RENAL, LIVER, AND BILIARY TRACT DISEASE

Question 1

1. What are some essential physiologic functions of the kidneys?

Answer 1

1. Essential physiologic functions of the kidneys include the excretion of metabolic
   wastes; the retention of nutrients; the regulation of water, tonicity, and
   electrolyte and hydrogen ion concentrations in the blood; and the production
   of hormones that contribute to water regulation and bone metabolism.

Question 2

2. Name some factors that place patients at an increased risk of acute renal failure in the perioperative period.

Answer 2

2. Factors that place patients at an increased risk of acute renal failure in the
   perioperative period include advanced age, emergent surgery, liver disease,
   high-risk surgery, body mass index, peripheral vascular occlusive disease, and
   COPD.

Question 3

3. What percent of the cardiac output normally goes to the kidneys? What fraction of this goes to the renal cortex?

Answer 3

3. Although the kidneys typically constitute only 0.5% of body weight, about 20%
   of the cardiac output normally goes to the kidneys. Of the 20%, more than
   two-thirds goes to the renal cortex and the remaining blood flow supplies the renal
   medulla

Question 4

4. Over what range of mean arterial blood pressures do renal blood flow and the
   glomerular filtration rate (GFR) remain constant? How is this accomplished by the
   kidneys? Why is it important?

Answer 4

4. Renal blood flow and the GFR remain constant when mean arterial blood pressures
   range between 80 and 180 mm Hg. This autoregulatory function of the kidneys
   is accomplished by the afferent arteriolar vascular bed. The afferent arterioles are
   able to adjust their tone in response to changes in blood pressure, such that
   during times of higher mean arterial blood pressure the afferent arterioles
   vasoconstrict, whereas the opposite occurs during times of lower mean arterial
   blood pressure. This is important for two reasons. The ability of the kidneys to
   maintain constant renal blood flow despite fluctuations in blood pressure ensures
   continued renal tubular function in the face of changes, especially decreases, in
   blood pressure. In addition, autoregulatory responses of the afferent arterioles
   protect the glomerular capillaries from large increases in blood pressure during
   times of hypertension, as may occur with direct laryngoscopy. When mean arterial
   blood pressures are less than 80 mm Hg or greater than 180 mm Hg renal blood
   flow is blood pressure dependent

Question 5

5. Even during normal kidney autoregulatory function, what two factors can alter renal blood flow?

Answer 5

5. Even during normal kidney autoregulatory function, renal blood flow can be altered
   by sympathetic nervous system activity and by circulating renin.

Question 6

6. What is renin? What is the secretion of renin usually in response to? What effect
   does renin have on renal blood flow?

Answer 6

6. Renin is a proteolytic enzyme secreted by the juxtaglomerular apparatus of
   the kidney. There are at least three things that stimulate the release of renin
   from the endothelial cells of the afferent arteriole:
   (1) Sympathetic nervous stimulation;
   (2) decreased renal perfusion; and
   (3) decreased delivery of sodium to distal convoluted renal tubules.
   • Renin increases efferent renal arterial
   arteriolar tone at low levels and causes afferent arteriolar constriction at higher
   levels.

Question 7

7. What is the physiologic effect of the secretion of renin?

Answer 7

7. Renin is the rate-limiting enzyme in the production of angiotensin II. After its
   secretion from the juxtaglomerular apparatus of the kidneys, renin acts on
   angiotensinogen. Angiotensinogen is a large glycoprotein released by the liver
   to the circulation. After being cleaved by renin, angiotensin I is formed from
   angiotensinogen. Angiotensin I is in turn cleaved by angiotensin converting
   enzyme in the lungs to form angiotensin II. Angiotensin II stimulates the release of
   aldosterone from the adrenal cortex and is a potent vasoconstrictor. It also inhibits
   renin secretion as part of a negative feedback loop

Question 8

8. What triggers the release of prostaglandins that are produced by the renal medulla?
   What is the effect of prostaglandins released by the renal medulla?

Answer 8

8. Prostaglandins are released from the renal medulla in response to angiotensin II, hypotension and sympathetic nervous system stimulation. Prostaglandins attenuate the actions of the sympathetic nervous system, arginine vasopressin,

Question 9

9. What is the renal effect of arginine vasopressin released by the hypothalamus?

Answer 9

9. Arginine vasopressin (previously known as antidiuretic hormone) release by the
   hypothalamus results in the renal tubular conservation of water, an increased urine
   osmolality, and a decrease in plasma osmolality. It is typically secreted in
   response to small increases in serum osmolality

Question 10

10. What is glomerular filtration? What is glomerular filtration dependent on?

Answer 10

10. Glomerular filtration is the filtration of water and low molecular weight substances from the blood in the renal afferent arterioles into Bowman’s space through
    the glomerulus. Glomerular filtration is dependent on two things: the permeability of the filtration barrier (the glomerular membrane) and the net difference
    between the hydrostatic forces pushing fluid into Bowman’s space and the
    osmotic forces keeping fluid in the plasma. (

Question 11

11. What is the normal hydrostatic pressure of the glomerular capillaries? What is the normal plasma oncotic pressure in the afferent and efferent arterioles?

Answer 11

11. The normal hydrostatic pressure of the glomerular capillaries is about 50 mm Hg.
    The normal plasma oncotic pressure in the afferent and efferent arterioles is 25 mm
    Hg and 35 mm Hg, respectively. The increase in oncotic pressure between the
    afferent and efferent arterioles reflects the effects of filtration.

Question 12

12. What is the average normal rate of glomerular filtration?

Answer 12

12. The average normal rate of glomerular filtration is 125 mL/min. (

Question 13

13. About what percent of the fluid shift from glomerular filtration is reabsorbed from renal tubules and ultimately returned to the circulation?

Answer 13

13. About 90% of the fluids that have been filtered by the glomerulus into
    Bowman’s capsule are reabsorbed from renal tubules and ultimately returned
    to the circulation

Question 14

14. How is the GFR influenced by the renal blood flow

Answer 14

14. The GFR is decreased during times of decreased renal blood flow or decreased mean
    arterial blood pressure

Question 15

15. What are the three mechanisms upon which the renal clearance of drugs depends?

Answer 15

15. The renal clearance of drugs or their metabolites depends on three things:
    glomerular filtration (GFR and protein binding), active secretion by the renal
    tubules, and passive reabsorption (favors nonionized compounds) by the
    tubules

Question 16

16. Name some tests used for the evaluation of renal function. How sensitive are tests of renal function?

Answer 16

16. Tests that are commonly used for the preoperative evaluation of renal function
    include a serum creatinine level, a BUN level, creatinine clearance, and urine protein levels. Tests that are commonly used for the preoperative evaluation of renal tubular function include the urine specific gravity, urine osmolarity, and urine sodium excretion. Most tests of renal function are not very sensitiv

Question 17

17. What degree of renal disease can exist before renal function tests begin to indicate possible decreases in renal function?

Answer 17

17. A significant degree of renal disease can exist before it is reflected in renal function tests. It is estimated that more than a 50% decrease in renal function may exist before these tests become abnormal.

Question 18

18. What is the normal level of blood urea nitrogen (BUN)?

Answer 18

18. The normal BUN level in serum varies among individuals, typically ranging between 10 and 20 mg/dL. Urea is freely filtered by the glomerulus of the kidney, but its reabsorption from the tubules varies greatly. Although the BUN varies with changes in GFR, it is influenced by multiple other factors that decrease its utility as a measure of the GFR and of renal function.

Question 19

19. What factors may influence the BUN level?

Answer 19

19. Factors that may influence the BUN level include dietary protein intake,
    gastrointestinal bleeding, decreased urinary flow, hepatic function, and increased catabolism as during trauma, sepsis, or febrile illness.

Question 20

20. Why does the BUN concentration increase in dehydrated states?
    What is the serum creatinine level under these circumstances?

Answer 20

20. The BUN concentration increases in dehydrated states as a result of the
    corresponding decrease in urinary flow through renal tubules. During low urinary
    flow rates, a greater fraction of the urea is reabsorbed by the kidney. During
    low urinary flow rates the serum creatinine level remains normal, such that the
    ratio of serum BUN to creatinine is increased during times of low urinary flow
    associated with hypovolemia.

Question 21

21. What do BUN concentrations higher than 50 mg/dL almost always indicate?

Answer 21

21. Blood urea nitrogen concentrations higher than 50 mg/dL are almost always
    a reflection of decreased GFR.

Question 22

22. What is the source of serum creatinine? How is the serum creatinine level related to the GFR?

Answer 22

22. Serum creatinine is a product of skeletal muscle protein catabolism. Serum
    creatinine levels are dependent on a patient’s total body water, creatinine
    generation rate, and creatinine excretion rate. The generation of creatinine is
    relatively constant within an individual, making its release into the circulation
    relatively constant as well. Serum creatinine levels are believed to be reliable
    indicators of the GFR, because its rate of clearance from the circulation is directly
    dependent on the GFR.

Question 23

23. Why might a normal creatinine level be seen in elderly patients despite a decreased GFR?

Answer 23

23. Elderly patients may have a normal creatinine level despite a decreased GFR
    secondary to the decrease in muscle mass that commonly accompanies aging.
    For this reason, even mild increases in the serum creatinine level of elderly patients
    may be an indication of significant renal dysfunction

Question 24

24. Why might normal serum creatinine levels not accurately reflect the GFR in patients
    with chronic renal failure?

Answer 24

24. Normal serum creatinine levels may not accurately reflect the GFR in patients with chronic renal failure for two reasons. First, patients with chronic renal failure
    may have decreased skeletal muscle mass, resulting in a decrease in creatinine
    production. Second, the excretion of creatinine occurs via nonrenal means in these patients

Question 25

25. What is the creatinine clearance a measurement of?

Answer 25

25. The creatinine clearance is a measurement of the excretion of creatinine into the
    urine after being filtered by the glomerulus. (

Question 26

26. Why is the creatinine clearance a more reliable measurement of the GFR than
    serum creatinine levels? What is a disadvantage of creatinine clearance
    measurements?

Answer 26

26. The creatinine clearance is a more reliable measurement of GFR than serum
    creatinine levels because the clearance does not depend on corrections for age or the
    presence of a steady state. A disadvantage of creatinine clearance measurements
    is the requirement of accurate, timed urine collections. (

Question 27

27. What are some nonrenal causes of proteinuria?

Answer 27

27. Intermittent proteinuria occurs in healthy individuals after standing for long
    periods of time and after strenuous exercise. Proteinuria may also occur during
    febrile states and congestive heart failure.

Question 28

28. What are the differences in site of action of thiazide, spironolactone, and loop and
    osmotic diuretics?

Answer 28

28. Thiazide diuretics cause diuresis by inhibition of reabsorption of sodium and
    chloride ions from the early distal renal tubules. Spironolactone, an aldosterone
    antagonist, blocks the renal tubular effects of aldosterone. Spironolactone is a
    potassium-sparing diuretic. Loop diuretics inhibit the reabsorption of sodium and
    chloride, and augment the secretion of potassium primarily in the loop of Henle.
    Osmotic diuretics, such as mannitol, produce diureses by being filtered at the
    glomeruli but not reabsorbed by the renal tubules. The excess osmolarity of the renal
    tubular fluid leads to excretion of water.

Question 29

29. What are the differences in pharmacologic action between dopamine and fenoldopam?

Answer 29

29. Dopamine dilates renal arterioles by its agonist action at the DA-1 receptor and
    causes adrenergic stimulation leading to an increase in renal blood flow and GFR.
    Dopamine therapy when used to augment urine output has not been shown to alter
    the course of renal failure. Dopamine also potentially leads to tachydysrhythmias,
    pulmonary shunting, and tissue ischemia. Fenoldopam is a dopamine analog
    which also possesses DA-1 agonist activity, but lacks the adrenergic activity of
    dopamine.

Question 30

30. What are the systemic changes that frequently accompany end-stage renal disease
    (ESRD)?

Answer 30

30. There are several systemic changes that accompany end-stage renal disease (ESRD).
    Cardiovascular disease is the predominant cause of death in patients with ESRD.
    Systemic hypertension is very common and can be severe and refractory to therapy.
    Acute MI, cardiac arrest/dysfunction and cardiomyopathy account for more than 50% of deaths in patients maintained on dialysis. Diabetes mellitus frequently presents concomitantly with ESRD. Electrolyte abnormalities also occur commonly
    as patients develop difficulty excreting their dietary fluid and electrolyte loads.
    A normochromic normocytic anemia is frequently present because of decreased erythropoiesis. Uremia-induced platelet dysfunction can lead to clinical coagulopathy.

Question 31

31. What are some anesthetic considerations for the anesthetic management of patients
    with ESRD?

Answer 31

31. There are several considerations for the anesthetic management of patients with ESRD. These patients may benefit from extensive monitoring, such as direct arterial
    blood pressure monitoring and perhaps central venous pressure monitoring depending on the surgical case, comorbidities, and other factors. Hypotension can commonly occur in patients with ESRD, particularly after hemodialysis.
    Patients with arteriovenous fistulas should have the presence of the thrill monitored during positioning and intraoperatively. Patients with gastroparesis should be considered at increased risk for the aspiration of gastric contents. Electrolytes,
    especially potassium, should be evaluated preoperatively and intraoperatively if necessary. Finally, drugs or their metabolites that are renally excreted should be administered judiciously or avoided if possible

Question 32

32. Should succinylcholine be avoided in patients with ESRD?

Answer 32

32. Succinylcholine is not contraindicated in patients with ESRD. The increase in serum
    potassium after a large dose of succinylcholine is approximately 0.6 mEq/L for
    patients both with and without ESRD. This increase can be tolerated without imposing a significant cardiac risk, even in the presence of an initial serum potassium concentration higher than 5 mEq/L

Question 33

33. What are some causes of prerenal oliguria?

Answer 33

33. Prerenal oliguria is indicative of a decrease in renal blood flow, the most common causes of which include a decrease in the intravascular fluid volume and a decrease in the cardiac output. Another cause may be surgical compression of the renal arteries leading to obstructed blood flow to the kidneys, either directly through
    clamping or inadvertently through retraction or manual traction. Whatever the cause, the duration of oliguria should be minimized to decrease the risk of acute renal failure.

Question 34

34. What is the treatment for prerenal causes of oliguria?

Answer 34

34. The treatment of prerenal causes of oliguria is dependent on whether the cause is secondary to a decrease in intravascular fluid volume or in cardiac output. A crystalloid fluid bolus would result in a brisk diuresis if in fact the cause was hypovolemia. A lack of response to the fluid bolus would indicate that perhaps the
    cause of the oliguria is a decrease in cardiac output or is a result of the secretion of antidiuretic hormone in response to surgical stress. A small dose of furosemide, 0.1 mg/kg intravenously, will lead to diuresis if the cause of the oliguria is antidiuretic hormone secretion. If there is no response to the intravenous administration of furosemide, a determination should be made as to whether the patient remains hypovolemic or there is a decrease in cardiac output. If the patient
    is at risk for a decrease in cardiac output, it may be worthwhile to monitor
    cardiac filling pressures to guide intravascular fluid replacement. If the cardiac
    filling pressures is high, a cause for the decrease in cardiac output should be
    sought.

Question 35

35. What are some causes of oliguria due to intrinsic renal disease?

Answer 35

35. Acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis are
    intrinsic renal causes of oliguria.

Question 36

36. For oliguria that is secondary to renal causes such as acute tubular necrosis, is the urine typically concentrated or dilute? Does the urine typically contain excessive or minimal stores of sodium?

Answer 36

36. Oliguria due to acute tubular necrosis is characterized by urine that is typically dilute and contains excessive sodium.

Question 37

37. What are some causes of postrenal oliguria?

Answer 37

37. Causes of postrenal oliguria include ureteral obstruction, bladder outlet obstruction, and obstruction or kinking of the Foley catheter. Postrenal causes of oliguria are frequently reversible.

Question 38

38. What are some physiologic functions of the liver?

Answer 38

38. Physiologic functions of the liver include protein synthesis, drug metabolism, fat
    metabolism, hormone metabolism, bilirubin formation and excretion, and
    glucose homeostasis.

Question 39

39. What is the blood supply to the liver? What percent of the cardiac output goes to the
    liver?

Answer 39

39. The liver receives its blood supply via the portal vein (70%) and hepatic artery
    (30%). Approximately 25% of the cardiac output goes to the liver. While the portal
    vein supplies 70% of hepatic blood supply, it only contributes 50% of the liver’s
    oxygen supply. The remaining 50% of the liver’s oxygen supply comes from
    the hepatic artery.

Question 40

40. What are some determinants of hepatic blood flow?

Answer 40

40. Total hepatic blood flow is directly proportional to the perfusion pressure across the
    liver and is inversely proportional to splanchnic vascular resistance. There are many
    determinants of hepatic blood flow. Determinants intrinsic to the liver include
    hepatic autoregulation, metabolic control, and the hepatic arterial buffer response.
    Determinants extrinsic to the liver include sympathetic nervous system activity,
    surgical stimulation, and humoral factors.

Question 41

41. What is hepatic autoregulation? How is hepatic autoregulation affected by surgery
    and anesthesia?

Answer 41

41. Hepatic autoregulation refers to the ability of the hepatic artery to alter its resistance
    in response to changes in arterial pressure to maintain hepatic artery blood flow.
    For example, hepatic artery resistance may decrease to maintain perfusion to
    the liver when portal vein flow is reduced. Of note, there does not appear to be
    autoregulation of the portal venous system. Instead portal venous blood flow
    parallels cardiac output. Surgery and anesthesia impair hepatic autoregulation
    and typically result in reduced hepatic perfusion

Question 42

42. What is the hepatic arterial buffer response? How is this hepatic response affected by
    anesthesia?

Answer 42

42. The hepatic arterial buffer response refers to the capacity of the liver to increase or
    decrease hepatic artery blood flow in response to decreases or increases in portal
    venous flow. For example, when portal venous flow decreases, the resistance of
    the hepatic artery decreases and hepatic artery blood flow increases. This reciprocal
    relationship allows for the hepatic oxygen supply and total hepatic blood flow
    to be maintained despite alterations in portal venous flow. This compensatory
    mechanism does not completely compensate for changes in portal venous flow,
    however. In addition, the hepatic arterial buffer response can be disrupted by several
    factors, including neural, humoral, and metabolic changes. This hepatic response
    is also disrupted by hepatic cirrhosis and volatile anesthetics.

Question 43

43. What results from sympathetic nervous stimulation of the liver?

Answer 43

43. Innervation of the liver is by both the parasympathetic nervous system and
    the sympathetic nervous system. Generalized sympathetic nervous system
    stimulation, as can occur with arterial hypoxemia or hypercarbia, pain or surgical
    stress, results in an increase in the splanchnic vascular resistance. The increase
    in splanchnic vascular resistance yields a decrease in liver blood flow and blood
    volume.

Question 44

44. How does positive pressure ventilation of the lungs affect hepatic blood flow?

Answer 44

44. Positive pressure ventilation of the lungs decreases hepatic blood flow through
    its increase in hepatic venous pressure. Hepatic blood flow is decreased further
    by the application of positive end-expiratory pressure through the same
    mechanism.

Question 45

45. How does congestive heart failure affect hepatic blood flow?

Answer 45

45. Congestive heart failure, particularly right-sided heart failure, decreases hepatic
    blood flow through its increase in hepatic venous pressure.

Question 46

46. How do changes in cardiac output or myocardial contractility affect hepatic blood
    flow?

Answer 46

46. Decreases in cardiac output or myocardial contractility result in decreases in hepatic
    blood flow

Question 47

47. How do changes in arterial blood pressure affect hepatic blood flow?

Answer 47

47. Decreases in arterial blood pressure result in decreases in hepatic blood flow.

Question 48

48. How does the liver store glucose?

Answer 48

48. The liver stores glucose as glycogen in the hepatocytes.

Question 49

49. How does the liver maintain glucose homeostasis in times of starvation?

Answer 49

49. Glucose homeostasis is maintained during times of starvation by the breakdown
    of the glycogen to glucose in the hepatocytes. Glucose is then released into the
    circulation. The glycogen stores of the liver correspond to 24 to 48 hours of glucose
    supply during times of starvation. Prolonged starvation that results in the
    depletion of the glycogen stores requires that the liver convert lactate, glycerol, and
    amino acids to glucose. This is termed gluconeogenesis.

Question 50

50. Why might patients with cirrhosis be more likely to develop hypoglycemia in the
    perioperative period?

Answer 50

50. Patients with cirrhosis may be more likely to develop hypoglycemia in the
    perioperative period as gluconeogenesis may be impaired.

Question 51

51. What role does the liver play in blood coagulation? What is the clinical implication
    of this for the patient with liver disease?

Answer 51

51. A normal liver synthesizes most of the proteins responsible for the coagulation of
    blood. A diseased liver may therefore manifest as coagulopathy in the patient

Question 52

52. How significant must liver dysfunction be before abnormal blood coagulation is
    noted? How can this be evaluated preoperatively?

Answer 52

52. Bleeding can be prevented with only 20% to 30% of normal levels of clotting
    factors, so that abnormal blood coagulation manifests only after significant liverdisease. The coagulation status of a patient can be evaluated preoperatively by
    checking the patient’s prothrombin time, partial thromboplastin time, and bleeding
    time. Indeed, the prothrombin time is frequently used as an evaluation of the
    synthetic function of the liver. (

Question 53

53. What is the role of vitamin K in coagulation?

Answer 53

53. Vitamin K plays an important role in the catalysis of some of the procoagulant
    proteins to produce factors II, VII, IX, and X

Question 54

54. How does the liver facilitate the renal excretion of lipid soluble drugs?

Answer 54

54. The liver facilitates the renal excretion of lipid soluble drugs by converting
    the drugs to more water soluble forms via mechanisms such as conjugation.

Question 55

55. How does chronic drug therapy affect the metabolism of anesthetic drugs by the
    liver?

Answer 55

55. Chronic drug therapy can inhibit anesthetic drug metabolism by inhibiting hepatic
    enzymes. Conversely, they can also enhance drug metabolism by inducing
    hepatic enzymes (particularly cytochrome P isoforms).

Question 56

56. How does chronic liver disease impact drug metabolism?

Answer 56

56. Chronic liver disease may interfere with the metabolism of drugs because of the
    decreased number of enzyme-containing hepatocytes or the decreased hepatic
    blood flow that typically accompanies cirrhosis of the liver.

Question 57

57. Why may hepatic drug metabolism be accelerated after the administration of certain
    medications?

Answer 57

57. Accelerated drug metabolism may be noted after the administration of certain
    drugs such as phenytoin. It is believed that exposure of the microsomal
    enzymes to these drugs causes an up-regulation, or induction, of their own
    synthesis.

Question 58

58. What role does the liver play in the excretion of bilirubin? What is the clinical
    implication of this for the patient with liver disease?

Answer 58

58. The conjugation of bilirubin with glucuronic acid takes place in the liver through
    the action of glucuronyl transferase. The conjugation of bilirubin allows it to
    become water soluble for renal excretion. Impairment of this function of the liver,
    as with liver disease, can lead to increased serum levels of unconjugated bilirubin.
    The liver is also responsible for the excretion of conjugated bilirubin into bile.
    This explains the elevated serum levels of conjugated bilirubin in the presence of
    liver disease.

Question 59

59. What proteins are synthesized in the hepatocytes?

Answer 59

59. All proteins are synthesized in hepatocytes except for gamma globulins and factor
    VIII

Question 60

60. What is the role of the urea cycle in the hepatocytes?

Answer 60

60. The urea cycle is used by hepatocytes to convert the end products of amino acid
    degradation, such as ammonia and other nitrogenous waste products, to urea
    which is readily excreted by the kidneys.

Question 61

61. What pathophysiologic changes are associated with end-stage liver disease
    (ESLD)?

Answer 61

61. End-stage liver disease (ESLD) is associated with portopulmonary hypertension,
    hepatopulmonary syndrome (shunting due to impairment of hypoxic pulmonary
    vasoconstriction), atelectasis, pleural effusions, hepatic encephalopathy,
    impaired drug binding, coagulopathy, ascites, and renal dysfunction (due to
    various factors including the hepatorenal syndrome).

Question 62

62. What are the hemodynamic changes associated with ESLD?

Answer 62

62. Severe liver disease that has advanced to cirrhosis is associated with a
    hyperdynamic circulation. Patients typically have normal to low systemic blood
    pressure, increased cardiac output and decreased systemic vascular resistance due to
    vasodilation and shunting.

Question 63

63. What are some consequences of the portal hypertension seen in ESLD?

Answer 63

63. Portal hypertension, as seen in ESLD, is the high resistance of blood flow through
    the liver. This results in an accumulation of blood in the vascular beds that normally
    drain to the liver, and these vessels become dilated and hypertrophy. Vessels
    draining the esophagus, stomach, spleen, and intestines are affected, resulting in
    varices.

Question 64

64. What are some of the symptoms of portal hypertension?

Answer 64

64. Some of the symptoms of portal hypertension include anorexia, nausea, ascites,
    esophageal varices, spider nevi, and hepatic encephalopathy

Question 65

65. What are some complications that can occur as a result of the portal hypertension
    seen in ELSD?

Answer 65

65. Complications that can occur as a result of the portal hypertension seen in
    ELSD include increased susceptibility to infection, renal failure, mental status
    changes, and massive hemorrhage through the rupture of the engorged dilated
    submucosal veins. Gastroesophageal varices are at the greatest risk of rupture.

Question 66

66. What are some pulmonary complications that can be seen in ESLD?

Answer 66

66. Pulmonary complications that can be seen in ESLD include pulmonary
    arteriovenous communications that are not ventilated, the impairment of hypoxic
    pulmonary vasoconstriction, atelectasis, and restrictive pulmonary disease due
    to ascites and pleural effusions. In less than 5% of patients with ESLD
    portopulmonary hypertension develops, whose cause is not well established.

Question 67

67. What are some reasons why a patient with hepatic cirrhosis may have arterial
    hypoxemia? Does the administration of supplemental oxygen increase the oxygen
    saturation in these patients?

Answer 67

67. Patients with hepatic cirrhosis may have arterial hypoxemia for several
    reasons. Often, patients with hepatic cirrhosis have right-to-left pulmonary
    shunting in response to the portal vein hypertension. Patients with ascites
    and hepatomegaly may also have impairment of diaphragmatic excursion due
    to the weight of the abdominal contents, particularly in the supine position.
    In patients with significant ascites, pleural effusions may impair lung expansion.
    In the early stages of ESLD, supplemental oxygen may improve arterial
    hypoxemia, but as the disease progresses oxygen therapy may not be
    effective.

Question 68

68. What are some causes of hepatic encephalopathy seen in patients with ESLD?

Answer 68

68. The cause of hepatic encephalopathy seen in patients with ESLD is multifactorial.
    Hepatic encephalopathy is in part due to increased serum concentrations of
    chemicals normally cleared by the liver, especially ammonia. Other factors include
    disruption of the blood–brain barrier, increased central nervous system inhibitory
    neurotransmission, and altered cerebral energy metabolism.

Question 69

69. What is the therapy for hepatic encephalopathy? Is it effective?

Answer 69

69. Therapy for hepatic encephalopathy revolves around reducing the production
    and absorption of ammonia. Neomycin is used to reduce ammonia production
    by urease-producing bacteria and lactulose is administered to reduce ammonia
    absorption. Some symptoms of hepatic encephalopathy are reversible with
    flumazenil therapy. These therapies are not completely effective because multiple
    other etiologic factors are associated with hepatic encephalopathy. It is also
    important to rule out other causes of altered mental status in the patient with
    ESLD. Other causes may include intracranial bleeding, hypoglycemia, or a postictal
    state.

Question 70

70. What role does the liver play in drug binding to serum proteins? What is the clinical
    implication of this for the patient with liver disease?

Answer 70

70. The liver synthesizes albumin, which binds drugs in the plasma. The binding of
    drugs to albumin decreases the free, or pharmacologically active, portion of the
    drug. When the liver is diseased the synthesis of albumin becomes impaired,
    decreasing the albumin available in the plasma for binding. As a result there is
    an increased concentration of free, unbound drug in the plasma. Patients
    with liver disease may manifest a more pronounced drug effect than patients
    with normal liver function after an intravenous injection of a specific drug
    dose. Increased drug effect secondary to a decrease in protein binding is more
    likely to be seen when the serum albumin concentration is less than 2.5 g/dL.

Question 71

71. Why is ascites thought to accumulate in patients with hepatic cirrhosis?

Answer 71

71. Ascites affects 50% of patients with hepatic cirrhosis. Ascites is thought to
    accumulate secondary to a decrease in plasma oncotic pressure, a corresponding
    increase in the hydrostatic pressure in the hepatic sinusoids, and an increase in
    sodium retention by the kidneys due to increased circulating levels of antidiuretic
    hormone.

Question 72

72. What are some complications associated with ascites?

Answer 72

72. Complications associated with ascites include marked abdominal distention that
    can lead to atelectasis and restrictive pulmonary disease, spontaneous bacterial
    peritonitis, and circulatory instability due to compression of the inferior vena cava
    and right atrium

Question 73

73. What is the treatment for ascites?

Answer 73

73. The treatment for ascites is initially fluid restriction, reduced sodium intake, and
    diuretic therapy. In severe cases abdominal paracentesis temporarily effectively
    reduces abdominal distention and restores hemodynamic stability

Question 74

74. How might renal function be affected in patients with hepatic cirrhosis?

Answer 74

74. Patients with hepatic cirrhosis tend to have a decrease in arterial blood volume,
    and consequently a decrease in renal blood flow and the GFR. Because of this
    patients with hepatic cirrhosisare at risk of developing hepatorenal syndrome, a seriouscomplication that is often fatal. The syndrome is characterized by intravascular
    fluid depletion, intrarenal vasoconstriction, worsening hyponatremia, hypotension,
    and oliguria. (

Question 75

75. What categories of hepatorenal syndrome have been described? Are there any
    therapies?

Answer 75

75. Two types of hepatorenal syndrome have been described. Type 1 hepatorenal
    syndrome presents as rapidly progressing prerenal failure. It is associated with
    a poor prognosis in the absence of therapeutic intervention. Type 2 hepatorenal
    syndrome presents with a milder degree of renal dysfunction. Treatment with
    octreotide, glucagon, and midodrine have shown promise at reversing type 1
    hepatorenal syndrome.

Question 76

76. In the absence of surgical stimulation, how do regional and inhaled anesthetics
    affect hepatic blood flow?

Answer 76

76. In the absence of surgical stimulation, regional and inhaled anesthetics decrease
    hepatic blood flow by 20% to 30%. Changes in hepatic blood flow in response to
    regional and inhaled anesthetics are believed to result from decreases in cardiac
    output, mean arterial pressure, or both. Volatile anesthetics may also decrease
    hepatic blood flow by impairing intrinsic hepatic mechanisms to maintain hepatic
    blood flow to varying degrees.

Question 77

77. Is there any evidence to suggest one inhaled anesthetic preserves hepatic
    autoregulation more than others?

Answer 77

77. There is some evidence to suggest that isoflurane inhibits hepatic autoregulation
    less than other inhaled anesthetics. (4

Question 78

78. What is halothane hepatitis? Are pediatric patients or adult patients more likely to
    develop halothane hepatitis?

Answer 78

78. There are two different forms of hepatotoxicity that can result from the
    administration of halothane. Halothane hepatitis typically refers to the more
    severe hepatotoxicity that can result in hepatic necrosis and death. Halothane
    hepatitis is extremely rare. Adult patients are more likely to develop halothane
    hepatitis than pediatric patients. Patients most likely to be affected are middle-
    aged, obese women who have had repeated administration of halothane
    anesthesia.

Question 79

79. What is the cause of halothane hepatitis?/

Answer 79

79. Although the exact cause of halothane hepatitis is unclear, it is believed to be due to
    an immunologic response to a toxic metabolite of halothane.

Question 80

80. How is the diagnosis of halothane hepatitis made?

Answer 80

80. The diagnosis of halothane hepatitis is made after other causes of hepatitis
    have been excluded. Its rare incidence and the disappearance of halothane in
    modern clinical practice make the likelihood of halothane hepatitis extremely
    unlikely. (

Question 81

81. Can volatile anesthetics, other than halothane, cause hepatotoxicity?

Answer 81

81. The administration of all volatile anesthetics can result in a mild, self-limited form
    of hepatotoxicity. It can be seen in up to 20% of patients, but is associated with
    minimal sequelae.

Question 82

82. What are some commonly ordered liver function tests? What is the utility of liver
    function tests in the perioperative period?

Answer 82

82. Commonly ordered liver function tests include serum bilirubin, aminotransferase
    enzymes, alkaline phosphatase, albumin, and the prothrombin time. Liver tests
    are very nonspecific, and significant liver dysfunction must occur before it is
    reflected in the majority of tests. Despite this, liver function tests have some utility
    in the perioperative period. Liver function tests may be useful preoperatively in
    detecting the presence of liver disease. Perioperatively, liver dysfunction may be
    classified as prehepatic, intrahepatic, or posthepatic through the evaluation of the
    results of the various liver function tests

Question 83

83. What are some preoperative findings in patients with liver disease that are
    associated with increased postoperative morbidity?

Answer 83

83. Preoperative findings in patients with liver disease that are associated with
    increased postoperative morbidity include marked ascites, markedly elevated
    prothrombin time and serum bilirubin level, markedly decreased serum albumin
    level, and encephalopathy.

Question 84

84. What monitoring may be useful intraoperatively for patients with hepatic cirrhosis
    undergoing surgical procedures?

Answer 84

84. Intraoperative monitoring for patients with hepatic cirrhosis should be guided by
    the surgical procedure. In general, monitoring of the arterial blood pressure
    with an intra-arterial catheter may be useful. This allows for monitoring of the
    arterial blood gases, pH, coagulation status, and glucose as well as the blood
    pressure. In addition, the urine output should be closely monitored due to the risk of
    postoperative renal dysfunction that can occur in patients with severe liver

Question 85

85. Why is the intraoperative maintenance of the arterial blood pressure particularly
    important in patients with hepatic cirrhosis?

Answer 85

85. The intraoperative maintenance of the arterial blood pressure is particularly
    important in patients with hepatic cirrhosis because these patients are dependent on
    hepatic arterial blood flow to provide oxygen to the hepatocytes. In the presence
    of portal hypertension, hepatic arterial blood flow is typically reduced from
    normal levels. The addition of anesthetics and the surgical procedure can exacerbate
    this reduction in hepatic blood flow and may contribute to postoperative liver
    dysfunction

Question 86

86. When liver function tests become abnormal postoperatively, what is the most
    likely mechanism for the postoperative liver dysfunction? In what patients and
    types of surgeries are liver function tests most likely to become elevated
    postoperatively?

Answer 86

86. Liver function tests are most likely to become abnormal secondary to an
    inadequate supply of oxygen to the hepatocytes intraoperatively. This is the
    most likely mechanism for mild, self-limited postoperative liver dysfunction.
    Abnormal postoperative liver function tests are most likely to occur in
    patients with preexisting liver disease whose hepatic oxygenation was marginal
    preoperatively or after surgery in which the operative site was in close proximity
    to the liver.

Question 87

87. What are the most likely causes of postoperative liver dysfunction?

Answer 87

.87. The most likely causes of postoperative liver dysfunction include drugs, arterial
hypoxemia, sepsis, congestive heart failure, cirrhosis, and a history of preexisting
hepatic viruses

Question 88

88. What laboratory values indicate an intrahepatic cause of liver dysfunction?

Answer 88

88. Elevated aminotransferase enzymes, decreased albumin, and a prolonged
    prothrombin time are all indicative of an intrahepatic cause of liver
    dysfunction. These alterations are reflective of direct hepatocellular damage.

Question 89

89. What are some causes of postoperative jaundice?

Answer 89

89. Operations on the liver or biliary tract, multiple blood transfusions, resorption
    of surgical hematoma, antibiotics and other perioperative drugs and metabolic and
    infectious causes can all lead to postoperative jaundice. Rarely, inhaled anesthetic
    agents may be implicated.

Question 90

90. What is delirium tremens? How does it usually present?

Answer 90

90. Delirium tremens is a severe withdrawal syndrome in patients with a history of
    chronic alcohol abuse. The onset of delirium tremens is typically 48 to 72 hours after
    cessation of the ingestion of alcohol. Delirium tremens presents clinically as
    tremulousness, hallucinations, agitation, confusion, disorientation, and increased
    activity of the sympathetic nervous system. Increased activity of the sympathetic
    nervous system in these patients is manifest as diaphoresis, fever, tachycardia,
    and hypertension. In severe cases the syndrome may progress to seizures and
    death.

Question 91

91. What is the treatment of delirium tremens?

Answer 91

91. The treatment of delirium tremens is primarily with the administration of central
    nervous system depressants, usually a benzodiazepine. If necessary, a b-adrenergic
    antagonist may be administered to offset sympathetic nervous system
    hyperactivity. The trachea may be intubated if indicated for airway protection.
    Other treatment is supportive as necessary, including hydration and the correction
    of electrolyte disorders.

Question 92

92. What is the mortality associated with delirium tremens? What is the usual cause of
    death in these patients?

Answer 92

92. The mortality associated with delirium tremens can be as high as 10%. The usual
    cause of death in these patients is cardiac dysrhythmias or seizures.

Question 93

93. What approximate percent of females and males aged 55 to 65 years are believed to
    have gallstones?

Answer 93

93. Approximately 20% of women and 10% of men aged 55 to 65 years are believed to
    have gallstones. Elevated serum bilirubin and/or alkaline phosphatase levels in
    these patients imply the presence of a stone in the common bile duct causing
    obstruction to the flow of bile.

Question 94

What is the potential problem with the use of opioids intraoperatively during a
cholecystectomy or common bile duct exploration?

Answer 94

94. Opioids such as morphine, meperidine, and fentanyl may produce spasm in the
    sphincter of Oddi. This increases the pressure in the common bile duct in a
    dose-dependent manner and may be painful to an awake patient. The
    administration of these medicines intraoperatively could hinder the passage of
    contrast medium for exploration of the common bile duct. In clinical practice,
    however, the administration of opioids to these patients rarely results in difficulty
    with intraoperative cholangiograms. (460

Question 95

95. How can intraoperative spasm of the sphincter of Oddi be treated?

Answer 95

95. Intraoperative spasm of the sphincter of Oddi can be treated with naloxone,
    glucagons, or nitroglycerin.

Question 96

96. What are some anesthetic considerations for patients undergoing laparoscopic
    procedures?

Answer 96

96. Anesthetic considerations for patients undergoing laparoscopic procedures are
    multiple. Included are the insufflation of the abdomen with carbon dioxide and the
    possible impairment of ventilation of the lungs in the presence of increased
    ventilatory requirements, the probable placement of the patient in the
    Trendelenburg position, the risk of puncture of bowel or vessels, and the potential
    for nitrous oxide to expand bowel gas.