Practice Questions (Given) Flashcards

(58 cards)

1
Q

What is the difference between catabolic and anabolic pathways?

A

Catabolic pathways break down complex molecules into simpler ones, releasing energy (exergonic). Examples include glycolysis, fatty acid oxidation, and protein degradation. Anabolic pathways synthesize complex molecules from simpler precursors, requiring energy input (endergonic). Examples include gluconeogenesis, fatty acid synthesis, and protein synthesis.

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2
Q

Compared with the resting state, vigorously contracting skeletal muscle shows an increased reduction of pyruvate to lactate. True or False?

A

True

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3
Q

List the three sources of plasma glucose.

A
  • Dietary intake
  • Glycogenolysis
  • Gluconeogenesis
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4
Q

What is Ketogenesis?

A

Ketogenesis is the synthesis of ketone bodies (acetoacetate, β-hydroxybutyrate, and acetone) from acetyl-CoA in the liver mitochondria.

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5
Q

How is ketogenesis regulated?

A

Activated by: High fatty acid oxidation, low insulin/glucagon ratio, fasting state, high glucagon, low malonyl-CoA. Inhibited by: High insulin, fed state, high malonyl-CoA.

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6
Q

What effect do ketone bodies have on brain metabolism?

A

During prolonged fasting/starvation, ketone bodies become the primary fuel for the brain, providing up to 70% of brain energy needs and sparing glucose and muscle protein.

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7
Q

Describe how glucose is metabolized to pyruvate in glycolysis.

A

Overall pathway: Glucose (6C) → 2 Pyruvate (3C) through 10 enzymatic steps.

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8
Q

What are the irreversible steps of glycolysis?

A
  1. Hexokinase: Glucose → Glucose-6-phosphate
  2. Phosphofructokinase-1: Fructose-6-phosphate → Fructose-1,6-bisphosphate
  3. Pyruvate kinase: Phosphoenolpyruvate → Pyruvate
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9
Q

What are the regulatory steps of glycolysis?

A
  1. Hexokinase (Step 1) - inhibited by product (G6P)
  2. Phosphofructokinase-1 (Step 3) - major control point
  3. Pyruvate kinase (Step 10)
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10
Q

The first reaction in glycolysis that results in the formation of an energy-rich compound is catalyzed by?

A

glyceraldehyde 3-phosphate dehydrogenase.

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11
Q

How do insulin and glucagon affect the rate of glycolysis?

A

Insulin stimulates glycolysis; glucagon inhibits glycolysis.

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12
Q

Which of the following statements is true for insulin but not for glucagon?

A

Its secretion is decreased by the catecholamines.

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13
Q

What would logically be characteristic of an insulinoma?

A

Decreased glucose in the blood.

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14
Q

What is the pentose phosphate pathway?

A

An alternative glucose oxidation pathway that occurs in the cytosol.

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15
Q

List the products of the pentose phosphate pathway.

A
  • NADPH
  • Ribose-5-phosphate
  • Glycolytic intermediates (G3P, F6P)
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16
Q

How is cytosolic pyruvate oxidized to acetyl-CoA and CO₂ in the mitochondria?

A

Pyruvate is transported into the mitochondrial matrix and catalyzed by pyruvate dehydrogenase complex.

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17
Q

What are the roles of pyruvate dehydrogenase complex (PDHc) enzymes?

A

E1 decarboxylates pyruvate; E2 transfers acetyl group to CoA; E3 regenerates oxidized lipoate.

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18
Q

Describe the regulation of PDH by allosteric effectors.

A

Activated by Ca²+ and ADP; inhibited by Acetyl-CoA, NADH, and ATP.

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19
Q

What are the symptoms of PDHC deficiency?

A

Lactic acidosis, neurological problems, developmental delays, muscle weakness.

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20
Q

What is a treatment for thiamine deficiency?

A

Ketogenic diet and thiamine supplementation

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21
Q

The reaction converting pyruvate to acetyl CoA is reversible. True or False?

A

False

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22
Q

Where does the conversion of pyruvate to acetyl CoA occur?

A

Mitochondria

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23
Q

What inhibits the TCA cycle dehydrogenases?

A

High NADH

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24
Q

What is the overall reaction of acetyl-CoA oxidation in the TCA cycle?

A

Acetyl-CoA + 3NAD+ + FAD + GDP + Pi + 2H₂O → 2CO₂ + 3NADH + FADH₂ + GTP + CoA

25
Name the enzyme that produces CO₂ from isocitrate in the TCA cycle.
Isocitrate dehydrogenase
26
Which coenzyme is used by dehydrogenases in both glycolysis and the TCA cycle?
NAD+
27
What are the four protein complexes in the electron transport chain?
* Complex I (NADH-CoQ reductase) * Complex II (Succinate-CoQ reductase) * Complex III (CoQ-cytochrome c reductase) * Complex IV (Cytochrome c oxidase)
28
Which complex in the transport chain does not pump protons?
Complex II
29
What is the role of FADH₂ in the electron transport chain?
Enters at Complex II and pumps fewer protons than NADH
30
What is the chemiosmotic theory of oxidative phosphorylation?
Energy from electron transport is stored as a proton gradient, then used for ATP synthesis
31
What is the significance of superoxide dismutase?
Converts superoxide radical to hydrogen peroxide, protecting against oxidative damage
32
What is gluconeogenesis?
Synthesis of glucose from non-carbohydrate precursors primarily in liver and kidney cortex
33
Name the bypass reactions in gluconeogenesis.
* Pyruvate → Oxaloacetate (pyruvate carboxylase) * Oxaloacetate → Phosphoenolpyruvate (PEPCK) * Fructose-1,6-bisphosphate → Fructose-6-phosphate (Fructose bisphosphatase-1) * Glucose-6-phosphate → Glucose (glucose-6-phosphatase)
34
Which reaction is unique to gluconeogenesis?
Oxaloacetate → phosphoenolpyruvate
35
What is the main function of the Cori cycle?
Regenerate NAD+ anaerobically
36
What is the main product of the Cahill cycle?
Alanine
37
Which metabolic conditions do the Cori cycle and Cahill cycle operate under?
* Cori Cycle: Intense exercise, hypoxia * Cahill Cycle: Fasting, starvation, prolonged exercise
38
What effect does glucagon have on gluconeogenesis?
Activates gluconeogenesis
39
What is the effect of increased NADH/NAD+ ratio on gluconeogenesis?
Inhibits gluconeogenesis
40
What is the role of ATP synthase in oxidative phosphorylation?
Uses proton flow back into matrix to drive ATP synthesis
41
What are the key inhibitors of the respiratory chain?
* Complex I: Rotenone, barbiturates * Complex II: Malonate * Complex III: Antimycin A * Complex IV: Cyanide, carbon monoxide, azide * ATP synthase: Oligomycin
42
What is the role of alcohol dehydrogenase in ethanol metabolism?
Ethanol → Acetaldehyde (produces NADH) ## Footnote Alcohol dehydrogenase is an enzyme that catalyzes the conversion of ethanol to acetaldehyde, producing NADH in the process.
43
What is the function of aldehyde dehydrogenase in ethanol metabolism?
Acetaldehyde → Acetate (produces NADH) ## Footnote Aldehyde dehydrogenase is responsible for converting acetaldehyde to acetate, also producing NADH.
44
What is the effect of an increased NADH/NAD+ ratio on lactate and pyruvate equilibrium?
Shifts lactate → pyruvate equilibrium toward lactate (less substrate) ## Footnote This shift results in a decreased availability of pyruvate due to increased lactate concentration.
45
What is the effect of an increased NADH/NAD+ ratio on oxaloacetate and malate equilibrium?
Shifts oxaloacetate ← malate equilibrium toward malate (less oxaloacetate for PEPCK) ## Footnote This results in less oxaloacetate available for gluconeogenesis.
46
What is the overall result of increased NADH/NAD+ ratio on gluconeogenesis?
Decreased gluconeogenesis → hypoglycemia (especially in fasted state) ## Footnote The inhibition of gluconeogenesis leads to lower blood glucose levels, particularly in individuals who are fasting.
47
What are the inputs of gluconeogenesis?
* 2 Pyruvate (or equivalent precursors) * 4 ATP * 2 GTP * 2 NADH ## Footnote These inputs are required to synthesize glucose from non-carbohydrate sources in the liver.
48
What are the outputs of gluconeogenesis?
* 1 Glucose * 4 ADP + 4 Pi * 2 GDP + 2 Pi * 2 NAD+ ## Footnote Gluconeogenesis is energetically expensive, requiring 6 high-energy phosphates to reverse glycolysis, which only produces 2 ATP.
49
What are the reasons glucose is stored as glycogen?
* Osmotic advantage - polymeric form doesn't affect osmolarity * Rapid mobilization - branched structure allows simultaneous glucose release * Space efficient - compact storage * Large glucose storage without increasing osmotic pressure ## Footnote Storing glucose as glycogen prevents osmotic pressure issues that would occur if glucose were stored in its free form.
50
What are the steps involved in glycogen synthesis (glycogenesis)?
* Glucose → Glucose-6-phosphate (hexokinase/glucokinase) * G6P → Glucose-1-phosphate (phosphoglucomutase) * G1P + UTP → UDP-glucose (UDP-glucose pyrophosphorylase) * UDP-glucose added to glycogen (glycogen synthase - rate-limiting) * Branching enzyme creates α-1,6 branches ## Footnote Glycogenesis is the process of synthesizing glycogen from glucose, involving several enzymatic steps.
51
What are the steps involved in glycogen breakdown (glycogenolysis)?
* Glycogen phosphorylase removes glucose residues as Glucose-1-phosphate * Debranching enzyme moves branches and hydrolyzes α-1,6 bonds * G1P → G6P (phosphoglucomutase) * Liver: G6P → Glucose (glucose-6-phosphatase) - released to blood * Muscle: G6P enters glycolysis (no glucose-6-phosphatase) ## Footnote Glycogenolysis allows the body to access stored glucose for energy, particularly during fasting or intense exercise.
52
What hormones regulate glycogen synthesis and glycogenolysis in the liver?
* Glucagon (fasting): Activates phosphorylase, inactivates glycogen synthase → breakdown * Insulin (fed): Inactivates phosphorylase, activates glycogen synthase → synthesis * Epinephrine: Activates breakdown ## Footnote These hormones help maintain glucose homeostasis by regulating glycogen metabolism based on the body's energy needs.
53
What hormones regulate glycogen synthesis and glycogenolysis in muscle?
* Epinephrine: Activates breakdown (via cAMP) * Ca²+ (contraction): Activates breakdown * Insulin: Promotes synthesis ## Footnote In muscle, the regulation of glycogen metabolism is closely tied to energy demand and muscle contraction.
54
What is von Gierke disease?
Deficiency: Glucose-6-phosphatase Pathophysiology: Cannot release glucose from liver → severe fasting hypoglycemia, hepatomegaly, lactic acidosis, hyperuricemia, hyperlipidemia ## Footnote Von Gierke disease is a glycogen storage disease characterized by the inability to convert glycogen to glucose due to a specific enzyme deficiency.
55
What is the pathophysiology of pyruvate carboxylase deficiency?
Deficiency: Pyruvate carboxylase (first step of gluconeogenesis) Pathophysiology: Impaired gluconeogenesis → fasting hypoglycemia, lactic acidosis, developmental delay, failure to thrive ## Footnote This condition affects gluconeogenesis and the TCA cycle due to the inability to convert pyruvate to oxaloacetate.
56
What is the mechanism behind alcohol-induced hypoglycemia?
Increased NADH/NAD+ ratio from ethanol metabolism Pathophysiology: Inhibits gluconeogenesis, depletes glycogen stores, hypoglycemia especially in fasted/malnourished individuals ## Footnote Alcohol metabolism affects glucose production and storage, leading to hypoglycemia.
57
Where are the major glycogen storage sites in the body?
* Liver: ~100-120g (10% of liver mass) * Skeletal Muscle: ~400-500g (1-2% of muscle mass) * Other tissues: Small amounts in cardiac muscle, kidney, brain (limited) ## Footnote The liver and skeletal muscle are the primary sites for glycogen storage, with distinct functions in glucose regulation and energy provision.
58
What is the function of glycogen stored in the liver?
Maintain blood glucose ## Footnote The liver can release free glucose into the bloodstream, helping to regulate blood sugar levels.