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hepatic pathophysiology and disease Flashcards

1
Q

what are basic characteristics of the liver?

A
  • largest internal organ
  • weights about 1400-1800 g
  • located right side under ribcage
  • ability to regenerate
  • over 500 vital functions
  • involved in many digestive, vascular, and metabolic activities
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2
Q

what is the basic functional unit of the liver?

A

hepatic lobules compromised of hepatocytes

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3
Q

what vessels supply blood to the liver?

A
  • portal vein (75%)

- hepatic artery (25% w/ 2/3 of O2 supply)

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4
Q

what percentage of CO does the liver receive?

A

25-30%

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5
Q

what is unique about the hepatic portal vein?

A

not a true vein b/c it conducts blood to capillary beds in the liver and not directly to the heart

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6
Q

what is hepatic perfusion pressure (HPP)?

A

the combination of hepatic arterial pressure and portal venous pressure vs. hepatic venous pressure (CVP)
(HAP + HPV) - CVP

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7
Q

what causes decreased hepatic blood flow?

A
  • increased CVP
  • circulating catecholamines
  • hypoxia
  • hypercarbia (vasoconstriction)
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8
Q

what type of receptors are found in the hepatic artery?

A

both alpha and beta

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9
Q

what receptors are found in the portal vein?

A

only alpha receptors

*most effected by alpha vasoconstriction, impacting liver BF

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10
Q

how does the liver usu. compensate for portal blood flow decrease? what blunts this response?

A
  • hepatic artery BF increases to compensate
  • halothane blunts this response
  • isoflurane does NOT*
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11
Q

how does regional and general anesthesia affect hepatic blood supply?

A

both reduce hepatic blood supply to varying degrees (regional 30%)

  • halothane, enflurane: decreased HPBF; may decrease or may not change HABF
  • isoflurane, desflurane: decreased HPBF, increased HABF
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12
Q

what does the liver filter and how?

A
  • filters blood from the GI tract

- Kupffer’s cells

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13
Q

what is the amount of circulatory reservoir held by the liver to be put back into circulation when needed?

A

350 ml

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14
Q

what are primary functions of the liver?

A
  • bile production
  • protein synthesis (albumin, coagulation factors)
  • glycogen storage
  • protein metabolism
  • insulin clearance
  • lactate conversion into glucose
  • drug metabolism and transformation
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15
Q

what are other functions of the liver?

A
  • filtering
  • circulatory reservoir
  • creation of bile pigments, synthesis and secretion of bile
  • synthesis of cholesterol
  • detoxification
  • deposition and exchange of vit. (A, B, D), and iron, copper, zinc ions
  • regulation/balance b/w coagulant and anticoagulant system; formation of heparin
  • destruction of some microorganisms, bacterial ,and other toxins
  • deposition of plasma in the blood; regulation of a total amt. of blood
  • hemopoiesis in the fetus
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16
Q

what are the four primary causes of liver damage?

A
  • inflammation: immune response
  • fibrosis: scar tissue
  • cirrhosis: liver cells destroyed & replaced w/ scar tissue
  • hepatocellular carcinoma: liver cancer
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17
Q

describe albumin

A
  • plasma protein
  • 3.0-3.5 gm/dL
  • provides majority of oncotic pressure of the plasma
  • 1/2 life 14-20 days
  • chief site where drugs are protein bound
  • unbound portion of drugs is the portion that interacts w/ receptor sites
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18
Q

what happens when albumin drops below 2.5 gm/dL?

A

results of drugs (esp. highly protein bound) is exaggerated

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19
Q

what are the main morphological types of damage of the liver?

A
  • hepatitis
  • cirrhosis
  • cancer
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20
Q

what acute and chronic diseases of the liver contribute to pathophysiology?

A
  • infectious diseases: viruses, bacteria, spirochetes, pathogenic fungi, elementary, helminthes
  • toxic substances: hepatotoxins (alcohol, drugs i.e. oncology and bone marrow suppression)
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21
Q

what are rare causes of hepatic dysfunction

A
  • hyperdynamic circulation: AV malformations, hypoviscosity d/t anemia, increased intravascular volme
  • hypoxemia: r-l intrapulmonary shunt, V/Q mismatch, ascites (restrictive), decreased FRC, hyperventilation w/ resp. alkalosis
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22
Q

what clinical manifestations are seen with hepatic dysfunction?

A
  • arrhythmias
  • increased intra abdominal pressure w/ decreased gastric emptying (ascites)
  • poor thermoregulation
  • immunocompromised
  • anemia
  • coagulopathy
  • electrolyte abnormalities
  • acute renal failure
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23
Q

what enzymes are produced in the liver?

A

pseudocholinesterase and plasma esterases

*severe liver disease may cause prolonged action of succinylcholine, esmolol, and ester local anesthetics

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24
Q

how does hepatic extraction ratio affect drug clearance?

A
  • drug clearance dependent on hepatic extraction ratio of the drug
  • higher extraction ratio depends more on liver blood flow for clearance (propranolol, lidocaine (300%), morphine, meperidine)
  • lower extraction ratio depends more on protein binding and the liver’s enzymatic activity
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25
Q

how does decreased BF affect hepatic extraction ratio?

A
  • affects high extraction ratio drugs

- causing to last longer

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26
Q

how does decreased protein (albumin) levels or protein binding issues affect hepatic extraction ratio?

A
  • affects low extraction ration drugs

- cause to last longer

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27
Q

what happens with enzyme induction?

A

increased tolerance to some drugs from overproduction of enzymes like CP450

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28
Q

what are some causes of enzyme induction?

A
  • smoking
  • ethanol
  • benzodiazepines
  • ketamine
  • barbiturates
  • phenytoin
29
Q

what are common drugs that show an increased tolerance d/t enzyme induction?

A
  • sedatives
  • opioids
  • induction agents
  • muscle relaxants
  • robinul
30
Q

what may cause enzyme inhibition?

A
  • cimetidine

* causes an increase in drug’s effect

31
Q

what is the difference b/w hepatitis and cirrhosis?

A
  • hepatitis: liver inflammation; infection
  • cirrhosis: intensified diffuse growth of new connective liver tissue (stroma) on the background of dystrophic and necrotic hepatocytes (parenchyma) damage (thicker and tighter; things cant pass through; filtering is an issue)
32
Q

describe carbohydrate metabolism disorder

A
  • slowing down of glycogen synthesis may happen when hepatocytes are affected (glycogen synthesis and splitting are main regulatory processes to help liver keep glucose homeostasis, esp. its blood level)
  • leads to simultaneous limitation of glucuronic acid formation, which is indispensable in detoxification of many poisons (industrial toxins) and final metabolites and unconjugated bilirubin
33
Q

describe fat metabolism disorder

A
  • liver regulates nutrient balance
  • if no balance in food ingredients, liver takes the surplus substances and stores them until the necessary product appears to construct macromolecules and to expel them into the blood
  • w/ pathology, liver stores mainly fats since fat is easier to store and wont be able to supply nutrients it usu. stores
  • called fatty liver infiltration
34
Q

describe albumin metabolism disorder

A
  • hypoproteinemia: blood level decrease of albumins, which are synthesized by hepatocytes; leads to hypooncia and edema results
  • hemorrhagic syndrome: decreased synthesis of blood coagulation factors (except VIII) (abnormal PT, PTTs)
  • increase in BUN: decreased urea synthesis and ammonia accumulation; seen when 80% of parenchyma are affected
  • increase of enzymes level in blood (aminotransperases)
35
Q

describe copper metabolism disorder

A

Wilson’s Disease

  • rare and treatable disorder of copper metabolism
  • abnormal accumulation of copper in the hepatocytes
  • affect the basal ganglia (balance and motor), eyes, kidneys
  • ceruloplasm carries the copper, but in Wilson’s it is low, so copper cannot be carried to be metabolized
  • give a drug that binds copper to be removed
36
Q

what is hepatocerebral coma?

A
  • syndrome d/t liver insufficiency
  • characterized by significant impact on CNS
  • loss of consciousness
  • loss of reflexes
  • cramps
  • blood flow and breathing disorders
37
Q

what are the four most frequent hepatocerebral coma reasons?

A
  • viral hepatitis
  • toxic liver dystrophy
  • cirrhosis
  • portal hypertension
38
Q

the accumulation of what four toxic neurotropic substances are the main mechanism of CNS damage in hepatocerebral coma?

A
  • ammonia
  • decaying products
  • low molecular fatty acids
  • pyroracemic acid derivatives
39
Q

describe jaundice

A
  • symptom

- yellowish discoloration of the skin and sclera seen as a result of excess bilirubin in the blood (more than 1.2 mg/dL)

40
Q

what is bilirubin?

A

product of RBC breakdown

41
Q

what are the three main types of jaundice?

A
  • hemolytic jaundice (excessive breakdown of RBCs)
  • intrahepatic jaundice (cirrhosis, infection, inflammation)
  • extrahepatic obstructive jaundice (gallstones obstructing common duct)
42
Q

describe cholelithiasis effects

A
  • obstructive jaundice d/t obstruction to outflow of bile
  • bile pigment metabolism issues: accumulation of pigments and stones formed in gallbladder; elevated bilirubin, liver enzymes altered, may see steatorrhea
  • pts. in an acute gallbladder episode will look like liver failure, except it is treatable
43
Q

describe cholemic syndrome

A
  • appears w/ obstructive and parenchimatous jaundices

- bile acids enter blood causing symptoms

44
Q

what are the main four symptoms of cholemic syndrome?

A
  • bradycardia
  • hypotension
  • excitability
  • skin itch (rash)
45
Q

why may hypoglycemia be seen with hepatic pathology?

A

d/t glugoneogenesis or glycolosis problems

46
Q

what clinical triad characterizes hepatopulmonary syndrome?

A
  • portal HTN
  • hypoxemia
  • pulmonary vascular dilatations
  • when liver malfunctions, the 30% of CO coming to it backs up to the lungs (pulm. edema) and then eventually the heart (CHF)
47
Q

what is portopulmonary HTN (POPH)?

A

pulmonary HTN syndrome w/ vascular obstruction and increased resistance to pulmonary arterial flow
*liver not able to function properly d/t blocked BF and increased pressures

48
Q

what is hepatorenal syndrome?

A

form of pre-renal acute kidney injury that occurs in decompensated cirrhosis

  • if liver cant filter blood, toxins reach kidneys
  • late symptoms of cirrhosis
49
Q

what is used to assess mortality risk with cirrhosis?

A

Child Pugh Classification: score based on
-bilirubin
-albumin
-prothrombin time (PT)
-ascites
-encephalopathy
1-2.5 low, 2.5-3.5 mod., 3.5-5 significant risk

50
Q

what other measures predict mortality w/ liver cirrhosis?

A
  • ascites
  • increased serum creatinine
  • pre-op GI bleed
  • high ASA physical status
  • previous abd. surgery
51
Q

what represents actual liver function?

A
  • albumin
  • prothrombin time (PT)
  • pseudocholinesterase concentrations
  • if these abnormal, even if LFT normal, treat as liver failure
52
Q

what is the most sensitive indicator of hepatocellular dysfunction?

A

INR

*could be result of meds; does not mean chronic damage

53
Q

what is the diagnostic criteria for portopulmonary HTN (POPH)?

A
  • mean pulmonary artery pressure (mPAP) greater than 25 mmHg at rest and
  • pulmonary vascular resistance (PVR) of more than 240 dynes/s/cm-5
  • better measure is transpulmonary gradient greater than 12 mmHg (mPAP-PAOP) as this reflects the obstruction to flow (PVR)
  • w/ any ICU pt., check for previous caths or measurements
54
Q

what may cirrhotic pts. w/ end stage liver disease also suffer from?

A

cirrhotic cardiomyopathy

*portal HTN backs up to lungs, then heart

55
Q

what are AIs with hepatic encephalopathy?

A
  • more sensitive to benzos d/t increase in number of cerebral GABA receptors
  • even small doses can cause apnea (0.5 mg versed)
  • w/ liver problems, do pre-op in an area where resuscitation equipment available
56
Q

what are AIs w/ hyperdynamic circulation?

A
  • CO increased a lot
  • SVR decreased
  • increased MVO2
  • sensitive to catecholamines
  • circulation is increased, not liver function, so don’t need more meds d/t increased CO
57
Q

what are hepatic considerations with sedatives?

A
  • use cautiously
  • exaggerated response including apnea
  • *highly protein bound and protein is low
58
Q

what are hepatic considerations w/ aspiration?

A
  • decreased gastric motility
  • ascites (full stomach like)
  • aspiration prophylaxis
59
Q

what needs to be avoided with hepatic disease?

A
  • hypoxia
  • hypotension
  • decreased CO
  • *all of which are caused by anesthesia drugs
60
Q

what are hepatic considerations with regional anesthesia?

A
  • effective if no coagulopathy
  • better at maintaining hepatic blood flow than GA if hypotension can be avoided
  • platelet function needs to be greater than 100,000
61
Q

what are hepatic considerations w/ volatile agents?

A
  • all decrease the mean arterial pressure and portal blood flow (vasodilation)
  • isoflurane maintains hepatic blood flow best (VOLATILE AGENT OF CHOICE)
  • limit N2O: sympathomimetic effects causes hepatic vasoconstriction
62
Q

what are hepatic considerations with IV anesthetics?

A
  • modest impact on hepatic blood flow
  • no meaningful adverse impact on post op liver function if the MAP is adequately maintained
  • give small amounts to see how tolerated
  • *give time to work
63
Q

how does ketamine affect hepatic blood flow?

A

little impact

64
Q

how does propofol affect hepatic blood flow?

A

increases total hepatic blood flow in both hepatic arterial and portal venous circulation, suggesting a significant vasodilator effect; but decreases systemic BP 20%

65
Q

how does etomidate and thiopental affect hepatic blood flow?

A

-decrease hepatic blood flow either from increased hepatic arterial vascular resistance or from reduced CO and/or BP

66
Q

what NMB should be used with hepatic dysfunction?

A
  • atracurium (most) and cisatracurium
  • Hofmann elimination (atracurium) and ester hydrolysis (cisatracurium)
  • have clinical duration of actions similar to those in normal patients
  • metabolites metabolized renally and hepatically
67
Q

what muscle relaxants should you take caution w/ in hepatic disease?

A
  • succinylcholine: may be prolonged r/t decreased enzyme production (don’t give)
  • vecuronium, rocuronium: prolonged effect
  • *drugs of choice: atracurium and cisatracurium
68
Q

what should be considered w/ opioids and hepatic dysfunction?

A
  • morphine: most closely associated w/ sphincter of Oddi spasm (give dilaudid or Demerol)
  • fentanyl, sufentanil, alfentanil are ok to use
  • hepatic metabolism: prolonged effects and side effects
  • remifentanil: nonspecific plasma esterase metabolism (wears off quickly, must provide other pain management before stopping)
  • give slowly and small doses to see reaction
69
Q

with any drug when giving to a liver diseased pt. remember?

A

start low and go slow!

advanced pathophysiology (3 decks)

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