Week 9 Flashcards

(58 cards)

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

Where does glycolysis occur?

A

Cytosol

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

Why are RBCs a good model for glycolysis?

A

They lack mitochondria → depend entirely on glycolysis for ATP.

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

Why do RBCs perform only anaerobic glycolysis?

A

No mitochondria → no TCA cycle or ETC.

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

What is the main function of glycolysis?

A

Convert glucose → pyruvate with ATP and NADH production.

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

When does anaerobic glycolysis occur?

A

When oxygen is limited or mitochondria absent.

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

What happens to pyruvate in anaerobic conditions?

A

Reduced to lactate by lactate dehydrogenase.

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

Why must NADH be reoxidized to NAD+?

A

NAD+ is required for step 6 (G3P dehydrogenase).

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

What tissues rely heavily on anaerobic glycolysis?

A

RBCs, lens, cornea, kidney medulla, testes, exercising muscle.

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

What enzyme catalyzes Step 1?

A

Hexokinase (most tissues) / Glucokinase (liver, β cells)

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

Is Step 1 reversible?

A

No (irreversible).

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

What inhibits hexokinase?

A

Glucose-6-phosphate (product inhibition)

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

Key properties of hexokinase?

A

Low Km, low Vmax, broad specificity.

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

How is glucokinase different?

A

High Km, high Vmax, not inhibited by G6P.

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

What is Step 2?

A

G6P → F6P (isomerization).

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

What is the rate-limiting step of glycolysis?

A

Step 3: PFK-1

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

Reaction of PFK-1?

A

F6P → F1,6-bisphosphate.

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

What enzyme splits F1,6BP?

A

Aldolase.

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

What is formed after Step 5?

A

2 molecules of G3P.

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

What happens in Step 6?

A

G3P → 1,3-BPG + NADH.

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

What type of reaction is Step 7?

A

Substrate-level phosphorylation.

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

What happens in Step 10?

A

PEP → Pyruvate (via pyruvate kinase).

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

Is Step 10 reversible?

A

No (irreversible).

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

ATP used in glycolysis?

A

2 ATP (Steps 1 and 3).

25
ATP produced?
4 ATP (2 per each 3-carbon fragment).
26
Net ATP in anaerobic glycolysis?
2 ATP per glucose.
27
What happens to NADH in aerobic glycolysis?
Oxidized via ETC → generates more ATP.
28
Why does anaerobic glycolysis require more glucose?
Only 2 ATP per glucose (less efficient).
29
From which intermediate is 2,3-BPG formed?
1,3-BPG.
30
Which enzyme forms 2,3-BPG?
Bisphosphoglycerate mutase.
31
What is the function of 2,3-BPG?
Decreases hemoglobin affinity for O₂ → increases O₂ delivery.
32
Does the 2,3-BPG shunt produce ATP?
No — it bypasses ATP production.
33
Why is 2,3-BPG high in PK deficiency?
Compensatory increase to improve O₂ delivery.
34
How is hexokinase regulated?
Product inhibition by G6P.
35
Is glucokinase inhibited by G6P?
No.
36
What regulates glucokinase?
GKRP (glucokinase regulatory protein).
37
What happens to glucokinase when glucose is high?
Released from GKRP → active in cytosol.
38
What inhibits PFK-1?
ATP, citrate.
39
What activates PFK-1?
AMP, fructose-2,6-bisphosphate.
40
What does high ATP signal?
Energy sufficient → inhibit glycolysis.
41
What hormone increases fructose-2,6-BP?
Insulin.
42
What hormone decreases fructose-2,6-BP?
Glucagon.
43
What activates pyruvate kinase?
Fructose-1,6-bisphosphate (feed-forward activation).
44
What inhibits liver pyruvate kinase?
Phosphorylation via cAMP (glucagon effect).
45
What does glucagon do to PK?
Inactivates it → promotes gluconeogenesis.
46
What does insulin do to glycolytic enzymes?
Increases synthesis of glucokinase, PFK-1, PK.
47
What does glucagon promote?
Gluconeogenesis and inhibition of glycolysis.
48
What type of anemia occurs?
Chronic hemolytic anemia.
49
Why do RBCs lyse in PK deficiency?
↓ ATP → membrane instability → splenic destruction.
50
Why is severity variable?
Depends on residual enzyme activity + 2,3-BPG compensation.
51
What enzyme does fluoride inhibit?
Enolase.
52
Why is fluoride used in blood collection tubes?
Prevents glycolysis after sample collection.
53
How does arsenate affect glycolysis?
Replaces Pi in Step 6 → no ATP formed.
54
What is the effect?
Glycolysis proceeds but no net ATP gain.
55
Causes of lactic acidosis?
MI, shock, PE, hemorrhage, hypoxia.
56
Why does hypoxia cause lactic acidosis?
Impaired ETC → ↑ anaerobic glycolysis → lactate accumulation.
57
Why does thiamine deficiency cause lactic acidosis?
Impaired PDH → pyruvate accumulates → converted to lactate.
58
Calculate ATP from 1 glucose anaerobically.
4 produced – 2 used = 2 ATP net.