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!!!!! Co-Existing Disease !!!!! > Liver > Flashcards

Liver Flashcards

1
Q

The liver is the site of synthesis of all clotting factors except

A

vWF

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2
Q

CV function in patients with cirrhosis

A
  1. Hyperdynamic circulation
    1. High CO and Low SVR
  2. Possible cardiomyopathy
  3. Decreased response to catecholamines
  4. Increased flow to splanchnic, pulm, muscular, cutaneous beds
  5. Decreased hepatic flow
  6. Portal HTN
  7. Arterial hypoxemia
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3
Q

S/S of cirrhosis

A
  • Fatigue /malaise
  • Anorexia/ weakness
  • Nausea/ vomiting
  • Abdominal pain
  • Jaundice /spider nevi
  • Hypoalbuminemia
  • Coagulation disorders
  • Endocrine disorders
  • Hepatic encephalopathy
  • Gastroesophageal variceal
  • Hepatomegaly /ascites
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4
Q

Many alcoholics can get cardiomyopathy. How does this affect your anesthetic?

A

Don’t give anything that depressed the myocardium

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5
Q

How do the majority of cirrhosis patients die during abdominal surgery?

A

60% die from bleeding

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6
Q

Coagulation in Cirrhosis

A

Treat bleeding with FFP, Vitamin K, Platelets

Cirrhosis patients will have:

  1. Prolonged PT/INR
  2. Vit K deficiency
  3. factors II, V, VII, IX, X deficiency
  4. Thrombocytopenia

(Bleeding accounts for 60% of deaths in abdominal surgery →syrgery contraindicated if Platelets < 50,000 or PT> 3 )

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7
Q

Pre-op considerations in cirrhosis

A
  1. Treat as full stomach →RSI
  2. Low albumin → decrease doses
  3. Ascites → fluid status
  4. Cardiomyopathy
  5. PaO2 60-70 (R->L pulm shunt)
  6. Hypoglycemia
  7. Pneumonia
  8. Encephalopathy
  9. Hepatorenal syndrome
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8
Q

monitoring for cirrhosis patients

A
  1. CVP, A-line, +/- PA
  2. UO→ foley
  3. Blood glucose
  4. AVOID esophageal temp probe
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9
Q

Why are cirrhosis patients considered full stomachs?

A
  • Alcohol use weakens the lower esophageal sphincter
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10
Q

Liver patients tend to be (hyper/hypo)glycemic

A
  • Hypoglycemic.
  • Give fluids with glucose
  • Pts are hypoglycemic d/t decreased hepatic gluconeogenesis.
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11
Q

How should we maintain anesthesia for the patient with cirrhosis?

A

IA at 1/2 MAC with N2O and opioids

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12
Q

In cirrhosis, we need a (higher/lower) dose of NMRs and why?

A

Need higher dose because Vd will be increased

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13
Q

What NMBs are best for cirrhosis

A
  • Mivacurium
  • atracurium
  • cisatracurium*
  • (the ones metabolized in blood)
  • Sux is apparently ok too
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14
Q

Reasons why liver patients are at risk for morbidities post-op

A
  • Pneumonia
  • Bleeding
  • Sepsis
  • Poor wound healing
  • Liver dysfunction
  • DT’s
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15
Q

Other comorbidities that alcoholics may have

A
  • Hypothermia
  • alcoholic poluneuropathy
  • Wernicke-Korsakoff syndrome
  • Pernicious anemia
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16
Q

Considerations for Maintinence of anesthesia ain cirrhosis patients

A
  1. Balanced technique:
    • Combine Volitile anesthetics (1/2 MAC), N2O and opioids.
  2. Manitain hepatic blood flow →
    • Sevo, Iso and Des are all safe to use
    • MUST maintain an adequate BP →hypotension will decrease oxygen delivery to the hepatoytes
  3. Use NMBs that are metabolized in the blood
    • mivacurium, atracurioum, cis-atratrcurium, sux
    • Will also need larger doses → d/t larger volume of distribution, but also the doses will last longer
  4. Don’t give anything that will depress the heart!
  5. Patients will have low protein binding
  6. Bleeding risk
  7. Considered full stomachs
    • poor lower esophageal sphincter tone
  8. ​Give fluids that contain glucose → often they become hypoglycemic
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17
Q

This enzyme is deficient in porphyria

A

ALA synthetase

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18
Q

S/S of porphyria attack

A
  • abd pain
  • N/V
  • ANS instability (HTN and tachycardia)
  • electorlyte (Na, K, MG) disturbances,
  • neuro psych manifestations
  • weakness
    • Weakness can progress to quadriparesis and respiratory failure.
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19
Q

Regional anesthesia and porhyria

A
  1. AVOID During an acute exacerbation
  2. itherwise no absolute contraindications
  3. Pre anesthetic neuro eval
  4. Keep in mined ANS blockade may lead to cardiovascular instibility (especially with hypovolemia)
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20
Q

Why do patients have hyperdynamic circulation with liver disease?

A

Accumulation of vasodilating compounds like prostaglandins and interleukins. Reduced blood viscosity may also play a role.

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21
Q

Any IAs that decrease hepatic BF will increase serum concentrations of

A

Alpha-GST

22
Q

Blood volume in liver disease

A
  • Decreased in central circulation
  • but increase in
    • splanchnic, pulmonary, muscle, and cutaneous corcualtion.
23
Q

GA Considerations in porphyria

A
  1. Use short acting agents
  2. Monitor for instability
  3. Induction
    • Propofol, ketamine → these are ok to use in porphyria
    • NO ETOMIDATE → trigger
  4. Maintenance
    • Nitrous, inhaled anesthetics, opioids, NDMR
  5. CP bypass is a stress → will need ICU after and VERY good post op management!
24
Q

Is cimetidine good or bad in porphyria?

A

GOOD. It decreases heme consumption and decreases ALA synthetase activity.

25
Q

These meds can be given to treat porphyria

A

Hematin 3-4 mg/kg IV, somatostatin, plasmapheresis

26
Q

Cholecystectomy Induction/Maintenance

A

Consider volume, e-lyte replacement RSI with cricoid pressure, cuffed tube Reverse tburg Mechanical ventilation Judicious use of opioids

27
Q

Cholecystectomy and opioids

A

Sphincter of Oddi spasm occurs in 3% of the population Antagonize spasm with: Naloxone (maybe not the best idea). glucagon, NTG

28
Q

Volatile anesthetics and hepatic dysfunctions

A

VA produce a self-limiting post-op liver dysfunction- transient increase in alpha-GST Halothane hepatitis: Immune mediated 1 in 10,000-30,000 Only Sevo does not metabolize into trifluoroacetylaed compounds

29
Q

What would you do if a patient has post-op hepatic dysfunction

A

Multi-factorial analysis

  1. Review all drugs administered
  2. Check for sepsis
  3. Check bilirubin
  4. Rule out occult hematomas → hyperbilirubinemia
  5. Review peri-operative record for hypotension, hypoventilation, hypoxemia, hypercarbia, and hypovolemia***
30
Q

What is hepatitis

A

Liver disorder of varying etiology that results in inflammation and necrosis for more than 6 months

31
Q

Common hepatitis causes

A

HBV, HDV, HCV, autoimmune, drug induced Graded on degree of inflammation, necrosis, progression, and degree of fibrosis

32
Q

Anesthesia for hepatitis

A

How long has the hepatitis been present What stage is it What type/mode of transmission Signs/symptoms the pt is experiencing Is patient optimized for anesthesia (fluids, e-lytes) Does everyone have proper vaccines in place?

33
Q

Pre-op considerations in hepatitis

A

Coags? Encephalopathy?

34
Q

Induction for hepatitis

A
  • NPO?
  • Volume status (often hypovolemic)
  • Other organ system involvement
35
Q

Viral hepatitis

A

5 types- HAV, HBV, HCV, HDV, HEV

  • C most common blood borne infection in US
  • D can only infect if the pt already has B
  • E for enteric transmission in Asia, Africa, Central America

S/S

  • anorexia, N/V, low grade fever, dark urine, clay colored stool, jaundice, acute liver failure
  • AST/ALT 400-4000
36
Q

Hep B Tx

A
  • Interferon
  • Lamivudine
  • Adefovir
37
Q

Hep C Tx

A
  • Interferon
  • Ribavirin
38
Q

Autoimmune hepatitis Tx

A
  • AZT
  • corticosteroids
39
Q

What is cirrhosis

A

Affects 3 million in US, 12th leading cause of death Mostly due to ETOH and Hep C Alters all organ systems in advanced stages

40
Q

Liver blood supply

A

Hep. artery gives 25% flow and 50% oxygen Portal vein gives 75% flow and 50% oxygen

41
Q

Pre-op/Induction cirrhosis

A
  1. volume status
  2. RSI
  3. Protein binding
  4. ETOH on board? (lowers anesthetic requirements)
  5. Cardiomyopathy
  6. Consider vitamin K, FFP, Platelets
  7. Administer glucose solutions
42
Q

Post-op cirrhosis considerations

A

Increased post-op morbidity

  1. Pneumonia
  2. Bleeding
  3. Sepsis
  4. Poor wound healing
  5. Liver dysfunction
  6. DTs
43
Q

DTs timeline

A
  • 6-8 hours of ETOH withdrawa pt may become tremulous
  • 24 hours hallucinations, grand mal seizures may occur
  • DTs within 72 hours
  • Treat with benzos
44
Q

What is Porphyria

A

Defective enzyme leads to overproduction of porphyrin Acute intermittent porphyria is most serious

45
Q

Porphyria Treatment

A
  1. Hematin 3-4mg/kg (drug of choice)
  2. Remove triggering agents
  3. Hydration
  4. Carbohydrates (b/c a trigger is fasting)
  5. Treat pain and N/V
  6. Beta blockers for HTN & tachycardia
  7. Benzodiazepines for seizures
  8. Fluid and electrolyte balance (10% glucose saline infusions)

(also somatostatin, plasmapheresis)

46
Q

Triggers in porphyria

A
  1. Drugs that have an Allyl group →barbs
  2. Drugs with a Steroid structure
    1. Pentathol, thiamylal, methohexital, etomidate​
  3. Hormonal fluctuations (everything we induce!)
    1. fasting
    2. dehydration
    3. stress
    4. infection
47
Q

Anesthetic management in porphyria

A
  1. Avoid known triggers
    • minimize use of multiple drugs
  2. Minimize stress
  3. Ensure proper hydration
    • use glucose solution
  4. Give anxiolytics
  5. Cimetidine
    • decreases heme consumption and inhibits ALA synthetase (good)
48
Q

What labs assess Liver function?

A
  • Biliruben
  • Aminotranferases
  • Alkaline Phosphatase
  • INR
  • Albumin
49
Q

Billiruben

A

Degreation procuct of hemoglobin and myoglobin

  • Unconjugated is formed in the periphery→transported to liver via albumin→conjugated into water soluble compounds (unable to cross membranes)→eliminated from body

​​Increased *UNconjugated* biliruben

  • Increased biliruben production (hemolysis, skeletal muscle breakdown)
  • Decreased Hepatic uptake (low albumin stores)
  • Decreased conjugation

Increased *Conjugated* Biliruben:

  • decreased canicular transport of biliruben (billiary tract problem)
  • Acute/chronic hepatocellular dysfunction
  • Obstruction of bile ducts
50
Q

Aminotransferase

A
  • Lacks liver specificity → found throughot the body
  • Cholestatic disorders: increased levels may indicate damage of hepatic membranes from bile salt
  • 5’NT = most specific to billiary damage
51
Q

International Normalized Ratio

A
  • Strong correlation of deteriorating hepatic function
  • Used in Child-Pough score
  • Incicates impairment of hepatic synthesis of coagulation factors and Vitamin K
  • Tests 2, 7, 9, 10 and proteins C and S
52
Q

Albumin

A
  • MOST abundant plasma protein (only made in liver)
  • Synthesized by hepatocytes
  • If levels are decreased may mean:
    • Protein manutrition
    • Loss of protein →nephrotic syndrome
    • severe reduction in synthesis from liver

(acute liver failure will have high levels of albmin → albumin half life = 21 days )

!!!!! Co-Existing Disease !!!!! (15 decks)

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