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Step 1 High Yield > Metabolism > Flashcards

Metabolism Flashcards

1
Q

NADPH is a product of the ___ shunt

NADPH is used in: (4)

A

NADPH is a product of the HMP shunt

1) Anabolic processes (steroid and fatty acid synthesis)
2) Respiratory burst
3) Cytochrome P450 system
4) Glutathione reductase

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2
Q

NAD+ is generally used in ________ reactions (breakdown of substances) to carry reducing equivalents away as NADH

A

Catabolic

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3
Q 
Answer Hexokinase or glucokinase to the following...
Low Km (higher affinity):
Feedback inhibited by glucose 6-P:
High Vmax:
Induced by insulin:
A

Low Km (higher affinity): Hexokinase
Feedback inhibited by glucose 6-P: Hexokinase
High Vmax: Glucokinase
Induced by insulin: Glucokinase

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4
Q

What steps of glycolysis produce ATP?

A

1,3 BPG (phosphoglycerate kinase) → 3-PG

PEP (Pyruvate kinase) → Pyruvate

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5
Q

Explain the actions of FBPase-2 and PFK-2 during the fasting state and the fed state (they are the same bifunctional enzyme)

A

Fasting state: ↑ glucagon → ↑ cAMP → protein kinase A →↑ FBPase-2, ↓PFK-2 → Less glycolysis, more gluconeogenesis

Fed state: ↑ insulin → ↓cAMP → ↓protein kinase → ↓FBPase-2, ↑PFK-2 → More glycolysis, less gluconeogenesis

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6
Q

What are the components of glycolysis? (Substrates and enzymes)
“Good Guy Fred Fucks Girls By Putting Protruding Penis Parallel”
“High Profile People Act Too Glamorous Picture Posing Every Place”

A

Glucose (hexokinase) → glucose 6-phosphate (phosphofructoisomerase) → Fructose-6-phosphate (PFK-1) → Fructose-1-6-bisphosphate (Aldolase B/TPI) → Glyceraldehye-3-P (G3PD) → 1,3-bis-phosphoglycerate (phosphoglycerate kinase) → 3-phosphoglycerate (phosphoglycerate mutase) → 2-phosphoglycerate (enolase) → PEP (pyruvate kinase) → pyruvate

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7
Q

How does arsenic affect pyruvate dehydrogenase?

How does exercise affect pyruvate dehydrogenase

A

Arsenic inhibits lipoic acid

Exercise activates PDH: Increases NAD+/NADH ratio, ↑ADP, ↑Ca2+

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8
Q

What pyruvate pathways occur in the mitochondria?

A 
Pyruvate dehydrogenase complex
Pyruvate carboxylase (forms oxaloacetate)
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9
Q

Which amino acids are purely ketogenic? (when should these be consumed)

A

Lysine and leucine (increased intake of ketogenic nutrients as treatment for PDH complex deficiency)

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10
Q

When is NADH produced in the TCA cycle? ATP consumed? GTP produced?

A

NADH: Isocitrate dehydrogenase, alpha-kg-dehydrogenase, malate dehydrogenase
ATP: consumed with citrate synthase
GTP: Succinyl CoA synthetase (post succinyl CoA)

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11
Q

What are the electron transport inhibitors (decrease ETC proton gradient and ATP synthesis)?

What does Oligomycin inhibit?

A

Rotenone, cyanide, antimycin A, CO

Oligomycin inhibits ATP synthase

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12
Q

What are the irreversible enzymes of gluconeogenesis?

A

(Pathway Produces Fresh Glucose)
Pyruvate carboxylase (in mitochondria - activated by acetyl CoA)
PEP carboxykinase (requires GTP) Oxaloacetate → PEP
F-1,6-BP (increased by citrate)
Glucose-6-phosphatase (in ER) Glucose-6-P → Glucose

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13
Q

What is produced in the oxidative step of the HMP shunt?

A

CO2, 2NADPH, Ribulose 5-P (enzyme: G6P dehydrogenase)

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14
Q

What is produced in the nonoxidative part of the HMP shunt?

A

Ribose-5-P (DNA synthesis), G3P, F6P (Phosphopentose isomerase transketolases (require B1))

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15
Q

What is the blue-green heme containing pigment that gives sputum its color? (It is also an enzyme in the respiratory burst)

A

Myeloperoxidase (forms HOCl)

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16
Q

What is lactoferrin?

A

A protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation

17
Q

Glucose-6-phosphate dehydrogenase deficiency
Inheritance:
Relation to hemolytic anemia:
Characteristic cells:

A

Inheritance: X-linked recessive disorder
Relation to hemolytic anemia: NADPH is necessary to keep glutathione reduced, which in turn detoxifies free radicals and peroxides which damage RBCs leading to hemolytic anemia
Characteristic cells: Heinz bodies (oxidized Hb), Bite cells

18
Q

Why is fructose intolerance (aldolase B deficiency) worse than essential fructosuria (fructokinase defect)?

A

Fructosuria: Benign, asymptomatic condition, since fructose is not trapped in cells
Fructose intolerance: Fructose-1-P accumulates, causing decrease in available phosphate (fructokinase uses ATP) resulting in inhibition of glycogenolysis and gluconeogenesis

19
Q

What enzyme is absent in classic galactosemia? What causes damage?

A

Galactose-1-phosphate uridyltransferase - damage cuased by accumulation of toxic substances (galacitol)

20
Q

What are the essential amino acids?

A

Glucogenic: methionine, valine, histidine
Glucogenic/Ketogenic: Isoleucine, phenylalanine, threonine, tryptophan
Ketogenic: Leucine, lysine

21
Q

What are the substrates of the urea cycle?

What are the enzymes?

A

“Orange Cats Always Ask For Awesome Umbrellas”

Ornithine (ornithine transcarbamylase) → Citrulline + Aspartate (arginosuccinate synthetase) → Arginosuccinate (Arginosuccinase) → Fumarate (TCA) and Arginine (Arginase) → Urea (to kidney)

22
Q

How is the excess nitrogen (NH3) from amino acid catabolism included into the urea cycle?

What provides the second nitrogen group to urea?

A

CO2 + NH3 (Carbamoyl phosphate synthetase I + N-acetylglutamate) → Carbamoyl phosphate + Ornithine (Ornithine transcarbamylase) → Citrulline

Aspartate provides the second nitrogen group

23
Q

How do glutamate and alanine help remove ammonia from amino acid catabolism?

A

Amino acids (NH3) + alpha-KG → Glutamate (NH3) → Alanine (NH3) → Alanine cycle (muscle → liver) → Glutamate (NH3) → Urea

24
Q

How does the Cori cycle contribute to transport of ammonia by alanine and glutamate?

A

Takes the pyruvate in the liver that remains from transfer of alanine NH3 to glutamate and converts it to glucose, then moves it back to the muscle and turns it back into pyruvate for re-use

25
Q

What is the difference in presentation between N-acetylglutamate deficiency and Ornithine transcarbamylase deficiency?

A

N-acetylglutamate deficiency: Hyperammonemia characterized by increased ornithine with normal urea cycle enzymes

Ornithine transcarbamylase deficieny (X-linked recessive): Excess carbamoyl phosphate is converted to orotic acid → increased orotic acid in blood and urine, decreased BUN

26
Q

What disorder occurs with a tyrosinase deficiency?
What enzyme is deficient in PKU?
What enzyme is deficient in alkaptonuria?

A

Albinism: DOPA (tyrosinase) → Melanin
PKU: Phenylalanine hydroxylase (or BH4) (Phenylalanine → Tyrosine)
Alkaptonuria: Homogentisate oxidase (Homogentisate → Maleylacetoacetic acid → fumarate)

27
Q

What are the two pathways of homocysteine?

A

1) Homocysteine (cystathionine synthase) → cystathionine → Cysteine
2) Homocysteine (homocysteine methyltransferase) → Methionine

28
Q

What cannot be transported due to cystinuria?

What can this lead to?

How is it treated?

A

What cannot be transported due to cystinuria?
- COLA: Cysteine, Ornithine, Lysine, Arginine
What can this lead to?
- Hexagonal cystine stones
How is it treated?
- After nitroprusside test - potassium citrate, acetazolamide

29
Q

___________ cleaves glucose-1-p residues off branched glycogen until 4 remain before a branch point, then ________ moves three glucose-1-Ps from the branch to the linkage. Then, ________ cleaves off the last glucose-1-P on the branch

A

Glycogen phosphorylase cleaves glucose-1-p residues off branched glycogen until 4 remain before a branch point, then de-branching enzyme (4-alpha-D-glucanotransferase) moves three glucose-1-Ps from the branch to the linkage. Then, alpha-1,6-glucosidase cleaves off the last glucose-1-P on the branch

30
Q

What is similar and what is different between Niemann Pick disease and Tay-Sachs disease?

A

Similar: Both consist of progressive neurodegeneration, cherry red spot on macula and are autosomal recessive
Different: NPD has foam cells and hepatosplenomegaly whereas TS has lysosomes with onion skin and no hepatosplenomegaly

31
Q

What lysosomal storage disease consists of peripheral neuropathy, developmental delay, optic atrophy and globoid cells?

What enzyme is deficient?

A

Krabbe disease

Galactocerbrosidase

32
Q

What disease presents with a deficiency of arylsulfatase?

A

Metachromatic leukodystrophy

33
Q

Hunters syndrome is Hurlers syndrome + _________ and without _________

A

Hunters syndrome is Hurlers syndrome + aggressive behavior and without corneal clouding

34
Q

What shuttles fatty acids out of the cytoplasm and into the mitochondria for degradation?

What happens if it is deficient?

A

Carnitine shuttle

Inability to transport LCFAs into the mitochondria resulting in toxic acumulation

35
Q

In starvation, glycogen reserves are depleted after __ days

What maintains glucose levels after this?

A

1 day

Adipose release of FFA
Muscle and liver shift fuel use from glucose to FFA
Hepatic gluconeogensis from peripheral tissue lactate and alanine and adipose tissue glycerol and propionyl CoA

36
Q 
What is the function of each of the following enzymes:
Pancreatic lipase:
Lipoprotein lipase:
Hepatic lipase:
Hormone sensitive lipase:
LCAT:
CETP:
A

Pancreatic lipase: degradation of dietary TG
Lipoprotein lipase: Degradation of TG circulating in chylomicrons and VLDL (found on vascular endothelial surfaces)
Hepatic lipase: Degradation of TG remaining on IDL
Hormone sensitive lipase: Degradation of TG stored in adipocytes
LCAT: Catalyzes esterification of cholesterol
CETP: Transfer of cholesterol esters to other lipoprotein particles

37
Q

Which apolipoprotein activates LCAT?
Which apolipoprotein binds the LDL receptor?
Which is an LPL co-factor?

A

Which apolipoprotein activates LCAT? - A-1 (HDL)
Which apolipoprotein binds the LDL receptor? - B-100
Which is an LPL co-factor? - C-II

Step 1 High Yield (21 decks)

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