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Phase 1 > IMMS: Week 5 > Flashcards

IMMS: Week 5 Flashcards

1
Q

Give three examples of fatty acids

A

Oleic
Palmitic
Stearic

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2
Q

Where is the electron transport chain locacted

A

Inner mitochondrial membrane

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3
Q

What is contained in the inner mitochondrial membrane surface

A

Cytochromes

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4
Q

What does a cytochrome contain

A

Iron and copper co-factors

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5
Q

Describe what happens in the Electron transport chain

A

Check book

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6
Q

How many molecules of ATP are produced for each molecule of NADH

A

2.5

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7
Q

How many molecules of ATP are produced for each molecule of FADH2

A

1.5

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8
Q

What is the overall reaction of aerobic respiration

A

C6H12O6 + 6O2 + 38ADP + 38 Pi -> 6CO2 + 6H20 + 34-38 ATP

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9
Q

What do we have to assume about oxidative phosphorylation, glycolysis and kerb’s cycle to state 38ATP molecules are produced from them

A

That all NADH produced in glycolysis and Kreb’s cycle enter oxidative phosphorylation and ALL H+ are used in chemiosmosis

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10
Q

Why does ketogenesis take place

A

Because some acetyl coA exceed the capacity of the Kreb’s cycle and so need to be used to make ketone bodies instead

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11
Q

Were are ketone bodies produced

A

Mitochondrial matrix

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12
Q

Describe the process of ketogenesis

A

Look in book

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13
Q

What happens to acetoacetate after ketogenesis

A

It is converted to acetone and expired by the lungs

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14
Q

What happens to the level of oxaloacetate when carbohydrate utilisation is low or deficient

A

Oxaloacetate levels will also be low

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15
Q

What happens to acetoacetate and b-hydroxybutyrate after ketogenesis

A

It is used as fuel in many tissues

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16
Q

What happens to acetoacetate and b-hydroxybutyrate in skeletal muscles

A
  1. Taken into cytosol and into mitochondrial matrix
  2. B-hydrobutyrate -> acetoacetate
  3. Acetoacetate -> Acetoacetyl CoA
  4. Acetoacetyl CoA -> Two molecules of Acetyl CoA
  5. Acetyl CoA used in Kreb’s Cycle
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17
Q

What converts acetoacetyl CoA to Acetyl CoA

A

Thiolase enzyme

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18
Q

Why can’t the liver use ketones as a fuel

A

No presence of SUCCINYL COA which is needed to convert acetoacetate to acetoacetyl CoA

Can’t be used to produce Acetyl CoA

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19
Q

How is ketogenesis controlled

A

By the rate of release of fatty acids from adipose tissue

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20
Q

In what organ does ketogenesis take place

A

Liver

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21
Q

What causes the rate of production of ketone bodies to increase

A

Decrease in carbohydrate stores

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22
Q

How does diabetic ketoacidosis occur

A

From reduced supply of glucose and increased in fatty acid oxidation

Increased Acetyl CoA -> Increased Ketogenesis

Kettles are strong acids so this lowers blood pH

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23
Q

What is the pH of ketone bodies

A

3.5

24
Q

What is the problem of diabetic ketoacidosis

A

Impairs ability for haemoglobin to bind to oxygen

25
Q

What are ROS

A

Reactive Oxygen Species:

Highly reactive oxygen containing compounds that are free radicals (unpaired electrons in their orbital)

26
Q

Why are radicals so reactive

A

Because they try to extract electrons from other compounds to fill their outer orbitals

27
Q

What is the most potent ROS

A

Hydroxyl

28
Q

Where are exogenous sources of ROS

A

UV, tobacco and drugs

29
Q

What are endogenous sources of ROS

A

NADPH and ECT

30
Q

How do Oxygen radicals form

A

Check book

31
Q

Why is H2O2 considered an ROS

A

Because it is readily converted to the OH radical in cells

Lipid soluble so can cause damage away from site of formation

32
Q

What compounds catalyse the formation of a hydroxyl radical from hydrogen peroxide

A

Fe2+ and Cu2+

33
Q

What is the reaction of formation of hydroxyl radicals from hydrogen peroxide

A

Fenton reaction

34
Q

Describe the Fenton Reaction

A

H2O2 + Fe2+ -> Fe3+ + OH- + OH (radical)

35
Q

What two reactions are found in the Haber-Weiss Reaction

A

Fenton Reaction

Haber-Weiss Reaction

36
Q

What two reactions do hydroxyl radicals initiate

A

Lipid Peroxides

Organic Radicals

37
Q

What compound do free radicals DAMAGE

A

Proteins, lipids, carbohydrates and nucleic acids

38
Q

What membranes do free radicals they damage

A

Cells
Nuclear
Mitochondrial
ER

39
Q

Is DNA affected by the hydroxyl radical

A

Yes, it damages DNA and causes mutations

40
Q

What are respiratory bursts

A

Immune system defence against bacteria

41
Q

When are ROS released by immune cells

A

Following phagocytosis

42
Q

How do ROS form through immune cells

A
  1. NADPH oxidase reduces oxygen to superoxide

2. Superoxide is reduced to H2O2 -> OH radical

43
Q

What happens to ROS produced by immune cells

A

Myeloperoxidases combine H2O2 with CL- to produce CLO-

44
Q

What is CLO- needed for

A

Destroying bacteria by damaging bacterial cell membranes

45
Q

What enzyme converts superoxide to hydrogen peroxide and oxygen

A

Superoxide dismutase

46
Q

What enzyme catalyses conversion of hydrogen peroxide to water and oxygen

A

Catalase

47
Q

What is the role of catalase in the immune system

A

Protects WBCs against own rest bursts

48
Q

What enzyme catalyses the reduction of H2O2 to water and a disulphide

A

Glutathione Peroxidase

49
Q

What are two antioxidant vitamins

A

E and C

50
Q

Role of E

A

Protects against lipid per oxidation and stops free radical propagation in membranes

51
Q

Role of C

A

Reacts with superoxide and hydroxyl radical

52
Q

What is the Henderson Hasselbalch Equation

A

pH = pKa + log([HCO3-]/[CO2])

53
Q

What is the role of protein matrix of the bone

A

Buffer large amounts of H+ in patients with chronic acidosis

54
Q

What pH results in academia

A

Less than 7.35

55
Q

What pH results in alkalaemia

A

More than 7.45

56
Q

What PaCO2 level is a sign of respiratory acidosis

A

> 6 kPa

57
Q

What PaCO2 level is a sign of respiratory alkalosis

A

<4.5 kPa

Phase 1 (30 decks)

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