Hepatic System (FINAL EXAM) Flashcards

(126 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The liver is composed of ___ lobules.

A

50,000 – 100,000 lobules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Vitamin K deficiency is manifested as _____.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Bile is produced by ____.

A

hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Bile drains into the ____

A

the bile ducts and converges to form the common hepatic duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The sphincter of Oddi controls the ____.

A

emptying of the common hepatic duct into the duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Innervation of the liver

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sympathetic activation results in _____.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The liver receives what percent of cardiac output?

A

25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Liver perfusion is supplied by which two vessels?

A

1) portal vein and 2) the hepatic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where are the majority of our cytochrome p450 enzymes located?

A

Zone 3 of the Acinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Intrinsic regulation revolves around ____

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Extrinsic regulation revolves around ____

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hypercarbia can do what to hepatic perfusion

A

increase it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

The liver is a reservoir for ___

A

blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Low resistance of hepatic sinusoids allows ___

A

large blood flow through the portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Small changes in hepatic venous pressure can result in ___.
large changes in hepatic blood volume
26
Chart comparing hepatic venous blood volume and hepatic venous pressure
27
What are some examples of how changes to hepatic venous pressure can influence blood volume?
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)
28
Function of Kupffer cells
Cleanse more than 99% of bacteria load Process antigens Release cytokines
29
The liver is the major organ for the storage of what?
Major organ for glycogen storage
30
What enhances glycogenesis?
Insulin
31
What enhances glycogenolysis?
Epinephrine and glucagon
32
The liver is responsible for the metabolism of ____.
macronutrients (like carbohydrates)
33
Glycogenesis = ____
Glycogenesis decreases the blood sugar level to normal.
34
Glycogenolysis = ____
Glycogenolysis increases the blood sugar level.
35
Glycogen stores are depleted after___.
24 hours of fasting
36
The liver and kidney can form glucose from ___.
lactate, pyruvate, amino acids and glycerol. Gluconeogenesis is vital for the maintenance of normal blood sugar.
37
Gluconeogenesis
Gluconeogenesis refers to synthesis of new glucose from noncarbohydrate precursors, provides glucose when dietary intake is insufficient or absent.
38
What enhances gluconeogenesis?
Glucocorticoids, catecholamines, glucagon and thyroid hormone
39
What inhibits gluconeogenesis?
Insulin
40
When carbohydrate stores are saturated, the liver converts the excess carbohydrates (and proteins) into _____.
fat (fatty acids), which can be used directly as fuel or stored in the liver or adipose tissue.
41
What can utilize only glucose?
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).
42
Discuss the liver and protein metabolism
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
43
Discuss the liver and the formation of plasma proteins
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)
44
Drug Metabolism in the liver (general info)
Most drugs undergo hepatic biotransformation. End products are inactivated or more soluble (more easily excreted in kidney or by bile) There are two phases
45
Phase I of drug metabolism in liver
Phase I: via oxidases and P-450 Oxidation Reduction Deamination Sulfoxidation Dealkylation Methylation
46
Phase II of drug metabolism in liver
conjugation
47
Enzymes systems, like the CYP450 system can be increased and decreased by ____.
exposure to other drugs
48
CYP450 inducers
Barbiturates, ketamine, benzodiazepines, phenytoin, chronic alcohol use, rifampin, glucocorticoids, "Bad kids bring pot causing risky games"
49
CYP450 inhibitors
Acute alcohol use, Omeprazole, erythromycin, Cimetidine "Always Offer Excellent Candy"
50
The liver converts ____
T4 to T3
51
The liver degrades ____
Thyroid Hormone, Insulin, Estrogen, Aldosterone, Cortisol, Glucagon and ADH
52
The liver stores ____
Vitamins A, B12, E, D, and K
53
The liver produces _____
transferrin, haptoglobin, and ceruloplasmin
54
The liver synthesizes
thrombopoietin which stimulates platelet production
55
Erythropoiesis = ____
**Erythropoiesis: Heme and Bilirubin Metabolism** * Primary erythropoietic organ of the fetus - 2 months of age * Metabolism of hemoglobin produces bilirubin Conjugation of bilirubin
56
What is one test that can evaluate all liver injury?
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
Liver abnormalities can often be divided into ____.
synthetic function, hepatocellular injury, hepatic clearance and biliary duct obstructions
58
Normal value for PT Additional info?
12-14 seconds *Very sensitive for acute injury (V and VII t1/2 is <25 hours) *Prolonged by vitamin K deficiency
59
Normal Albumin value Additional info?
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
Which two tests assess synthetic function?
PT and Albumin
61
Which tests assess hepatic function?
AST and ALT
62
Normal AST
10-40 units/L
63
Normal ALT
10-55 units/L
64
MArked elevation of ALT/AST suggests ___
hepatitis
65
AST/ALT ratio >2 suggests ___
cirrhosis or alcoholic liver disease
66
Normal Bilirubin Additional Info?
0-11 units/L Confounding factors: hemolysis or hematoma reabsorption
67
Normal Alkaline phosphatase Additional info?
45-115 units/L AP is not very specific (it's also in bone, placenta and tumors)
68
Normal Y Glutamyl transpeptidase
0-30 units/L GGTP is more sensitive than AP (its not present in bone)
69
Normal 5'-Nucleotidase
0-11 units/L
70
Which test is the most specific indicator for bile duct obstruction?
5'-Nucleotidase When there is a bile duct obstruction, these enzymes spill into the systemic circulation
71
What is prehepatic liver failure caused by? Which LFTs would be abnormal?
Caused by: hemolysis & hematoma reabsorption Bilirubin would be increased
72
What is liver failure r/t hepatocellular injury caused by? Which LFTs would be abnormal?
Causes: cirrhosis, alcohol abuse, drugs, viral infection, sepsis, hypoxemia Bilirubin, AST, ALT, PT, & AlkPhos would be increased Albumin would be decreased
73
What is liver failure r/t cholestatic problems caused by? Which LFTs would be abnormal?
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
Hepatic blood flow usually ______ during regional and general anesthesia.
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
How do volatiles decrease hepatic flow?
All volatiles decrease portal blood flow in proportion to MAP and CO Most with Halothane Least with Isoflurane
76
How does neuraxial anesthesia decrease hepatic flow?
Neuraxial anesthesia decreases blood flow by lowering arterial BP
77
How does PEEP decrease hepatic flow?
Controlled positive pressure ventilation and high peak airway pressures decrease hepatic blood flow by decreasing venous return
78
What are other medications/conditions that decrease hepatic flow?
* 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
Stress response from surgery causes _____
increased catecholamines, glucagon, and cortisol This can be reduced by regional anesthesia, deep general, or blockade of the sympathetic system.
80
Mobilization of glucose stores causes ___
hyperglycemia
81
Mobilization of protein stores causes ____.
negative nitrogen balance This can be reduced by regional anesthesia, deep general, or blockade of the sympathetic system.
82
Mild postoperative liver dysfunction in healthy people is ____.
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
What is the most likely cause of postoperative jaundice?
overproduction of bilirubin because of resorption of a large hematoma or red cell breakdown following transfusion is the most likely cause
84
Which type of hepatitis does not cause cirrhosis and hepatocellular carcinoma?
Hepatitis A
85
Which type of hepatitis causes cirrhosis and hepatocellular carcinoma?
B & C
86
Which type of Hepatitis is a co-infection with type B?
Type D
87
How is Hepatitis A spead? What is the prophylaxis after exposure?
Spread via fecal/oral Treated with: Pooled gamma globulin Hep A vaccine
88
How is Hepatitis B spread? What is the prophylaxis after exposure?
Spread via Percutaneous/ permucosal Tx: Hep B immunoglobulin Hep B vaccine
89
How is Hepatitis C spread? What is the prophylaxis after exposure?
Spread via Percutaneous/ permucosal Tx: Interferon + ribavirin
90
Timeline for Acute Hepatitis
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
Drug-Induced Hepatitis
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
Volatile agents and hepatitis
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
Pre-Op Eval for Acute Hepatitis
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
Intra-Op Considerations for Acute Hepatitis
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
Chronic Hepatitis
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
Chronic Persistent Hepatitis
Resolves Hepatic cellular integrity is preserved
97
Chronic Lobular Hepatitis
Involves recurrent exacerbations of acute inflammation Progression to cirrhosis is rare
98
Chronic Active Hepatitis
Hepatocyte destruction 20 – 50% develop cirrhosis Ultimately hepatic failure Death (hemorrhage from esophageal varices, multiorgan system failure, & encephalopathy).
99
Anesthetic Considerations for Chronic Hepatitis
Chronic Persistent Hepatitis and Chronic Lobular Hepatitis is treated like acute hepatitis Chronic Active Hepatitis is treated like Cirrhosis
100
Acute alcohol intoxication anesthetic considerations
decreased MAC requirement Impaired pharyngeal reflexes Considered full stomach
101
MAC for chronic alcohol abuse
increased MAC requirement
102
Alcohol and its effects on receptors
Alcohol potentiates the GABA receptor and inhibits the NMDA receptor
103
Alcohol withdrawal
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
Cirrhosis general info
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
Possible complications of cirrhosis
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
What diseases can cause hepatic fibrosis without necrosis?
Schistosomiasis Idiopathic Portal Fibrosis Congenital Hepatic Fibrosis Budd Chiari Syndrome (obstruction of the portal vein)
107
Portal hypertension (greater than 10 mm Hg) leads to ____.
extensive portal- systemic venous collateral channels Gastroesophageal ➡️ major source of morbidity and mortality Hemorrhoidal Periumbilical Retroperitoneal
108
Treatment of variceal bleed
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
Cirrhosis Hematological Considerations
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
Cirrhosis Circulatory Considerations
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
Cirrhosis Respiratory Considerations
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
What is the pathophysiology of ascites?
Portal hypertension ➡️ increases hydrostatic pressure Hypoalbuminemia ➡️ decreases oncotic pressure Renal sodium and water retention due to relative hypovolemia and secondary hyperaldosteronism
113
Electrolyte disturbances seen with renal failure/cirrhosis
hyponatremia and hypokalemia
114
Hepatorenal syndrome
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
Cirrhosis CNS Considerations
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
Altered drug responses with cirrhosis
Increased Vd (expanded ECF): Need higher loading doses Changes in CNS sensitivity Decreased protein binding Decreased drug metabolism Decreased drug elimination
117
Anesthetic consierations for cirrhosis
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
Cirrohis monitoring and intra-op considerations
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
Child’s & Pugh Classification
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
MELD = ___
(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
MELD scores and risk
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
Older surgical procedure to decompress liver
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
Modern technique to decompress liver
Interventional Radiologic TIPS (trans-jugular intra-hepatic porto-systemic shunt) Hepatic vein accessed via internal jugular vein → where shunt is deployed
124
Basics of TIPs procedure, risks?
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
Hepatic surgery for tumors
Repair of lacerations - Drainage of abscesses - Resections for tumors – Up to 80-85% of the liver may be resected
126
Hepatic surgery anesthetic management
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