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Clin Med III Unit 2 > 5 Alcoholic Liver Disease and Liver Cancer > Flashcards

5 Alcoholic Liver Disease and Liver Cancer Flashcards

1
Q

Damage to your liver function due to alcohol abuse

A

Alcoholic Liver Disease (ALD)

Occurs in about 25-30% of heavy drinkers

Gene mutations have been linked to the risk of alcoholic liver disease

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2
Q

____% of all deaths from liver disease are attributed to alcohol

A

45%

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3
Q

ALD has replaced HCV as the leading cause of …

A

Liver transplantation in the USA

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4
Q

What are the three main patterns of injury in ALD?

A

Fatty liver (Simple Steatosis

Alcoholic Hepatitis

Chronic Hepatitis with fibrosis or cirrhosis

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5
Q

The risk of developing cirrhosis increases with daily consumption of _____ for men and _______ for women

A

Men: >3 drinks per day > 5 years

Women >2 drinks per day > 5 years

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6
Q

_____ are more sensitive to alcohol

A

Women

Twice as sensitive to EtOH hepatotoxicity
Develop more severe ALD at lower doses with shorter duration

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7
Q

What is the incidence of ALD like between ethnic groups?

A

African Americans>Hispanic>Caucasian males

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8
Q

____ and _____ act together to increase risk of liver disease

A

Obesity and excess body weight

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9
Q

______ and alcohol is associated with a more rapid progression of liver disease

A

Hep C

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10
Q

ALD and smoking is associated with ….

A

Increased risk of hepatocellular cancer

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11
Q

Risk factors for ALD

A

Amount of alcohol ingested**

Type of alcohol may influence risk
• Beer or spirits > wine

Pattern of drinking
• Outside of meal times increases risk 2.7 times

Relationship of quantity and ALD is not completely linear

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12
Q

Accumulation of fat (small or large droplets) in the cytoplasm of the liver cells

A

Fatty liver or hepatic steatosis

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13
Q

Simple uncomplicated fatty liver is usually …

A

Asymptomatic and self-limited

Clinical findings minimal to absent but hepatomegaly may be detectable

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14
Q

Fatty liver may ____________ with abstinence after about 4-6 weeks

A

Be completely reversible

Some studies show 5-15% progression to fibrosis or cirrhosis despite abstinence though

Continued alcohol use increases the risk of progression to cirrhosis

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15
Q

Inflammation of the liver characterized by necrosis and fibrotic scaring in the setting of history of chronic or current heavy alcoholic consumption

A

Alcoholic hepatitis

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16
Q

Clinical features of alcoholic hepatitis

A

Spectrum is asymptomatic to mild to severe

In severe cases, may see:
Fever
Leukocytosis
Hepatic encephalopathy***** (b/c inability to clear ammonia)
Spider angiomas***
Jaundice
Hepatosplenomegaly with liver tenderness
Edema (scrotal or LE)
Ascites
Variceal bleeding
Oliguria
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17
Q

Lab findings for alcoholic hepatitis

A 
Leukocytosis w/ left shift
Macrocytosis 
Thrombocytopenia
AST/ALT ratio >2********* with AST 2-6x ULN
ALP mildly elevated
Bilirubin elevated
PT/INR elevated
Low albumin
Hyponatremia, hypokalemia
GTP elevated
Low Folate
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18
Q

What are some histologic findings for alcoholic hepatitis?

A

Fatty infiltration

Neutrophil infiltration around clusters of necrotic hepatocytes

Clumps of intracellular material (Mallory bodies)***

Fibrosis around hepatic venules (precursor to cirrhosis)

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19
Q

How is ALD diagnosed?

A

Liver biopsy is only required for Dx of alcoholic hepatitis when there is an unclear history of alcohol use and elevated LFTs

Confounded by other risk factors for liver disease and considering pharmacotherapy

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20
Q

Failure of the liver to detoxify noxious agents of gut origin b/c of hepatocellular dysfunction and portosystemic shunting —> impaired brain function with advanced liver disease

A

Hepatic encephalopathy

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21
Q

_____ is the best known neurotoxin that precipitates hepatic encephalopathy

A

Ammonia

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22
Q

How do you manage hepatic encephalopathy?

A

Treat any precipitating factors: GI bleed, infection, sedating meds, electrolyte abnormalities, constipation, renal failure

Don’t use benzos or opioids if possible

Lactulose for acute over HE and secondary prophylactic therapy for an indefinite period

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23
Q

What are the clinical signs of hepatic encephalopathy?

A

EEG changes and flapping tremor (asterxisis)

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24
Q

What grade of hepatic encephalopathy:

Changes in behavior, mild confusion, slurred speech, disordered sleep pattern

A

Grade I (Subclinical or covert encephalopathy)

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25
Q

What grade of hepatic encephalopathy:

Lethargy, moderate confusion, +/- asterixsis

A

Grade II

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26
Q

What grade of hepatic encephalopathy:

Marked confusion (stupor), incoherent speech, sleeping but can be aroused

A

Grade II

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27
Q

What grade of hepatic encephalopathy:

Coma, unresponsive to pain

A

Grade IV

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28
Q

Brief cognitive screening tools which do not require psychological expertise in administration and interpretation, used to evaluate psychomotor speed and cognitive flexibility

A

Strop Test

Able to diagnose minimal hepatic encephalopathy with excellent sensitivity/specificity

29
Q

Which patients with alcoholic hepatitis require hospitalization?

A

Those with high mortality rate based on risk assessment calculators:
• Model of End Stage Liver Disease (MELD) score > 20
• Maddery (Modified) Discriminant Factor (MDF) ≥ 32
• Lillie Score (labs over time) used to determine if steroids should be continued

30
Q

What is essential to the management of alcoholic hepatitis?

A

D/C ALL ALCOHOL and maintain complete abstinence

31
Q

How do you manage mild-sever alcoholic hepatitis?

A

Treatment of alcohol withdraw and infection surveillance

Fluid overload management (diuretics)

Meds for HE (Lactulose, Rifaximin)

Severe disease (MDF ≥32 or MELD >20) consider steroid tx and d/c if not effective on day 7 using Lillie score
\+/- liver transplant

Nutritional assessment and therapy

Do not limit protein intake

Sodium restriction (<2000 mg per day)

Address vitamin deficiencies/malnutrition

32
Q

What med do you need to d/c in patients with alcoholic hepatitis?

A

Non-selective beta blockers, as they are associated with increased risk of AKI

33
Q

Widespread destruction and regeneration of liver tissue with marked increase in fibrotic connective tissue, nodules, and permanent alterations in the structure of the organ

A

Cirrhosis

Scarring and increased connective tissue —> impairment of liver function

34
Q

Cirrhosis is considered compensated if…

A

Portal pressure <10

35
Q

Median survival with compensated cirrhosis

A

~12 years

36
Q

Clinical manifestations of compensated cirrhosis

A

Splenomegaly (thrombocytopenia, leukopenia, anemia, AST elevation)

37
Q

Decompensated cirrhosis is characterized by …

A

Increased portal pressure (>10) and decreased liver function

Median survival <2 years

38
Q

Clinical manifestations of decompensated cirrhosis

A 
Ascites
Esophageal and rectal varicose
Splenomegaly (leukopenia, thrombocytopenia)
Dilated abdominal veins
Encephalopathy
Jaundice
39
Q

Increased pressure within the portal venous system

A

Portal HTN

40
Q

What are the three possible sites of obstruction to flow that can lead to portal hypertension?

A

Prehepatic - portal vein thrombosis

Intrahepatic - cirrhosis**

Posthepatic - CHF, constrictive pericarditis

41
Q

Clinical manifestations of portal HTN

A

Caput medusae
Varies
Ascites

42
Q

Lab findings for alcoholic cirrhosis

A

Similar to alcoholic hepatitis

AST elevation or can be normal in compensated

Anemia of chronic disease, from folate deficiency, suppression of hematopoiesis, hemolysis, GI blood loss, or Splenomegaly

Thrombocytopenia

Coagulation abnormalities (reduced synthesis of clotting factors)

Thrombocytopenia, leukopenia

43
Q

Treatment for cirrhosis

A

Treat/prevent complications of portal HTN and cirrhosis

Variceal surveillance (EGD) +/- banding

HCC surveillance (AFP q6 months)

Non-selective beta blocker prophylaxis for prevention of variceal bleeding - HR 55-60 and SBP <90 is the goal

44
Q

How do you treat ascites associated with cirrhosis?

A

Adherence to less than 2g/d sodium

Diuretics (Lasix, spironolactone)

Fluid restriction ONLY if sodium is <125

For Refractory ascites:
•Stop Beta Blocker
• Therapeutic paracentesis (with albumin if >5-6 L drained)
• TIPS (transjugular intrahepatic portosystemic shunt)

45
Q

During therapeutic paracentesis, _______ is infused for each liter >5L removed to prevent ________.

A

6-8g albumin

Kidney injury

46
Q

Who gets liver transplants for cirrhosis?

A

Patients with decompensated cirrhosis and a MELD score ≥15

Requires 6 months abstinence before can be considered for transplant

Begin AA immediately

47
Q

If a patient with alcoholic cirrhosis continues to drink…

A

4 year survival with a major complication is <20%

48
Q

Complications of cirrhosis

A

Portal HTN

Spontaneous bacterial peritonitis - once they’ve had one episode, should be given abx prophylaxis after d/c

Hepatic encephalopathy

Hepatorenal syndrome

49
Q

Functional renal failure in the setting of decompensated cirrhosis

A

Hepatorenal syndrome

50
Q

What are the two types of hepatorenal syndrome?

A

Type 1 - rapidly and progressive renal failure with severe multi-organ failure
• Median survival ≤4 weeks
• Prognosis: 3-month probably of survival 10%

Type 2 - usually associated with refractory ascites
• Median survival ~6 months (better but still bad)

51
Q

Diagnostic criteria for hepatorenal syndrome

A

Cirrhosis with ascites
Absence of shock
Renal impairment (inc Cr of 0.3mg/dL within 48 hours or 50% inc from baseline within 7 days)
No improvement with correction of volume status + albumin x 2 days
Absence of other causes of AKI

52
Q

Clinical features of hepatorenal syndrome

A 
Ascites
Serum Creatinine levels >1.5 mg/dL
Azotemia (increased BUN)****
Oliguria (urine volume <500 ml/d)
Hyponatremia (<130 mEq/L)
Hypotension
53
Q

How do you prevent hepatorenal syndrome?

A

Use albumin IV with large volume paracentesis

Protect against GI bleeding with EGD surveillance or beta blocker use

Do not use NSAIDs or supplements

SBP prophylaxis
• Pt with previous Hx of SBP
• Pt with variceal bleed x 3-7 days
• Pt with ascetic protein <1.5 g/dL

54
Q

Why do you still need to exclude other diseases of acute/chronic liver disease with serologic testing +/- liver bx in patients who are chronic alcoholics?

A

As many as 20% of alcoholics have a secondary or co-existing etiology of liver disease

55
Q

What are the three categories of liver masses?

A

Benign lesions —> no further testing required

Benign lesions —> that need further investigation/therapy

Malignant lesions requiring appropriate management

56
Q

What is considered a benign liver lesion?

A

Cavernous hemangioma <4 cm

Focal nodular hyperplasia

Simple cyst <4 cm and asymptomatic

Focal fatty change/sparing

57
Q

________ are associated with use of oral birth control pills

A

Adenoma (malignant potential only 5% but increased risk of bleeding)

58
Q

Benign liver lesions that require further management

A

Adenoma
Liver abscess (pyogenic, amebic)
Inflammatory pseudo tumor
Atypical/complex cysts and large symptomatic simple cysts

Refer to GI/Hep for further workup to confirm Dx and recommend treatment

59
Q

Which malignancy is considered the Great Masquerader?

A

Lymphoma

60
Q

What are the three types of primary liver neoplasm

A

Hepatocellular carcinoma (in the liver cells themself)

Cholangiocarcinoma (in bile ducts)

Other rare tumors (cystadenocarcinoma, angiosarcoma)

61
Q

Neoplasms arising from parenchymal cells of the liver

A

Hepatocellular carcinoma

62
Q

Neoplasms arising from biliary duct cells

A

Cholangiocarcinomas

63
Q

You should have a high index of suspicions of HCC in what patients?

A

Cirrhotic patients

Patients with non-cirrhotic Hep B with liver lesion on imaging

64
Q

Who is at risk for HCC

A

All suspected cirrhotic patients from any liver disease

Chronic Hep B

65
Q

Sx of HCC

A

Cachexia, weakness, and weight loss

Sudden appearance of ascites

Elevated Alk Phos

Elevated alpha-fetoprotein****

66
Q

What diagnostic tests do you want for HCC?

A

Tri-phasic CT scan first

If non-diagnostic then tri-physic MRI with gadolinium based contrast

Liver biopsy is diagnostic, but may not need if imaging is typical and AFP is elevated

67
Q

Screening of cirrhotic patients with US imaging and AFP should occur…

A

Q 6 months

68
Q

How is HCC managed?

A

Resection rarely feasible due to background cirrhosis

Liver transplant evaluation for early stage cancer
• 1 lesion up to 5 cm or 3 lesions up to 3 cm AND no vascular invasion or distant spread

RFA for small tumors in non-operative candidates

TACE/TARE or XRT for large tumors if sufficient hepatic reserve

Clin Med III Unit 2 (6 decks)

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