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MODHIII - Unit 3 > Liver & Biliary Disorders > Flashcards

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- most common complication of cirrhosis
- 50% of cirrhotics will die within 2 yrs of onset of ascites
- physical exam worthless, ultrasound is the way to go
- paracentesis part of physical exam


Indications for paracentesis

- new onset ascites
- signs of infection
- any evidence of clinical deterioration
- relief of symptoms due to tense ascites


Lab tests on ascitic fluid

- cirrhotic: serum ascites-albumin gradient, cell count w/ differential, ascitic fluid cultures in addition to the above
- absence of liver disease: cytology, AFB culture, triglycerides, amylase


Serum-ascites albumin gradient (SAAG)

- SAAG > 1.1 = portal hypertension


SAAG levels

- SAAG > 1.1: high portal pressure; portal HTN or CHF


Spontaneous Bacterial Peritonitis (SBP)

- result of bacterial translocation from gut due to impaired barrier
- 2/3 of pts present with abdominal pain, fever, diarrhea NOT peritonitis
- 1/3 asymptomatic


Diagnosis of SBP

- >250 PMNs/mm3 in ascitic fluid
- cultures negative 50% of the time
- monomicrobial: E coli, klebsiella
- polymicrobial: anaerobic or fungal (secondary peritonitis i.e. perforated viscus)


Treatment of SBP

- antibiotic: Cefotaxime
- IV albumin infusion: 1.5g/kg bw on day 1, 1g/kg bw on day 3
- aminoglycosides should NOT be used


Candidates for prophylaxis of SBP

- hospitalized cirrhotics w/ GI bleeding
- non bleeding cirrhotics w/ ascites and: protein 2.5, SBP
- various antibiotic regimen are effective


Management of Ascites

- sodium restricted diet (2g/d)
- diuretics: spironolactone (K+ sparing) with furosemid (K+ wasting)
- NO IV diuretics: too rapid volume loss = renal hypoperfusion


Causes of poor response to treatment of ascites

- inadequate sodium restriction
- inadequate diuretic dosage


Endpoints of ascites treatment

- weight loss of .5-1 kg/day
- urinary Na:K ratio > 1 indicates good response
- fluid restriction not necessary except for significant hyponatremia (Na 120, creatinine >2, or encephalopathy


Large volume paracentesis

- rapid relief of symptoms but does not treat underlying cause
- if used w/ out sodium restriction ascites reaccumulates
- not first line therapy
- albumin infusions used to blunt changes in volume (8g/L removed)
- smaller volume taps


Variceal bleeding

- 1/3 who have varices will bleed from them
- bleeding associated w/ 30% risk of mortality
- accounts for 80% of GI bleeding in cirrhotics


Management of suspected variceal hemorrhage

- life threatening event: admit to ICU
- hemodynamic resuscitation: large bore IVs, blood products
- consider intubation, call GI
- begin somatostatin or octreotide (decreases portal pressure)


Treatment of variceal bleeding

- endoscopic therapy: ligation
- TIPS when can't be stopped endoscopically
- antibiotic prophylaxis (quinolone)


Transjugular intrahepatic portosystemic shunt (TIPS)

- shunt to bypass the liver vasculature: portal vein to IVC


Primary prophylaxis of variceal hemorrhage

- screen cirrhotics for varices
- nonselective B-blockers: propranol or nadolol
- Goal: reduction in hepatic venous pressure gradient by 25%/below 12
- Alternate: 25% decrease in HR or HR of 50-60bpm


Hepatic encephalopathy (HE)

- due to impaired hepatic clearance of neurotoxic molecules (ammonia)
- most cases precipitating cause can be identified, treatment of cause usually results in complete resolution


Evolution of hepatic encephalopathy

- first sign: sleep disturbance
- asterixis: flapping hand tremor
- altered reflexes


Diagnosis of HE

- CLINICAL diagnosis: based on signs of liver disease, asterixis, hyperreflexia
- elevated blood ammonia levels NOT required to make diagnosis


Precipitants of hepatic encephalopathy

- GI bleed, infection, constipation, hypoxia, electrolyte imbalance, use of sedatives, or tranquilizers


Treatments of HE

- lactulose: osmotic laxative
- neomycin or rifaximin: if no response to lactulose
- sodium benzoate rarely used


Hepatocellular carcinoma (HCC)

- primary liver cancer: 80% occur in setting of cirrhosis
- incidence in cirrhotics is 3-5%/year
- risk is even higher with cirrhosis due to chronic viral hepatitis


HCC screening and treatment

- cirrhotic patients: ultrasound q 6mos +/- serum alpha fetaprotein
- treatment: liver transplant if limited tumor burden, local Rx, systemic Rx


Liver transplantation in HCC

- can be life saving
- timing of transplant is KEY
- MELD score used to predict 3 month mortality, thus priority for transplant


Model for end stage liver disease: MELD Score

- based on 3 lab scores: objective
- serum creatinine, serum bilirubin, INR


Liver function tests

- not tests of liver function
- estimate metabolic function
- indicate cholestasis
- reflective of hepatocellular injury


Indices of metabolic function

- serum albumin, bilirubin, prothrombin time
- estimate severity of liver disease in pts WITH cirrhosis


Cholestasis lab values

- hallmark is elevation of alkaline phosphatase: bone and placenta can be other sources as well
- bilirubin need not be elevated for pattern to be cholestatic