38. Conference 5 Flashcards
Liver tests: generally, what do AST/ALT elevations indicate? what about alkaline phosphatase elevation?
What do we consider to be “true” liver function tests?
AST/ALT elevations are a sign of liver injury (not function) – ie, necrosis.
Alkaline phosphatase elevation is a sign of bile duct injury (or obstuction).
True liver function tests are albumin, PT, INR which assess the liver’s ability to synthesize protein and to conjugate bile acids.
Evaluation of a patient with abnormal liver tests: what are the possible causes, listed from most likely to least likely?
Medications- review all prescription and OTC’s
Viral hepatitis- tests to order: HCV antibody, hepatitis B surface antigen
Alcohol- clue can be an increased AST/ALT ratio. (SAKE = alcohol!)
NASH- there is no blood test for this – diagnosis based on risk factors and on exclusion of other causes of liver test abnormalities.
Autoimmune hepatitis- often one can see other autoimmune conditions associated with this such as autoimmune thyroiditis
Primary Biliary Cirrhosis- usually cholestatic lft’s, look for history of other autoimmune conditions
Hemochromatosis
Wilson’s disease
Alpha one antitrypsin deficiency
Risk factors for NASH?
Metabolic syndrome: obesity (often truncal), hyperlipidemia, diabetes, hypertension
Eval of elevated LFTs: what should I look for on physical exam?
- BP, wt/BMI to assess risk factors for fatty liver
- any signs of chronic liver disease such as spider angiomas, nail abnormalities, palmar erythema
Evaluation of elevated LFTs: once these come back elevatd, what other tests should I order?
Viral serologies
iron tests
autoimmune markers
ceruloplasmin
alpha one antitrypsin level and phenotype
We diagnose NASH in a patient. Why might the ferritin level be elevated even if transferrin sat is normal?
Likely it’s a sign of inflammation in the liver rather than iron overload given that transferrin saturation is normal.
This is a very common finding in both alcoholic and non alcoholic fatty liver disease.
We diagnose NASH. Will a liver biopsy be helpful?
It would confirm the diagnosis and assess the severity. If NASH is present vs steatosis alone, prognosis is worse with 30% chance of developing cirrhosis over the next 10 years.
We diagnose NASH in a patient. What do we recommend as treatment?
Treat the metabolic syndrome:
- Lose weight
- Change diet- we have good animal data that diets high in fructose (mainly in juices, sodas) and in trans fats (partially hydrogenated oils) lead to steatohepatitis with a lot more inflammation in the liver compared to similar calorie diets that don’t contain these foods.
- Exercise
- Screen for diabetes and treat aggressively if present with an insulin sensitizing agent.
- Treat hypercholesterolemia- statins are perfectly safe to use.
- Consider treating with vitamin E 800 IU/day. In one large study and several smaller studies this has shown to improve LFT’s and histology in patients with NASH. (The reason we may not prescribe it to everyone is that large cardiology trials have shown increased mortality from cardiac reasons in patients treated with vitamin E.)
If diuretics have failed to treat a patient’s ascites, what options do we have?
Large Volume Paracentesis: drain the fluid directly from the abdomen.
Banding: with endoscopy, tie off the esophageal varices within the esophagus
TIPS surgery: create a trans-hepatic shunt to decrease portal pressure.
What is this? features?
Close-up histology of NASH.
Steatosis.
Upper left: ballooning hepatocytes (degeneration)
Center: mixed inflammatory cells.
Gastroesophageal Varices: what % of cirrhotic patients do they happen to?
How many of them bleed?
- De novo varices develop in 5-15% of cirrhotic patients per year
- One third of patients with varices experience variceal bleeding
Primary prophylaxis of variceal hemorrhage: what may prevent the first bleed?
•Non-selective beta blockers (nadolol, propranol, carvedilol) are first line treatment for primary prophylaxis
•They block vasodilatory beta adrenergic receptors, permitting unopposed alpha-adrenergic vasoconstriction in the mesenteric arterioles- reducing portal venous inflow and pressure
Endoscopic therapy for variceal bleeding?
- EVL is the preferred endoscopic modality for control of acute esophageal variceal bleeding and for prevention of rebleeding
- Varices at the GE junction are banded initially, and then more proximal varices are banded in a spiral manner about every 2 cms.
- 80-90% of patients will stop bleeding with EVL and octreotide.
Secondary treatment to prevent variceal bleeding if banding does not work?
- Eradication of esophageal varices by EVL (every 2-3 weeks until varices eradicated)
- Non selective beta blocker
- Endoscopy/banding every 3 to 6 months for treatment of recurrent varices
•TIPS if pharmacologic and endoscopic therapy fail
•Transplant evaluation for Child B or C pt
TIPS Procedure: what is it?
Major complication?
Treatment of early rebleeding, or of uncontrolled active bleeding.
Go in through the hepatic vein, dilate a channel, place an stent and create a shunt.
Decreases portal pressure.
Can cause encephalopathy since you are basically bypassing the liver.
Management of moderate ascites?
Low sodium diet
Diuretics (spironolactone, furosemide)
Management of refractory ascites?
(definition of refractory ascites?)
Def’n: lack of response to high dose diuretics.
Treatment = Repeated LVP with albumin (monthly).
TIPS surgery. Works by decreasing portal pressure, thus decreasing the activity of sodium-retaining mechanisms and improving renal response to diuretics.
(sorry I just realized these are redundant cards)
Define hepatic encephalopathy
A reversible decrease in neurologic function caused by liver disease, occurring most notably in patients with portal hypertension and shunting of blood away from the liver.
Hepatic encephalopathy: what are the symptoms?
Subtle neuropsych changes
Normal EEG
diagnosed by psychomotor testing
Reversible with treatment
(from Robbins) Hepatic encephalopathy = a spectrum of disturbances in consciousness (subtle behavioral abnormalities; marked confusion and stupor; deep coma and death). These changes may progress over hours or days in acute hepatic failure, or more insidiously in a person with marginal hepatic function due to chronic liver disease. Neurologic signs include rigidity, hyper-reflexia, and asterixis (nonrhythmic, rapid extension-flexion movements of the head and extremities, best seen when the arms are held in extension with dorsiflexed wrists).
Hepatic encephalopathy: what is the pathogenesis? (wtf????)
Paraphrased from Robbins:
Hepatic encephalopathy = a spectrum of disturbances in consciousness (subtle behavioral abnormalities; marked confusion and stupor; deep coma and death). These changes may progress over hours or days in acute hepatic failure, or more insidiously in a person with marginal hepatic function due to chronic liver disease. Neurologic signs include rigidity, hyper-reflexia, and asterixis (nonrhythmic, rapid extension-flexion movements of the head and extremities, best seen when the arms are held in extension with dorsiflexed wrists).
Hepatic encephalopathy is regarded as a disorder of neurotransmission in the central nervous system and neuromuscular system, and seems to be associated with elevated ammonia levels in blood and the central nervous system, which impair neuronal function and promote generalized brain edema
Hepatic encephalopathy: some causes?
Hepatic encephalopathy usually occurs in a patient with chronic liver disease and often a precipitant can be found such as:
Hypovolemia
Gastrointestinal bleeding
Hypokalemia and/or metabolic alkalosisHypoxiaSedatives or tranquilizers
Hypoglycemia
Infection (including SBP)
Hepatic encephalopathy: treatment?
Find and treat the cause
Correct potassium levels
Correct ammonia levels - by either inhibiting GI ammonia production with antibiotics, or by increasing the removal of ammonia (via lactulose)
HCC: treatment?
- Radiofrequency ablation (for lesions up to 3cm)
- Surgical resection (if they don’t have portal hypertension)
- Transplant. Transplant status determined by MELD score
What is the MELD score? what are its components?
Model for End stage Liver Disease
Creatinine, INR, Bilirubin
HCC: how do we test for it?
Labs: if serum AFP is > 500, definitive for HCC
Ultrasound: looking for poorly-defined margins and irregular internal echoes
CT/MRI: Hyper-vascular, high attenuation lesion with contrast administration with rapid washout of contrast
