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

Liver Flashcards

(52 cards)

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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

22
Q

Blood volume in liver disease

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

GA Considerations in porphyria

Study These Flashcards
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?

Study These Flashcards
A

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

25
These meds can be given to treat porphyria
Hematin 3-4 mg/kg IV, somatostatin, plasmapheresis
26
Cholecystectomy Induction/Maintenance
Consider volume, e-lyte replacement RSI with cricoid pressure, cuffed tube Reverse tburg Mechanical ventilation Judicious use of opioids
27
Cholecystectomy and opioids
Sphincter of Oddi spasm occurs in 3% of the population Antagonize spasm with: Naloxone (maybe not the best idea). glucagon, NTG
28
Volatile anesthetics and hepatic dysfunctions
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
What would you do if a patient has post-op hepatic dysfunction
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
What is hepatitis
Liver disorder of varying etiology that results in **inflammation** and **necrosis** for more than **6 months**
31
Common hepatitis causes
HBV, HDV, HCV, autoimmune, drug induced Graded on degree of inflammation, necrosis, progression, and degree of fibrosis
32
Anesthesia for hepatitis
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
Pre-op considerations in hepatitis
Coags? Encephalopathy?
34
Induction for hepatitis
* NPO? * Volume status (often hypovolemic) * Other organ system involvement
35
Viral hepatitis
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
Hep B Tx
* Interferon * Lamivudine * Adefovir
37
Hep C Tx
* Interferon * Ribavirin
38
Autoimmune hepatitis Tx
* AZT * corticosteroids
39
What is cirrhosis
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
Liver blood supply
Hep. artery gives 25% flow and 50% oxygen Portal vein gives 75% flow and 50% oxygen
41
Pre-op/Induction cirrhosis
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
Post-op cirrhosis considerations
**Increased post-op morbidity** 1. Pneumonia 2. Bleeding 3. Sepsis 4. Poor wound healing 5. Liver dysfunction 6. DTs
43
DTs timeline
* **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
What is Porphyria
Defective enzyme leads to overproduction of porphyrin Acute intermittent porphyria is most serious
45
Porphyria Treatment
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
Triggers in porphyria
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
Anesthetic management in porphyria
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
What labs assess Liver function?
* Biliruben * Aminotranferases * Alkaline Phosphatase * INR * Albumin
49
Billiruben
**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
Aminotransferase
* 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
International Normalized Ratio
* 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
Albumin
* **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 )

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