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Year 3 - Clinical > 31 - Cirrhosis > Flashcards

31 - Cirrhosis Flashcards

1
Q

Causes in the Western world

A
  • Chronic alcohol abuse
  • Chronic hepatitis C
  • Less common = non-alcoholic steatohepatitis, chronic hepatitis B, medications (isoniazid, amiodarone, methotrexate), etc.
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2
Q

Pathophysiology of cirrhosis

A
  • Liver receives blood from hepatic artery & portal vein
  • Chronic liver disease can lead to liver scarring (hepatic fibrosis)
  • Ongoing disease & deterioration of hepatocyte function can progress to cirrhosis
  • Portal vein flow to liver is altered
  • *Understand that flow is altered going through the liver
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3
Q

Complications from cirrhosis

A
  • Portal hypertension
  • Esophageal & gastric varices w/ risk of variceal bleeding
  • Ascites
  • Spontaneous bacterial peritonitis (SBP) – when fluid causing ascites becomes infected
  • Hepatic encephalopathy – confusion due to poor liver function that causes toxins to build up & flow around the body
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4
Q

Describe portal hypertension

A
  • Increased BP in portal venous system
    • Hepatic venous pressure gradient (HVPG) > 5 mmHg
  • Develops b/c:
    • Scarring of liver causing mechanical obstruction of blood flow from portal vein to liver
    • Splanchnic (GI) arterial vasodilation & decreased response to vasoconstrictors increases blood flow to portal vein
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5
Q

Describe varices

A
  • Portal hypertension w/ HVPG > 10 mmHg can lead to esophageal & gastric varices
  • Small veins in lower esophagus & stomach become distended as blood is redirected
  • High mortality rate; high recurrence rate
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6
Q

Describe ascites

A
  • Portal HTN can lead to cascade of events resulting in ascites (accumulation of fluid in peritoneal cavity)
  • Sodium retention, low serum albumin (decreased oncotic pressure – less fluid to hold protein in the vessels, so fluid spills out), fluid leaks into peritoneal cavity
  • W/in 10 years, about ½ of all px w/ cirrhosis develop ascites & ½ of those px die w/in 2 years
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7
Q

Describe spontaneous bacterial peritonitis (SBP)

A
  • Infection of ascitic fluid w/o obvious surgically treatable source
  • Bacteria from GI tract end up in ascitic fluid
  • Exact mechanism not been definitely elucidated (possibly bacterial translocation or hematogenous transmission)
  • E. coli, K. pneumoniae, & pneumococci are most commonly isolated
  • High mortality rate (< 50% survival 1 year after 1st episode)
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8
Q

Describe hepatic encephalopathy

A
  • Decreased liver function causes neurotoxins to accumulate, affects brain function
  • Most commonly implicated = ammonia; increased levels in arterial blood due to:
    • Decreased liver function
    • Shunting of blood around liver
  • Ammonia believed to play key role as attempting to lower levels improves encephalopathy, yet blood levels don’t correlate w/ mental status
  • Glutamine & endogenous benzodiazepines are among other substances that may play a role
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9
Q

Diagnosis of cirrhosis

A
  • Biopsy is most accurate way to confirm cirrhosis, but usually not necessary
  • Can usually diagnose from signs & sx, lab values/ abnormal endoscopy/ abnormal radiographic tests
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10
Q

Sx of cirrhosis

A
  • Weight loss
  • Fatigue
  • Anorexia
  • Jaundice
  • Men – impotence, decreased libido
  • Abdominal distention (ascites)
  • Confusion/mental status changes (encephalopathy)
  • Pruritus
  • GI bleeding, dark coloured urine
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11
Q

Signs of cirrhosis on physical exam

A
  • Hepatomegaly, splenomegaly
  • Spider angiomata
  • Caput medusae (distended veins from umbilicus)
  • Digital clubbing/ nail clubbing (enlargement of fingernails or distal ends of fingers)
  • Gynecomastia & testicular atrophy in men (b/c of circulating levels of estrogen)
  • Jaundice
  • Asterixis (associated w/ encephalopathy & increased levels of toxins in blood; when you close your eyes & hold your arms up w/ hands pointing up at 90-degree angle, person can’t hold hands still & will flap & try to go straight)
  • Ascites
  • Fetor hepaticus (breath has strong, musty smell)
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12
Q

Lab value abnormalities in cirrhosis

A
  • Moderately elevated aminotransferases (AST:ALT ~2:1 (up to 3:1) common in alcoholic liver disease)
  • Elevated alkaline phosphatase (2-3x normal) w/ concomitant GGT rise
  • Decreased serum albumin (test of liver function)
  • Prolonged prothrombin time & elevated INR
  • Hyperbilirubinemia
  • Thrombocytopenia, leukopenia, anemia (RBCs go into spleen so that’s why splenomegaly can occur)
  • Increased serum creatinine (decreased renal function)
  • Hyponatremia (would think hyper b/c more sodium is in blood vessels, but more water too so causes hypo)
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13
Q

2 tools for grading severity of liver disease

A
  • Child-Pugh classification – used for recommending drug dosage adjustments in liver failure
    • Considers bilirubin, albumin, degree of ascites, degree of encephalopathy, & degree of prolongation of PT
  • Model for end-stage liver disease score (MELD score) – used in allocation of liver transplants
    • Considers creatinine, bilirubin, & INR (more objective info than Child-Pugh)
    • Predicts 3-month mortality
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14
Q

Tx goals of cirrhosis

A
  • Slow rate of progression, modify causative factors (EtOH)

- Treat complications that develop (varices, ascites, SBP, hepatic encephalopathy)

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15
Q

Varices tx

A
  • 3 aspects to treating varices caused by portal hypertension
    1) Primary prophylaxis of varices
    2) Tx of acute variceal bleeding
    3) Secondary prophylaxis of varices
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16
Q

Primary prophylaxis of varices

A
  • No varices = no tx
  • Small varices w/ no risk factors = no tx
  • Small varices w/ risk factors for variceal hemorrhage (red wales, Child-Ugh score C) = treat pt w/ nonselective beta-blocker
  • Medium to large varices w/ no bleeding = treat pt w/ nonselective beta blocker or endoscopic variceal ligation (EVL aka banding)
    • EVL = tying off vessels so that they fall off & supposed to reduce risk of bleeding; preferred in cases of beta-blocker intolerance
    • Non-selective beta blockers = propranolol or nadolol; titrate as tolerated (~ q3days) to HR 55-60 bpm, continue indefinitely except in end stage liver disease (no benefit & may actually cause harm)
    • Mechanism = decrease portal venous inflow by decreasing cardiac output (beta-1) & by decreasing splanchnic blood flow (beta-2)
17
Q

Tx of acute variceal bleeding

A
  • Medical emergency
  • Need to maintain BP w/ fluids, control/correct bleeding (RBCs, platelets as needed)
  • Octreotide ASAP 50 mcg IV x1, then 50 mcg/h IV continuous infusion x3-5 days (inhibits vasodilatory glucagon & has local splanchnic vasoconstrictive effect)
  • EVL in conjunction
  • Prophylaxis for SBP = ciprofloxacin or ceftriaxone up to 7 days
  • If still bleeding w/ octreotide & EVL, transjugular intrahepatic portosystemic shunt (TIPS) – shunt bypasses the liver, but can cause encephalopathy b/c toxins aren’t being broken down by liver)
18
Q

Secondary prophylaxis of varices

A
  • More than ½ of px re-bleed
  • Tx = nonselective beta-blocker (propranolol or nadolol) + chronic EVL
  • If pt previously had TIPS, then possible liver transplant candidate
19
Q

Ascites tx

A
  • W/ new onset ascites, need a diagnosis
  • Medication tx = diuresis & sodium restriction to 2 g daily (fluid restriction usually not necessary unless sodium < 120 mmol/L)
  • Diuresis = furosemide (loop diuretic) + spironolactone (K+ sparing diuretic) in a 40 mg:100 mg ratio (to maintain normokalemia)
    • Titrate diuretics up every 3-5 days for goal of 0.5 kg weight loss daily (max dose 160 mg furosemide to 400 mg spironolactone)
    • Monitor electrolytes (K+ and Na+) and sCr
  • For ascites refractory to diuretics – therapeutic paracentesis (can sometimes drain well over 5 L)
  • Avoid NSAIDs, generally avoid ACEi/ARB
  • Beta-blockers for varices – weigh risk vs. benefit in refractory ascites
20
Q

SBP tx

A
  • May be asymptomatic, but often presents w/ one of more of – fever, abdominal pain, encephalopathy, confusion, renal failure
  • Diagnosis if PMN (polymorphonuclear leukocyte) > 250 cells/mm3 and positive ascitic fluid bacterial cultures
  • Treat empirically if PMNs > 250 or if signs/sx of infection
  • Use broad spectrum antibiotics to cover E. coli, K. pneumoniae, & pneumococci = 3rd gen cephalosporins preferred (cefotaxime) over ciprofloxacin
    • 5-day tx course (10 days usually not necessary)
  • Following episode of SBP, give long-term prophylaxis w/ quinolone or TMP-SMX (lower dosing than standard tx dose – once daily, 5 days/week, weekly dosing)
21
Q

Hepatic encephalopathy tx

A
  • Can present acutely (episodic), continually (persistent), or recurring (more than 1 episode < 6 months apart)
  • Precipitating factors = electrolyte abnormalities (dehydration, diuretic overuse), infection, GI bleeding, constipation
  • Mainstay of therapy = reduce ammonia levels
  • Lactulose (non-absorbable disaccharide)
    • Can give orally (30 mL/dose), NG, or PR – PO/NG preferred b/c dose for rectal administration is 1 L
    • Lowers ammonia by – laxative effect (less time for systemic ammonia absorption from gut); decreased pH leaves NH4+ cations “trapped” in acidified colon
    • Acutely can give q1h to initiate laxative effect, then titrate for ~ 3 soft stools daily; monitor for improved mental status
  • Rifaximin – poorly absorbed synthetic antibiotic, believed to reduce ammonia-producing bacteria in gut
  • Neomycin/metronidazole – not commonly used anymore b/c higher risk of side effects

Year 3 - Clinical (30 decks)

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