Cirrhosis - Franco Flashcards
Describe the lab findings seen in chronic liver disease resulting in cirrhosis.
Elevated bilirubin, transaminases, and alkaline phosphatases.
Elevated PT/INR and decreased albumin.
Thromobocytopenia, leukopenia.
Renal insufficiency & hyponatremia.
Name three physical exam findings in cirrhosis that are caused by elevated estrogens.
Spider angiomas (harder to see with obscuring makeup, darker complexion)
Palmar erythema
Male gynecomastia
When is cachexia seen in the timeline of cirrhotic liver disease?
How high must bilirubin be elevated to perceive scleral icterus indoors?
Found in final-stage liver disease.
About 5 mg/L
How does edema occur in cirrhotic liver disease?
Ascites?
Loss of serum proteins (hypoalbuminemia) due to loss of liver synthetic function results in starling forces that favor fluid outflow.
In ascites, this imbalance is exacerbated by activation of the RAAS and Vasopressin systems to increase water retention.
Compare and contrast Child-Pugh scoring with MELD.
Child-Pugh: Points for factors such as lab values and encephalopathy/ascites total to a grading of A/B/C liver function. Subjective.
MELD: More complex algorithm considering INR/bilirubin/Cr and dialysis only. Less subjective and preferred to assess the survival of patients with ESLD.
Cirrhosis is a very common cause of portal hypertension. Can you name 3-4 others?
- Portal vein thrombosis (“pre-hepatic”, uncommon)
- Hepatic vein thrombosis (Budd-chiari syndrome)
- Right-sided heart failure (congestion)
- Valvular heart disease
Describe the pathophysiology of esophageal varices in portal hypertension.
Does this affect other locations?
Increased portal vein resistance causes porto-caval shunting; the veins of the lower esophagus experience higher flow as they drain to the Azygos vein.
Rectal veins (hemorrhoids), varicose superficial veins (caput medusae), and others
How are esophageal varices treated? (prophylactic and active)
Prophylactic: Non-selective beta blockers to reduce cardiac output and constrict the splanchnic circulation.
Active: Octreotide (reduce portal venous pressure) and band ligation.
Which predominates in ascites: Vasopressin, or the RAAS axis?
Why is this important?
Vasopressin.
Water retention exceeds sodium retention via aldosterone; the result is hyponatremia.
How is ascites managed?
Sodium restriction and diuretics (spironolactone and furosemide)
How does spontaneous bacterial peritonitis present?
What are the usual causes?
Abdominal pain and fever, plus other symptoms associated with the overlying cirrhosis…
E. Coli > Streptoccocci >> Klebsiella and other G- bacilli
Explain the pathophysiology behind hepatorenal syndrome.
What would be the results on urinalysis?
The decreased systemic circulation resulting from splanchnic dilation would cause renal artery clamping to maintain glomerular pressure, reducing renal blood flow.
Urine sodium and microscopy are normal, indicating a healthy kidney. Urine production is reduced, and venous pressure is decreased.
What is hepatopulmonary syndrome?
Inappropriate vasodilation of the pulmonary capillaries results in overperfusion (V<q></q>
<p>(unknown cause; maybe lost hepatic clearance of vasodilators?)</p>
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Describe the pathophysiology of hepatic encephalopathy.
How does it present on physical exam?
Neurotoxins derived from gut flora, which are normally cleared by the liver, accumulate and cross the BBB. Swelling of the brain occurs with accumulation of ammonia and glutamate in the astrocytes (converted to glutamine) and may cause herniation.
Asterixis.
Describe the treatments generally prescribed for hepatic encephalopathy and the basis of their action.
Lactulose: Non-absorbed carbohydrate which becomes lactate due to colonic bacterial action; sterilizes bacteria (acidic), traps NH3, and increases “catharsis”, heh.
Rifaximin: Second-line, a non-absorbed antibiotic.
(reduction of gut flora > reduction of toxins)
