic infx response to tx?

A

RVR (rapid viral response): HCV RNA undetectable by wk 4 of trx

EOT (end of tx response): HCV RNA undetectable at the end of treatment

**SVR (sustainedvirologic response): undetectable HCV RNA at 12 wks after treatment completion

Nonresponse: failure to attain undetectable HCV RNA at any point during therapy

Relapse: EOT response followed by return of HCV RNA after completion of treatment

70
Q

Factors that reduce likelihood of attaining HCV SVR?

A

Cirrhosis

Previous nonresponse to interferon therapy

HCV genotype 3

If Yes –> tx extended to 24 wks, adding Ribavirin

71
Q

What is Drug-induced Liver Injury (DILI)/
Toxic Hepatitis?

A

one of the MCC of elevated LFTs

greater incidence in older pts

72
Q

What drugs commonly cause drug induced liver injury?

A

Antimicrobials (46%)

CNS Agents

Immunomodulating agents

Analgesics

Lipid-lowering agents

LOTS more

73
Q

Presentation of DILI?

A

subclinical LFT elevation –> acute liver failure

May develop in days or within several wks of substance ingestion

Liver labs may reveal: hepatoxic injury, cholestatic, or mixed

74
Q

Dx of DILI?

A

hx of patient consuming a causative drug or toxin

Exclude other causes of liver disease

75
Q

Tx of DILI?

A

Remove causative agent and monitor for resolution of liver injury

In severe cases of Acute Liver Failure – liver transplantation may be required

76
Q

What is the MCC of ALF from DILI?

A

OD of Tylenol

toxic dose: 10-20g (lower in alcoholics or pts w/ liver disease)

77
Q

Presentation of toxic ingestion of Acetaminophen?

A

30mins – 24 hrs after ingestion: GI sxs

2 days after: R sided abd pain & oliguira, elevated LFTs and prolonged PT/INR

3-5 days after: hepatic necrosis with elevated aminotransferases, renal failure in 20% of cases, ALF in 30% of cases

5-10 days after: recovery phase

78
Q

What can indicate likelihood of death/need for liver transplant after Tylenol OD?

A

pH lower than 7.3

Stage 3-4 encephalopathy with PT/INR > 6.5 and Cr >3.4

Factor V level of 10% or less

79
Q

Management of toxic Tylenol ingestion?

A

Obtain serum acetaminophen level

IV N-acetylcysteine (NAC) for serial doses

Charcoal can be used if it is within 1 hr of ingestion

Gastric lavage can be used within 4 hrs of ingestion

80
Q

Spectrum of alcoholic liver disease?

A

Steatosis (fatty liver)

Steatohepatitis (alcoholic hepatitis)

Cirrhosis (predominate fibrogensis/scarring)

due to: chronic/excessive alcohol intake

81
Q

Clinical features of alcoholic liver disease?

A

asxs-advanced liver failure

Portal hypertension can occur in alcoholic hepatitis without cirrhosis

Other sxs: fever, anorexia, nausea, RUQ pain, tender hepatomegaly, jaundice

82
Q

Labs seen in alcoholic liver disease?

A

AST is usually elevated (usually not above 300)

AST > ALT, usually by a factor of 2 or more.

Alk Phos…increased

+/- other LFTs elevated

High TGs

Low: Potassium, phosphate, magnesium

High glucose

83
Q

Dx of alcoholic liver disease? Tx?

A

hx alcohol abuse

exclude other liver disease

liver bx

Abstinence!

84
Q

What can be used to dx short term px w/ worsening alcohol hepatitis?

A

Maddrey’s discrimination function (DF)

DF = 4.6 x (the difference between the patient’s and control prothrombin time) + serum bilirubin

> 32 = 50% mortality

85
Q

Management of acute worsening of alcoholic hepatitis?

A

Alcohol Abstinence!

sufficient carbs/calories

Nutrional support

Admin micronutrients

Methoprenisone DF >32

Pentoxifylline

86
Q

What is included in Nonalcoholic Fatty Liver Disease (NAFLD)?

A

Hepatic steatosis

Non-alcoholic steatohepatitis(NASH)

87
Q

What is Hepatic Steatosis?

A

accumulation of triglyceride droplets in hepatocytes

If no significant inflammation or fibrosis on bx = benign condition

88
Q

What is NASH?

A

necroinflammatory changes on liver bx, may progress to cirrhosis

Pathogenesis: lipotoxic injury to hepatocytes

89
Q

RF for NASH?

A

Insulin resistance

Obesity

DM2

Lipid abnormalities

Medications such Tamoxifen and corticosteroids

90
Q

Presentation of NAFLD and NASH?

A

usually asxs, +/- RUQ pain

elevated aminotransferase levels and/or hepatomegaly

bx needed

91
Q

Tx NASH?

A

lifestyle changes:

Weight loss
dietary fat restriction
exercise

92
Q

What is autoimmune hepatitis?

A

Usually young to middle-aged women

Chronic hepatitis with high serum globulins and characteristic liver histology.

Positive antinuclear antibody (ANA) and/or smooth muscle antibody in most common type

93
Q

Autoimmune hepatitis responds to…

A

corticosteroids

94
Q

s/s of autoimmune hepatitis?

A

onset is usually insidious

If sxs/signs do occur, may include fatigue, jaundice, and/or hepatomegaly

May present as acutely severe/fulminant

95
Q

Labs seen in autoimmune hepatitis?

A

Serum aminotransferase levels may be > 1000

total bilirubin is usually increased

Alkaline phos: usually elevated

Serum gamma-globulin levels are typically elevated

Auto abs (need at least 1: ANA or smooth muscle abs, auto abs to soluble liver antigen, Anti-LMKK1)

+/- elevated serum gamma globulin

liver bx: dx, eval severity

96
Q

Tx of autoimmune hepatitis?

A

Prednisone with or without azathioprine improves symptoms

97
Q

Standard tx for autoimmune hepatits?

A

Prednisone taper from 30mg QD down to 10mg QD over 1 month. Then 10mg maintenance until end point.
+
Azathioprine 50mg daily until endpoint
OR
-Prednisone taper from 60mg QD to 20mg QD over 1 month. Then 20mg maintenance.

98
Q

When do you stop tx for autoimmune hepatitis?

A

Ideal (satisfactory) Remission: no sxs, nl liver tests (AST/ALT ≤2 ULN, nl liver tissue (no interface hepatitis)

99
Q

FU for autoimmune hepatitis?

A

If remission is achieved will need to follow with hepatologist every 3-6 months due to high-likelihood of relapse

100
Q

What is wilson’s disease?

A

due to a genetic abnormality inherited in an autosomal recessive manner that leads to impairment of cellular copper transport.

101
Q

Classic presentation for wilson’s disease?

A

age 5 -35 years

decreased serum ceruloplasmin

detectable Kayser-Fleischer rings

102
Q

Tx for wilson’s disease?

A

D-penicillamine

Liver transplant: indications –>
Fulminant hepatitis

Hepatic insufficiency unresponsive to medical therapy

Severe neurologic sxs

103
Q

What is Hereditary Hemochromatosis?

A

An inherited disorder with impaired intestinal iron absorption that leads to iron-mediated tissue injury, iron is deposited in multiple organs

Usually suspected because of elevated iron saturation or serum ferritin or a family history.

104
Q

Presentation of hereditary hemochromatosis?

A

most sxs

Cardiac disease, DM, joint disease, infx

105
Q

What gene mutation is seen with Hereditary Hemochromatosis?

A

HFE gene mutation (usually C282Y/C282Y)

106
Q

Tx for Hereditary Hemochromatosis?

A

serial phlebotomy to achieve iron depletion

107
Q

What is Alpha-1 antitrypsin (AAT) deficiency?

A

174

108
Q

Dx of Alpha-1 antitrypsin (AAT) deficiency?

A

174

109
Q

Tx of Alpha-1 antitrypsin (AAT) deficiency?

A

174

110
Q

Patho of primary biliary cirrhosis?

A

T-cell attack on bile ducts those genetically susceptible cannot suppress the attack gradual bile duct loss and portal scarring  cirrhosis

111
Q

Presentation of primary biliary cirrhosis?

A

middle-aged women

Often asxs

Fatigue and pruritis

+/-jaundice, features of cirrhosis, xanthelasma (yellow plaques on eyelid), xanthoma (yellow deposits throughout skin) , steatorrhea.

112
Q

Labs seen in primary biliary cirrhosis?

A

elevated alk phos

(+) antimitochondrial antibodies (AMA)- 95%

elevated IgM
increased cholesterol.

norm biliary imaging

liver bx

113
Q

Tx for primary biliary cirrhosis?

A

Cholestyramine (a bile acid resin) taking 4 g in water or juice three times daily may be beneficial for pruritus

Ursodeoxycholic acid (slows progression of damage to cells)

Liver transplant for intractable pruritis or liver failure

114
Q

What is PSC?

A

181

115
Q

PSC has a strong assoc with…

A

ulcerative colitis (UC) and cholangiocarcinoma

116
Q

Presentation for PSC?

A

182

117
Q

What labs are seen with PSC?

A

183

118
Q

Dx for PSC?

A

184

119
Q

Management for PSC?

A

187

120
Q

Comps of PSC?

A

190

121
Q

Px for PSC?

A

191

122
Q

What diseases can lead to cirrhosis (ESLD)?

A

192

123
Q

Comps of ESLD?

A

jaundice

palmar erythema

spider angioma

encephalopathy w/ asterixis

portal HTN

Ascites and muscle wasting

Spontaneous bacterial peritonitis

124
Q

What causes hepatic encephalopathy?

A

portosystemic and hepatocellular dysfunc that leads to increased serum ammonia levels.
Ammonia in a normal liver would have been converted to urea, but in HE crosses into the blood brain barrier.

125
Q

Tx of HE?

A

aimed at reducing ammonia derived from gut/gut bacteria

Grade I – II: Lactulose 30mL BID or TID with a goal of 2 bowel movements per day and/or Rifaximin 550mg BID

Grade III – IV: in hospital, lactulose 15mL oral or via NG tube q 2hours until patient has BM and mental status improving

126
Q

What causes portal vein thrombosis?

A

200

127
Q

Dx of portal vein thrombosis? tx?

A

Doppler US, CT, or MRI

anticoagulation with heparin or low-molecular-weight heparin

128
Q

tx for Fluid Overload: Ascites, LE edema and pleural effusion secondary to ESLD?

A

1st line: Diuretics: furosemide and spironolactone, usu. at a ratio of 40mg and 100mg respectively

Compression stockings for LE edema

2nd line: paracentesis/thoracentesis

3rd line: Transjugular Intrahepatic Portosystemic Shunt (TIPS)

129
Q

What is spontaneous bacterial peritonitis?

A

An infection in the abdominal ascites fluid and/or the pleural fluid

130
Q

s/s of spontaneous bacterial peritonitis?

A

fever, abdominal pain, change in mental status, or asymptomatic

131
Q

Dx of SBP?

A

204

132
Q

tx of SBP?

A

204

133
Q

What labs do you want to monitor in a pt with ESLD?

A

PT-INR, Na, Cr

134
Q

What can be used to determine deg of ESLD?

A

Model of End-Stage Liver Disease (MELD)

mortality

135
Q

MC risk factor for HCC?

A

cirrhosis

136
Q

Dx of HCC?

A

US and/or CT

AFP

Liver biopsy to confirm

137
Q

Tx of HCC?

A

If cancer is not metastatic and lesion/s are within a certain size criteria can be treated with liver transplant

monitor with alternative CT/MR Q6mo

prevention of growth with TACE

138
Q

What is Cholangiocarcinoma?

A

CA arising from the bile duct epithelium

139
Q

Epidemiology of Cholangiocarcinoma?

A

225

140
Q

Etiology of cholangiocarcinoma?

A

226

141
Q

s/s of cholangiocarcinoma?

A

Painless jaundice, weight loss, and abdominal pain in patient >55 years old

pruritus, triad of fever/jaundice, RUQ pain

Foundations III-GI (8 decks)

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