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43 Cards in this Set
- Front
- Back
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what is cirrhosis?
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chronic, degenerative disease characterized by diffuse hepatic disease, fibrosis, and abnormal nodules
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cirrhosis etiology
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most common: alcohol and viral hep B and C
metabolic liver disease, cholestatic liver disease, drugs/herbals (INH, amiodarone, methyldopa, MTX, anabolic steroids, black cohosh) |
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central vein purpose
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collects filtered blood, empties into larger hepatic vein and inferior vena cava
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portal triad
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portal vein (entry of blood from spleen, intestine, and stomach circulation)
hepatic artery (entry of oxygenated blood to the liver from heart) bile duct (collects bile to store in gall bladder) |
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pathophysiology of a fatty liver
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fat deposits from ETOH oxidation accumulate in hepatocytes
no functional impairment, may be reversible |
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pathophysiology of hepatitis
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inflammation, immune reaction, necrosis, and death of hepatocytes
may be functional impairment, less reversible |
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pathophysiology of liver fibrosis and cirrhosis
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collagen and scar tissue formation replace functional tissue
functional impairment, not reversible |
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progression of alcoholic liver disease
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normal --> steatosis (fatty liver) --> fibrosis or alcoholic hepatitis or both
fibrosis --> cirrhosis (not reversible) |
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pathophysiology of alcoholic liver disease
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fibrosis and scarring of liver tissue within the sinusoids --> obstruction/resistance of blood flow through the lobules --> increased pressure in portal vein resulting in portal HTN --> release of vasodilators (NO) in splanchnic circulation leads to vasodilation and pooling of blood
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effects of portal HTN
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ascites, spontaneous bacterial peritonitis (SBP), esophageal varices and variceal bleeding, hepatic encephalopathy, thrombocytopenia
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effects of liver cell death and failure
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coagulation disorders, hepatic encephalopathy, hypoalbuminemia
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cirrhosis clinical presentation: physical exam
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-N, V, malaise, anorexia
-jaundice, icteric (yellow skin/eyes) -dark urine/pale stool -spider angiomatas -gynecomastia, palmar erythema -altered mental status -abdominal distention, ascites, edema |
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cirrhosis lab findings
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-increased transaminases (AST & ALT)
-severe > 10-20 x ULN (drugs/toxins, viral hep, ischemia) -mild < 10 x ULN (EtOH, obstruction, broad dx) EtOH ration of AST:ALT > 2:1 -increased bilirubin -increased ALP (non specific) -increased GGT (non specific) -decreased albumin ***increased PT/INR -increased aldosterone -decreased platelets -anemia (decreased Hg and Hct) |
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complications of cirrhosis
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portal HTN, gastroesophageal varices, ascites, SBP, hepatic encephalopathy
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characteristics of portal HTN
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-resistance to portal blood flow
-increased portal pressure (>10mmHg) -formation of collateral vessels (shunts blood away from liver) -splanchnic vasodilation -NO and glucagon -blood pooling -increased capillary pressure & permeability, pooling fluids into interstitial space |
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systemic effects of portal HTN
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"effective hypovolemia"
-decreased blood volume, hypoperfusion -decreased BP -activation of RAAS system |
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portal HTN drug tx
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1st line: decrease splanchnic blood flow
-propranolol 20 mg PO BID (max 80 mg BID) -nadalol 40 mg PO daily -titrated dose every 2 days until goals achieved ***non selective BB are preferred 2nd line: alter intrahepatic circulation -isosorbide mononitrate 20 mg PO BID (ADJUNCT ONLY) |
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portal HTN tx monitoring
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efficacy:
-goal to decrease portal pressure < 12mmHg and decrease HR by 25% baseline but not less than 55 bpm ADRs: bradycardia, hypotension, SOB, bronchoconstriction, fatigue, vivid dreams |
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gastroesophageal varices characteristics
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-result of increased portal pressure and collateral formation
-high mortality with every bleed -↓ plts, ↑ PT/INR, high pressure behind pt of rupture, ↓ systemic BP |
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gastroesophageal varices primary prevention
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goal: prevent 1st bleed and ↓ portal pressure
-propranolol 20 mg PO BID (max 80 mg BID) -nadalol 40 mg PO daily -vasoconstriction of mesenteric arteries, 50% reductions in risk of 1st bleed, pts at highest risk = most benefit |
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gastroesophageal varices acute bleed tx overview/goals
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-med ER
-presents as hematemesis or melena (blood in stool) -goal is to stop or slow blood loss, fluid resuscitation, correct coagulopathy, prevent infection, and prevent rebleeding |
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gastroesophageal varices acute bleed: stop/slow blood loss tx
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1st line:
1. octreotide 50-100 mcg IV bolus then IV infusion of 25-50 mcg/hr x 48 hours -analog of somatostatin -reduces splanchnic and hepatic blood flows, increases splanchnic arteriolar resistance, and decreases portal and intravariceal pressures -short t1/2, start ASAP 2. Endoscopic Band Ligation (EBL): wraps 2+ rubber bands around esophageal mucosa that contains the bleeding varix; leads to necrosis within a few days and ulcer healing in 14-21 days ***both 1st line and used together in ER |
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gastroesophageal varices acute bleed: supportive tx
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-fluid resuscitation (prevent shock): IVF, blood products
-correct coagulopathy: Vit K, platelets, FFP -prevent infection: prophylactic ABx -any acute bleed gets ABx for 5-10 days |
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gastroesophageal varices acute bleed: secondary prevention
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goal: prevent rebleed; highest risk in first 72 hours after initial bleed (after 6 wks risk returns to normal)
-propranolol or nadolol: increased likelihood of being bleed free and reduced death from rebleeding -non pharm: -sclerotherapy -band ligation -TIPS (last line, shunts blood around liver) |
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ascites general characteristics
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-accumulation of fluid in peritoneal cavity
-affect 50% pts within 10 years of dx -most common complication -associated with decreased QoL, infection, renal dysfunction, and poor long term outcome |
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ascites development
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portal HTN --> splanchnic arterial vasodilation --> 1 or 2
1. increase splanchnic capillary pressure and permeability --> lymph formation exceeds lymph return --> ascites 2. arterial vascular underfilling; activation of RAAS system, ADH --> Na and H2O retention --> ascites |
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ascites management: pre tx
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1. baseline measurements: renal function, electrolytes, arterial blood pressure
2. assess ascitic fluid: SAG = ALBs - ALBa -gradient >/= 1.1 g/dL suggests portal HTN -rule out SBP |
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ascites management: drug tx
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1. aldosterone blockage
-mod vol: spironolactone 50-200 mg daily -lg vol: spironolactone 200-400 mg daily 2. diuresis -mod vol: lasix 20-40 mg daily -lg vol: lasix up to 160 mg daily ***ratio of spironolactone:lasix = 100 mg : 40 mg 3. albumin: only if > 5 L removed during paracentesis |
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ascites management: nonpharm tx
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-abstain from EtOH
-low sodium diet < 1-2 g/day -fluid restriction < 1000 mL/day (with serum Na <120 mmol/L) -paracentesis: rapid removal of fluid from peritoneal space, preferred for large volumes, fluid shifts from vascular space to peritoneal space occur rapidly |
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ascites management: monitoring
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efficacy: wt loss (0.5 kg/day vs 1-2 kg/day), ins/outs, edema, belly size
ADRs: electrolytes and renal function |
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furosemide ADRs
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-decreases: K, Cl, Mg
-dehydration (↑SCr and BUN) -orthostasis |
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spironolactone ADRs
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↑ K
gynecomastia |
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SBP: general characteristics
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-20-30% of pts with ascites
-70% recurrence within 1 year -associated with significant renal damage -risk factors: ascitic fluid protein concentration < 1 g/dL and hx of SBP |
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SBP: pathophysiology
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1. bacterial translocation: migration of gut flora thru intestinal barrier --> mesenteric lymph or extraintestinal organs
2. persistent bacteremia: ↓phagocytic activity, ↓hepatic flow to protective kupffer cells (cells fight infections) 3. bacterial colonization: bacterial growth/colonization of ascitic fluid, inflammation of peritoneum |
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SBP: dx
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***need either ↑PMN or (+) culture for dx
-ascitic fluid: ↑PMN > 250, cultures (e. coli, k pneumoniae, enterococci, pneumococcus, streptococci) -s/s of infection: ↑WBC, fever, abdominal pain, N/V, new onset, rapid ascites, new onset encephalopathy, GI bleed, renal dysfunction |
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SBP: empiric ABx tx
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-3rd gen cephalosporin:
-cefotaxime 2g q8 hrs -CTX 2g q24 hrs -FQs (pcn allergy only) -norfloxacin 400 mg q12 hrs -duration: 5 days if blood cultures remain negative; 5-10 days if culture positive or acute GI bleed |
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SBP: prophylaxis
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goal: intestinal decontamination
target pts: hx of SBP (tx forever) or cirrhotic pts with upper GI bleed (short term tx) -norfloxacin 400 mg daily -cipro 750 mg weekly -bactrim DS 5 days/wk |
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hepatic encephalopathy: pathophysiology
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-major neuropsych complication of cirrhosis
-↑ammonia circulation: impaired hepatic fxn and metabolism, portosystemic shunting -production of false NTs -activation of GABA receptors -manganese deposits in brain |
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hepatic encephalopathy: precipitating factors
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-oral protein load
-GI bleed -sedative use (benzos) -TIPS, shunting procedures -infection -progression of cirrhosis -hypokalemia, systemic alkalosis |
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hepatic encephalopathy: dx
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clinical features: hx of cirrhosis, hepatic encephalopathy, exposure to precipitating factors; mood change, dementia, sleep disturbance, speech, memory deficits
PE: asterixis, rigidity, ataxia, coma Labs: ammonia blood levels (norm = 55); not always indicative, focus more on sxs |
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hepatic encephalopathy: dietary mods
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goals: ↓ammonia and clinical improvement
-protein restriction (not less than 1g/kg/day) -substitution of vegetable protein; use of branched chain AAs -zinc supplementation |
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hepatic encephalopathy: ammonia lowering
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-lactulose syrup (10g/15mL): nonabsorbable disaccharide; 1st line in acute and chronic tx
-lactulose converted to organic acids = ↓gut pH = protonation of ammonia and bacterial killing -cathartic effect = ammonia elimination lactulose 15-45 mL PO q8 hrs (enemas ok if NPO or no NG sol'n) -titrate dose to produce 2-4 soft, formed BMs daily -ADRs: flatulence, D, hyperglycemia, abdominal pain |
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hepatic encephalopathy: decrease ammonia production
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1. neomycin 1-2 g TID acutely (enemas ok if PO unavailable)
-inhibit gut bacteria ammonia production ADRs: nephrotoxic, ototoxic, malabsorption syndrome; limit use 2. metronidazole 250 mg q8 hrs -inhibit gut bacteria ammonia production -ADRs: GI intolerance, neuropathy, metallic taste 3. rifaximin 400 mg TID -PO non absorbable ABx -inhibits ammonia production -recent use in hepatic encephalopathy |
