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AU13 Biochemistry Final > Stiner - The Role of the Liver in Metabolism > Flashcards

Stiner - The Role of the Liver in Metabolism Flashcards

1
Q

This organ is where all ingested materials are filtered through, the cells have a broad range of synthetic, catabolic, and excretory function; where most drug metabolism takes place

A

the liver

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2
Q

With ______ liver disease there are typically ___ outward symptoms, but with ______ liver disease, ______ symptoms are present

A

mild
no
severe
many

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3
Q

The ______ of the liver facilitates the exchange of metabolites between _______ and _______

A

structure

hepatocytes and plasma

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4
Q

The liver plays a central role in _______ metabolism by maintain the circulating concentration of it

A

glucose

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5
Q

This enzyme permits the release of ___ _____ to the blood by hydrolysis of itself resulting in the creation of a ____ ____ and ____ _____

A

glucose-6-phosphate

free glucose
phosphate group
free glucose

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6
Q

_____ store more glycogen than the liver

A

muscles

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7
Q

The majority of plasma proteins (albumin, coagulation factors, α/β globins, acute phase proteins) are synthesized in the _______

A

liver

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8
Q

Genetic deficiency of _________ presents in infancy as liver disease or in adulthood as lung disease

A

α1-antitrypsin

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9
Q

Genetic deficiency of ______ leads to Wilson’s disease, a condition associated with liver and CNS damage

A

ceruloplasmin

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10
Q

Liver cancer is associated with particularly high plasma concentrations of __________

A

α-fetoprotein

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11
Q

Plasma proteins and membrane receptors are ________ and then ______ by acid proteases within intracellular organelles known as _________

A

endocytosed
hydrolyzed
lysosomes

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12
Q

Intracellular proteins are degraded within structures known as _______, by the ______-_______ system

A

proteasomes

ubiquitin-proteasome (UPS)

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13
Q

________ marks intracellular proteins for degradation

A

ubiquitin

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14
Q

UPS involves three enzymes, what are they?

A

an ATP-dependent ubiquitin-activating enzyme (E1)
ubiquitin-conjugating enzyme (E2)
ubiquitin-protein ligase (E3)

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15
Q

The UPS is important in the activation of the ______ ______ pathway and the function of UPS is _______ by ROS

A

NFκB proinflammatory

modified

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16
Q

The ____ ____ is essential for the removal of nitrogen generated via amino acid metabolism; detoxification of ammonia/alanine to _____ in the liver

A

urea cycle

urea

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17
Q

Ammonia is toxic, particularly to the _______; impaired clearance of ammonia can cause ______ ______

A

CNS

brain damage

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18
Q

_______, a constituent of hemoglobin, myoglobin, and cytochromes, is synthesized in most cells of the body (the liver is the main non erythrocyte source of its synthesis)

A

heme

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19
Q

Heme synthesis-1: glycine and succinyl-coenzyme A condense to form _____________ and this reaction is catalyzed by _______; located in the __________

A

5-aminolevulinate (5-ALA)
5-ALA synthase
mitochondria

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20
Q

The rate limiting step of heme synthesis is the inhibition of _________

A

5-ALA synthase

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21
Q

Heme synthesis-2: In the ________, two molecules of 5-ALA condense to form a molecule containing a pyrrole ring, ______________

A

cytosol

porphobilinogen (PBG)

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22
Q

Heme synthesis-3: Four molecules of PBG combine to form a _______ ______ compound which cyclize to yield ____________ and then __________

A

linear tetrapyrrole
uroporphyrinogen III
coporphyrinogen III

23
Q

Heme synthesis: Final stages (1 of 2) occur in the _______ where a series of carboxylation/decarboxylation of side chains in uroporphyrinogen III yield _________

A

mitochondria

protoporphyrin IX

24
Q

Heme synthesis: The last stage is where iron (Fe2+) is added by _________ to _________ to form heme

A

ferrocheltase

protoporphyrin IX

25
Q

________ is the catabolic product of heme; it is excreted into bile and urine and responsible for the yellow color of bruises, jaundice, etc; coagulation of it in the gut is catabolized by bacteria

A

bilirubin

26
Q

Bilirubin, when oxidized, reverts to become _______; and this cycle has led to the theory of bilirubin as a cellular ________

A

biliverdin

antioxidant

27
Q

True or False

Bilirubin is soluble and biliverdin is not

A

False; biliRUBIN is NOT soluble and biliVERDIN is soluble; bilirubin must be transported by a carrier protein

28
Q

_______ is clinically obvious when plasma bilirubin concentration exceed 50μmol/L; result of an imbalance between production and secretion; there are 3 main causes

A

jaundice

29
Q

Three main causes of jaundice;
________ is the increased production of bilirubin
________ is impaired hepatic uptake, conjugation, or secretion of bilirubin
______ is the obstruction of biliary drainage

A

prehepatic
intrahepatic
posthepatic

30
Q

_______ _______ results from excess production of bilirubin as a result of hemolysis, or a genetic abnormality

A

prehepatic jaundice

31
Q

_______ ______ reflects a generalized hepatocyte disfunction; lack of bilirubin processing; common in newborns

A

intrahepatic jaundice

32
Q

______ _______ is caused by an obstruction of bilirubin “tree,” the plasma bilirubin is conjugated and other biliary metabolites, such as bile acids, accumulate

A

posthepatic jaundice

33
Q

Metabolism of drugs proceeds in 2 phases:
phase 1 –> the addition of a _____ group mediated by _______
phase 2 –> _______ mediated by cytoplasmic enzymes, ______, ______, _____

A

polar
cytochrome C P-450 (CYP)

conjugation
sulfination, acetylation, methylation

34
Q

Active site of CYP contains a ____ ____ center; important for the ________ of organic substances; accounts for ~75% of total ____ _____

A

heme iron
oxidation
drug metabolism

35
Q

The __________ enzyme family is responsible for drug breakdown; present in the ______ _____ mainly in the liver; can be inhibited by agents such as grapefruit juice; these enzymes can also exhibit _____ _____ that can alter catalytic activity

A

cytochrome P-450
endoplasmic reticulum
allelic variance

36
Q

The commonly prescribed drug _______ can be hepatotoxic in excess; an overdose can cause free radical mediated peroxidation of membrane lipids

A

acetaminophen

37
Q

Excess intake of ____ ____ remains the most common cause of liver disease in the western world; it can also affect the ubiquitin system

A

ethyl alcohol

38
Q

________ deaths associated with liver disease in the US annually and _____% of these are linked to alcoholic cirrhosis

A

25,000

40%

39
Q

Ethanol is oxidized in the liver by _____ ________ to form ________

A

alcohol dehydrogenase

acetaldehyde

40
Q

Acetaldehyde is oxidized by ________ to form ______

A 
acetaldehyde dehydrogenase (ALDH)
acetate
41
Q

______ ______ _____ is the cofactor for the ethanol –> acetaldehyde –> acetate reaction

A

nicotinamide adenine dinucleotide (NAD+); is reduced to NADH

42
Q

Liver damage in patients who abuse alcohol may arise from the toxicity of _________

A

acetaldehyde

43
Q

Both alcohol dehydrogenase and acetaldehyde dehydrogenase are susceptible to _____ _____; which can increase/decrease rise of liver disease/alcoholism

A

genetic polymorphisms

Increase

44
Q

Biochemical tests to measure “liver function” work by testing levels of ______ ______; fluctuations in these can be an indicator of disease

A

liver enzymes (bilirubin, albumin, etc)

45
Q

____ _____ is a good indicator of liver synthetic function

A

prothrombin synthesis

46
Q

_______ ______ and ______ ___-_____ are involved in the interconversion of amino and ketoacids, and are required for metabolism of nitrogen and carbohydrates; both are in the mitochondria and serum activity increases in liver disease

A 
aspartate aminotransferase (AST)
alanine amino-transaminase (ALT)
47
Q

In liver disease, the synthetic functions of ________ are likely affected, and so the patient would be expected to have a ______ prothrombin time (clotting) and a ______ serum albumin concentration

A

hepatocytes
prolonged
low

48
Q

An increased level of ________ is indicative of impairment of heme catabolism

A

Bilirubin

49
Q

A decreased level of _________ is indicative of impaired Carbohydrate metabolism

A

Glucose

50
Q

An increased level of ______ and a decreases level of ________ is indicative of impairment of Protein synthesis

A

Prothrombin time

Albumin

51
Q

An increased level of ___________ and a decreased level of __________ is indicative of impairment of protein catabolism

A

Ammonia

Urea

52
Q

An increase of _______ and ______ is indicative of an impairment of lipid metabolism

A

Cholesterol

Triglycerides

53
Q

An increase of _________ is indicative of an impairment with drug metabolism

A

Drug half time

54
Q

An increase in ____ _____ is indicative of an impairment of bile acid metabolism

A

Bile acids

AU13 Biochemistry Final (14 decks)

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