Hepatic pearls part 2 Flashcards

1
Q

Hepatic arterial blood flow is dependent on

A

metabolic demand- autoregulation

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2
Q

Hepatic blood flow promotes sufficient time for the blood to be in contact with

A

Kupffer cells & hepatocytes

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3
Q

Describe bridging fibrosis.

A

fibrous tissue contracts around the blood vessels & greatly impedes portal vein blood flow

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4
Q

Sympathetic activation results in

A

hepatic artery & mesenteric vessel vasoconstriction & decreased hepatic blood flow

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5
Q

Kupffer cells that line the hepatic venous sinusoids

A

cleanse the blood as it passes through the sinuses

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6
Q

Pores in the sinusoids are very permeable and allow easy passage of

A

fluid & protein into the spaces of Disse–> permits large amounts of lymph to form

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7
Q

A 10 to 15 mmHg increase in hepatic venous pressure can increase

A

lymph flow to 20x normal

-produces “sweating” from the liver surface with large amounts of free fluid entering the abdominal cavity= ascites

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8
Q

The liver has the following metabolic functions:

A

carbohydrate, fat, protein, drug, & miscellaneous metabolism

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9
Q

Specific liver functions associated with CHO metabolism:

A
  1. conversion of galactose & fructose to glucose
  2. storage of large amounts of glycogen
  3. gluconeogenesis
  4. formation of many chemical compounds from intermediate products of CHO metabolism
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10
Q

Glycogen is a readily available source of glucose that does

A

not contribute to intracellular osmolality

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11
Q

Describe the glucose buffer function:

A

storage of glycogen allows the liver to remove excess glucose from the blood, store it, & return it to the blood when BG concentration decreases

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12
Q

Hepatic glycogen stores are depleted after

A

a 24 hour fast

after this period we need gluconeogenesis to supply glucose

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13
Q

____ enhances glycogen storage

A

insulin

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14
Q

___ enhances glycogen breakdown

A

epinephrine & glucagon

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15
Q

Specific liver functions associated with fat metabolism:

A
  1. oxidation of fatty acids to supply energy for other body functions
  2. synthesis of large amounts of cholesterol, phospholipids & lipoproteins
  3. synthesis of fat from CHO & proteins
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16
Q

To derive energy from fat (triglycerides):

A

they must be split into glycerol & FAs
FAs are then split by beta oxidation into 2 carbon acetyl radicals that form acetyl coenzyme A
Acetyl Co-A enters the citric acid cycle & yields energy

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17
Q

Since the liver cannot use all of the acetyl co-A it produces:

A

it is converted to acetoacetic acid (combination of 2 acetyl co-A enzymes)
highly soluble and enters the blood & is absorbed by other tissues
reconverted back into acetyl co-A & enters the citric acid cycle
this is the way the liver is responsible for a major part of fat metabolism

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18
Q

Specific liver functions associated with protein metabolism:

A
  1. deamination of proteins
  2. formation of urea for removal of ammonia from the body fluids
  3. formation of plasma proteins
  4. synthesis of amino acids & synthesis of other compounds from amino acids
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19
Q

Deamination of _____ plays a major role in hepatic gluconeogenesis

A

alanine

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20
Q

All of the plasma proteins with the exception of the

A

immunoglobulins are formed by hepatocytes

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21
Q

Quantitatively the most important plasma proteins are

A

albumin

& alpha 1 anti-trypsin

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22
Q

Qualitatively the most important plasma proteins are

A

coagulation factors

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23
Q

Among one of the most important functions of the liver is the

A

synthesis of AAs and synthesis of other compounds from AAs

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24
Q

Describe transamination

A
  • keto acid is formed & similar to AA but has keto oxygen

- amino radical is transferred from an available AA to the keto acid to take the place of the keto oxygen

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25
Q

The most common cause of postoperative jaundice is

A

over-production of bilirubin due to reabsorption of a large hematoma or RBC breakdown following transfusion

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26
Q

All opioids can potentially cause spasm

A

of the sphincter of Oddi & increase biliary pressure

order of effect: fentanyl, morphine, meperidine, butorphanol, nalbuphine

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27
Q

The endocrine stress response may be at least partially blunted by

A
regional anesthesia 
(blocks afferent signals to the brain so the body doesn't release catecholamines)
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28
Q

All _____ decrease portal blood flow

A

volatile agents–> greatest with halothane, least with isoflurane

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29
Q

Spinal & epidural anesthesia (effects on hepatic blood flow)

A

decrease hepatic blood flow by decreasing blood pressure

30
Q

General anesthesia (effect on hepatic blood flow)

A

usually decreases hepatic blood flow by decreasing blood pressure & CO & resulting SNS stimulation

31
Q

Describe lab values that are changed in pre-haptic liver dysfunction

A

bilirubin overload
increased unconjugated bilirubin
(no change to other values)

32
Q

Describe lab values that are change in intrahepatic liver dysfunction:

A
parenchymal/hepatocellular dysfunction
increased- conjugated bilirubin
increased aminotransferase 
prolonged PT
decreased albmin
slightly increased alk phosph
33
Q

Describe the lab values that are changed in post-hepatic liver dysfunction:

A

cholestasis
increased-conjugated bilirubin
slightly increased aminotransferase
increased alk phosph

34
Q

PT measures the activity of

A

factors II, V, VII, & X

35
Q

Factor VII has

A

a short half-life & therefore the PT is useful in evaluating hepatic synthetic function

36
Q

In the presence of biliary obstruction, more

A

alk phos is synthesized & released into the circulation

37
Q

Which is the more specific of the serum aminotransferases?

A

ALT- primarily located in the liver

38
Q

Serum aminotransferases are

A

enzymes that are released into the circulation as a result of hepatocellular injury

39
Q

Which bilirubin is toxic to cells?

A

conjugated

40
Q

A primarily unconjugated hyperbilirubinemia may be seen with

A

hemolysis or with congenital or acquired defects in bilirubin conjugation

41
Q

A predominantly conjugated hyperbilirubinemia is associated with

A

an increased urobilinogen & may reflect:
intrahepatic cholestasis
extrahepatic biliary obstruction
a & b may lead to hepatocellular dysfunction

42
Q

Generally liver “function” tests are

A

not very sensitive or specific

43
Q

Tests that measure the liver synthetic function include:

A

serum albumin, PT, cholesterol, & pseudocholinesterase

44
Q

Describe phase I reactions

A

modify substances through CYP450 enzymes & mixed function oxidases
oxidation & reduction

45
Q

Describe cross-tolerance

A

enzyme induction can promote tolerance to other drugs metabolized by the same enzymes

46
Q

Products of phase 1 reactions may be

A

more active than the parent compound or may be rendered cytotoxic

47
Q

For drugs that have a high rate of hepatic extraction from the circulation,

A

a decrease in metabolic clearance is a product of reduce hepatic blood flow (not hepatocyte dysfunction)

48
Q

Describe phase II reactions.

A

may or may not follow a phase 1 reaction
involve conjugation of a substance with a H2O soluble metabolite
glucuronide is the most common

49
Q

The liver stores large quantities of these vitamins:

A

A, B12, D, E, & K

50
Q

Describe how the liver stores iron

A

iron is stored in the liver as ferritin
hepatic cells produce apoferritin which binds excess iron in body fluids
apoferritin + iron= ferritin- stored in hepatocytes until iron is needed in body
during low levels of iron in the circulation ferritin releases iron
iron is carried in the blood by transferrin
apoferritin-ferritin system therefore acts as an iron storage & buffer system

51
Q

Vitamin K is a required cofactor for the synthesis of factors

A

II, VII, IX, & X

52
Q

Hepatocytes secrete_____ into the bile canniculi

A

conjugated bilirubin

53
Q

Flow of bile from the common bile duct is controlled by

A

the sphincter of Oddi

54
Q

The gallbladder serves as a

A

reservoir for bile

55
Q

Cholecystokinin is a hormone

A

released from the intestinal mucosa in response to fat & protein that causes contraction of the gallbladder, relaxation of the Sphincter of Oddi & ejection of bile into the small intestine

56
Q

Bilirubin is the major end product of

A

end product of hemoglobin degradation

57
Q

Bilirubin provides a valuable tool for diagnosing

A

hemolytic blood disease & various types of liver disease

58
Q

Describe the formation of bilirubin

A

hemoglobin is split into globin & heme
heme ring is opened and the Fe is released & transported by transferrin
4 pyrrole rings of the prophyrin structure are converted to biliverdin
biliverdin is rapidly converted to free bilirubin
free bilirubin combines with plasma albumin

59
Q

Describe the summary of conversion of hemoglobin to bilirubin.

A

hemoglobin–> globin + heme–> Fe + pyrrole rings–> biliverdin–> free bilirubin–> bilirubin + albumin

60
Q

Bilirubin bound to plasma albumin is called

A

“free bilirubin”, unconjugated or indirect bilirubin

61
Q

Free bilirubin is absorbed by hepatocytes, released from albumin, and conjugated with:

A

glucuronide

or sulfate

62
Q

Conjugated bilirubin is excreted from

A

or direct bilirubin is excreted from hepatocytes by active transport into the bile canaliculi

63
Q

1/2 of the conjugated bilirubin in the intestines is converted by bacteria to

A

urobilinogen which is reabsorbed back into the blood

majority of urobilinogen is reexcreted by the liver back into the intestines & eliminated in the feces

64
Q

Excess bilirubin in the ECF produces

A

jaundice

-large quantities of unconjugated or conjugated bilirubin

65
Q

Common causes of jaundice include:

A

hemolytic jaundice- increased destruction of RBCs

obstructive jaundice- obstruction of bile ducts or damage preventing bilirubin from being excreted

66
Q

In hemolytic jaundice, RBCs are

A

hemolyzed rapidly
-increased production of bilirubin by macrophages
-increased unconjugated bilirubin in blood- hepatocytes cannot conjugate all of the bilirubin
results in primarily an increase in unconjugated bilirubin in the blood
-excretory function of the liver is not impaired

67
Q

Hemolytic jaundice results primarily in an increase in

A

unconjugated bilirubin

68
Q

With obstructive jaundice, unconjugated bilirubin enters

A

the hepatocytes & is conjugated in the usual way
the rate of conjugated bilirubin formation is normal but it cannot pass from the liver into the intestines
the conjugated bilirubin enters the blood via rupture of the bile canaliculi & direct emptying of bile into the lymph system

69
Q

Most of the bilirubin in the plasma in obstructive jaundice is in the

A

conjugated form

70
Q

The diagnostic differences between hemolytic & obstructive jaundice include

A

hemolytic jaundice–> unconjugated or free bilirubin form

obstructive jaundice–> conjugated form

71
Q

When there is total obstruction of bile flow, diagnostically we will see

A

test for urobilinogen in the urine is completely negative
because: no conjugated bilirubin can reach the intestines to be converted to urobilinogen
no urobilinogen is reabsorbed into the blood and excreted by the kidney