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Flashcards in Liver- Disease Deck (28)
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1

What is associated with acute liver disease? Most common cause?

Chronic?  Most common cause?

  • Acute- elective surgery has high M&M
    • encephalopathy- req ICP management
    • Coagulopathy (INR > 1.5)
    • No history of liver disease
    • illness <26 weeks to be considered acute
    • most common: acetaminophen toxicity
  • Chronic
    • Hepatic inflammation and necrosis continued for >6 months
    • need liver biopsy for grading (inflammation and necrosis)
    • most common: HBV, HCV, and autoimmune

2

What are the five types of viral hepatitis?

  • **Varied presentation ranging from asymptomatic to acute hepatic failure
    • flue like symptoms, malaise, muscle pain, jaundice, dark urine
  • Hep A- enteric, contaminated food
    • usually get better after 21 days if previously healthy
  • Hep B (50% of US cases)
    • Bodily fluids, IV drug abuse
  • Hep C (30% of US cases)
    • sexually transmitted, needlesticks
  • Hep D (20% of US cases)
    • RNA strand requires Hep B at same time
  • Hep E- similar to hep A
  • Miscellaneous causes- CMV, epstein Barr, Herpes

3

Toxin and drug-induced hepatitis

What is directly toxic?

What cause idiosyncratic reactions?

  • Directly toxic:
    • carbon tetrachloride
    • acetaminophen- tx with N-acetylcysteine
    • alpha-amanitin (toxic mushroom)- tx with HD
  • Idiosyncratic reactions: unpredictable and not dose dependent
    • NSAIDS
    • VA
    • anti-HTN meds
    • anticonvulsants

4

VA induced hepatitis:

How does it present?

What are risk factors?

  • Presentation:
    • fever
    • anorexia
    • nausea
    • chills
    • myalgias
    • rash
    • fever 
    • arthralgia
    • eosinophilia followed by jaundice 3-6 days later
  • Risk factors:
    • PRIOR EXPOSURE!
    • >40 yrs old
    • obesity
    • female
    • mexiican ethnicity
    • multiple brief procedures within brief duration of time
    • enzyme induction

5

VA induced hepatitis:

What causes it?

  • Immune theory
    • Cytochrome P450 2EI oxidizes each anesthetic (exc Sevo) to yield highly reactive (toxic) intermediates that bind covalently (acetylation) to a variety of hepatocellular macromolecules
    • Altered hepatic proteins may trigger an immunologic response that causes massive hepatic necrosis
    • Causes halothane hepatitis

6

How much of each VA is hepatically metabolized?

 

KNOW THIS!  Board question!

  • Halothane 20-46%
  • Enflurane 2.5-8.5%
  • Sevoflurane 2-5%- NOT going to cause halothan hepatitis
  • Isoflurane 0.2-2%
  • Desflurane 0.02%

7

How do the VA affect hepatic blood flow?

  • HBF and oxygenation decrease with general anesthesia with VA
    • Halo > Enfl > Des > Iso > Sev
  • Decreased CO and stress response = catecholamine induced vasoconstriction (???)
  • Metabolic demands do decrease, improving the supply demand balance

8

How does N2O affect HBF and oxygen delivery?

  • Increase in SNS activity = mild vasoconstriction of splanchnic vasculature (decreased portal flow) and hepatic arterial system
  • inhibition of methionine synthase activity 
    • prolonged exposure leads to B12 deficiency
  • No concrete evidence it causes hepatic toxicity if supply-demand O2 is normal
    • does cause hepatic disease in providers that use it often

9

How do IV anesthetics affect HBF and O2 delivery?

  • only have modest impact on HBF and no meaningful adverse influence on postoperative liver function when BP is maintained
  • Opioids increase tone of CBD and SOO
    • also increase number of phasic contractions leading to increased biliary tract pressure and spasm

10

How does neuraxial anesthesia affect HBP and O2 delivery?

  • HBF decreases during spinal and epidural anesthesia parallel to reductions in BP
  • Reduced PBF and unchanged HABF causes a decrease in THBF
  • Changes may NOT be reversed with fluids and vasopressors 
    • vasopressors may drop splanchnic blood forr wihich will further reduce portal blood flow

11

What are other causes of peri-operative liver dysfunction?

  • Inflammation and sepsis- less blood flow to liver, but liver is producing the inflammatory mediators....set up for failure
  • hypoxia and ischemia
  • cardiac disease
  • surgical stress

12

What is nonalcoholic fatty liver disease?

  • Most common US chronic liver disease
    • associated with DM II and obesity
    • Bariatric surgery often improves
  • Fat accumulation in liver >5% of weight
    • may have increased M&M with abdominal procedures
  • Sx range from asymptomatic to cirrhosis

13

What are the different types of alcoholic liver disease?

  • Steatosis- caused by binge drinking; if they stop they will recover (Octoberfest)
  • Alcoholic hepatitis
  • Cirrhosis
  • ***alcohol abusers have a 2-3x increase in peri-op morbidity

14

What is cirrhosis?

 

Sx?

  • Parenchymal liver disease
  • Most commonly caused by HCV and alcoholism
  • Chronic inflammation/necrosis results in fibrotic changes
  • Sx:
    • anorexia
    • weakness
    • N&V
    • abdominal pain
    • hepatosplenomegaly
    • ascites
    • varices
    • jaundice
    • spider nerves
    • metabolic encephalopahty
  • EVERY organ and body system is altered

15

What are the hepatic vascular abnormalities seen in cirrhosis?

  • Hallmark of end-stage cirrhosis = portal HTN
  • Portal HTN results in porto-systemic collaterals which develop by dilation and hypertrophy of existing vascular channels
  • Ascites
  • hepatic encephalopathy
  • varices
  • susceptibility to bacterial infections
  • altered drug metab

16

What are the cardiovascular abnormalities seen in cirrhosis?

  • Hyperdynamic circulation:
    • high CO
    • low SVR
    • low normal BP
    • normal or increased SV
    • normal filling pressures
    • high normal HR
  • Systolic and diastolic dysfunction correlates with degree of disease
  • prolonged QT in 30-60% of end stage pts
  • Increased TBV with decreased central "effective volume and hypervolemic splanchnic circulation
  • Extensive arteriovenous collateralization
  • decreased response to catecholamines
    • high concentrations of circulating endogenous vasodilators

17

What are esophageal varices?

How can they be handled?

  • Portosystemic collaterals formed after pre-existing vascular channels are dilated by portal HTN
    • 1/3 of initial bleeding episodes are fatal
  • Non-selective B-blockers (propranolol and nadolol) reduce risk of bleeding by 40-50%
  • IV somatostatin (octreotide) for acute or suspected bleed
  • Endoscopic band ligation/scelrotherapy is sometimes done if the patient cannot tolerate medical therapy
    • 90% effective in stopping active blddding

18

What are the pulmonary implications of cirrhosis?

  • Hepatopulmonary syndrome- progressive hypoxemia
    • intrapulmonary shunting
  • VQ mismatch- impaired hypoxic pulmonary vasoconstriction, pleural effusions, ascites, and diaphragm dysfunction
  • Right shift of oxyhgb diss curve- increased erythrocyte 2,3 DPG levels
  • Altered pulmonary diffusion capacity- secondary to increased ECF, interstitial pneumonitis, and porto-pulmonary HTN

19

What are the different theories of ascites in cirrhosis?

  • "Overflow theory"- primary renal tubular retention of Na as a result of portal HTN
    • increased plasma volume results and ascites develops as fluid is translocated out of splanchnic circulation
  • "Underfill theory"- reflects the normal homeostatic response to intravascular volume depletion (Na and H2O retention)
    • decrease in effective volume because of ascites/portal HTN
    • renal tubular reabsorption of Na and increased ECF volume = increased ascites and edema
  • "Peripheral arterial vasodilation hypothesisi"
    • portal HTN causes the production of mediators such as NO to vasodilate and enlarge the intravasc compartment and decreasing the effective volume
    • Baroreceptors are then activated causing SNS, RAAS, and vasopressin release, causing Na and H2O retention

20

Explain the flow chart of Cirrhosis-induced portal hypertension

21

How is cirrhosis with Portal HTN and ascites treated?

  • Na and fluid restriction
  • diuretics (spironolactone or amiloride)
  • Repeated paracentesis with albumin adminstrated only if >5L removed
    • administer 6-8 g albumin/L of ascites removed
  • Peroneal-venous shunt now uncommon
  • TIPS- improves quality of life but increaases risk of encephalopathy and high shunt failure rate

22

What are the renal abnormalities seen with cirrhosis?

  • Dramatic reduction in Na and free H2O excretion
    • d/t chronic SNS and RAAS activation
    • endogenous vasodilators very important
  • Decrease in renal perfusion and glomerular filtration
    • hepatorenal syndrome seen in extreme cases

23

Cirrhosis can cause hepatorenal syndrome.

What is it?

What are the two types?

How are they treated?

  • Prerenal failure characterized by intense vasoconstriction of the renal circulation, low GFR, preserved renal tubule function and normal renal histology
  • Type 1- progressive oliguria with a rapid rise in serum Cr.
    • poor prognosis
    • vasopressin, somatostatin or analogue w/volume expansion can help treat
  • Type 2- moderate, more stable impairment in renal function sually seen in pts with refractory ascites
  • Treatment aimed at reversing the pathophysiological cause (splanchnic arterial vasodilation
    • Vasoconstrictor therapy (AVP)
    • Octreotide
    • Albumin
    • transplant is usually curative

24

What are the hematologic and coagulation implications of cirrhosis?

  • Anemia- may occur because of:
    • plasma volume expansion
    • GI bleed
    • malnutrition
    • vit deviciency
    • hemolysis
    • hypersplenism
    • bone marrow dep
  • Synthesis of Vit K dependent factors decreases
    • II, VII, IX, X, Proteins C and S
    • factor VII must be decreased by 60-70% before the PT will be prolonged
  • Thrombocytopenia
    • splenic sequestration syndrome
    • bone marrow depression (ETOH, interferon, other meds)
    • immune mediated platelet destruction (plt-associated IgG)
  • Dysfibrinogenemia (activation of fibrinolysis)
    • abnormal fibrinogen functioning leading to increased FDPs and D-dimer
    • pt may have prolonged thrombin time, normal to slightly prolonged PT, PTT and "nml" fibrinogen levels but still have coagulation issues

25

What are the endocrine disorders caused by cirrhosis?

  • Abnormal glucose utilization
    • increased fatty acid concentration in plasma antagonizes insulin's ability to promote glucose uptake by skeletal muscle
  • growth hormone and glucagon levels are increased causing decreased glucose tolerance
  • Hypoglycemia- caused by:
    • glycogen depletion
    • failure of gluconeogenesis
    • impairment of hepatic conversion of lactate to glucose
  • Abnormal sex hormone metabolism leads to feminization of males, amenorrhea in females

26

What are the Sx of hepatic encephalopathy caused by cirrhosis?

What causes it?

  • Hepatic encephalopathy in cirrhotic pt is complex but reversible
  • clinical manifestations range from small personality changes to confusion, lethargy, somnolence and coma
    • Neuropsychologic and neuromotor Sx: hyperreflexiveness, nystagmus, posturing
    • Ammonia accumulation leads to inappropriate levels of inhibitory and/or excitatory neurotransmitters
  • 50-70% of cirrhotic pts have at least minimal symptoms

27

What are the factors associated with hepatic encephalopathy?

  • Increased ammonia production- excessive dietary protein, constipation, GI bleed, infection, azotemia
  • Fluid, electrolyte, and acid-base imbalance generates ammonia
    • surgical stresses, GA-related reduction in hepatic perfusion
    • vomiting, diarrhea
    • diuretics
    • paracentesis
  • Altered liver and brain function
    • hypoxia
    • hypotension
    • anemia
    • hypoglycemia
    • sedation
  • Reduced hepatic metabolism- creation of portal-systemic shunt

28

What can cause cholestatic disease?

Signs and symptoms?

  • Impaired biliary flow
    • dysfunction of the bile transporter is the main cause of intrahepatic cholestasis
    • mechanical obstructions to bile flow is the chief cause of extrahepatic cholestasis
    • unconjugated bilirubin disrupts essential matabolic pathways (oxidative phosphorylation, tricarboxylic acid cycle, glycogenesis)
      • at high concentrations can cause membrane dysfunction
    • Cholestatic disorders can induce pathologic changes throughout the body affecting elimination and pharmacokinetics
  • Signs and symptoms:
    • pruritis, jaundice, lighter colored stool, dark urine (bile diverted from GI to GU tract