LIver

Question 1

How does chronic liver disease typically present clinically?

Answer 1

Often cirrhosis is asymptomatic unless one or more complications occurs. Include Portal HTN, Varices, Ascites, gynecomastia, testicular atrophy, palmar erythema, spider angiomas, hemorrhoids

Question 2

What is the most serious complication of portal HTN?

Answer 2

Bleeding secondary to hemhorraged esophagogastric varices is the most life-threatening.

Question 3

How do you screen for esophagogastric varices? Why would you do this?

Answer 3

Upper GI endoscopy. Do this in patients with portal HTN or if pt presents with evidence of upper GI bleed (hematemesis, melena) after they have been stabilized.

Question 4

Prophylaxis for esophagogastric varices:

Answer 4

Non-selective beta blocker, though evidence is limited for small varices.

Question 5

How should bleeding esophageal varices be managed?

Answer 5

1. Hemodynamic stabilization w/ fluids
2. IV octreotide (splanchnic vasoconstrictor)
3. Emergent upper GI endoscopy to perform variceal ligation/banding or sclerotherapy.

Question 6

What is the MOST COMMON complication of cirrhosis?

Answer 6

Acites. Note that portal HTN must be present to diagnose ascites.

Question 7

How is a diagnosis of cirrhosis confirmed?

Answer 7

Liver biopsy.

Question 8

What are some other potential causes of ascites (aside from portal HTN/cirrhosis)?

Answer 8

CHF, Chronic renal disease, fluid overload, tuberculous peritonitis, malignancy, hypoalbuminemia, peripheral vasodilation secondary to endotoxin-induced release of nitrous oxide (leads to inc. renin, inc. aldosterone), impaired liver inactivation of aldosterone.

Question 9

What diagnostic test should you use to confirm ascites is due to cirrhosis?

Answer 9

Paracentesis and examination of the fluid: cell count, albumin, gram stain, and culture (r/o infection). Serum ascites albumin gradient = Serum albumin - ascites albumin.
>1.1 g/dL suggests portal HTN. <1.1 makes it unlikely.

Question 10

How is ascites managed?

Answer 10

Low Na diet and diuretics. Therapeutic paracentesis if tense, SOB, or early satiety are present.
Transjugular intrahepatic portal-sustemic shunt (TIPS) will reduce portal HTN.

Question 11

An alcoholic patient presents with confusion, decreased mental function, and poor concentration following a bout of “flu”. What is the likely cause? What are some clinical signs?

Answer 11

Hepatic encephalopathy- build up of toxic metabolites (esp Ammonia) builds up in brain.

Signs: asterixis, rigidity, hyperreflexia.

Question 12

How is hepatic encephalopathy treated?

Answer 12

Lactulose promotes excretion of ammonia via gut. Protein restricted diet is important (less than 30-40g/day).

Question 13

Describe the pathogenesis of hepatorenal syndrome:

Answer 13

Essential process is renal hypoperfusion due to vasoconstriction of renal vessels. RAA is activated in response to perceived low blood volume–it seems blood volume is sequestered in splanchnic circulation where vasodilation and reduced resistance are present.

Syndrome involves no direct kidney damage and is reversible with liver transplant.

Question 14

You obtain paracentesis on a patient in the hospital with ascites caused by end stage liver disease and on microscopy see that it contains lots of WBCs and PMNs. You suspect____ and treat with _____

Answer 14

Spontaneous bacterial peritonitis (SBP). Tx w/ broad-spectrum Abx (Coverage of E Coli, Klebsiealla, S pneumo) then narrow once culture and sensitivity are returned.

Question 15

Hyperestrinism- what is it and what are the clinical consequences?

Answer 15

Increase in systemic amounts of estrin-containing hormones. Causes Spider angiomas, palmar erythema, gynecomastia, testicular atrophy.

Question 16

How do coagulopathies develop from cirrhosis? How are they treated?

Answer 16

Decreased synthesis of clotting factors by diseased liver. PT is prolonged first, followed by PTT.
Treat with fresh frozen plasma.

Question 17

Cirrhosis predisposes patients to this type of cancer:

Answer 17

Hepatocellular carcinoma (HCC) occurs in 10-25% of patients with cirrhosis.

Question 18

What is Wilson’s disease?

Answer 18

An autosomal resessive disease of copper metabolism also associated with ceruloplasmin deficiency. Result is inability to secrete copper and its excessive deposition in end organs, including the liver, kidney, cornea, brain.

Question 19

How does Wilson’s disease present clinically?

Answer 19

Pt. is usually child, adolescent, or young adult (5-35). Most common disease at presentation is liver (acute hepatitis, cirrhosis, fulminant hepatic failure). Others are Kayser-Fleischer rings (yellow rings in cornea), extrapyramidal neuron signs (parkinsonian syndrome, chorea, drooling, dyskinesia) or psychiatric disturbances. Renal involvement (aminoaciduria and nephrocalcinosis) can occur.

Question 20

How is Wilson’s disease treated?

Answer 20

Chelating agents (D-penicillamine), Zinc (prevents dietary copper uptake), Liver transplant if unresponsive to Tx or fulminant liver failure.

Question 21

Hemochromatosis: definition

Answer 21

An autosomal recessive disease of iron absorption. Excessive absorption of iron in the intestine leads to increased accumulation of iron in various organs (as hemosiderin and ferritin).