1 - Nutrition, Diet + Bodyweight Flashcards

1
Q

what are the major components of energy expenditure (and rough values)

A

of average 70kg male, approx 12,000kJ
of average 58kg female, approx 9,500kJ

1 BMR (Basal Metabolic Rate) is the basal amount of energy required to maintain life (BMR = 100 x weight in kg)
- Skeletal Muscle 30%
- CNS 20%
- Liver 20%
- Heart 10%

2 Voluntary Physical Activity (BMR + 30% for sedentary, + 65% for moderate, and +100% for very active)

3 Diet Induced Thermogenesis (DIT) ie the amount of energy required to digest, absorb, distribute and store nutrients. Around 10% of energy content of food ingested.

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2
Q

list the essential components of the diet and explain why they are essential

A
  • Carbohydrates as organs require a constant source of energy (or can make glucose via gluconeogenesis)
  • Fats as lipids can be used as energy but also structurally as components of cell membrane. Fats have an energy yield 2.2x greater than carbs or proteins, but high levels of fat are associated with high BP and choslesterol.
  • Proteins as they contain amino acids that are vital for protein synthesis and N-containing compounds. Can also be used as an energy source
  • Water for cellular and metabolic processes, and for osmoregulation. Need to keep hydrated as 2.5 L of water is lost per day (urine, skin, faeces, sweat, expired air).
  • Dietary fibre for normal bowel function
  • Minerals and vitamins in more detail on seperate card

water is required as 30ml/kg/day

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3
Q

minerals required by the body (and some examples why)

A

electrolytes eg sodium, potassium and chloride
- establish ion gradients
- maintain water balance

minerals eg calcium, magnesium, phosphorus, sulphur, iron
- calcium + phosphorus essential for structure eg bone/teeth
- calcium for signalling
- enzyme co-factors eg iron, magnesium, manganese, cobalt, copper, zinc + molybdenum
- iron is essential for haemoglobin

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4
Q

vitamins required by the body, their deficiencies, and why

A

fat soluble
A - xerophthalmia
D - Rickets
E - Neurologic abnormalities
K - Blood clotting issues

water soluble
B1 - Beriberi
B12 - Anaemia
B6 - Dermatitis + Anaemia
Biotin - Alopecia, Scaly skin, CNS defects
C - Scurvy
Choline - Liver damage
Folate - Neural tube defects, anaemia
Niacin - Pellagra
Pantothenic Acid - Fatigue, apathy
Riboflavin - Aribofavlinosis

required in micro or milligram quanitities. Can have deficiency diseases if inadequate intake. Can also have hypervitaminosis where too much is toxic

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5
Q

why is dietary fibre important and where is it found

A
  • found in cereals (bread, beans, fruit and veg)
  • cellulose, lignin, pectins + gums
  • can’t be broken down by human digestive enzymes but essential for normal functioning of GI tract
  • recommended average intake for adults is 18g daily
  • low fibre intake associated with bowel cancer and constipation
  • high fibre diet can reduce cholesterol and risk of diabetes
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6
Q

what are the main factors affecting BMR (Basal Metabolic Rate)

A

this is energy required to maintain the resting activities of the body ie biochemical reactions and ion transport across membranes

  • body size + surface area
  • gender (males have higher BMR than females)
  • environmental temp (increases in cold)
  • endocrine status (increases in hyperthyroidism)
  • body temperature (increases with higher temp)
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7
Q

what are the main energy stores

A
  • very short term stores of energy rich molecules (few seconds), ie ATP too unstable to be transported around body
  • carbohydrate stores (ie glycogen) for immediate use (minutes or hours depending on activity). Glycogen is not for long term storage as capacity is limited
  • long term stores in adipose tissues (fat), around 40 days worth
  • under extreme conditions, muscle proteins can also be converted to energy
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8
Q

how to calculate BMI and what is it for

A

BMI = weight (in kg) / height squared (m^2)

always write units
kg/m^2

used to clinically evaluate weight, shows good correlation with body fat measurements. Major weakness with very muscular individuals who might be wrongly classified as obese. Also can measure waist to hip ratio.

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9
Q

BMI value table and classifications

A

less than 18.5 underweight
18.5 - 24.9 desirable weight
25 - 29.9 overweight
30 - 34.9 obese
over 35 severely obese

not for kids or pregnant women, can’t be relied on. Always measure kg/m2

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10
Q

what is obesity, and what are the factors involved

A

excessive fat accumulation in adipose tissues, which impairs health, with a BMI over 30 kg/m^2

result of energy intake exceeding energy expenditure over a number of years.

  • body fat distribution is clinically important
  • greater proportion of fat above waist (apple shaped) is higher risk
  • T2 diabetes, hypertension, hyperlipaedemia, stroke and premature death

factors involved
- lifestyle and working hours
- socioeconomic status
- education
- access to healthy foods
- genetics
- endocrine disorders
- drug therapy

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11
Q

explain the clinical consequences of protein + energy deficiency in humans

A

protein-energy malnutrition covers a spectrum of clinical conditions seen in starving people. Leads to loss of weight due to loss of subcutaneous fat + muscle wasting. Cold and weakness, GI tract and lung infections common

marasamus
- most commonly seen in children under 5
- looks emaciated, obvious muscle wasting + body fat loss
- no oedema
- hair is thin + dry, diarrhoea is common, anaemia may be present

kwashiorkor
- typically in young child displaced from breastfeeding by a new baby, and fed a diet with some carbohydrate but low protein
- child is lethargic, anorexic + apathetic
- pitting oedema, and generalised oedema
- distended abdomen due to hetatomegaly and/or ascites
- serum albumin low
- anaemia is common

…mechanism for kwashiorkor on another card

pitting oedema = when an indentation is left behind when pressure applied to area
hepatomegaly = enlarged liver
ascites = accumilation of fluid in peritoneal cavity

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12
Q

what is the mechanism for kwashiorkor

A
  • inadequate intake of protein
  • low serum albumin concentration (protein produced by liver)
  • therefore decreased plasma oncotic pressure in blood
  • increases the flow of fluid from the capillaries into the interstitium
  • results in water retention and oedema

fatty liver, why?
- production of lipoproteins are decreased
- fat is unable to be carried away from the liver as usual
- lipids accumulate in liver
- causes fatty liver and hepatomegaly

starling’s law of the capillary

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13
Q

what is re-feeding syndrome

A
  • can occur when nutritional support given to severely malnourished patients
  • electrolyte abnormalities, eg hyophosphataemia my occur
  • re-feed at 5-10 kcal/kg/day and gradually increase over a week
  • need to give the body time to adjust

rough mechanism
- rise in blood glucose level
- increased insulin
- increased stimulation of the sodium-potassium pump, driving K+ into cells
- decrease in amount of extracellular K+ (hypokalaemia)
- increase in insulin and effects on electrolyte migration are compounded by nutritional electrolyte deficiencies

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14
Q

define cell metabolism and explain its functions

A

the highly integrated network of chemical reactions that occur within cells and the network consists of a number of distinct metabolic pathways which link together

functions
- energy for cell functions and the synthesis of cell components (ATP)
- building block molecules that are used in the synthesis of cell components needed for the growth, maintenance, repair and ÷ of the cell
- organic precursor molecules that are used to allow the interconversion of building block molecules (eg acetyl CoA)
- biosynthetic reducing power used in the synthesis of cell components

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15
Q

describe the relationship between catabolism and anabolism

A

catabolic
- breaks down larger molecules into smaller ones (intermediary metabolites)
- release large amounts of free energy
- oxidative - release H atoms (reducing power)

anabolic
- synthesise larger important cellular components from intermediary metabolites
- use energy released from catabolism
- reductive (ie use H released in catabolism)

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16
Q

explain why cells need a continous supply of energy

A
  • energy and reducing power are used to drive the synthesis of new molecules (anabolic metabolism) or to produce work (eg exercise)
  • lots of process are endergonic, so require energy to take place (ie in the form of ATP → ADP + Pi)
  • also need for transport of ions and substances in/out of the cell
  • energy stores such as glycogen and adipose tissue are longer-term stores, and need to be broken down and carried in the form of ATP
17
Q

what is exergonic and endogonic

A

all cellular activities are expressions of chemical reactions in which chemical bonds are broken or formed

exergonic release energy -ΔG and react spontaneously, providing the energy to drive the endergonic reactions
endergonic requires energy +ΔG

endo and exothermic only talks about heat

18
Q

what is the definition of metabolism

A

the set of processes which derive energy and raw materials from food stuffs and use them to support repair, growth and activity of the tissues of the body to sustain life

19
Q

what are redox equations

A

redox = oxidation reactions accompanied by reduction reaction

oxidation = removal of electrons (e-) or removal of H-atoms (H+ and e-)

OIL RIG = oxidation is loss of e-, reduction is gain

19
Q

what are H-carrier molecules

A

when fuel molecules are oxidised, electrons and protons are transferred to carrier molecules aka co-enzymes or co-factors

  • nicotinamide adenine dinucleotide NAD+ (or NADH + H+)
  • nicotinamide adenine dinucleotide phosphate NADP+ (or NADPH + H+)
  • flavin adenine dinucleotide FAD (or FADH2)

Info:
- complex molecules (synthesised from vitamins)
- total concentration of carriers is constant - cycle between oxidised and reduced forms
- need to be continuously regenerated so that metabolic processes can continue
- act as carriers of reducing power for…

ATP Production (NADH + H+ and FADH2)
Biosynthesis (NADPH)

oxidised form in bold, reduced form in ()

ATP production requires NADH + H+ (or FADH2) and converts it back to NAD+ (or FAD)

20
Q

what are high and low energy signals

A
  • Catabolic pathways are generally activated when the concentration of ATP falls and the concentration of ADP and/or AMP increases
  • Anabolic pathways tend to be activated when the concentration of ATP rises
  • ATP is known as a high-energy signal because it signals that the cell has adequate energy levels for its immediate needs
  • Other high-energy signals include NADH, NADPH and FADH2
  • ADP and AMP are low-energy signals because they signal that the cell doesn’t have enough energy for its immediate needs
  • Other low-energy signals include NAD+ and NADP+ and FAD
  • This is an example of negative feedback

AMP is important for initiating glycolysis

21
Q

how and why is ATP re-synthesised

A
  • there is a limited amount of ATP and ADP in the cell and the concentration of ATP is only sufficient for a few seconds of energy
  • ATP must be rapidly resynthesissed from ADP
  • the free energy available when fuel molecules are oxidised during catabolism is used to drive the synthesis of ATP from ADP and Pi
  • reducing power is converted to ATP by oxidative phosphorylation
  • ATP acts as a carrier of free energy, not a store
  • ADP + Pi → ATP + H20 ΔG+ 31kJ/mol
  • ATP + H2O → ADP + Pi ΔG- 31kJ/mol
  • ADP + H2O → AMP + Pi ΔG- 31kJ/mol
22
Q

what is creatine kinase used for in the body

A
  • some cell types need to increase metabolic activity very quickly (eg skeletal muscle)
  • because not enough O2 getting to muscles to generate ATP quickly
  • creatine phosphate is a reserve of high energy stores that can be used immediately

creatine + ATP → creatine phosphate + ADP
reaction catalysed by creatine kinase

  • when ATP conc is high, CP is formed
  • if ATP conc falls suddenly, reaction reverses providing short term boost to ATP
23
Q

creatine kinase and a marker of muscle damage

technically not in ILOs

A
  • CK is found in high concentration in muscle cells
  • muscle damage causes CK to be released into serum
  • CK is cytosolic enzyme, so will appear in blood soon after damage
  • therefore can use blood tests to check for muscle damage
  • not very specific (can’t tell where muscle damage has occured, as CK is in skeletal and cardiac muscle)
  • therefore can’t confirm if someone has had myocardial infarction, but useful marker

cytosolic = found in cytoplasm

24
Q

why is creatinine a useful clinical marker

technically not in ILOs

A
  • breakdown product of creatine and creatine phosphate
  • produced by a spontaneous reaction at a constant rate (unless muscle wasting)
  • excreted via kidneys
  • used to assess kidney function (kidney faliure = high levels of creatinine in urine vs blood)
  • creatinine excretion per 24 hr is proportional to muscle mass of individual (so provides measure of muscle mass)
  • creatinine concentration in urine is marker of urine dilution