Alcoholic Hepatitis, NAFLD, and Cirrhosis Flashcards
Alcoholic liver disease includes:
(clinical spectrum)
Fatty liver
EtOH hepatitis
EtOH cirrhosis
Fatty liver
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
Alcoholic Hepatitis RF
Pts who drink 6-8 drinks/day for years
This is variable–some will develop with far less alcohol consumption
Alcoholic Hepatitis Clinical Presentation
(Sxs and PE)
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
Alcoholic Hepatitis Lab Findings
Low Hgb
High MCV
Transaminitis (AST>ALT)
High total bilirubin
High TGs
High white count
May have elevated INR
CAGE Questions
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)?
Tx of Alcoholic Hepatitis
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
NAFLD/NASH
What they stand for
Non-Alcoholic Fatty Liver Disease
Non-Alcoholic Steatohepatitis
What is the MC chronic liver disease in the western world?
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
Spectrum of NAFLD
Fatty liver (hepatic steatosis)- fat accumulates in the liver
NASH- fat plus inflammation and scarring
Cirrhosis-scar tissues replaces liver cells
NAFLD Pathophysiology
Accumulation of fat (mainly TGs) in hepatocytes from insulin resistance
Insulin resistance classified by HOMA score
NAFLD RFs/Associations w/ NAFLD
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
Clinical presentation of NAFLD
Almost always asymptomatic
Mild to moderate ALT/AST elevations usually found w/ routine screening
Diagnosis of NAFLD
Can use US, CT or MRI to detect fatty infiltration
Gold standard is liver biopsy–reveals lobular and portal inflammation, Mallory bodies and ballooning
Tx of NAFLD
Gradual weight loss (rapid can worsen liver ftn)
Prevention/tx of DMII and hyperlipidemia
Cirrhosis Definition/Pathophysiology
Progressive hepatic fibrosis that distorts hepatic architecture
Irreversible in advanced stages
Can be compensated or decompensated
Causes of cirrhosis
MC: EtOH, NASH, Hep C
Others: Hep B, PBC/PSC, autoimmune, hemochromatosis, R sided HF
PE Findings Cirrhosis
Hepatosplenomegaly
Spider angiomata
Palmar erythema (always)
Hepatic tenderness
Sclera icterus
More severe disease: ascites, muscle wasting, edema, asterixis, hepatic encephalopathy
Lab findings in Cirrhosis
Decreased hemoglobin and platelets
Decreased albumin
Increased INR
Increased total Bilirubin
Complications of Cirrhosis
**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
HCC
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)
Liver transplant
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
