Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biochem > Metabolism Part II > Flashcards

Metabolism Part II Flashcards

1
Q

What are the 4 fates of pyruvate?

A
  1. Acetyl CoA
  2. Oxaloacetate
  3. Alanine
  4. Lactate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What enzyme converts pyruvate to Acetyl CoA

A

Pyruvate Dehydrogenase

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

What factors regulate pyruvate dehydrogenase?

A 
TLC for Nobody
Thiamine pyrophosphate (TPP) - active B1
Lipoic acid
Coenzyme A - B5
FAD - B2
NAD+ - B3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What B vitamins are needed to make Acetyl CoA?

A

B1, B2, B3, B5

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

What factor does arsenic inhibit

A

Lipoic acid - cofactor for PDH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Arsenic poisoning features

A

Garlic breath, vomiting, rice water stool

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

What happens in PDH deficiency and what clinical features result

A

Back up of pyruvate that gets converted to other things: Lactate, Alanine.
Lactic acidosis
Neurologic defects

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

What is treatment of PDH deficiency

A

Increase intake of ketogenic nutrients (high fat, high lysine and leucine) - so can make Acetyl CoA from something else. Ketone bodies can be used for energy instead of glucose.

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

How is PDH deficiency acquired?

A

Arsenic exposure, B vitamin deficiency (especially B1)

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

What does TCA enzyme citrate synthase do

A

Makes citrate from Acetyl CoA and oxaloacetate

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

What does isocitrate dehydrogenase do

A

Converts isocitrate into alpha ketoglutarate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the rate limiting enzyme in the TCA cycle

A

Isocitrate dehydrogenase

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

What does alpha ketoglutarate dehydrogenase do

A

Converts alpha ketoglutarate to succinyl-CoA

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

Why is alpha ketoglutarate dehydrogenase so regulated

A

Requires same cofactors as PDH complex: TPP, lipoic acid, coenzyme A, NAD, FAD+

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

How many moles of ATP are produced per NADH in ETC?

A

2.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How many moles of ATP are produced per FADH2 in ETC?

A

1.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What effect does Amytal (a barbiturate) have on ETC?

A

Blocks Complex I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What effect does Rotenone have on ETC?

A

Blocks Complex I

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

What effect does MPP have on ETC?

A

Blocks Complex I

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

What effect does Antimycin A have on ETC?

A

Blocks Complex III

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

What effect does CN have on ETC?

A

Blocks Complex IV

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

What can inhibit complex IV of the ETC?

A

CO, N3-, CN, H2S (hydrogen sulfide)

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

What can inhibit the ATPase of ETC?

A

Oligomycin A (macrolide antibiotic)

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

What affect do uncoupling agents have on inner mitochondrial membrane

A

Make it more permeable to H+ ions - generate more heat in the bottom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is thermogenin

A

An uncoupling agent for heat in hibernation - found in brown fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are some uncoupling agents?

A

Aspirin
Thermogenin
2,4-Dinitrophenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What enzymes convert lactate and pyruvate?

A

Lactate dehydrogenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What happens to lactate in the liver

A

Lactate (from anaerobic glycolysis in muscles, RBCs) gets converted back to pyruvate via LDH.
Pyruvate can be used for gluconeogenesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How are the alanine cycle and cori cycle similar?

A

Muscles make something that goes to the liver to be made into glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe steps of alanine cycle

A

Pyruvate gets converted to alanine in muscle It goes in serum to liver, where it is uptaken, converted back to pyruvate -> glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why are alanine and glutamine found in such high concentrations in the blood?

A

Ala and glutamine are two major carriers of nitrogen from tissues. Liver uses glutamine to make urea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is generally involved in transamination?

A

transfer of amino group of an amino acid to alpha ketoglutarate to form glutamate.
the remaining deaminated amino acid is a ketoacid (eg pyruvate) that is used in energy metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What enzyme catalyzes transamination?

A

Aminotransferases

34
Q

How are aminotransferases named?

A

By donor of the amino group (alanine aminotransferase converts alanine to pyruvate and forms glutamate)

35
Q

In addition to substrates, what is required by all aminotransferases?

A

Pyridoxal phosphate (a derivative of B6)

36
Q

What are the substrates and products of alanine aminotransferase?

A

Alanine+aKG -> Glutamate + Pyruvate

37
Q

What are the substrates and products of aspartate aminotransferase?

A

Aspartate+aKG -> Glutamate + oxaloacetate

38
Q

What are the two main carriers of nitrogen in the blood?

A

Alanine + Glutamine

39
Q

What is NADPH needed for? 4 reasons

A

Make FA’s and Cholesterol
Make O2 free radicals
Inside RBCs to protect from O2 free radicals
Cytochrome p450

40
Q

Most important enzyme of the HMP shunt

A

G6PD

41
Q

What does G6PD do

A

Converts G-6-P to Ribulose 5-P and get 2 NADPH

42
Q

What is needed to create oxygen free radicals

A

Oxygen, NADPH, and NADPH oxidase

43
Q

What converts free radical oxygen to hydrogen peroxide

A

Superoxide dismutase

44
Q

What does myeloperoxidase do

A

Converts hydrogen peroxide to hypochlorus acid HOCl

45
Q

What disease results from deficiency of NADPH oxidase

A

Chronic granulomatous disease - susceptible to catalase positive organisms because neutralize environmental hydrogen peroxide to water

46
Q

What does glutathione peroxidase do

A

Converts hydrogen peroxide into water, by letting H2O2 react with reduced glutathione (GSH)

47
Q

What is reduced glutathione

A

An antioxidant required to neutralize H2O2 into water

48
Q

How is glutathione disulfide converted back to reduced glutathione?

A

Glutathione reductase

49
Q

What does glutathione reductase use as an electron donor

A

NADPH (to reduce glutathione)

50
Q

What keeps the steady supply of NADPH around in order to continue to reduce glutathione for antioxidation?

A

G6PD

51
Q

What are some drugs that “oxidize” red blood cells and so are problematic in G6PD deficiency (-> hemolytic anemia)

A 
Anti malarial drugs primaquine and chloroquine
Nitrofurantoin
Dapsone
Sulfonamide
Isoniazid
Naphthalene (moth balls)
Fava beans
Ibuprofen
High dose ASA
52
Q

What enzyme is deficient in essential fructosuria

A

Fructokinase

53
Q

What enzyme is deficient in fructose intolerance

A

Aldolase B

54
Q

Why is essential fructosuria benign

A

Fructose doesn’t get trapped in cells - have it spilling out into blood and urine

55
Q

What is pathophysiology of fructose intolerance/ aldolase B deficiency?

A

Cannot correct fasting hypoglycemia - accumulation of fructose 1-P in cells causes decreased available phosphate(using it up), inhibits glycogenolysis and gluconeogenesis.

56
Q

What are clinical symptoms of fructose intolerance

A

Hypoglycemia
Vomiting - after fructose or sucrose
Hepatomegaly, jaundice

57
Q

What enzyme is deficient in galactokinase deficiency

A

Galactokinase - can’t convert galactose to galactose-1-p

58
Q

What is pathophysiology and clinical features of galactokinase deficiency

A

Galactose converts to galactitol which accumulates in the blood and can appear in blood and urine, cause infantile cataracts

59
Q

What enzyme is deficient in classic galactosemia

A

Absence of galactose-1-phosphate uridyltransferase

60
Q

Pathophysiology of classic galactosemia

A

Accumulation of toxic substances galactose-1P and galactitol

61
Q

Clinical features of galactosemia

A

Hepatomegaly, jaundice, FTT, infantile cataracts, intellectual disability

62
Q

What is the treatment for galactosemia

A

Exclude galactose and lactose from diet

63
Q

Rate limiting step of pentose phosphate pathway

A

G6PD

64
Q

Which tissues use pentose phosphate pathway

A

RBCs, Liver, Adrenal cortex, Mammary glands (during lactation)

65
Q

What disease is caused by deficiency of galactokinase

A

Galactokinase deficiency

66
Q

What disease is caused by deficiency of aldolase B deficiency

A

Fructose intolerance

67
Q

What disease is caused by deficiency of galactose-1-phosphate uridyltransferase

A

Classic galactosemia

68
Q

What disease is caused by deficiency of fructokinase

A

Essential fructosuria

69
Q

What is the primary energy source in a patient who has not eaten in 2 days

A

Fatty acids

70
Q

Rate limiting enzyme in ketone body synthesis

A

HMG CoA synthase

71
Q

Why do people get hypoglycemic after drinking alcohol?

A

NADH produced which shunts pyruvate toward production of lactate, shunts oxaloacetate toward production of malate, so pyruvate and oxaloacetate are not available to undergo gluconeogenesis

72
Q

Hallmark features of Kwashiorkor

A 
FLAME
Fatty Liver
Anemia
Malnutrition (protein)
Edema
Skin lesion, skin and hair depigmentation
73
Q

When does gluconeogenesis start in the post-absorptive period?

A

Starts 4-6 hours after last meal

Full active when glycogen stores are depleted

74
Q

When are glycogen stores depleted

A

10-18 hours

75
Q

What are the two main ketone bodies made in the liver

A

Acetoacetate and Beta-hydroxybutyrate are made from fatty acids and amino acids using NADH

76
Q

What causes fruity breath smell in ketosis

A

Acetoacetate spontaneously becomes acetone

77
Q

What does urine test for ketones test for

A

Acetoacetate only

78
Q

When do you start making ketones?

A

When you have so many fatty acids and so much acetyl coA that TCA cycle can’t handle it all;
Oxaloacetate depleted for gluconeogenesis

79
Q

What metabolic scenario favors synthesis of ketone bodies

A

When production of acetyl CoA from beta oxidation of FA’s exceeds oxidative capacity of the TCA cycle

80
Q

What is marasmus

A

Total energy malnutrition (deficient in everything)

81
Q

What is refeeding syndrome

A

Drop in serum Mg, Phosphate, and K+, can lead to arrhythmias and neurologic problems
Overall ATP depletion - phosphorylating glucose in cells depletes it.

Biochem (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions