Alcoholic Hepatitis, NAFLD, and Cirrhosis Flashcards

1
Q

Alcoholic liver disease includes:

(clinical spectrum)

A

Fatty liver

EtOH hepatitis

EtOH cirrhosis

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2
Q

Fatty liver

A

Develops in response to short periods of alcohol abuse (days). Resolves within a month of abstinence.

Asymptomatic

Risk Factors:

  • Alcohol ingestion (3/day men; 2/day women)
  • Genetics: mutation in alcohol metabolizing enzyme systems
  • Gender: women more severe than men
  • Obesity: also have NAFLD/NASH
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3
Q

Alcoholic Hepatitis RF

A

Pts who drink 6-8 drinks/day for years

This is variable–some will develop with far less alcohol consumption

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4
Q

Alcoholic Hepatitis Clinical Presentation

(Sxs and PE)

A

Mild-Moderate

  • Tachycardia
  • Weakness
  • N/V
  • Fever
  • Anorexia

Severe: above plus:

  • portal HTN
  • GI bleeding
  • Hepatic encephalopathy
  • Ascities

PE:

  • hepatomegaly
  • fever
  • tachycardia
  • jaundice
  • abdominal distention
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5
Q

Alcoholic Hepatitis Lab Findings

A

Low Hgb

High MCV

Transaminitis (AST>ALT)

High total bilirubin

High TGs

High white count

May have elevated INR

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6
Q

CAGE Questions

A

Have you ever felt you should cut down on your drinking?

Have people annoyed you by criticizing your drinking?

Have you ever felt bad or guilty about your drinking?

Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover (eye opener)?

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7
Q

Tx of Alcoholic Hepatitis

A

Model for End Stage Liver Dz (MELD Score)

  • predicts survival based on total bilirubin, INR, creatinine

Abstinence!!

  • Watch for withdrawal and tx appropriately

Monitor and Tx complications as they arise:

  • Infection
  • Portal HTN
  • Corticosteroids to control inflammation–encephalopathy
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8
Q

NAFLD/NASH

What they stand for

A

Non-Alcoholic Fatty Liver Disease

Non-Alcoholic Steatohepatitis

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9
Q

What is the MC chronic liver disease in the western world?

A

NAFLD

By 2020 will be most likely cause of decompensated cirrhosis–these pts most likely won’t be able to receive liver transplant b/c multiple comorbidities

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10
Q

Spectrum of NAFLD

A

Fatty liver (hepatic steatosis)- fat accumulates in the liver

NASH- fat plus inflammation and scarring

Cirrhosis-scar tissues replaces liver cells

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11
Q

NAFLD Pathophysiology

A

Accumulation of fat (mainly TGs) in hepatocytes from insulin resistance

Insulin resistance classified by HOMA score

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12
Q

NAFLD RFs/Associations w/ NAFLD

A

Metabolic Syndrome. Three or more of:

  • Elevated fasting glucose
  • Waist circumference >40 men, >35 women
  • BP >130/85
  • Elevated TGs
  • Low HDL

Age >40

BMI >30

DMII

HTN

Elevated ALT

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13
Q

Clinical presentation of NAFLD

A

Almost always asymptomatic

Mild to moderate ALT/AST elevations usually found w/ routine screening

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14
Q

Diagnosis of NAFLD

A

Can use US, CT or MRI to detect fatty infiltration

Gold standard is liver biopsy–reveals lobular and portal inflammation, Mallory bodies and ballooning

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15
Q

Tx of NAFLD

A

Gradual weight loss (rapid can worsen liver ftn)

Prevention/tx of DMII and hyperlipidemia

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16
Q

Cirrhosis Definition/Pathophysiology

A

Progressive hepatic fibrosis that distorts hepatic architecture

Irreversible in advanced stages

Can be compensated or decompensated

17
Q

Causes of cirrhosis

A

MC: EtOH, NASH, Hep C

Others: Hep B, PBC/PSC, autoimmune, hemochromatosis, R sided HF

18
Q

PE Findings Cirrhosis

A

Hepatosplenomegaly

Spider angiomata

Palmar erythema (always)

Hepatic tenderness

Sclera icterus

More severe disease: ascites, muscle wasting, edema, asterixis, hepatic encephalopathy

19
Q

Lab findings in Cirrhosis

A

Decreased hemoglobin and platelets

Decreased albumin

Increased INR

Increased total Bilirubin

20
Q

Complications of Cirrhosis

A

**Ascities **

  • MC complication
  • hepatic sinusoidal pressure inc–> splanchnic and systemic vasodilation–> RAAS system retains more sodium and water
  • Tx w/ diuretics

Peripheral pitting edema

Hepatic encephalopathy

  • sign of decompensation, usually induced by some event
  • due to liver not metabolizing toxins–> build up causing a range of sxs from behavioral changes to confusion to coma

Esophageal Varices

  • From portal HTN
  • If >5mm use endoscopic banding
  • If refractory bleeding: TIPS procedure

**Spontaneous Bacterial Peritonitis **

  • Normal barriers to bacterial movement across intestinal lining are decreased
  • Present with fever, abdominal pain, sxs of decompensation
  • *DX: CBC + differential, fluid culture from paracentesis *
  • After tx, require life long ppx b/c high recurrence rate

Hepatorenal Syndrome

  • Type 1 (rapidly progressive renal failure) vs. Type 2 (stable moderate renal failure)
  • Should try to be prevented by avoiding nephrotoxic drugs, excessive diuretics, and large volume paracentesis w/o albumin in pts with cirrhosis
  • Tx: liver transplant
21
Q

HCC

A

Hepatocellular Carcinoma

80-90% arise in context of cirrhosis

Surveillance: US and alpha-fetoprotein q6months; MRI if US is inconclusive or suspect for liver lesion

Dx: made with MRI–avoid bx b/c tumor seeding

Tx:

  • liver transplant
  • surgical resection–if no cirrhosis or well preserved ftn with cirrhosis
  • percutaneous ethanol–HCC<3cm. Induces tumor necrosis
  • radiofrequency ablation–necrosis of 3-4cm area, caution if close to blood vessels or biliary tree (doesn’t work well)
  • Transarterial chemoembolization: injection of chemo into branch of hepatic artery that supplies the tumor to induce necrosis (CI with complete portal vein obstruction)
22
Q

Liver transplant

A

Pt survival is excellent, demand >>supply

Indications:

  • MC some form of decompensated liver disease–hepatitis C (MC), EtOH liver disease, PBC/PSC
  • Allocation based on short term mortality and different statuses: LT-Status 1 (acute liver failure) and MELD score (higher score=higher mortality; used for cirrhosis)

CI

  • extrahepatic malignancy
  • untreated alcoholism
  • severe multi-organ failure
  • severe psychological disease
  • severe pulmonary HTN
  • advanced cardiopulmonary disease