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Metabolism > Nurtition, Diet And Bodyweight > Flashcards

Nurtition, Diet And Bodyweight Flashcards

1
Q

What is the SI unit for energy?

A

KJ

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2
Q

How many KJ in 1 KCal?

A

4.2

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3
Q

What are sucrose, fructose, lactose and maltose made up of?

A

Sucrose: glucose- fructose
Fructose: sugar monosaccharide
Lactose: glucose- galactose
Maltose: glucose- glucose

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4
Q

What’s the difference between starch and glycogen?

A

Starch: glucose- glucose with 1-4 and a bonds only
Glycogen: glucose- glucose 1-4 and 1-6 bonds, making it branched

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5
Q

What are the 9 essential amino acids, not synthesised by the body?

A
  • isoleucine
  • lysine
  • threonine
  • histidine
  • leucine
  • methionine
  • phenylalanine
  • tryptophan
  • valine
    If learnt, this huge list may prove truely valuable
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6
Q

What amino acids become essential in pregnancy and as a child?

A

Argentina, tyrosine, cysteine

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7
Q

Why is animal meat a ‘high quality’ source of protein and plants a ‘low quality’ source

A

Animal meats contain all 20 amino acids, plant sources are missing some

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8
Q

What are lipids composed of?

A

Triglycerides- 3 fatty acids + glycerol

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9
Q

What is a trans fat?

A

where there are C=C bonds in the fatty acid chain but the H are on difffent sides (trans not cis isomer)

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10
Q

Other than high energy yields, why else are fats important in diet?

A

Needed for vitamins A, D, E and K absorption

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11
Q

Give roles for Ca, PO4 and iron

A

Ca- signalling and teeth and bone development
Iron- heamoglobin
PO4- teeth and bone

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12
Q

What minerals are needed from diet for cofactors?

A

Mg, Mn, Co, Cu, Zn

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13
Q

What are the requirements per Kg per day for Na, K, Cl and water in an IV?

A

Na, K and Cl- 1mmol/kg/day

Water- 30 my/Kg/day

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14
Q

What does niacin deficiency cause?

A

Pellagra - dermatitis, light sensitivity, dementia, diarrhoea

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15
Q

Where can fibre be found in the diet?

A

Cereal, breads, beans, fruit, veg

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16
Q

How much fibre is needed per day?

A

18g

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17
Q

What does too much and too little fibre cause?

A

Too much= low cholesterol –> diarrhoea as less water reabsrobed from bile salts. Also lower diabetes risk.
Too little- constipation and bowel cancer

18
Q

What is the reference nutrient intake (RNI) recommendations? What % of pop does it cover?

A

Amount of vitamins, minerals and proteins needed for 97% of population

19
Q

What is estimated average intakes (EAR)?

A

Energy needed for 50% of people (avg)

20
Q

What are the lower reference nutrient intakes?

A

Minimum intake for bottom 2.5% of people, amount needed depends on age, ethnicity and gender

21
Q

How many KJ of energy does the avg male and female need/ use per day?

A 
M= 12,000
F= 9,500
22
Q

What 3 things contribute to the daily energy expenditure?

A
  • basal metabolic rate
  • voluntary physical activity
  • diet induced thermogenesis (energy required to process food)
23
Q

How is BMI calculated?

A

Weight (kg)/ height (M) squared

24
Q

What are the health risks associated with obesity?

A

Increased risk of cancer, CVD, T2 diabetes, stroke, osteoarthritis ect

25
Q

What is desirable BMI ?

A

18.5- 24.9

26
Q

What is overweight, obese and severely obese categories for BMI?

A

Overweight: 25- 29.9
Obese: 30-34.9
Severely obese: >35

27
Q

What is an alternative to BMI?

A

Hip: waist ratio

28
Q

What distribution of fat (body shape) is associated with the biggest risk fo T2 diabetes, hypertension, stroke and high cholesterol?

A

Apple shape- lots of upper body fat

29
Q

What is the normal blood glucose range?

A

3.3-6 mmol/L

30
Q

What is the presentation of someone with marasmus disorder?

A

Thin, Wasted limbs with no muscle definition or fat. NO OEDEMA.
Usually in 1st year of life

31
Q

Describe the pathology behind marasmus disorder.

A

Decreased energy intake means fat, liver glycogen and muscle is being broken down. They have low (but enough) protein intake to stop odema and the fluid intake is very low so there isn’t much extra water intake to create oedema.
Main thing here in ENERGY INTAKE LOW

32
Q

Describe the presentation of kwashiorkor syndrome

A

Oedema in abdomen, swollen legs and arms, muscle wasting is present but hidden. Onset after breast feeding stopped. Fatty liver disease present .

33
Q

Why does kwashiorkor syndrome occur?

A

PROTEIN INTAKE VERY LOW.
Means lipoproteins not produces so lipids not transported out liver–> fatty liver disease
Albumin cannot be made in liver due to fatty liver and no protein intake. Leads to decrease oncotic pressure of blood, so more water move out into interstitial space–> oedema.
Fluid and energy intake normally low or normal

34
Q

How are kwashiorkor and marasmus managed?

A
  • glucose, rehydration and replace electrolytes then slowly start to refeed
  • Do not give protein in kwashiorkor because the protein will be converted to ammonia but the liver is damaged so it will not be able to convert the ammonia to urea and the high ammonia conc will kill them
35
Q

Why does refeeding symptom occur?

A
  • All stored low, including phosphorus store. So when meal given all PO4-2 will be used up to store the nutrients from the meal. The PO4-2 will then become VERY low, leading to cardiac arrest
  • Also, enzymes for urea cycle down regulated as previously a low protein diet. So when lots protein intaken and converted to ammonia it cannot be converted to urea fast enough so they get ammonia toxicity
36
Q

How are dietary carbohydrates such as starch or glycogen digested?

A

Amylase in saliva breaks down into dextrins.
Pancreatic amylase degrades detrixins into mono/ disaccharides.
Disacchardies attach to bush boarder where sucrase/ lactase/ amylase (1- 4 bonds)/ isomaltase (1-6 bonds) break down into monosaccharides

37
Q

How is glucose absorbed into blood at epethilia and in liver, kindest and B cells of pancreas? How does this differ to muscle and adipose cells?

A
  • Sodium cotransport at apical membrane and then GLUT2 facilitates diffusion into blood stream
  • GLUT4 present in adipose and muscle cells- only on surface when insulin present.
38
Q

What is the difference between primary and secondary lactase deficiency?

A

Primary- abcense of lactase persistence allele, so lactase at brith but none in adults
Secondary- caused by injury to small intestine (crones, coeliac ect).

39
Q

Is congenital lactase deficiency (no lactase allelles) rare or common cause of lactose intolerance?

A

rare

40
Q

What are symptoms of lactose intolerance?

A

Bloating, cramps, flatulance, diarrhoea, vomiting, rumbling stomach. Goes away when lactose ruled out of diet.

41
Q

Which cells cannot create energy from other sources so have an ‘absolute requirement’ for glucose?

A
  • RBCs
  • Neutrophils
  • Innermost cells of kidney medulla (low O2 supply)
  • Lens of eye (no capillaries, no O2)
42
Q

Does the CNS have an absolute requirement of glucose?

A

No, it can use ketone bodies to create energy but prefers glucose.

Metabolism (8 decks)

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