Liver Flashcards

1
Q

How might liver dysfuntion typically present?

What are some labs that are essential to determine the cause and severity?

A
  • typically presents as flu-like symptoms followed by jaundice
  • Labs
    • bilirubin
    • aminotransferases (ALT, AST)
    • alkaline phosphatase
    • INR
    • albumin
    • serologic and genetic testing
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2
Q

What is bilirubin?

What is its “pathway?”

A
  • Bilirubin is the pruduct of broken down hemoglobin and myoglobin
  • Unconjugated bilirubin is formed in the periphery, it is transported to the liver bound to albumin
    • In the liver it is conjugated, making it water soluble so it can be excreted
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3
Q

What increases unconjugated bilirubin?

What increases conjugated bilirubin?

A
  • Unconjugated
    • increased bilirubin production
    • decreased hepatic uptake
    • decreased conjugation
  • Conjugated
    • decreased canalicular transport of bilirubin
    • acute/chronic hepatocellular dysfunction
    • obstruction of bile ducts
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4
Q

What is the difference between AST and ALT?

What can the ratio of AST to ALT tell us?

A
  • AST represents Liver AND extrahepatic tissues
  • ALT is highly specific to the liver
  • Ratio of AST:ALT
    • 2:1 is seen in patients with Alcoholic liver disease (ALD)
    • <1 is seen in patients with non-alcoholic steatohepatitis (NASH)
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5
Q

What can an elevated alkaline phosphatase tell us?

A
  • Increases in serum Alk phos levels lack specificity because it is found in cell membranes throughout entire body
  • In Cholestatic disorders, increased levels may indicate that bile salts are damaging hepatocyte membranes
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6
Q

What can the INR tell us regarding liver disease?

A
  • INR is a good test of the liver’s ability to synthesize things
    • if clotting time is prolonged, the liver may not be making adequate clotting factors
  • INR depends a lot on factor VII, which is produced in the liver and relies on Vit K
    • other vitamin K clotting factors are II, IX, X, proteins C and S
  • INR is part of MELD score because it is a reliable independent risk factor for mortality
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7
Q

What is another scoring tool used to determine mortality with ESLD?

A

Child-Pugh score

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8
Q

How is albumin used to assess liver function?

What else can cause decreased albumin levels?

A
  • Albumin is the most abundant plasma protein and is synthesized exclusively by hepatocytes
  • decreased albumin levels also seen in:
    • protein malnutrition
    • protein-losing disease (nephrotic syndrome)
    • severe reduction in synthetic capacity of liver
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9
Q

What lab differences would you see between prehepatic, intrahepatic, and posthepatic dysfunction? (chart)

Bili

AST/ALT

Alk phos

causes of changes

A
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10
Q

What are the different types of liver disease?

A
  • Biliary disease (acute cholecystitis)
  • acute hepatitis
  • chronic hepatitis
  • cirrhosis
  • acute liver failure
  • porphyria
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11
Q

What are the functions of the liver?

A
  • Glucose homeostasis
  • coagulation
  • metabolism of:
    • drug/toxin
    • heme
    • cholesterol/lipid
    • protein
  • production of thrombopoietin
  • **impaired liver function affects nearly every organ system in the body
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12
Q

What is cholecystitis?

Who is at greatest risk?

symptoms

How is it treated?

A
  • gallbladder or biliary tract stone
  • Fat, fair, female, forty, fertile
  • symptoms:
    • N/V
    • fever
    • abdominal pain
    • RUQ tenderness radiating to back
    • dark urine
    • scleral icterus
  • Surgery when condition has stabled
    • laparoscopic–>5% convert to open
    • ERCP (endoscopic retrograde cholangiopancreatography)
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13
Q

What are some considerations for all laparoscopic procedures?

A
  • insufflation will increase intraabdominal pressure
    • risk for inadequate ventilation- decrease TV, increase RR
    • decreased venous return leading to decreased CO and increased MAP and SVR
    • bradycardia due to peritoneal stretching
  • Risk for vascular injury and acute blood loss
  • CO2 embolism
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14
Q

General considerations for Liver patients

A
  • Consider volume and electrolyte replacement before procedure
  • Consider how pt will be positioned
    • trendelenburg- increases venous return and CO
    • reverse trendelenberg- aids surgical access and may improve ventilation but decreases venous return and CO
  • support HR and BP
  • Ventilation-watch PIP and MV
    • adjust accordingling: decrease TV, increase RR
  • NG/OG tube
  • avoid N2O
  • careful use of opioids- risk of sphincter of oddi spasm
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15
Q

How do inhaled agents affect blood flow to the liver?

A
  • Halothane: vasoconstriction of hepatic arterial bed, decreased O2 delivery to liver
    • also a concern for halothane hepatitis
    • NO Halothane, isoflurane, or sevoflurane
  • Isoflurane- increased flow velocity in hepatic sinusoids
  • Sevoflurane- equal or superior to Isoflurane in maintaining Hepatic artery blood flow (HABF)
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16
Q

What is the Hepatic artery buffer response (HABR)?

A
  • Autoregulatory
  • matches a drop in portal bloodflow (PBF) with an increase in hepatic artery blood flow (HABF)
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17
Q

What are the different types of hepatitis?

acute vs chronic?

A
  • Inflammation of the liver parenchyma
  • viral
  • autoimmune
  • drug induced
  • Acute- usually self limiting
    • most often viral
    • can be caused by drugs/toxins
  • Chronic- hepatic inflammation >6 months
    • cirrhosis, hepatocellular carcinoma or liver failure
  • Symptoms can range from minimal (malaise/jaundice) to severe with multiple organ compromise
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18
Q

What is autoimmune hepatitis?

How is it diagnosed?

How is it cured?

Treatment goals?

A
  • cellular immune response against self-antigens in the liver
  • diagnosis is confirmed with clinical findings, lab testing, and histologic evaluation
  • no curative intervention
  • Goal is to induce remission with corticosteroids and immunosuppressive drugs or liver transplantation
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19
Q

What are some drugs that induce hepatitis?

What is APAP? How does it cause problems?

A
  • Drugs that can induce hepatitis: (NOT a complete list)
    • analgesics
    • anticonvulsants
    • antibiotics
    • antihypertensives
  • APAP is acetaminophen
    • uses up all the glutathione stores leading to inability to conjugate substances (free radicals??)
    • Administer N-acetylcysteine within 8 hours (it provides cystein to make more glutathione)
  • Drug induced hepatitis resembles viral hepatitis so prompt diagnosis is important
  • remove offending agent
20
Q

What is Halothane Hepatitis?

A
  • An immune mediated hepatitis caused by all inhaled agents except sevoflurane
    • Trifluoroacetyl halide metabolites covalently bond with microsomal proteins on hepatocytes, changing them from “self” to “non-self”
  • IgG antibody mediated
  • Halothane is the most common culprit d/t high degree of liver metabolism
  • Sensitized ppl may show cross-reactivity with other volatile anesthetics (except sevo)
    • use TIVA or Sevo
21
Q

What is cirrhosis?

What are some signs and symptoms?

A
  • Chronic, progressive parenchymal damage leads to scarring and nodular formation
  • Signs/symptoms
    • fatigue/malaise
    • jaundice
    • anorexia, weakness, N/V
    • spider angiomata
    • hypoalbuminemia
    • ascites/hepatomegaly
    • coagulation disorders
    • endocrine disorders
    • hepatic encephalopathy
    • gastoresophageal varices
    • hyperdynamic circulation
    • hepatorenal syndrome
22
Q

What labs would you expect to see elevated in a pt with cirrhosis?

decreased?

A
  • elevated:
    • bilirubin
    • aminotransferase (AST/ALT)
    • alk phos
    • INR
  • decreased
    • serum albumin
    • platelets
    • blood sugar
23
Q

What is the Child-Pugh score?

A
  • People with severe liver disease have a decreased ability to respond to stress
  • Child-Pugh score is used to predict surgical mortality with cirrhosis based on extent of liver damage and type of surgery
    • total bili, serum albumin, INR, ascites, and hepatic encephalopathy
  • Class A- 10% mortality rate with intrabdominal surg
  • Class B- 30% mortality
  • Class C- 80% mortality
  • Class A&B ok for surgery if optimized, Class C avoid or delay elective surgery
24
Q

How can the liver pt be optimized prior to surgery?

A
  • improve diet with protein and caloric intake
  • blood glucsoe control pre/intra/post op
  • aldosterone antagonist
    • cirrhosis is associated with increased aldosterone secretion
  • electrolyte and fluid status
25
Q

What should you consider if your patient has hepatic encephalopathy?

Ascites?

A
  • encephalopathy
    • RSI!
    • Use sedatives and induction agents judiciously (or not at all)
  • Ascites
    • RSI
    • mechanical ventilation
    • pulmonary artery pressures
    • fluid status
26
Q

What should you consider if your patient has esophageal varices?

A
  • NO esophageal temp probe or NG/OG
  • If bleeding, RSI
    • octreotide 50 mcg/hr or vasopressin 20 units over 5 minutes
27
Q

How can you prepare for the coagulopathy common in liver patients?

A
  • type and cross
  • vitamin K non-emergently
  • FFP, cryo, platelets
    • the only factors NOT produced in the liver are factors III, IV, and XII
  • PRBCs
    • impaired ability to handle citrate loads
    • monitor ionized Ca
    • may need to administer Ca– especially if they are not responding to pressors
28
Q

How could liver disease affect pharmacokinetics of some drugs?

A
  • low albumin will cause decreased protein binding and increased volume distribution
  • decreased clearance
    • Ex. larger initial dose of NDMR to compromise for the increased VD bt decreased subsequent dosing due to decreased clearance
  • use caution with drugs dependend on liver for clearance
29
Q

What muscle relaxants are good choices?

A
  • Cisatracurium
  • atracurium
  • mivacurium
30
Q

What is importing regarding hepatic blood flow and anesthetics?

A
  • Need to maintain liver blood flow
  • Hepatic artery is 25% of blood flow and 50% of O2 delivery
  • Portal vein is 75% of blood flow and 50% O2 delivery
  • IV anesthetics maintain hepatic blood flow if arterial pressure is maintained
  • All inhalational agents maintain hepatic blood flow except halothane
  • avoid SNS stimulation
31
Q

What are some post-op concerns for patients with cirrhosis?

A
  • Post-op morbidity is increased
    • liver dysfunction/failure (#1 problem)
    • pneumonia
    • bleeding
    • sepsis
    • poor wound healing
    • DTs
    • electrolyte disturbances
    • renal failure
    • frequent aspiration
32
Q

What is the difference in anesthetic needs between acute and chronic ETOH use?

A
  • Chronic ETOH causes enzyme induction = increased anesthetic needs
  • Acute ETOH decreases anesthetic needs due to additive effects
    • RSI
33
Q

What are the symptoms of alcohol withdrawal syndrome?

A
  • increased SNS/catecholamine release
  • agitation
  • tachycardia
  • delirium tremors- 48-72 hours post ETOH; this is a medical emergency
  • hallucinations
  • diaphoresis
  • cardiac dysrhythmias
  • hemodynamic instability
  • grand mal seizures and hypoglycemia
34
Q

How is alcohol withdrawal syndrome treated?

A
  • benzos
  • beta blockers (propranolol or esmolol)
  • airway protection
  • correct fluid/electrolyte and metabolic disturbances
  • DTs mortality rate is 10% d/t hemodynamic instability, cardiac dysrhythmias and seizures
35
Q

What is porphyria?

A
  • A metabolic disorder that results from deficiency of specific enzyme in the heme synthetic pathway
  • results in overproduction of porphyrins
    • accumulation of intermediate forms of porphyrin at the site of blocked enzyme
36
Q

What are porphyrins essential for?

How is heme production regulated?

A
  • oxygen transport and storage
  • Heme is the most important porphyrin
    • heme is bound to proteins to form hemoproteins (including hemoglobin and CYP450 isoenzymes)
  • Heme production is regulated by aminolevulinic acid (ALA) synthase, which is in mitochondria
    • formation of ALA is controlled by endogenous concentrations of Heme in a feedback loop
  • ** In porphyria, an increase in heme requirements results in accumulation of pathway intermediates
37
Q

What can induce ALA synthetase?

What will that cause in a pt with porphyria?

A
  • Any metabolism that relies on CYP450 will induce ALA synthetase
  • this will result in increased intermediates in a pt with porphyria
38
Q

What is the most serious porphyria?

A
  • Acute intermittent porphyria
    • affects central and peripheral nervous system
      • systemic HTN and renal dysfunction
    • this is life threatening!
39
Q

What are some porphyria triggers?

A
  • Enzyme inducing drugs
    • allyl group on barbiturates
    • steroid structure
    • avoid pentathol, thiamylal, methohexital, etomidate
  • hormonal fluctuations
    • menstruation/menopause/ pregnancy
    • fasting (pre-op)
    • dehydration
    • stress
    • infection
40
Q

What are signs and symptoms of porphyria?

A
  • Severe abdominal pain, N/V, due to autonomic neuropathy
  • ANS instability
  • electrolyte imbalances (Na, K, Mg)
  • skeletal muscle weakness- respiratory failure
  • cardiovascular instability resulting in hypertension and tachycardia (hypotension less likely)
  • seizures
41
Q

How is porphyria treated?

A
  • remove triggering agents
  • hydration
  • carbohydrates
  • treat pain, N/V
  • BB for HTN and tachycardia
  • benzos for sz
  • fluid and electrolyte balance
    • 10% glucose saline infusion
  • Hematin 3-4 mg/kg IV
  • Somatostatin
  • plasmapharesis
42
Q

Anesthetic management of porphyria

A
  • Pre-op prep: identify and avoid triggers
  • assess skeletal and CN function
  • assess cardiac- HTN, tachycardia
  • minimize multiple drug exposure
  • fluid/electrolyte management
  • anticipate post-op ventilation
  • minimize stress of pre-op fasting: glucose-saline infusion
  • preop meds:
    • anxiolytics, aspiration porphylaxis
43
Q

What drug inhibits ALA synthetase activity and decreases heme consumption?

A

Cimetidine

44
Q

GA in a pt with porphyria:

A
  • Use short acting agents
  • moniors!
  • induction with propofol or ketamine
  • maintenance with N2O, IA, opioids or NDMR
  • cardiopulmonary bypass is a stressor
45
Q

Is regional contraindicated in a pt with porphyria?

A
  • Same contraindications and risks as other pts
  • Avoid regional in acute exacerbation of porphyria
46
Q

What are the unsafe drugs for patients with porphyria?

A
  • barbs
  • etomidate
  • sulfa antibiotics
  • ETOH
  • diazepam
  • Nifedipine
  • ketorolac
  • phenacetin