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Concepts 3 > Hepatic System (FINAL EXAM) > Flashcards

Hepatic System (FINAL EXAM) Flashcards

1
Q

Basic anatomy of the liver

A

The liver consists of a right and left lobe, separated by the falciform ligament

The right lobe has 2 additional lobes, the caudate and quadrate lobes

The liver is also described as having 8 different segments

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2
Q

The liver is composed of ___ lobules.

A

50,000 – 100,000 lobules

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3
Q

Each lobule in the liver consists of ___

A

Hepatocytes
Many portal tracts
Hepatic arterioles
Portal venules
Bile canaliculi
Lymphatics
Nerves
One Centrilobular vein

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4
Q

The acinus is ________

A

The functional unit of the liver
Includes same anatomical structures as the lobule, but the portal tract is in the middle and the centrilobular veins at the periphery
Consists of three zones
* Zone 1 is most sensitive to hepatoxic agents. Zone 3 is least sensitive to hepatotoxic agents.
* Zone 3 is most sensitive to ischemic injury. Zone 1 is the most protected in an ischemic event.

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5
Q

Kupffer cells

A
  • Are macrophages found within the sinusoidal channels of the liver
  • Essential to filtering bacteria, viruses, proteins and particulate from blood
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6
Q

What is bile?

A

A dark green fluid that aids in the digestion of lipids and absorption of vitamins A, D, E and K

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7
Q

Vitamin K deficiency is manifested as _____.

A

a coagulopathy due to impaired formation of prothrombin and of factors VII, IX, and X

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8
Q

Bile is produced by ____.

A

hepatocytes

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9
Q

Bile drains into the ____

A

the bile ducts and converges to form the common hepatic duct

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10
Q

The sphincter of Oddi controls the ____.

A

emptying of the common hepatic duct into the duodenum

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11
Q

Innervation of the liver

A

supplied by T6–T11 sympathetic nerve fibers, vagal nerve parasympathetic fibers, and right phrenic nerve fibers

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12
Q

Some autonomic fibers synapse first in the _______, whereas others reach the liver directly via ______.

A

celiac plexus

splanchnic nerves and vagal branches before forming the hepatic plexus

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13
Q

Sympathetic activation results in _____.

A

vasoconstriction of the hepatic artery and mesenteric vessels, decreasing hepatic blood flow

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14
Q

The liver receives what percent of cardiac output?

A

25%

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15
Q

Liver perfusion is supplied by which two vessels?

A

1) portal vein and 2) the hepatic artery

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16
Q

Details on the portal vein

A

supplies 70% of the liver blood flow and 50% of the oxygen
* Vasoconstriction: a1 receptors
* Vasodilation: D1 receptors

Receives venous blood that has passed through splanchnic circulation
blood flow dependent on spleen and GI tract flow

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17
Q

Details on the hepatic artery

A

supplies 30% of the liver blood flow and 50% of the oxygen content
* Vasoconstriction: a1 receptors
* Vasodilation: b2, D1, and cholinergic receptors

The hepatic artery is a branch from the aorta
* Blood flow dependent on autoregulation

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18
Q

Unique properties of blood flow with the hepatic artery and portal vein

A

Some **compensation **between portal vein and hepatic artery blood flow
Decrease in flow flow from one increases the flow the another

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19
Q

Where are the majority of our cytochrome p450 enzymes located?

A

Zone 3 of the Acinus

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20
Q

Intrinsic regulation revolves around ____

A

Intrinsic regulation = hepatic arterial buffer response
By adenosine
Limited by things like portal venous pressure

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21
Q

Extrinsic regulation revolves around ____

A

Extrinsic regulation = by metabolic state
↓ pH, pO2, ↑ pCO2 of portal blood→ ↑ hepatic artery flow to sustain metabolism

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22
Q

Hypercarbia can do what to hepatic perfusion

A

increase it

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23
Q

The liver is a reservoir for ___

A

blood

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24
Q

Low resistance of hepatic sinusoids allows ___

A

large blood flow through the portal vein

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25
Q

Small changes in hepatic venous pressure can result in ___.

A

large changes in hepatic blood volume

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26
Q

Chart comparing hepatic venous blood volume and hepatic venous pressure

A
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27
Q

What are some examples of how changes to hepatic venous pressure can influence blood volume?

A
  1. Intraoperative hemorrhage ➡️ decrease CVP ➡️ decrease hepatic venous pressure ➡️ shifts blood from liver to circulation (300 mL)
  2. Congestive heart failure ➡️ increase CVP ➡️ increase hepatic venous pressure ➡️ shifts blood from circulation to liver (1 L)
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28
Q

Function of Kupffer cells

A

Cleanse more than 99% of bacteria load
Process antigens
Release cytokines

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29
Q

The liver is the major organ for the storage of what?

A

Major organ for glycogen storage

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30
Q

What enhances glycogenesis?

A

Insulin

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31
Q

What enhances glycogenolysis?

A

Epinephrine and glucagon

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32
Q

The liver is responsible for the metabolism of ____.

A

macronutrients (like carbohydrates)

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33
Q

Glycogenesis = ____

A

Glycogenesis decreases the blood sugar level to normal.

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34
Q

Glycogenolysis = ____

A

Glycogenolysis increases the blood sugar level.

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35
Q

Glycogen stores are depleted after___.

A

24 hours of fasting

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36
Q

The liver and kidney can form glucose from ___.

A

lactate, pyruvate, amino acids and glycerol. Gluconeogenesis is vital for the maintenance of normal blood sugar.

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37
Q

Gluconeogenesis

A

Gluconeogenesis refers to synthesis of new glucose from noncarbohydrate precursors, provides glucose when dietary intake is insufficient or absent.

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38
Q

What enhances gluconeogenesis?

A

Glucocorticoids, catecholamines, glucagon and thyroid hormone

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39
Q

What inhibits gluconeogenesis?

A

Insulin

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40
Q

When carbohydrate stores are saturated, the liver converts the excess carbohydrates (and proteins) into _____.

A

fat (fatty acids), which can be used directly as fuel or stored in the liver or adipose tissue.

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41
Q

What can utilize only glucose?

A

Only RBCs and the renal medulla can utilize only glucose (even neurons can switch to fatty acid breakdown products – ketone bodies – after several days of starvation).

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42
Q

Discuss the liver and protein metabolism

A

The liver performs CRITICAL steps in protein metabolism. Without this function, death occurs in a matter of days.
* Deamination of amino acids (converts them to carbs and fats – “transamination”)
* Formation of Urea (formed from ammonia)
* Interconversions between nonessential amino acids

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43
Q

Discuss the liver and the formation of plasma proteins

A

Nearly all plasma proteins (except for immunoglobulins)
Albumin
ALL COAGULATION FACTORS (except for Factor III, IV and VIII
Anticoagulants: protein C and S, antithrombin III
Plasma Cholinesterase (pseudocholinesterase)

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44
Q

Drug Metabolism in the liver (general info)

A

Most drugs undergo hepatic biotransformation.
End products are inactivated or more soluble (more easily excreted in kidney or by bile)
There are two phases

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45
Q

Phase I of drug metabolism in liver

A

Phase I: via oxidases and P-450
Oxidation
Reduction
Deamination
Sulfoxidation
Dealkylation
Methylation

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46
Q

Phase II of drug metabolism in liver

A

conjugation

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47
Q

Enzymes systems, like the CYP450 system can be increased and decreased by ____.

A

exposure to other drugs

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48
Q

CYP450 inducers

A

Barbiturates, ketamine, benzodiazepines, phenytoin, chronic alcohol use, rifampin, glucocorticoids,

“Bad kids bring pot causing risky games”

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49
Q

CYP450 inhibitors

A

Acute alcohol use, Omeprazole, erythromycin, Cimetidine

“Always Offer Excellent Candy”

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50
Q

The liver converts ____

A

T4 to T3

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51
Q

The liver degrades ____

A

Thyroid Hormone, Insulin, Estrogen, Aldosterone, Cortisol, Glucagon and ADH

52
Q

The liver stores ____

A

Vitamins A, B12, E, D, and K

53
Q

The liver produces _____

A

transferrin, haptoglobin, and ceruloplasmin

54
Q

The liver synthesizes

A

thrombopoietin which stimulates platelet production

55
Q

Erythropoiesis = ____

A

Erythropoiesis: Heme and Bilirubin Metabolism
* Primary erythropoietic organ of the fetus - 2 months of age
* Metabolism of hemoglobin produces bilirubin
Conjugation of bilirubin

56
Q

What is one test that can evaluate all liver injury?

A

Trick question!

There is not one laboratory test to evaluate overall hepatic function, therefor one test must be interpreted with other results and clinical assessment of the patient

57
Q

Liver abnormalities can often be divided into ____.

A

synthetic function, hepatocellular injury, hepatic clearance and biliary duct obstructions

58
Q

Normal value for PT

Additional info?

A

12-14 seconds

*Very sensitive for acute injury (V and VII t1/2 is <25 hours)
*Prolonged by vitamin K deficiency

59
Q

Normal Albumin value

Additional info?

A

Normal = 3.5-5.0 g/dL

Not sensitive for acute injury (t1/2 is 21 days)
Poor specificity for liver disease
Decreased by impaired synthesis or increased consumption/loss
Conditions that reduce albumin include: infection, nephrotic syndrome, malnutrition, malignancy, and burns

60
Q

Which two tests assess synthetic function?

A

PT and Albumin

61
Q

Which tests assess hepatic function?

A

AST and ALT

62
Q

Normal AST

A

10-40 units/L

63
Q

Normal ALT

A

10-55 units/L

64
Q

MArked elevation of ALT/AST suggests ___

A

hepatitis

65
Q

AST/ALT ratio >2 suggests ___

A

cirrhosis or alcoholic liver disease

66
Q

Normal Bilirubin

Additional Info?

A

0-11 units/L

Confounding factors: hemolysis or hematoma reabsorption

67
Q

Normal Alkaline phosphatase

Additional info?

A

45-115 units/L

AP is not very specific (it’s also in bone, placenta and tumors)

68
Q

Normal Y Glutamyl transpeptidase

A

0-30 units/L

GGTP is more sensitive than AP (its not present in bone)

69
Q

Normal 5’-Nucleotidase

A

0-11 units/L

70
Q

Which test is the most specific indicator for bile duct obstruction?

A

5’-Nucleotidase
When there is a bile duct obstruction, these enzymes spill into the systemic circulation

71
Q

What is prehepatic liver failure caused by?
Which LFTs would be abnormal?

A

Caused by: hemolysis & hematoma reabsorption

Bilirubin would be increased

72
Q

What is liver failure r/t hepatocellular injury caused by?
Which LFTs would be abnormal?

A

Causes: cirrhosis, alcohol abuse, drugs, viral infection, sepsis, hypoxemia

Bilirubin, AST, ALT, PT, & AlkPhos would be increased
Albumin would be decreased

73
Q

What is liver failure r/t cholestatic problems caused by?
Which LFTs would be abnormal?

A

Causes: Biliary tract obstruction & Sepsis

Bilirubin, AST, ALT, PT, AlkPhos, 5’-NT would all be increased (late disease)
Albumin would be decreased (late disease)

74
Q

Hepatic blood flow usually ______ during regional and general anesthesia.

A

Decreases!

and multiple factors are responsible, including both direct and indirect effects of anesthetic agents, the type of ventilation employed, and the type of surgery being performed.

75
Q

How do volatiles decrease hepatic flow?

A

All volatiles decrease portal blood flow in proportion to MAP and CO
Most with Halothane
Least with Isoflurane

76
Q

How does neuraxial anesthesia decrease hepatic flow?

A

Neuraxial anesthesia decreases blood flow by lowering arterial BP

77
Q

How does PEEP decrease hepatic flow?

A

Controlled positive pressure ventilation and high peak airway pressures decrease hepatic blood flow by decreasing venous return

78
Q

What are other medications/conditions that decrease hepatic flow?

A
  • Hypoxemia (via sympathetic stimulation)
  • Surgical procedures near the liver can decrease blood flow 60%
  • Beta blockers, α1 agonists, H2 receptor blockers and vasopressin Low dose
  • Dopamine may increase liver blood flow
  • All opioids can cause contraction of the sphincter of Oddi
79
Q

Stress response from surgery causes _____

A

increased catecholamines, glucagon, and cortisol

This can be reduced by regional anesthesia, deep general, or blockade of the sympathetic system.

80
Q

Mobilization of glucose stores causes ___

A

hyperglycemia

81
Q

Mobilization of protein stores causes ____.

A

negative nitrogen balance

This can be reduced by regional anesthesia, deep general, or blockade of the sympathetic system.

82
Q

Mild postoperative liver dysfunction in healthy people is ____.

A

not uncommon and it is likely due to decreased hepatic blood flow.

When the results of LFTs are elevated postoperatively, it’s usually due to underlying liver disease or the surgical procedure itself.

83
Q

What is the most likely cause of postoperative jaundice?

A

overproduction of bilirubin because of resorption of a large hematoma or red cell breakdown following transfusion is the most likely cause

84
Q

Which type of hepatitis does not cause cirrhosis and hepatocellular carcinoma?

A

Hepatitis A

85
Q

Which type of hepatitis causes cirrhosis and hepatocellular carcinoma?

A

B & C

86
Q

Which type of Hepatitis is a co-infection with type B?

A

Type D

87
Q

How is Hepatitis A spead?
What is the prophylaxis after exposure?

A

Spread via fecal/oral
Treated with: Pooled gamma globulin
Hep A vaccine

88
Q

How is Hepatitis B spread?
What is the prophylaxis after exposure?

A

Spread via Percutaneous/ permucosal

Tx: Hep B immunoglobulin
Hep B vaccine

89
Q

How is Hepatitis C spread?
What is the prophylaxis after exposure?

A

Spread via Percutaneous/ permucosal

Tx: Interferon + ribavirin

90
Q

Timeline for Acute Hepatitis

A

Viral - Timeline
1- 2 week: mild prodromal symptoms (fever, malaise, N/V) that may evolve into jaundice
2– 12 weeks: jaundice may develop
4 months: Serum transaminase levels return to baseline, suggesting a complete recover
The timeline for Hep B or C can be prolonged and more complex
Fulminant hepatic necrosis is uncommon

91
Q

Drug-Induced Hepatitis

A

Onset is late and presents around 2 – 6 weeks after insult, sometimes even six months
Alcoholic helaptitis is the most common
Acetaminophen (25 grams is usually fatal dose) +/;.[Halothane hepatitis

92
Q

Volatile agents and hepatitis

A

HALOTHANE HEPATITIS
The liver metabolizes desflurane, isoflurane and halothane to inorganic flourides and triflouroacetic acid (TFA)
Desflurane and isoflurane are metabolized 0.02% and 0.2% into TFA respectively by the liver, unlike halothane, where 40% of it is metabolized by the liver into TFA
Sevoflurane does not produce TFA
The risk factors for halothane hepatitis are obesity, middle age, female, repeat exposure to halothane (esp within 28 days)

93
Q

Pre-Op Eval for Acute Hepatitis

A

Patients with acute hepatitis should have any elective procedure postponed until the acute phase has resolved (normalized LFTs).
Risk of deterioration of hepatic function, encephalopathy, coagulopathy, or hepatorenal syndrome
Acute viral hepatitis: Morbidity 12% and Mortality 10%
Alcohol withdrawal: Mortality 50%
BUN, CMP, PT, platelet count, HBsAg
Transaminases don’t correlate with disease severity
Persistent elevation of PT after Vitamin K is indicative of severe liver disease
Determine the cause and extent of liver disease
Drug exposures
Recent Transfusions
Prior Anesthetics
May need Vitamin K or FFP to correct coagulopathy

94
Q

Intra-Op Considerations for Acute Hepatitis

A

Avoid factors that are detrimental to the liver
Avoid factors that are known to decrease blood flow to the liver (hypotension, excessive sympathetic activation, high mean airway pressures)
Inhalational agents are preferred to IV because they don’t require metabolism by the liver
Isoflurane
Standard doses of induction agents can be used because termination of their effect is due to redistribution not metabolism
NMBA considerations: decrease pseudocholinesterases, decreased biliary excretion, increased volume of distribution

95
Q

Chronic Hepatitis

A

Elevated transaminases for 6 months (note that transaminases correlate poorly with severity of disease)
3 Types
* Chronic Persistent Hepatitis
* Chronic Lobular Hepatitis
* Chronic Active Hepatitis

96
Q

Chronic Persistent Hepatitis

A

Resolves
Hepatic cellular integrity is preserved

97
Q

Chronic Lobular Hepatitis

A

Involves recurrent exacerbations of acute inflammation
Progression to cirrhosis is rare

98
Q

Chronic Active Hepatitis

A

Hepatocyte destruction
20 – 50% develop cirrhosis
Ultimately hepatic failure
Death (hemorrhage from esophageal varices, multiorgan system failure, & encephalopathy).

99
Q

Anesthetic Considerations for Chronic Hepatitis

A

Chronic Persistent Hepatitis and Chronic Lobular Hepatitis is treated like acute hepatitis
Chronic Active Hepatitis is treated like Cirrhosis

100
Q

Acute alcohol intoxication anesthetic considerations

A

decreased MAC requirement
Impaired pharyngeal reflexes
Considered full stomach

101
Q

MAC for chronic alcohol abuse

A

increased MAC requirement

102
Q

Alcohol and its effects on receptors

A

Alcohol potentiates the GABA receptor and inhibits the NMDA receptor

103
Q

Alcohol withdrawal

A

Onset 6-8 hours and peaks at 24-36 hours after blood alcohol concentration returns to normal
Early: tremors and disordered perception (eg hallucinations)
Late: Increased SNS activity, N/V, insomnia, confusion
Delirium tremens occurs after 2-4 days without alcohol

104
Q

Cirrhosis general info

A

Most common cause in the US is alcohol
Hepatocyte necrosis is followed by fibrosis and nodular regeneration
Distortion of the liver’s normal cellular and vascular structure leads to portal hypertension
Impairment of synthetic functions lead to multisystem disease
Clinical signs and symptoms often do not correlate well with severity of disease

105
Q

Possible complications of cirrhosis

A

Variceal hemorrhage from portal hypertension
Intractable fluid retention (ascites and hepatorenal syndrome)
Hepatic encephalopathy or coma
10% also develop at least one episode of spontaneous bacterial peritonitis

106
Q

What diseases can cause hepatic fibrosis without necrosis?

A

Schistosomiasis
Idiopathic Portal Fibrosis
Congenital Hepatic Fibrosis
Budd Chiari Syndrome (obstruction of the portal vein)

107
Q

Portal hypertension (greater than 10 mm Hg) leads to ____.

A

extensive portal- systemic venous collateral channels
Gastroesophageal ➡️ major source of morbidity and mortality
Hemorrhoidal
Periumbilical
Retroperitoneal

108
Q

Treatment of variceal bleed

A

Reduce the rate of blood loss
Vasopressin
Somatostatin
Propranolol
Fluids/Blood Products
Balloon Tamponade
Endoscopic Sclerosis
TIPS may decrease portal hypertension but increases risk of encephalopathy

109
Q

Cirrhosis Hematological Considerations

A

Anemia – due to blood loss increased destruction, bone marrow suppression, nutritional deficiencies
Splenomegally
Thrombocytopenia
Leukopenia
Decreased synthesis of coagulation factors ➡️ coagulopathy
Excessive blood transfusions can increase nitrogen load and worsen encephalopathy
Consider platelet transfusions if less than 100,000

110
Q

Cirrhosis Circulatory Considerations

A

Hyperdynamic state
Generalized peripheral vasodilation
AV shunting + decreased viscosity secondary anemia = increased CO
Cirrhotic cardiomyopathy: CO is dependent on higher-than-normal filling pressures and below normal SVR
Intravascularly depleted

111
Q

Cirrhosis Respiratory Considerations

A

Hyperventilation ➡️ respiratory alkalosis
Hypoxemia due to left-right shunting (up to 40% of CO)
Pulmonary AV shunts
V/Q mismatching
Elevation of the diaphragm from ascites decreases lung volumes, especially FRC and predisposes to atelectasis
Ascites causes a restrictive effect
Consider paracentesis if severe ascites

112
Q

What is the pathophysiology of ascites?

A

Portal hypertension ➡️ increases hydrostatic pressure
Hypoalbuminemia ➡️ decreases oncotic pressure
Renal sodium and water retention due to relative hypovolemia and secondary hyperaldosteronism

113
Q

Electrolyte disturbances seen with renal failure/cirrhosis

A

hyponatremia and hypokalemia

114
Q

Hepatorenal syndrome

A

Usually follows GI bleeding, aggressive diuresis, sepsis or surgery.
* Progressive
* Oliguria
* Sodium retention
* Azotemia
* Very high mortality
* Treatment is supportive; usually unsuccessful unless liver transplantation

115
Q

Cirrhosis CNS Considerations

A

Hepatic Encephalopathy
AMS
Fluctuating CNS signs: asterixis, hyperreflexia, inverted plantar reflex
EEG changes: symmetric high voltage, slow wave activity
Increased ICP (some)
Related to the amount of hepatic damage and the amount of blood shunted away from the liver directly into systemic circulation
Toxins: Ammonia, Mercaptans, short chain fatty acids, phenols
Increased permeability of BBB
Precipitate encephalopathy: GI bleeding, increased dietary protein, hypokalemic alkalosis (vomiting or diuresis), infections
Treat aggressively
* Lactulose – osmotic laxative and inhibits GI bacterial ammonia production
* Neomycin – inhibits GI bacterial ammonia production

116
Q

Altered drug responses with cirrhosis

A

Increased Vd (expanded ECF): Need higher loading doses
Changes in CNS sensitivity
Decreased protein binding
Decreased drug metabolism
Decreased drug elimination

117
Q

Anesthetic consierations for cirrhosis

A

Barbituate or Propofol followed by Isoflurane (avoid Halothane)
Opioid supplementation (caution b/c decreased metabolism)
Cisatricurium
RSI with Ketamine or Etomidate with SCh for unstable and/or actively bleeding patients

118
Q

Cirrohis monitoring and intra-op considerations

A

Monitoring
* Aline
* May require PEEP (if intrapulmonary shunts)
* CVP or Pulmonary Artery Catheter (monitor volume status)
* Follow UOP closely (mannitol)
Preop, usually are sodium restricted, but intraop preservation of intravascular volume is the priority
Following the removal of large amounts of ascites often requires subsequent colloid replacement to prevent hypotension and renal failure
Blood transfusions ➡️ citrate toxicity (normally metabolized by the liver) ➡️ hypocalcemia

119
Q

Child’s & Pugh Classification

A

Goal – Correlate relationship between liver disease & peri-op outcome
Classification system – Class A, B, & C (highest risk)

Score based on Total Bilirubin, serum albumin, Prothrombin time, Ascites, and hepatic encephalopathy

120
Q

MELD = ___

A

(Model for End-Stage Liver Disease)

Subsequent studies have shown MELD to be best predictor of peri-op mortality in cirrhotic patients undergoing major surgery
Used to predict 3-month survival in patients with liver disease
Has no subjective data
Uses creatinine, bilirubin and INR

121
Q

MELD scores and risk

A

Those with MELD scores < 10 (Low Risk) or Class A, may proceed with surgery
Those with MELD scores 10-15 (Intermediate Risk) or Class B, proceed ONLY if necessary (not elective)
Those with MELD score > 15 (High Risk) or Class C should avoid surgery & may be candidates for transplantation

122
Q

Older surgical procedure to decompress liver

A

Decompress the portal system
Very extensive surgery decompresses the PV system → Spleno-renal shunt procedure
Shunt was placed between the splenic vein & left renal vein to reduce portal hypertension
Associated with severe morbidity & mortality

123
Q

Modern technique to decompress liver

A

Interventional Radiologic
TIPS (trans-jugular intra-hepatic porto-systemic shunt)
Hepatic vein accessed via internal jugular vein → where shunt is deployed

124
Q

Basics of TIPs procedure, risks?

A

TIPS – to treat bleeding varices & refractory ascites → bypassing cirrhotic liver
Risks:
Typical of CVP insertion
Inadvertent puncture of liver capsule →hemo-peritoneum
Portosystemic encephalopathy incidence is 30% after TIPS

125
Q

Hepatic surgery for tumors

A

Repair of lacerations - Drainage of abscesses - Resections for tumors –
Up to 80-85% of the liver may be resected

126
Q

Hepatic surgery anesthetic management

A

Complicated by
* Large amounts of blood loss
* Cirrhosis
Management
* Multiple large-bore IV catheters
* Fluid warmer
* Rapid infusion devices
* Invasive monitoring
* Antifibrinolytics (amicar or tranexamic acid)
* Postoperative mechanical ventilation

Concepts 3 (12 decks)

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