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Gastro nutrition > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Outline the 3 main components to protein metabolsim

A

Protein synthesis
Amino acid synthesis adn metabolism
Nitrogenous waste excretion

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2
Q

Outline the role the liver plays in protein synthesis

A
  • Protein synthesis - the dominant site of protein synthesis for all major protein groups aside from immunoglobulins
    ◦ Albumin synthesis - key transport protein for acidic drugs and intrinsic hormones + electrolytes; the dominant source of intravascular plasma oncotic pressure
    ◦ Globulin protein synthesis
    ‣ Alpha globulins including haptoglobin for plasma free haemoglobin binding, serine protease inhibitors e.g. alpha 1 anti trypsin
    ‣ Beta globulins - transferrin binding and transferring iron in its ferric form
    ‣ Complement synthesis
    ◦ Clotting factors - vitaminK dependent clotting factors + independent factors
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3
Q

What role does the liver play in amino acid synthesis

A
  • Amino acid synthesis and metabolism
    ◦ Oxidative deamination forming energy and urea from surplus amino acids - remaining keto acid can be transformed by transamination to another amino acid, used as a substrate for gluconeogenesis or utilised in the citric acid cycle
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4
Q

What 3 phases are there to starvation

A
  1. Glycogenolytic phase
  2. Gluconeogenesis
  3. Ketogenic
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5
Q

Describe the glycogenolytic phase of starvation

A

Glycogenlysis can buffer glucose for 8-12 hours of fasting systemically from liver stores, muscle glycogen utilised within muscles only. Free fatty acids are metabolised by beta oxidation with release of acetoacetate and beta hydroxybutyrate in small amounts. Minor gluconeogenesis from lactate and glycerol

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6
Q

Define starvation

A
  • Relative or absolute inadequate energy supply causing the body to harness endogenous reserves
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7
Q

Describe the gluconeogenic phase of starvation

A

‣ after 24 hours glucose is produced from gluconeogenesis primarily from amino acids from lean tissues, glycerol from adipose, lactate from RBCs.
* In muscle tissues, protein is broken down to alanine as a substrate for gluconeogenesis by the alanine-glucose cycle
* Alanine formed by transamination of pyruvate derived from oxidation of isoleucine, leucine, valine
* Protein is also broken down into glutamine in muscle tissues which is used by the kidneys as a gluconeogenesis substrate
‣ Increased cortisol concentration reduced protein synthesis in skeletal muscle

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8
Q

Describe the ketogenic phase of starvation

A

‣ Ketone bodies gradually rise and replace glucose as the fuel for the CNS as gluconeogenesis declines adn fat becomes the dominant source of energy as lipolysis becomes overwhelmingly stimulated by glucagon stimulation, reducing insulin stimulation, reducing T3 stimulation
‣ Carnititine synthesis requires methyl from methionine derived from muscle breakdown
‣ Brain energy comes from ketones and residual glucose
‣ Cardiac and skeletal muscle derived energy from fatty acid oxidation
‣ Gluconeogenesis declines as a protein sparing mechanism - due to glucagon concentration decline at 10 days of starvation
* Protein breakdown is 75g/day during the first few days but decreased to 20g/day by the third week due to ketone body formation

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9
Q

When does the 2nd phase of starvation start

A

◦ Gluconeogenesis phase -
‣ after 24 hours glucose is produced from gluconeogenesis primarily from amino acids from lean tissues, glycerol from adipose, lactate from RBCs.

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10
Q

How long does glycogen supplies last in starvation

A

8-12 hours

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11
Q

What do muscles use as substrate for energy in the gluconeogenesis phase of starvation

A
  • In muscle tissues, protein is broken down to alanine as a substrate for gluconeogenesis by the alanine-glucose cycle
    * Alanine formed by transamination of pyruvate derived from oxidation of isoleucine, leucine, valine
    * Protein is also broken down into glutamine in muscle tissues which is used by the kidneys as a gluconeogenesis substrate
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12
Q

How is alanine formed

A
  • In muscle tissues, protein is broken down to alanine as a substrate for gluconeogenesis by the alanine-glucose cycle
    * Alanine formed by transamination of pyruvate derived from oxidation of isoleucine, leucine, valine
    * Protein is also broken down into glutamine in muscle tissues which is used by the kidneys as a gluconeogenesis substrate
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13
Q

Why is alanine important in starvation

A
  • In muscle tissues, protein is broken down to alanine as a substrate for gluconeogenesis by the alanine-glucose cycle
    * Alanine formed by transamination of pyruvate derived from oxidation of isoleucine, leucine, valine
    * Protein is also broken down into glutamine in muscle tissues which is used by the kidneys as a gluconeogenesis substrate
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14
Q

What is the dominant source of metabolic fuel in the 3rd phase of starvation

A

‣ Ketone bodies gradually rise and replace glucose as the fuel for the CNS as gluconeogenesis declines adn fat becomes the dominant source of energy as lipolysis becomes overwhelmingly stimulated by glucagon stimulation, reducing insulin stimulation, reducing T3 stimulation

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15
Q

What are ketones derived from

A

‣ Ketone bodies gradually rise and replace glucose as the fuel for the CNS as gluconeogenesis declines adn fat becomes the dominant source of energy as lipolysis becomes overwhelmingly stimulated by glucagon stimulation, reducing insulin stimulation, reducing T3 stimulation

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16
Q

What stimulates lipolysis in the 3rd phase of starvation

A

‣ Ketone bodies gradually rise and replace glucose as the fuel for the CNS as gluconeogenesis declines adn fat becomes the dominant source of energy as lipolysis becomes overwhelmingly stimulated by glucagon stimulation, reducing insulin stimulation, reducing T3 stimulation

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17
Q

What is carnitine? What is its role in starvation response

A

‣ Carnititine synthesis requires methyl from methionine derived from muscle breakdown

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18
Q

Where does energy for cardiac and skeletal muscle come from in prolonged starvation

A

Fatty acid oxidation

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19
Q

Why is gluconeogenesis not a prolonged factor in energy production

A

‣ Gluconeogenesis declines as a protein sparing mechanism - due to glucagon concentration decline at 10 days of starvation
* Protein breakdown is 75g/day during the first few days but decreased to 20g/day by the third week due to ketone body formation

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20
Q

In what form are most TG once they are absorbed

A

◦ 50% of dietary triglycerides are hydrolysed to glycerol and fatty acids, and 40% are hydrolysed to monoglycerides and fatty acids

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21
Q

What is the fate of short chain fatty acids absorbed from the gut

A

‣ Short chain fatty acids are transported directly to the liver without re-esterification in portal circulation

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22
Q

What is the fate fo longer chain fatty acids absorbed from the gut?

A

‣ Longer chain fatty acids are re-esterified to triglycerides, covered with phospholipids and transprted in chylomicrons —> lipoprotein lipases hydrolyse the chylomicrons producing free fatty acids that may be taken up by adipocytes for storage or metabolised within body tissues for energy; glycerol left over from hydrolysis is taken to the liver for gluconeogenesis

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23
Q

What is beta oxidation? What is its product?

A

◦ Beta oxidation - free fatty acid conversion to acetyl CoA which proceed through the Kreb’s cycle in mitochondria; or alternatively stored as acetic acid to transport energy to peripheral tissues to undergo conversion back to Acetyl CoA for energy utilisation

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24
Q

What is cholesterol made from

A

‣ Acetyl CoA can be converted back to triglycerides for storage, through triglycerides be converted to cholesterol or directly to cholesterol, can be used to create phospholipid or produce ketone bodies where critic acid cycle cannot be conducted

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25
Q

Once beta oxidation occurs can Acetyl CoA be converted back to TG?

A

Yes

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26
Q

Where can beta oxidation be performed?

A

All tissues
It is fastest in the liver

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27
Q

Excess Acetyl CoA in the liver is converted to?

A

Acetoacetic acid
COnverted back to ACetyl CoA in peripheral tissues

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28
Q

How is a ketone body formed?

A

◦ Where there is excessive Acetyl CoA formation from fat metabolism ketone bodies are formed by condensation of 2 acetyl-CoA molecules which can be utilised by the liver, heart and brain as an energy source

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29
Q

What is a ketone body sturcturally?

A

◦ Where there is excessive Acetyl CoA formation from fat metabolism ketone bodies are formed by condensation of 2 acetyl-CoA molecules which can be utilised by the liver, heart and brain as an energy source

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30
Q

What is the source of new fatty acids? What does the body do with them?

A

‣ Fatty acids can either be ingested or synthesised in the liver from excess glucose
* Fatty acids are esterified with glycerol to form triglycerides (lipogenesis) when insulin levels are high, glycogen storage is full in the liver
* These are then packaged in VLDL and released into circulation distributing endogenous triglyceride to tissues mainly stored in adipose cells

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31
Q

WHat is the fate of fatty acids once they reach the liver

A

‣ Fatty acids can either be ingested or synthesised in the liver from excess glucose
* Fatty acids are esterified with glycerol to form triglycerides (lipogenesis) when insulin levels are high, glycogen storage is full in the liver
* These are then packaged in VLDL and released into circulation distributing endogenous triglyceride to tissues mainly stored in adipose cells

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32
Q

Where does cholesterol come from?

A

‣ A combination of cholesterol directly ingested , but mostly synthesised in the liver from acetyl CoA

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33
Q

WHat is the fate of cholesterol?

A
  • converted to bile (80%)
    * Transported with lipoproteins to peripheral tissues to
    ◦ Used as a precursor for steroid hormone synthesis
    ◦ Used for creation of cell membranes or intracellular structures
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34
Q

Why is lactate produced?

A
  • Energy is required for cellular processes to function and is principally produced from aerobic metabolism. However when there is insufficient oxygen for the Kreb’s cycle and electronic transport chain to proceed, energy production is halted after glycolysis leaving pyruvate produced
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35
Q

Draw the pathway of glucose to lactate?

A
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36
Q

How is lactate made

A
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37
Q

How much ATP does 1 glucose molecule produce if converted to lactate?

A

2 ATP

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38
Q

How much ATP does 1 glucose molecule produce if aerobic metabolism occurs

A

38 ATP

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39
Q

What is the metabolic fate of lactate?

A

◦ If PO2 is restored peripherally or at the site of production —> oxidised back to pyruvate from which it can enter the citric acid cycle
◦ Lactate can leave the cell cytoplasm and circulate to the liver where it can
‣ Oxidised back to pyruvate
‣ Undergo gluconeogenesis to convert it to Glucose (Cori cycle)
◦ Converted to ethanol to regenerate NAD+ in a process called fermentation in non humans

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40
Q

How does lactate production differ in peripheral tissues to in RBC

A

Peripheral tissues have the capacity to aerobically metabolise and can utilise their own lactate to regenerate pyruvate and proceed down glyocolysis however RBC do not

◦ If PO2 is restored peripherally or at the site of production —> oxidised back to pyruvate from which it can enter the citric acid cycle
◦ Lactate can leave the cell cytoplasm and circulate to the liver where it can
‣ Oxidised back to pyruvate
‣ Undergo gluconeogenesis to convert it to Glucose (Cori cycle)
◦ Converted to ethanol to regenerate NAD+ in a process called fermentation in non humans

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41
Q

Define basal metabolic rate

A

the resting energy output or heat production over time in a subject in a state of mental and physical rest,in a comfortable environment 12 hours after a meal

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42
Q

What is the units used to express Basal metabolic rate

A
  • Expressed as watts or watts/metres squared of body surface area
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43
Q

What is basal metabolic rate for a 70kg man

A
  • BMR of a 70kg man is 100w or 58 watts/metre squared (1.43 kcal/min) or 2000kcal/day; or 200kJ/metres square x height
  • Usually corrected for age and surface areaWh
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44
Q

What important corrective factors are there to basal metabolic rate?

A
  • BMR of a 70kg man is 100w or 58 watts/metre squared (1.43 kcal/min) or 2000kcal/day; or 200kJ/metres square x height
  • Usually corrected for age and surface area
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45
Q

Outline the factors affecting basal metabolic rate?

A

Factors which affect it
* Body size as reflected in surface area
* Body fat - higher proportion of body fat reduces BMR proportionally to body size. This accounts for gender differences as lean body mass BMR is the same
* Age - newborn has a higher BMR twice that of an adult now eight basis due to growth
◦ BMR decreases 2% per decade through adult life
* Exercise
* Proximity to meal
◦ BMR rises for 4-6 hours after a meal by about 10-15% called specific dynamic action of food (oxidative deamination of food in the liver)
◦ Greater for protein compared with carbohydrates or fat
* Starvation - reduced BMR due to reduced metabolism a nd decreased cell mass
* Climactic - tropical environment reduces BMR by 10% compared to temperate environments
◦ Fever causes increased BMR
* Hormonal
◦ Thyroxine - increased heat production and oxidation
◦ Epinephrine - stress response to emotional or physical circumstances
* Pregnancy - increasing BMR by 20% especially in 2nd and 3rd trimester
◦ Required for metabolism of placenta and foetus e.g. increased cardiac and respiratory work, metabolism of additional uterine and breast tissue
◦ Lactation increases BMR

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46
Q

How would you divide the types of factors that alter basal metabolic rate?

A

Baseline characteristcis - age, gender, body surface area nd fat

Food and exercise - proximity to a meal, starvation, exercise

Hormonal and climactic - including pregnance

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47
Q

If you wanted to reduce basal metabolic rate what are factors that could be performed to do this

A
  • Body size as reflected in surface area
  • Body fat - higher proportion of body fat reduces BMR proportionally to body size. This accounts for gender differences as lean body mass BMR is the same
  • Age - newborn has a higher BMR twice that of an adult now eight basis due to growth
    ◦ BMR decreases 2% per decade through adult life
  • Food and exercise
    ◦ Exercise
    ◦ Proximity to meal
    ‣ BMR rises for 4-6 hours after a meal by about 10-15% called specific dynamic action of food (oxidative deamination of food in the liver)
    ‣ Greater for protein compared with carbohydrates or fat
    ◦ Starvation - reduced BMR due to reduced metabolism a nd decreased cell mass
  • Changed internal or external conditions
    ◦ Climactic - tropical environment reduces BMR by 10% compared to temperate environments
    ‣ Fever causes increased BMR
    ◦ Hormonal
    ‣ Thyroxine - increased heat production and oxidation
    ‣ Epinephrine - stress response to emotional or physical circumstances
    ◦ Pregnancy - increasing BMR by 20% especially in 2nd and 3rd trimester
    ‣ Required for metabolism of placenta and foetus e.g. increased cardiac and respiratory work, metabolism of additional uterine and breast tissue
    ‣ Lactation increases BMR
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48
Q

If you wanted to increase basal metabolic rate how might this be performed

A
  • Body size as reflected in surface area
  • Body fat - higher proportion of body fat reduces BMR proportionally to body size. This accounts for gender differences as lean body mass BMR is the same
  • Age - newborn has a higher BMR twice that of an adult now eight basis due to growth
    ◦ BMR decreases 2% per decade through adult life
  • Food and exercise
    ◦ Exercise
    ◦ Proximity to meal
    ‣ BMR rises for 4-6 hours after a meal by about 10-15% called specific dynamic action of food (oxidative deamination of food in the liver)
    ‣ Greater for protein compared with carbohydrates or fat
    ◦ Starvation - reduced BMR due to reduced metabolism a nd decreased cell mass
  • Changed internal or external conditions
    ◦ Climactic - tropical environment reduces BMR by 10% compared to temperate environments
    ‣ Fever causes increased BMR
    ◦ Hormonal
    ‣ Thyroxine - increased heat production and oxidation
    ‣ Epinephrine - stress response to emotional or physical circumstances
    ◦ Pregnancy - increasing BMR by 20% especially in 2nd and 3rd trimester
    ‣ Required for metabolism of placenta and foetus e.g. increased cardiac and respiratory work, metabolism of additional uterine and breast tissue
    ‣ Lactation increases BMR
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49
Q

How is basal metabolic rate measured

A

Measurement - performed indirectly as heat output is related to oxygen utilisation it is used as an indirect measure
* Benedict Roth spirometer - closed circuit breathing system filled with 6L of O2, held in a drum floating on a water seal
◦ SUBjects breaths in from the drum through an inspiratory valve and expired air is passed back to the drum through an expiratory valve and soda lime canister removing CO2
◦ As oxygen is consumed volume of drum decreases and this is recorded and rate of oxygen consumption determined
* Douglas bag technique
◦ All expired air is collected using a mouthpiece with inspiratory and expiratory valves
◦ Expired air collected in the Douglas bag is analysed for content of oxygen and carbon dioxide so oxygen utilisation and carbon dioxide production can be calculated
* Max Planck respirometer
◦ Based on Douglas bag technique and the volume of expired gas is measured directly in a dry gas meter
◦ A device within the spirometer diverts an adjustable volume of expired gas into a breathing bag from which it may be sampled and analysed
◦ Used for measuring high rates of oxygen consumption for prolonged periods

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50
Q

What is a benedict Roth spirometer and how does it work?

A

Measurement - performed indirectly as heat output is related to oxygen utilisation it is used as an indirect measure
* Benedict Roth spirometer - closed circuit breathing system filled with 6L of O2, held in a drum floating on a water seal
◦ SUBjects breaths in from the drum through an inspiratory valve and expired air is passed back to the drum through an expiratory valve and soda lime canister removing CO2
◦ As oxygen is consumed volume of drum decreases and this is recorded and rate of oxygen consumption determined
* Douglas bag technique
◦ All expired air is collected using a mouthpiece with inspiratory and expiratory valves
◦ Expired air collected in the Douglas bag is analysed for content of oxygen and carbon dioxide so oxygen utilisation and carbon dioxide production can be calculated
* Max Planck respirometer
◦ Based on Douglas bag technique and the volume of expired gas is measured directly in a dry gas meter
◦ A device within the spirometer diverts an adjustable volume of expired gas into a breathing bag from which it may be sampled and analysed
◦ Used for measuring high rates of oxygen consumption for prolonged periods

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51
Q

What does direct and indirect basal metabolic rate measurement refer to”?

A

Measurement - performed indirectly as heat output is related to oxygen utilisation it is used as an indirect measure
* Benedict Roth spirometer - closed circuit breathing system filled with 6L of O2, held in a drum floating on a water seal
◦ SUBjects breaths in from the drum through an inspiratory valve and expired air is passed back to the drum through an expiratory valve and soda lime canister removing CO2
◦ As oxygen is consumed volume of drum decreases and this is recorded and rate of oxygen consumption determined
* Douglas bag technique
◦ All expired air is collected using a mouthpiece with inspiratory and expiratory valves
◦ Expired air collected in the Douglas bag is analysed for content of oxygen and carbon dioxide so oxygen utilisation and carbon dioxide production can be calculated
* Max Planck respirometer
◦ Based on Douglas bag technique and the volume of expired gas is measured directly in a dry gas meter
◦ A device within the spirometer diverts an adjustable volume of expired gas into a breathing bag from which it may be sampled and analysed
◦ Used for measuring high rates of oxygen consumption for prolonged periods

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52
Q

WHat is the Douglas bag technique for basal metabolic rate measurement

A

Measurement - performed indirectly as heat output is related to oxygen utilisation it is used as an indirect measure
* Benedict Roth spirometer - closed circuit breathing system filled with 6L of O2, held in a drum floating on a water seal
◦ SUBjects breaths in from the drum through an inspiratory valve and expired air is passed back to the drum through an expiratory valve and soda lime canister removing CO2
◦ As oxygen is consumed volume of drum decreases and this is recorded and rate of oxygen consumption determined
* Douglas bag technique
◦ All expired air is collected using a mouthpiece with inspiratory and expiratory valves
◦ Expired air collected in the Douglas bag is analysed for content of oxygen and carbon dioxide so oxygen utilisation and carbon dioxide production can be calculated
* Max Planck respirometer
◦ Based on Douglas bag technique and the volume of expired gas is measured directly in a dry gas meter
◦ A device within the spirometer diverts an adjustable volume of expired gas into a breathing bag from which it may be sampled and analysed
◦ Used for measuring high rates of oxygen consumption for prolonged periodsW

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53
Q

What is the Max Planck respirometer? What is it used to measure? How does it do this?

A

Measurement - performed indirectly as heat output is related to oxygen utilisation it is used as an indirect measure
* Benedict Roth spirometer - closed circuit breathing system filled with 6L of O2, held in a drum floating on a water seal
◦ SUBjects breaths in from the drum through an inspiratory valve and expired air is passed back to the drum through an expiratory valve and soda lime canister removing CO2
◦ As oxygen is consumed volume of drum decreases and this is recorded and rate of oxygen consumption determined
* Douglas bag technique
◦ All expired air is collected using a mouthpiece with inspiratory and expiratory valves
◦ Expired air collected in the Douglas bag is analysed for content of oxygen and carbon dioxide so oxygen utilisation and carbon dioxide production can be calculated
* Max Planck respirometer
◦ Based on Douglas bag technique and the volume of expired gas is measured directly in a dry gas meter
◦ A device within the spirometer diverts an adjustable volume of expired gas into a breathing bag from which it may be sampled and analysed
◦ Used for measuring high rates of oxygen consumption for prolonged periods

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54
Q

What is the highest energy expenditure for cells?

A

Na/K ATPase

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55
Q

How much ATP is produced in the body per day?

A

100mol

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56
Q

How much ATP is in storage?

A

None really, but the amount of ATP present at any one time could sustain the energy needs of the body for 1.5minutes

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57
Q

At resting energy production what level of efficiency is it operating at>

A

60%

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58
Q

What chemical process is behind the releasing of energy?

A
  • Oxidation = removal of e– at high potential & transferring them to a lower potential ∴releasing E
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59
Q

What is the electron acceptor in cells?

A

O2

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60
Q

What is the problem with O2 as an electron acceptor

A

◦ But O2 is too reactive to be immediate oxidising agent → ∴intermediates NAD+ + FAD are e– carriers between metabolic pathways and O2 is used in the mitochondria
‣ NAD+ = nicotinamide adenine dinucelotide
‣ FAD+ = flavin adenine dinucleotide

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61
Q

What intermediate carriers are used for electrons in energy harnesing? WHy?

A

◦ But O2 is too reactive to be immediate oxidising agent → ∴intermediates NAD+ + FAD are e– carriers between metabolic pathways and O2 is used in the mitochondria
‣ NAD+ = nicotinamide adenine dinucelotide
‣ FAD+ = flavin adenine dinucleotide

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62
Q

What does NAD stand for?

A

◦ But O2 is too reactive to be immediate oxidising agent → ∴intermediates NAD+ + FAD are e– carriers between metabolic pathways and O2 is used in the mitochondria
‣ NAD+ = nicotinamide adenine dinucelotide
‣ FAD+ = flavin adenine dinucleotide

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63
Q

WHat does FAD stand for

A

◦ But O2 is too reactive to be immediate oxidising agent → ∴intermediates NAD+ + FAD are e– carriers between metabolic pathways and O2 is used in the mitochondria
‣ NAD+ = nicotinamide adenine dinucelotide
‣ FAD+ = flavin adenine dinucleotide

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64
Q

NAD+ and FAD+ undergo what process during glycolysis? WHat does this produce>

A

◦ NAD+ and FAD are reduced by Glycolysis & Krebs to NADH + H+ + FADH2 → these carry e– to ETC

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65
Q

What happens if O2 is not available to NAD and FAD? What level fo O2 is required?

A

◦ If O2 is N/A, NAD+ & FAD are converted to NADH + H+ & FADH2 by Law of Mass Action, the equation STOPS
‣ Oxygen partial pressure of 3mmHg ensures adequate availability at the mitochondria

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66
Q

Why is lactate production even required in anaerobic conditions?

A

◦ NADH + H+ produced during gluycolysis transfers its electrons to pyrvuate producing lactate and regenerating NAD+ allowing glycolysis to continue

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67
Q

What happens to NADH produced during glycolysis under anaerobic conditions?

A

◦ NADH + H+ produced during gluycolysis transfers its electrons to pyrvuate producing lactate and regenerating NAD+ allowing glycolysis to continue

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68
Q

What is ATP? Where is the energy stored? How is it released?

A
  • ATP - adenosine triphosphate
    ◦ two high energy phosphate bonds
    ◦ Energy released by hydrolysis of these bonds
    ◦ To produce 1mol of ATP from ADP required 7kcal of energy
    ◦ The aorbvic metabolism of 1mol of glucose produces 686kcal of energy - of which 40% is harnessed to produce 38moles of ATP the rest is lost as heat
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69
Q

How much energy is in 1mol of ATP?

A
  • ATP - adenosine triphosphate
    ◦ two high energy phosphate bonds
    ◦ Energy released by hydrolysis of these bonds
    ◦ To produce 1mol of ATP from ADP required 7kcal of energy
    ◦ The aorbvic metabolism of 1mol of glucose produces 686kcal of energy - of which 40% is harnessed to produce 38moles of ATP the rest is lost as heat
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70
Q

In aerobic metabolism 1mol of glucose makes how much energy? WHat % is harnesed? What is made?

A
  • ATP - adenosine triphosphate
    ◦ two high energy phosphate bonds
    ◦ Energy released by hydrolysis of these bonds
    ◦ To produce 1mol of ATP from ADP required 7kcal of energy
    ◦ The aorbvic metabolism of 1mol of glucose produces 686kcal of energy - of which 40% is harnessed to produce 38moles of ATP the rest is lost as heat
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71
Q

What energy compounds exist other than ATP

A
  • GTP and other triphosphate nuclotides to a lesser extent
  • Creatine phosphate in the brain and muscle
  • Intermediates - conserve energy as ATP and function as coenzymes reoxidised to generate ATP
    ◦ NADH - 1x molecule equivalent to 3ATPs
    ◦ NADPH - - 1x molecule equivalent to 3ATPs
    ◦ Flavoproteins - - 1x molecule equivalent to 2ATPs
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72
Q

NADH is equivalent to how many ATPs?

A
  • Intermediates - conserve energy as ATP and function as coenzymes reoxidised to generate ATP
    ◦ NADH - 1x molecule equivalent to 3ATPs
    ◦ NADPH - - 1x molecule equivalent to 3ATPs
    ◦ Flavoproteins - - 1x molecule equivalent to 2ATPs
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73
Q

NADPH is equivalent to how many ATPs?

A
  • Intermediates - conserve energy as ATP and function as coenzymes reoxidised to generate ATP
    ◦ NADH - 1x molecule equivalent to 3ATPs
    ◦ NADPH - - 1x molecule equivalent to 3ATPs
    ◦ Flavoproteins - - 1x molecule equivalent to 2ATPs
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74
Q

FADH is equivalent to how many ATPs

A
  • Intermediates - conserve energy as ATP and function as coenzymes reoxidised to generate ATP
    ◦ NADH - 1x molecule equivalent to 3ATPs
    ◦ NADPH - - 1x molecule equivalent to 3ATPs
    ◦ Flavoproteins - - 1x molecule equivalent to 2ATPs
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75
Q

Glycolysis occurs in what part of the cell?

A

Cytoplasm

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76
Q

Glycolysis in absence of oxygen is enabled to continue by?

A

NADH + H+ electrons transferred to pyruvate with production of lactate

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77
Q

How many reactions are there in glycolysis

A

10

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78
Q

How many carbons does Pyruvate have?

A

3

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79
Q

How many pyruvate are made for 1 molecule of glycose?

A

2

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80
Q

Glycolysis energy equation equates to what being produced?

A

◦ 2x ATP net –> 2 used, 4 created
◦ Pyruvate which under aerobic conditions enters the citric acid cycle
◦ NADH + H+ –> to mitochondrial ETC indirectly as unable to cross membrane itself regenerating cytosol NAD+

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81
Q

Draw the energy aspects of glycolysis as equations and pathway diagram

A
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82
Q

What is the pathway to produce lactate?

A
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83
Q

Anaerobic conditions make how mcuh ATP from glucose?

A

2 ATP

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84
Q

How do you make Acetyl CoA from pyruvate?

A
  • Starting point = Acetyl CoA
    ◦ CoA from vitamin B - transfers two carbon acetyl groups between molecules
    ◦ When pyruvate (3x carbons) enters mitochondrion it reacts with CoA to produce
    ‣ Acetyl CoA
    ‣ carbon dioxide
    ‣ NADH + H+
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85
Q

What happens to pyruvate under aerobic conditions

A
  • Starting point = Acetyl CoA
    ◦ CoA from vitamin B - transfers two carbon acetyl groups between molecules
    ◦ When pyruvate (3x carbons) enters mitochondrion it reacts with CoA to produce
    ‣ Acetyl CoA
    ‣ carbon dioxide
    ‣ NADH + H+
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86
Q

Where does CoA come from in Acetyl CoA

A
  • Starting point = Acetyl CoA
    ◦ CoA from vitamin B - transfers two carbon acetyl groups between molecules
    ◦ When pyruvate (3x carbons) enters mitochondrion it reacts with CoA to produce
    ‣ Acetyl CoA
    ‣ carbon dioxide
    ‣ NADH + H+
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87
Q

What is the product from pyruvate + NAD_ and CoA

A
  • Starting point = Acetyl CoA
    ◦ CoA from vitamin B - transfers two carbon acetyl groups between molecules
    ◦ When pyruvate (3x carbons) enters mitochondrion it reacts with CoA to produce
    ‣ Acetyl CoA
    ‣ carbon dioxide
    ‣ NADH + H+
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88
Q

What enzyme catalyses creation of Acetyl CoA

A

Pyruvate dehydrogenase

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89
Q

How does the citric acid cycle begin?

A
  • The citric acid cycle begins with acetyl group of Acetyl CoA being transferred to 4 carbon molecule oxaloacetate producing citrate
    ◦ 2 carbons lost as CO2
    ◦ Electrons are donated to produce NADH + H+ and FADH2 reactions
    ◦ One ATP is formed
    ◦ At the end of the cycle oxaloacetate is reproduced
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90
Q

What does Acetyl CoA combine with at the start of the citric acid cycle

A

OxaloacetateW

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91
Q

What is formed from oxaloacetate and Acetyl CoA

A

Citrate

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92
Q

How many carbons does citrate have

A

6

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93
Q

What is the fate of citrate in the citric acid cycle

A

Becomes alpha ketoglutarate after removal of CO2 and reduction of NAD+ –> NADH + H+

Therefore becomes a 5 carbon molecule

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94
Q

Alpha ketoglutarate has how many carbons

A

5

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95
Q

Alpha ketoglutarate’s fate in the citric acid cycle?

A

Loses CO2 and reduces NAD+ to NADH + H+

Therefore losing another carbon becomes a 4 carbon molecule as succinyl CoA

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96
Q

What does alpha ketoglutarate become

A

Loses CO2 and reduces NAD+ to NADH + H+

Therefore losing another carbon becomes a 4 carbon molecule as succinyl CoA

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97
Q

Succinyl CoA in the citric acid cycle ahs how many carbons

A

4

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98
Q

Syccinyl CoA becomes what in the citric acid cycle

A

Loses water, reduces ADP to ATP and loses CoA becoming succinate

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99
Q

Succinate has how many carbons?

A

4

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100
Q

What is succinate produced from in the citric acid cycle?

A

Succinyl CoA via loss of water, reduces ADP to ATP and loses CoA becoming succinate

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101
Q

Succinate becomes what in the citric acid cycle?

A

Fumarate via loss of FADH2

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102
Q

Fumarate is made from what in the citric acid cycle?

A

Succinate via removal of FADH2

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103
Q

Fumarate becomes waht in the citric acid cycle? How?

A

Addition of water becomes Malate

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104
Q

Malate is made from what in the citric acid cycle?

A

Fumarate via addition of H20

105
Q

What happens to Malate in the citric acid cycle

A

Becomes Oxaloacetate vai NAD+ being reduced to NADH + H+

106
Q

Oxaloacetate is made from?

A

Malate via reduction of NAD+ to NADH + H+

107
Q

Oxaloacetate reacts with what to become what in the citric acid cycle?

A

Reacts with Acetyl CoA and water to make citrate

108
Q

Draw the citric acid cycle?

A
109
Q

Where does the citric acid cycle occur?

A
110
Q

At what point in aerobic metabolism can a process not be reversed

A

Pyruvate moving into inner mitochondrial membrane is an irreversible process producing Acetyl CoA

111
Q

Acetyl CoA has how many carbons

A

2

112
Q

Where does the electron transport chain occur?

A

Inner mitochondrtial membrane is the inside surface

113
Q

What is the electron transport chain

A
  • Series of 4 cytochrome enzymes that pump H+ across into intermembrane space as electrons are transferred from NADH and FADH2 from an energy gradient of high to low potential
114
Q

What is the electron transport chain made up of

A
  • Series of 4 cytochrome enzymes that pump H+ across into intermembrane space as electrons are transferred from NADH and FADH2 from an energy gradient of high to low potential
115
Q

What happens to electrons in the electron transport chain?

A

◦ Energy released as electrons pass down the chain is used to pump hydrogen ions across inner mitochondrial membrane to the cytoplasmic side
‣ NADH donates electrons at the beginning of the chain –> 3ATP
‣ FADH2 donates electrons at the 2nd site –> 2 ATP

116
Q

Draw the electron transport chain

A
117
Q

How is electron movement related to energy production?

A

◦ Molecular pores allow hydrogen ions to flow back down their concentration gradient into the matrix releasing energy producing ATP from ADP and phosphate ions (oxidative phosphorylation) –> 3 distinct points this occurs

118
Q

What happens to electorns at the end of the electron transport chain

A

Accepted by oxygen

119
Q

How is the majority of energy stored in the body?

A
  • Fats 80% of the stored energy in the body
    ◦ Beta oxidation in mitochondrial matrix
    ◦ Removal of 2 carbon atoms at a time to form acetyl CoA and hydrogen atoms are combined with coenzymes to enter the ETC
    ‣ By weight 2.5x the amount of energy created
120
Q

Where does beta oxidation occur?

A
  • Fats 80% of the stored energy in the body
    ◦ Beta oxidation in mitochondrial matrix
    ◦ Removal of 2 carbon atoms at a time to form acetyl CoA and hydrogen atoms are combined with coenzymes to enter the ETC
    ‣ By weight 2.5x the amount of energy created
121
Q

How does fat compare to carbohydrates as a mechanism of storing energy?

A
  • Fats 80% of the stored energy in the body
      ‣ By weight 2.5x the amount of energy created
122
Q

How does beta oxidation occur?

A

◦ Beta oxidation in mitochondrial matrix
◦ Removal of 2 carbon atoms at a time to form acetyl CoA and hydrogen atoms are combined with coenzymes to enter the ETC

123
Q

In catabolism what is a phase 1 reaction

A
  • 1/3 of energy release from these reactions
  • Simple units
    ◦ Carbohydrates - hexoses
    ◦ Fat - FFA
    ◦ Protein - amino acids
  • These simple units are oxidised to
    ◦ Major compounds –> Acetyl CoA, alpha ketoglutarate and oxaloacetate
    ◦ Minor compounds –> Pyruvate, fumarate, succinyl CoA
124
Q

What % of energy released from catabolism occurs in phase 1 reactions?

A

x* 1/3 of energy release from these reactions
* Simple units
◦ Carbohydrates - hexoses
◦ Fat - FFA
◦ Protein - amino acids
* These simple units are oxidised to
◦ Major compounds –> Acetyl CoA, alpha ketoglutarate and oxaloacetate
◦ Minor compounds –> Pyruvate, fumarate, succinyl CoA

125
Q

Describe phase 1 of lipid catabolism?

A
126
Q

How does a fatty acid actually become acetyl CoA

A
127
Q

Is production of Acetyl CoA from fatty acids an energy consuming or gaining process?

A
128
Q

What enzyme breaks down glycogen?

A

Glycogen phosphorylase

129
Q

What promotes activity of glycogen phosphorylase

A

Insulin inhibits
Glucagon and adrenaline promote

130
Q

What hormones increase activity of beta oxidation

A

Growth hormone
Glucocorticoids

131
Q

What is phase 2 of catabolism

A

Citric acid cycle

132
Q

What do amino acids enter the citric acid cycle as?

A

◦ Alpha ketoglutarate
◦ Fumarate
◦ Succinyl CoA
◦ Oxaloacetate

133
Q

What accumulation product from the citric acid cycle will inhibit enzymatic function? Why might this accumulate? Which enzymes does it inhibit?

A
  • Accumulation of NADH inhibits the dehydrogenases of the cycle–> main limitation is O2 supply
134
Q

What drives the breakdown of protein for energy?

A
135
Q

Which hormone drives muscle protein breakdown for metabolic fuel

A

GC

136
Q

Explain the pathway for protein catabolism for energy

A
137
Q

Describe the glucose alanine cycle

A
138
Q

What is the utility of muscle producing and releasing alanine?

A
139
Q

What hormones drive gluconeogenesis?

A

GC
Glucagon

Inhibited by insulin

140
Q

WHat substrates are used for gluconeogenesis by the liver

A
141
Q

What amino acids can pyruvate be made from

A

Alanine
Cysteine

142
Q

Oxaloacetate can be made from what amino acids

A

Arginine
Glutamate
Methionine
Histidine

143
Q

How is fructose useful to the body?

A

It is converted to glucose via the final few steps of gluconeogenesis

144
Q

What happens to glycerol after free fatty acids are utilised?

A
145
Q

Explain how ketone bodies are formed

A
146
Q

Explain how ketone bodies are used in peripheral circulation

A
147
Q

What ketone bodies are there

A

Acetoacetate
Beta hydroxybutyrate
Acetone

148
Q

What is the ketoacid formed first

A

Acetoacetate

149
Q

Beta hydroxybutyrate is produced from

A

Acetoacetate

150
Q

What ketoacid is the most useful to peripheral circulation

A

Acetoacetate

151
Q

How are ketone bodies utilised for energy

A
152
Q

Under normal conditions why are ketone bodies not made?

A

Acetyl CoA is generated by beat oxidation of fatty acids or from glucose. In th presence of ample carbohydrate fule there is plenty of oxaloacetate to react with Acetyl CoA and enter the Kreb’s cycle

153
Q

In a glucose poor environment why are ketone bodies made

A
  • In glucose poor environment too much oxaloacetate is diverted away into gluconeogenesis restricting entry into Kreb’s cycle for Acetyl CoA in the liver

Excess acetyl CoA is proudced and ketones are made

154
Q

What are ketone bodies made from

A

Acetyl CoA when in excess
◦ High amounts of FFA due to lipolysis (inhibited by insulin usually, driven by catecholamines) into mitochondria and ability of mitochondria to remove acetyl CoA.

155
Q

What is actually involved in forming acetoacetate?

A
  • 2 Acetyl CoA units condense to form acetoacetate vai intermediaries and loss of Coenzyme A
156
Q

Acetoacetate has what pKa? Acid or base?

A

◦ Acetoacetate - pKa 3.77 –> acid

It is an anion decreasing the strong ion difference

157
Q

How is acetoacetate changed back to energy

A

◦ Acetoacetate converted back to 2x acetyl Coa via succinyl CoA giving up CoA to become succinate (catalysed by transferase enzyme only present in peripheral tissues esp heart, kidneys, CNS and skeletal muscle - not in the liver preventing hepatic utilisation of ketones) to create Acetoacetate CoA –> via thiolase to Acetyl Coa
‣ This enters the citric acid cycle to proceed towards oxidative phosphorylation –> 19 molecules of ATP per Acetyl CoA i.e. 38 ATP per acetoacetate

158
Q

How much energy do you get from acetoacetate?

A

38 ATP

159
Q

How is beta hydroxybutyrate formed?

A

may be reduced with NADH to Beta hydroxybutyrate in mitochondria

160
Q

Which ketone is predominantly found in ketoacidosis? Why?

A

‣ prevalent ketone in ketoacidosis and normal ratio is 3:1 to acetoacetate and can rise to 10:1. More NADH = more Beta hydroxybutyrate

		* Dominates in alcoholics compared to acetoacetate because metabolism of alcohol produces NADH from NAD+ favouring beta hydroxybutyrate production
161
Q

What ketone body do you find in alcoholics? Why?

A

Beta hydroxybutyrate Dominates in alcoholics compared to acetoacetate because metabolism of alcohol produces NADH from NAD+ favouring beta hydroxybutyrate production

162
Q

What chemically is beta hydroxybutyrate

A

‣ Technically a carboxylic acid not a ketone
‣ Plasma half life of 110 minutes

163
Q

What is the half life of beta hydroxybutyrate?

A

‣ Technically a carboxylic acid not a ketone
‣ Plasma half life of 110 minutes

164
Q

What is the 3rd amino acid?

A

◦ Acetone far less common and not acidic - it is exhaled and cleared by kidneys, or incorporated into lipids, proteins
‣ Produced by non enzymatic decarboxylation of acetoacetate (release of CO2)

165
Q

where are ketones synthesised

A

Liver only

166
Q

What is the one location unable to utilise ketones at all for energy?

A
  • However the liver is unable to utilise them as it lacks oxo-acid CoA transferase enzyme that catalyses the transfer of CoA from succinyl CoA to acetoacetic acid
167
Q

How does beta hydroxybutyrate get converted back to acetoacetate?

A

‣ Beta hydroxybutyrate dehydrogenase does this

168
Q

What is acetoacetate converted back to

A

2x acetyl CoA via syccinyl CoA giving up CoA to become succinate as part of the citric acid cycle

169
Q

How does a urine dipstick correlate to blood ketone levels?

A

When you dipstick-test somebody’s urine, the ketone levels return as “+”, “++” or “+++”. One “+” equates to about 0.5 mmol/L of acetoacetate, whereas “+++” equates to about 3.0 mmol/L.

170
Q

What is the dominant anabolic hormone

A

Insulin

171
Q

Is insulin required for glucose entry into muscle cells?

A

Yes

172
Q

What enzyme catalyses the production of glycogen

A

Glycogen synthase

173
Q

Liver stores how much glycogen

A

70-100g

174
Q

Muscle stores how much glycogen?

A

400g

175
Q

Does the brain store glycogen?

A

Yes
Enough for 4 minutes

176
Q

What enzyme does the liver have that other locations do not have that allows glycogen to be broken down to glucose?

A

‣ Muscle also lacks glucose 6 phosphatase so it cannot be released into blood

177
Q

What are FFA made from? What catalyses this?

A

Insulin promotes

Glycogen, lactate and glucose the main sources

178
Q

What sources of Acetyl CoA are used for creation of FFA

A

‣ Pyruvate the source of acetyl CoA- important substrate for FFA synthesis under Acetyl CoA carboxylase converting to a fatty acid through intermediaries
‣ Citrate from the citric acid cycle diffuses out fo the mitochondrion and splits into acetyl CoA and oxaloacetate in the cytoplasm

179
Q

What is the hexose monophosphate shunt

A
  • The hexose monophosphate shunt is a paralell pathway to glycolysis generating NADPH as well as ribose 5 phosphate as a precurser to nucleotides oxidising glucose in an anabolic role. Important in RBC as NADPH prevents oxidative stress by reducing glutathione
180
Q

Where is the hexose monophosphate shunt important?

A

RBC

		* The hexose monophosphate shunt is a paralell pathway to glycolysis generating NADPH as well as ribose 5 phosphate as a precurser to nucleotides oxidising glucose in an anabolic role. Important in RBC as NADPH prevents oxidative stress by reducing glutathione
181
Q

What does the hexose monophosphate shunt have to do with FFA synthesis?

A

NADPH provision which is required for FFA creation comes from the hexose monophosphate shunt (and from citrate conversion to pyruvate in the cytoplasm)

182
Q

Where is TG synthesised in the cell?

A

Cytoplasm in fat cells and endoplasmic reticulum

183
Q

What inhibits oxidative phosphorylation

A

ATP
NADH inhibits dehydrogenase enzymes of the citric acid cycle

184
Q

What promotes oxidative phsophorylation

A

ADP

185
Q

Where does cyanide affect the production of energy?

A

Final cytochrome A3

186
Q

In what state are TG post absorption?

A

◦ 50% of dietary triglycerides are hydrolysed to glycerol and fatty acids, and 40% are hydrolysed to monoglycerides and fatty acids

187
Q

What happens to short and longer chain fatty acids post absorption?

A

‣ Short chain fatty acids are transported directly to the liver without re-esterification in portal circulation
‣ Longer chain fatty acids are re-esterified to triglycerides, covered with phospholipids and transprted in chylomicrons —> lipoprotein lipases hydrolyse the chylomicrons producing free fatty acids that may be taken up by adipocytes for storage or metabolised within body tissues for energy; glycerol left over from hydrolysis is taken to the liver for gluconeogenesis

188
Q

What lipids are synthesed in the liver

A

Fatty acids
Triglycerides from fatty acids and glycerol
Phospholipids
Cholesterol

189
Q

What process brings together fatty acids and glycerol

A

Esterification

190
Q

Describe the relative sources of fuel for the brain, skeletal muscle and heart

A

◦ Brain and CNS - glucose primarily, ketones if prolonged fasting
◦ Skeletal muscle oxidises free fatty acids and ketone bodies
‣ Glucose if anaerobic
◦ Cardiac muscle - free fatty acids, lactate and ketone bodies

191
Q

What is the fate of nutrients when there is an excess of glucose in the liver?

A
  • High glucose meal causes insulin secretion –>
    ◦ Glucose conversion in liver and adipose tissue to glycogen
    ◦ Remainder broken down to triose phosphate by glucolytica nd hexone monophosphate pathways
    ‣ Alpha glycerophosphate produced in adipose cells and esterifies FFA to TG
    ‣ This reduces FFA availability for beta oxiditation increasing glucose utilisation for oxidation
    ◦ Excess AcetylCoA converted to FFA in liver and adipose cells once glycogen storage maxed out
192
Q

How is lactate produced?

A
193
Q

How much lactate is produced per day?

A

1500mmol

0.8mmol/kg/hr (20mmols/kg/day)

194
Q

Why is lactate made

A

Pyruvate reduced to lactate, NADH is oxidised to NAD+ allowing glycolysis to continue as it requires NAD+

195
Q

WHich organs are responsible for lactate proudction

A

◦ Skin 25%
◦ Red cells 20%
◦ Brain 20%
◦ Muscle 25% - at rest 22mg/kg/hr of glucose metabolised 50% returned as lactate
◦ Gut 10%

196
Q

What enhances lactate production?

A

catecholamines, exercise, sepsis, lack of mitochondria due to excess pyruvate

197
Q

What is th extraction ratio of lactate in the liver?

A

55% of lactate passing through is extracted

198
Q

Is lactate metabolism in the liver high or low capacity? Is it high or low affinity?

A

high affinity enzymes and high capacity for metabolism. Lactate metabolism thus almost entirely dependent on rate of hepatic blood flow

199
Q

What happens to circulating lactate?

A

80% through the Cori cycle in the liver and kidney (30% kidney, remainder in the liver)
20% used as fuel by the heart
Minimal to ethanol
Minimal oxidised at its site of production

200
Q

What is the eponymous name for lactate production occurs in the RBC

A

the production from glucose in RBC is the Embden Meyerhoff pathway

201
Q

What happens to lactate in the kidney?

A

30% of lactate metabolism occurs in the kidney
‣ Small amount renally filtered 180mmol/day is fully reabsorbed - unless lactate >6

202
Q

What converts lactate back to pyruvate?

A

◦ Lactate can leave the cell cytoplasm and circulate to the liver where it can
‣ Oxidised back to pyruvate by lactate dehydrogenase where it can either
* Be used locally for energy production 50%
* Undergo gluconeogenesis (50%) to convert it to Glucose (Cori cycle) - at a cost of 6ATP per molecule. This shifts the cost of tissue metabolism ot the liver

203
Q

When lactate is converted back to pyruvate in the liver what happens to the pyruvate?

A

◦ Lactate can leave the cell cytoplasm and circulate to the liver where it can
‣ Oxidised back to pyruvate by lactate dehydrogenase where it can either
* Be used locally for energy production 50%
* Undergo gluconeogenesis (50%) to convert it to Glucose (Cori cycle) - at a cost of 6ATP per molecule. This shifts the cost of tissue metabolism ot the liver

204
Q

Intracellular lactate vs pyruvate concentrations

A

10:1
More lactate

205
Q

Lactate pKa

A

4
so at physiological pH most is fully dissociated into lactate conjugate base and H_ –> thus for every 1mmol of lactate expect bicarbonate to decrease by 1mmol

206
Q

Glycolysis vs acid base

A
  • Glyclolysis is decreased by acidosis, and alkalosis increases it
    ◦ Thus in intracellular alkalosis more pyrvuate produced which in oxygen poor environment will be metabolised into lactate instead of being oxidised
  • Note that the production of lactate from pyruvate consumes a hydrogen ion
207
Q

Draw the Cori cycle

A
208
Q

What does direct calimotry refer to?

A
  • Direct calorimetry - measures heat energy produced by the body, using an insulated room known as a Atwater Benedict chamber measuring heat production per hournd
209
Q

Indirect calorimetry refers to

A
  • Indirect techniques as heat output is related to oxygen utilisation it is used as an indirect measure - based on assumption that 1L of O2 is equivalent to production of 4.8kcal of energy. –> can be divided by surface area
    ◦ typical value is 40kcal/metre square./hr for a 70kg adult
    ◦ It works because heart production is vastyl aerobic metabolism - production of ATP via oxidative phosphorulation in mitochondria is assocaited with fixed oxygen consumption
    ◦ The oxygen consumption reaction is the final reaction in the ETC catalised by cytochrome oxidase (2H+ + 1/2 O2 –> H2O)
    ◦ Assumes all oxygen used for oxidation of substrate, complex, expensive, requires special equipoment, measure of consumption not demand. Inaccurate at high PEEP or high FIO2
210
Q

What is a baseline value for indirect calorimetry?

A
  • Indirect techniques as heat output is related to oxygen utilisation it is used as an indirect measure - based on assumption that 1L of O2 is equivalent to production of 4.8kcal of energy. –> can be divided by surface area
    ◦ typical value is 40kcal/metre square./hr for a 70kg adult
    ◦ It works because heart production is vastyl aerobic metabolism - production of ATP via oxidative phosphorulation in mitochondria is assocaited with fixed oxygen consumption
    ◦ The oxygen consumption reaction is the final reaction in the ETC catalised by cytochrome oxidase (2H+ + 1/2 O2 –> H2O)
    ◦ Assumes all oxygen used for oxidation of substrate, complex, expensive, requires special equipoment, measure of consumption not demand. Inaccurate at high PEEP or high FIO2
211
Q

Why does indirect calorimetry work?

A
  • Indirect techniques as heat output is related to oxygen utilisation it is used as an indirect measure - based on assumption that 1L of O2 is equivalent to production of 4.8kcal of energy. –> can be divided by surface area
    ◦ typical value is 40kcal/metre square./hr for a 70kg adult
    ◦ It works because heart production is vastyl aerobic metabolism - production of ATP via oxidative phosphorulation in mitochondria is assocaited with fixed oxygen consumption
    ◦ The oxygen consumption reaction is the final reaction in the ETC catalised by cytochrome oxidase (2H+ + 1/2 O2 –> H2O)
    ◦ Assumes all oxygen used for oxidation of substrate, complex, expensive, requires special equipoment, measure of consumption not demand. Inaccurate at high PEEP or high FIO2
212
Q

WHat does indirect calorimetry assume? When is it inaccurate?

A

◦ Assumes all oxygen used for oxidation of substrate, complex, expensive, requires special equipoment, measure of consumption not demand. Inaccurate at high PEEP or high FIO2

213
Q

What is a Benedict Roth spirometer?

A
  • Benedict Roth spirometer - closed circuit breathing system filled with 6L of O2, held in a drum floating on a water seal
    ◦ SUBjects breaths in from the drum through an inspiratory valve and expired air is passed back to the drum through an expiratory valve and soda lime canister removing CO2
    ◦ As oxygen is consumed volume of drum decreases and this is recorded and rate of oxygen consumption determined
214
Q

What is a Douglas bag technique

A
  • Douglas bag technique
    ◦ All expired air is collected using a mouthpiece with inspiratory and expiratory valves
    ◦ Expired air collected in the Douglas bag is analysed for content of oxygen and carbon dioxide so oxygen utilisation and carbon dioxide production can be calculated
215
Q

How can a pulmonary artery catehter be used for oxygen consumption?

A
  • Pulmonary artery catheter reverse Fick method using cardiac output, VO2, DO2 to calacuate energy expenditure however it neglects energy expenditure in the lungs (important in ARDS), invasive
    ◦ VO2 = (COx Ca) - (CO x Cv)
    ‣ Ca = arterial oxygen content approx 200ml/litre
    ‣ Cv venous oxygen concentration about 150 ml/lite
    ‣ If the equation is solved using cardiac output data and calculate oxygen extraction and thus its rate of metabolism
216
Q

What is a Max Planck repsirometer?

A
  • Max Planck respirometer
    ◦ Based on Douglas bag technique and the volume of expired gas is measured directly in a dry gas meter
    ◦ A device within the spirometer diverts an adjustable volume of expired gas into a breathing bag from which it may be sampled and analysed
    ◦ Used for measuring high rates of oxygen consumption for prolonged periods
217
Q

What estimate is often used for energy expenditure per day

A
  • Estimates can also be used
    ◦ 25 kcal/kg/day. This is the so-called “ACCP standard” (after the American College of Chest Physicians). The precise estimate is 25-30kcal/kg/day of actual body weight, or 21kcal/kg of ideal body weight.
    ◦ Predictive equations - input is gender, heigh,a ge, weight and specific abnormalitie sfactored in as multipliers) –> cheap, quick, requires no expertise, accurate for many circumstances however tend be inaccurate the sicker the patient
    ‣ Being unwell earns a multiplier of 1.2; severe catabolic state is 1.9x
218
Q

What factor does being unwell add to the your resting energy expendtiure?

A
  • Estimates can also be used
    ◦ 25 kcal/kg/day. This is the so-called “ACCP standard” (after the American College of Chest Physicians). The precise estimate is 25-30kcal/kg/day of actual body weight, or 21kcal/kg of ideal body weight.
    ◦ Predictive equations - input is gender, heigh,a ge, weight and specific abnormalitie sfactored in as multipliers) –> cheap, quick, requires no expertise, accurate for many circumstances however tend be inaccurate the sicker the patient
    ‣ Being unwell earns a multiplier of 1.2; severe catabolic state is 1.9x
219
Q

What does an ICU stay add to your resting energy expenditure?

A
  • Estimates can also be used
    ◦ 25 kcal/kg/day. This is the so-called “ACCP standard” (after the American College of Chest Physicians). The precise estimate is 25-30kcal/kg/day of actual body weight, or 21kcal/kg of ideal body weight.
    ◦ Predictive equations - input is gender, heigh,a ge, weight and specific abnormalitie sfactored in as multipliers) –> cheap, quick, requires no expertise, accurate for many circumstances however tend be inaccurate the sicker the patient
    ‣ Being unwell earns a multiplier of 1.2; severe catabolic state is 1.9x
220
Q

Where is CO2 produced in the body?

A

Mitochondria in the Krebs cycle during aeorbic respiration

221
Q

How much CO2 is produced per day?

A

200ml/hr compared to O2 250ml/hr

222
Q

What is a respiratory quotient

A

CO2 production related to O2 consumption Baseline 0.8
Depends on fuel substrate

223
Q

What is the respiratory quotient of fat

A

0.7

224
Q

What is the respiratory quotient of carbohydrates?

A

1

225
Q

What quantiity of carbon dioxide and bicarbonate is in the body?

A

120L (100x O2)

226
Q

CO2 is carried in the blood in what forms?

A
  • CO2 is carried in the blood in 3 forms – dissolved (5%), as bicarbonate (70-80%) and as carbamino compounds (20-25%).
227
Q

For every 1 molecule fo ATP in the Citric acid cycle how much CO2 is produced?

A

2

228
Q

CO2 is related to respiration how?

A
  • PACO2 = VCO2/VA x k (rearranging the alveolar ventilation equation)
    ◦ PaCO2 = alveolar pressure of CO2
    ‣ Where PACO2 ≈ PaCO2 if minimal dead space and at equilibrium
    ◦ VCO2 = CO2 production
    ◦ VA = alveolar ventilation
    ◦ And K = 0.863, derived from ideal gas laws
    ◦ Therefore –> PACO2 ∝ production/elimination
    ◦ Note negative feedback loop: ↑PaCO2 -> ↑VA -> ↓PaCO2
    ◦ Note metabolic rate matched to VA via control of PaCO2
229
Q

What is the alveolar ventilation equation?

A
  • PACO2 = VCO2/VA x k (rearranging the alveolar ventilation equation)
    ◦ PaCO2 = alveolar pressure of CO2
    ‣ Where PACO2 ≈ PaCO2 if minimal dead space and at equilibrium
    ◦ VCO2 = CO2 production
    ◦ VA = alveolar ventilation
    ◦ And K = 0.863, derived from ideal gas laws
    ◦ Therefore –> PACO2 ∝ production/elimination
    ◦ Note negative feedback loop: ↑PaCO2 -> ↑VA -> ↓PaCO2
    ◦ Note metabolic rate matched to VA via control of PaCO2
230
Q

CO2 production is increased by?

A

◦ Increased metabolic rate –> increased temperature, exercise, neonates/male/pregnant
◦ High respiratory quotient consumption

231
Q

CO2 elimination is affected by

A
  • CO2 elimination will be affected by alveolar ventilation
    ◦ Reduced alveolar ventilation increases CO2 –> VA = RR x (VT – VD)
    ‣ Reduced RR/Reduced TV –> Can be causes by neurological disorders, muscular weakness, severe respiratory impairment, metabolic alkalosis
    ‣ Dead space - apparatus, PE, or increased west zone 1 areas with reduced perfusion or increased alveolar pressure
232
Q

How does temperature affect CO2

A
  • Temperature - increased temperature reduces solubility increasing PaCO2 to CaCO2
233
Q

What factors increased CO2 productino

A
  • ↑MR -> ↑VCO2:
    ◦ ↑temp (7% per 1°C) e.g. sepsis, malignant hyperthermia
    ◦ Exercise
    ◦ Youth: neonate 2x
    ◦ Male
    ◦ Increased size
    ◦ Pregnancy 1.2x
234
Q

Alveolar ventilation equation

A
  • VA = (VCO2/ PACO2).k,
    ◦ where VCO2 = CO2 production,
    ◦ VA = alveolar ventilation
    ◦ k is a constant.
  • Rearranging, PACO2 = (VCO2/VA).k
235
Q

What is the respiratory quotient of key metabolic substrates/

A
  • Respiratory quotient i.e. ratio VCO2:VO2
    ◦ Carbohydrate: RQ 1.0
    ◦ Fat: RQ 0.8
    ◦ Protein: RQ 0.7
    ◦ Alcohol 0.7
    ◦ Ketones 0.7
236
Q

Why might alveolar ventilation decrease? or increase?

A

VA = RR x (VT – VD)
* ↑RR or VT
◦ CNS: pain, anxiety, pregnancy (progesterone)
◦ Hypoxia (synergistic with ↑PaCO2 at peripheral chemoreceptors)
◦ Metabolic acidosis: PaCO2 = 8 + 1.5 x HCO3- (also synergistic)
* ↓RR or VT
◦ Drugs: general anaesthetics, opioids
◦ CNS: e.g. stroke
◦ Metabolic alkalosis PaCO2 = 40 + 0.7 x (HCO3- - 24)
◦ Muscular: e.g. dystrophy
◦ Skeletal: e.g. scoliosis
◦ Pulmonary: e.g. severe COPD
* ↑VD
◦ Apparatus: e.g. long tubing distal to Y piece
◦ Anatomical: reasonably fixed
◦ Alveolar: (i.e. West zone 1)
‣ ↑alveolar pressure: positive pressure ventilation, PEEP
‣ ↓pulmonary arterial pressure: e.g. haemorrhage
* Perfusion limitation
◦ CO2 30x more soluble than O2
◦ Small partial pressure gradient from mixed venous blood to alveolar air (46 -> 40mmHg)

237
Q

Describe the control of alveolar ventilation

A
  • Afferents
    ◦ Peripheral chemoreceptors: sense PaCO2 directly
    ◦ Central chemoreceptors: sense PaCO2 indirectly via pH in brain ECF (CO2 crosses blood-brain barrier)
  • Controller- Respiratory centre in medulla
  • Efferents - Inspiratory +/- expiratory muscles
  • Circuit - ↑PaCO2 -> ↑afferent stimulation -> ↑discharge from resp centre -> ↑RR, ↑VT -> ↓PaCO2
238
Q

What factors make up the Haldane effect?

A
  • Haldane effect -
    ◦ ↓ PaO2/SaO2 -> ↑Hb affinity for CO2 -> ↓PaCO2:CaCO2
    ◦ 70% of increment due to ↑carbamino formation
    ◦ 30% of increment due to ↑pKa imidazoles to 8.2 hence better buffer
239
Q

What is the carbon dioxide reverse cascade>

A
  • Mitochondrial and cellular PCO2:
    ◦ Essentially the same
    ◦ The mitochondrial membrane is incredibly permeable to CO2
    ◦ Microscopic distances allow CO2 to equilibrate
    ◦ Depending on the metabolism of the tissue, PCO2 ranges from 20-100 mmHg
  • Tissue CO2:
    ◦ Drops slightly by diffusion distance no nearest capillary
    ◦ Diffusion is highly variable and tissue-specific
    ◦ Slowly equilibrating tissues (bone, fat) will take up to 30-60 minutes to equlibrate with the rest of the body
    ◦ Fast tissues (brain, blood, kidney) equilibrate over minutes and seconds
  • Capillary PCO2
    ◦ Highly variable, depending on tissue perfusion and metbaolic activity
    ‣ Anywhere from 42mmHg to 100mmHg
    ◦ PCO2 drops slightly because of storage in deoxyhaemoglobin and as bicarbonate
  • Mixed venous CO2
    ◦ Usually said to be ~ 46 mmHg
    ◦ usually 6mmHg higher than arterial PCO2
  • Alveolar capillary PCO2
    ◦ Theoretically, should be higher than mixed venous because of reverse Haldane effect (release of CO2 from haemoglobin and bicarbonate stores)
    ‣ High oxygen environment causes CO2 to becarried more porely
    ‣ Oxygenated haemoglobin a poorer buffer affecting the bicarbonate equation
    ◦ Practically, trends towards arterial values because of rapid diffusion into the alveolus
  • Expired CO2
    ◦ Alveolar CO2 essentially equal to pulmoanry end capillary PCO2 50mmHg
    ◦ End tidal CO2
  • Atmospheric PCO2
    ◦ 0.3 mmHg
  • Arterial CO2 6mmHg lower than venous
240
Q

What is atmospheric PCO2

A

0.3mmHg

241
Q

What is alveolar PCO2

A

50

242
Q

What is mixed venous CO2

A

46mmHg

243
Q

PCO2 of tissue

A

20-100mmHg

◦ Drops slightly by diffusion distance no nearest capillary
◦ Diffusion is highly variable and tissue-specific
◦ Slowly equilibrating tissues (bone, fat) will take up to 30-60 minutes to equlibrate with the rest of the body
◦ Fast tissues (brain, blood, kidney) equilibrate over minutes and seconds
244
Q

What is the overall reaction of the citric acid cycle?

A
  • AcCoA + 3NAD+ + FAD + GDP + Pi + 2H2O –> 2CO2 + 3NADH + FADH2 + GTP + CoA
245
Q

Where does the citric acid cycle take place

A

Mitochondrial matrix

246
Q

What converts pyruvate to Acetyl CoA? How?

A
  • Pyruvate generated in glycolysis is converted to Acetyl CoA by pyruvate dehydrogenase releasing 1 NADH per pyruvate molecule (leading to the generation of 6 ATP equvalents per glucose molecule)
247
Q

What are the products of the citric acid cycle?

A

2CO2 + 3NADH + FADH2 + GTP + CoA

248
Q

How many ATP are created per Acetyl CoA molecule?

A

12 ATP generated for each Acetyl CoA molecule

249
Q

Citric acid cycle intermediates are also used for?

A
  • Malate and oxaloacetate –> Gluconeogenesis
  • Citrate –> fatty acid and cholesterol biosynthesis
  • Oxaloacetate and alpha ketoglutarate –> Amino acid biosynthesis via reductive amination and transamination
  • Succinyl CoA –> Porphyrin production for Haem
  • Purine and pyrimidine synthesis as precursers of DNA and RNA
250
Q

What is malate also used for?

A

Citric acid cycle
Gluconeogenesis

251
Q

What is oxaloacetate used for?

A

Citric acid cycle
Gluconeogenesis
Amino acid biosynthesis via reductive amination and transamination

252
Q

What is citrate used for?

A

Citric acid cycle
Fatty acid and cholesterol biosynthesis

253
Q

What citric acid cycle intermeiates are used for amino acid biosynthesis?

A
  • Malate and oxaloacetate –> Gluconeogenesis
  • Citrate –> fatty acid and cholesterol biosynthesis
  • Oxaloacetate and alpha ketoglutarate –> Amino acid biosynthesis via reductive amination and transamination
  • Succinyl CoA –> Porphyrin production for Haem
  • Purine and pyrimidine synthesis as precursers of DNA and RNA
254
Q

Ketones bodies water soluble or lipid soluble?

A

Water soluble but can cross BBB

255
Q

What is acetoacetate oxidised to? Where does this happen?

A

Mitochondria of extrahepatic organs back to Succinyl CoA

256
Q

How much energy is made from acetoacetate?

A
  • 2 GTP and 22 ATP molecules per acetoacetate molecule when oxidized in the mitochondria.
257
Q

What sign of DKA is acetone responsible for?

A
  • Acetone also increases but it does not dissociate, it is highly fat soluble and excreted slowly via lungs (aromatic smell of DKA patients)
258
Q

What is different about acetone as compared to other ketones?

A

◦ Acetone is the decarboxylated form of acetoacetate which cannot be converted back into acetyl-CoA except via detoxification in the liver where it is converted into lactic acid, which can, in turn, be oxidized into pyruvic acid, and only then into acetyl-CoA.

Gastro nutrition (7 decks)

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