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Malnourishment and Obesity > Minerals > Flashcards

Minerals Flashcards

1
Q

Name the macronutrients:

A
  • Carbohydrates
  • Proteins
  • Fat
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2
Q

Name the micronutrients:

A
  • vitamins

- minerals (macrominerals = major; microminerals = trace)

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3
Q

What is the % of children less than 5yo that are stunted? - WHO

A

20%

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4
Q

How do you access the adequacy of a population’s…. lets say… Zn intake?

A
  1. Take into account the physiological requirements for absorbed Zn
  2. Account for an estimate of % of absorbable dietary Zn (to calculate EAR)
  3. Account for an estimate of coefficient of variation (CV) of usual intakes of zinc in the population
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5
Q

What is the result of calcium deficiency?

A
  • Rickets
  • Osteomalacia
  • Osteoporosis
  • Tetany
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6
Q

What is the result of Magnesium deficiency?

A
  • Neuromuscular hyperexcitability
  • muscle weakness
  • tetany
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7
Q

What is the result of phosphorus deficiency?

A
  • neuromuscular, skeletal, haematological, and cardiac manifestations
  • rickets
  • osteomalacia
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8
Q

What is the result of sulfur deficiency?

A

(unknown.. hahaha)

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9
Q

What are the ‘functions’ of calcium?

A
  • Bone structure
  • muscle contraction
  • nerve impulse transmission
  • wound healing
  • cellular metabolism
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10
Q

In lifetime, when is absorption in great levels?

A

childhood and pregnancy

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11
Q

What are the % levels of absorption at childhood and adulthood respectively?

A 
childhood = 75%
adulthood = 30%
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12
Q

What facilitates absorption?

A

lactose

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13
Q

What reduces absorption?

A

Phytates, NSP and oxalates

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14
Q

Is absorption energy-dependant?

A

Yes

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15
Q

In what way can vitamin deficiency develop?

A
  • lack of exposure to sunlight
  • inadequate dietary intake
    (or both)
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16
Q

What is reduced in vitamin deficiency?

A
  • efficiency of intestinal Ca2+ absorption

- decreased serum ionized calcium

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17
Q

From animal studies, what happens in excessive Ca2+ intake?

A

Can impair Fe, Zn and Mg nutritional status

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18
Q

From Human studies, what happens in excessive Ca2+ intake?

A
  • Ca2+ interacts and reduces absorption of Mg and P
  • inhibits absorption of Fe in a dose-dependent and dose-saturable fashion
  • reduces absorption of Zn and Zn balance = increase Zn requirement
  • NO EVIDENCE that it’s associated with nutrient deficiencies
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19
Q

Does calcium deficiency exist?

A

No. (at least not as a nutritional disorder)

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20
Q

What does inadequate intake/poor intestinal absorption of Ca2+ cause?

A
  • circulating ionized calcium concentration declines acutely
  • triggers increase in PTH synthesis and release
  • restores the circulating calcium concentration to normal via targeting 3 organs
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21
Q

How fast does it take for plasma calcium concentration levels to be restored?

A

within minutes to hours

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22
Q

Circulating Ca2+ concentration is maintain largely at the expense of?

A

Skeletal mass

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23
Q

In regard to bones, what happens from vitamin D deficiency?

A
  • increased rate of bone resorption

- over years, reduced bone mass and osteoporosis

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24
Q

What is tetany?

A

Muscle pain, spasm, numbness in hands and feet

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25
Q

What are the outcomes in terms of the link between calcium deficiency and osteoporosis?

A
  • affects post-menopausal women
  • loss of trabecular bone
  • public health significance
  • evidence for oestrogen, vit D and low PA
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26
Q

What are the 3 main outcomes from calcium toxicity?

A
  1. Kidney stone formation (nephrolithiasis)
  2. Syndrome of hypercalcaemia and renal insufficiency (with or w/out alkalosis)
  3. Effects on absorption of other essential minerals (Fe, Zn, Mg, P)
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27
Q

What is alkalosis?

A
  • historically referred as milk alkali syndrome

- associated with peptic ulcer, dyspepsia, osteoporosis treatments

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28
Q

What is the tolerable upper intake level (UL) of calcium?

A

2500mg/day

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29
Q

What is genetic hypocalcaemia?

A

Inborn erros of metabolism associated with hypocalcaemia that can impair the bone calcification process

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30
Q

What are the 2 outcomes of genetic hypocalcaemia?

A
  1. Vitamin D-dependent rickets (type I and II)

2. Familial benign hypercalcaemia (type I and III)

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31
Q

What causes vit. D-dependent rickets and what is its treatment?

A
  • mutation in enzyme enzyme 25(OH)D3-1α-hydroxylase
  • changes in the vitamin D receptor molecule

Treatment = daily vitamin D3 administration

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32
Q

What causes familial benign hypercalcaemia?

A
  • mutation in the gene encoding the calcium-sensing receptor

- renal tubular defect in calcium reabsorption

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33
Q

What substance enhances intestinal phosphorus absorption?

A

Vitamin D

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34
Q

What substances inhibit intestinal phosphorus absorption?

A
  • Phytic acid

- excessive intakes of: Mg, Al, Ca

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35
Q

What are the functions of phosphorus?

A
  1. Bone mineralisation
  2. Nucleotide/nucleoside phosphates
  3. Phosphoproteins and phosphorylated forms of vitamins (e.g. B6)
  4. Phospholipids
  5. Acid-base balance
  6. Oxygen availability
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36
Q

What does phosphorus inhibit?

A

polyphosphates in food additives can interfere with the absorption of Fe, Cu and Zn

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37
Q

What are the roles of nucleotide/nucleoside phosphates?

A
  1. Structural role
  2. Energy storage and transfer
  3. Intracellular second messenger
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38
Q

Is phosphorus ubiquitous in various food?

A

Yes

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39
Q

What is hypophosphataemia?

A

Limited P stored within cells, tissue depend on ECF inorganic P for their metabolic phosphate (ECF P < 0.3 mmol/l)

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40
Q

What does hypophosphataemia cause?

A
  • cellular dysfunction

- severe manifestations

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41
Q

What are some symptoms of hypophosphataemia?

A
  • anorexia, anaemia, muscle weakness, bone pain, rickets and osteomalacia
  • general dibility
  • increased susceptibility to infection, paresthesia, ataxia, confusion and even death
  • skeleton will exibit either rickets in childern or osteomalacia in adults
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42
Q

What happens in rickets and osteomalacia?

A
  • failure of bone mineralisation

- impairment of chondroblasts and osteoblast function

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43
Q

State the bioavailability % of different sources of P:

A

Plant P (phytates) = absorption rate 40-50%

Animal P (casein) = Absorp. rate 60-70%

Inorganic P (food additives) = Absorp. rate 100%

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44
Q

In what way is inorganic P helping patients with advanced CKD?

A

can measurably elevate the serum P concentration

high absorp. rate = 100%

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45
Q

What are the effects of hyperphosphotaemia?

A
  1. Adjustments in hormonal control system regulating Ca economy
  2. Ectopic calcification, particularly of kidney
  3. Increased porosity of skeleton (in some animal models)
  4. May decrease Ca calcium absorption by complexing calcium (limited evidence)
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46
Q

What are the 3 phosphorus-related genetic diseases?

A
  1. X-linked hypophosphataemia
  2. Hypophosphatemic bone disease
  3. Fanconi’s syndrome
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47
Q

What is X-linked hypophosphataemia?

A

Primary inborn error of phosphate transport, probably located in the proximal nephron (Xp22.2-p.22.1)

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48
Q

Specifically in hemizygous male patients, what are the results of X-linked hypophosphataemia?

A
  • hypophosphataemia
  • lower limb deformities
  • stunted growth rate
  • low serum P evident early after birth
49
Q

In patients with x-linked hypophsphataemia, when are leg deformities observed?

A

at time of weight bearing progressive departure from normal growth

50
Q

How is Hypophosphatemic bone disease clinically characterised?

A
  • modest shortening of stature
  • bowing of lower limbs
  • nonachitic bone changes (chondrodysplasia)
  • hypophosphataemia
  • defect in renal transport of P, which is diff from the x-linked hypophos.
51
Q

What is Fanconi’s syndrome?

A

Autosomal dominant disorder, characterised by lactic aciduria and tubular proteinuria in childhood.

52
Q

What develops in the second decade of Fanconi’s syndrome?

A

glycosuria and aminoaciduria

53
Q

What develops at start of fourth decade of Fanconi’s syndrome?

A

osteomalacia

54
Q

What are the functions of magnesium?

A
  1. Neuromuscular activity transmission
  2. Cardiac muscle contraction
  3. Cellular (second messenger) role
55
Q

What are the cellular roles of magnesium?

A
  • activates enzymes for CHO and Protein metabolism
  • Transportation of Na and K across the cell membranes
  • influences utilisation of K, Ca and proteins
  • Mg deficits are frequently accompanied by K and/or Ca deficit
56
Q

What is the role that Mg plays?

A

Stabilisation of ATP and other molecules

57
Q

Is Mg deficiency rare?

A

YES. Occurs only in clinical settings as secondary consequences of another disease

58
Q

What risk factors has marginal deficiency in Mg proposed?

A

Chronic diseases such as

  • osteoporosis
  • cardiovascular disease
  • diabetes
59
Q

What are Mg deficiency symptoms?

A
  1. Progressive reduction in plasma Mg (10-30% below controls)
  2. RBC Mg slower, less extreme than fall in plasma Mg
  3. Hypocalcaemia and hypocalciuria
  4. Hypokalaemia, from exceds K+ excretion, leading to negative K+ balance
  5. Abnormal neuromuscular function
60
Q

How are all Mg deficiency symptoms reversed?

A

with dietary Mg repletion

61
Q

What are the two conditions Mg deficiency is seen in humans?

A
  • as a secondary complication of primary disease state (cardiovascular and neuromuscular function, endocrine disorders, malabsorption syndromes, muscle wasting)
  • resulting from rare genetic abnormalities of Mg homeostasis
62
Q

What are the effects of Mg depletion?

A
  • effect on serum PTH and 1,25(OH)2D3

- disrupted Ca2+ metabolism

63
Q

What is the tolerable UL Mg for adolescents/adults?

A

350mg of non-food Mg

64
Q

What are the high intakes of Mg salts (pharmacological purposes) linked to?

A

adverse effects of excess Mg (diarrhea, nause, abdominal cramping)

65
Q

What are some examples of trace and ultratrace minerals?

A
  • Iron
  • Iodine
  • Zinc
  • Chromium
  • Copper
  • Manganese
  • Molybdenum
  • Selenium
66
Q

What is the result of iodine deficiency?

A

Enlarged thyroid gland (goitre)

67
Q

What is the result of iron deficiency?

A
  • anaemia
  • fatigue
  • impaired work performance
  • decreased resistance to infection
68
Q

What is the result of zinc deficiency?

A
  • Poor wound healing
  • subnormal growth
  • anorexia
  • abnormal taste/smell
  • impaired reproductive system development
69
Q

What are the sources of iron?

A
  • organ meats (liver)
  • meat
  • molasses, clam, oysters
  • nuts, legumes, green leafy vegetables, dried fruits
  • enriched/whole grains
70
Q

What are the sources of iodine?

A
  • iodised salt, salt-water seafood
  • milk
  • liver, eggs, yoghurt
  • legumes
  • sea/shell fish
  • seaweed
71
Q

What are the sources of zinc?

A
  • oysters, beef, liver, poultry

- wheat germ, whole grains

72
Q

what are the 3 stages of IDA progression (iron deficiency anaemia)?

A
  1. Depletion of storage Fe
  2. Decrease in transported Fe
  3. Supply of Fe insufficient to provide enough Hb for new erythrocytes, insufficient to fulfill other physiological functions
73
Q

In the first stage of IDA progression, what is the specific name of the serum that decreases?

A

serum ferritin

74
Q

What stage of life is iron deficiency anaemia most common at?

A
  • infants
  • preschool children
  • adolescents
  • child-bearing age
75
Q

What is the prevalence of IDA?

A

in UK:
men = 3%
women = 8%

76
Q

Which category of people is IDA most common?

A

pre-menopausal women

77
Q

What percentage of non-pregnant women aged 16-49yo had iron deficiency?

A

11%

78
Q

What percentage of non-pregnant women aged 16-49yo had IDA?

A

3-5%

79
Q

Why are infants and adolescents at high risk of iron deficiency?

A

due to increased demand related to growth spurts

80
Q

What are the reasons for iron deficiency of infants and young children?

A
  • low iron content of milk and other preferred foods
  • rapid growth rate
  • insufficient body reserves of iron to meet needs beyond 6mths
81
Q

What are the reasons for iron deficiency of adolescents?

A
  • rapid growth

- need of expanding RBC mass

82
Q

What are the reasons for iron deficiency of females @ child-bearing years?

A

menstrual iron losses

83
Q

What are the reasons for iron deficiency of pregnant women?

A
  • expanding blood volume
  • demands of fetus and placenta
  • blood losses incurred at childbirth
84
Q

What are the physical features of anaemia?

A

pallor of skin, eyes, mucous membranes

85
Q

Which groups are most at risk of anaemia in developed countries?

A
  • children, adolescents
  • pregnant women
  • women of childbearing age
  • vegetarians
86
Q

What are the signs and symptoms of Iron deficiency

A
  • Fatigue
  • Headaches
  • disrupted sleep
  • reduced libido
  • reduced energy levels
  • dizziness/vertigo
  • loss of appetite
  • concentration/memory problems
87
Q

What are consequences of anaemia?

A
  • decreased work capacity
  • breathlessness on exertion
  • lethargy, tiredness
  • reduced intellectual performance
  • lowered resistance to infection
  • poor thermoregulation
  • child/fetal development
88
Q

What is the dietary reference value for iron in men and women?

A 
men = 8.7 mg/d
women = 14.8 mg/d
89
Q

What are two results of iron toxicity?

A
  • haemochromatosis (Fe overload w/tissue damage)

- haemosiderosis (Fe overload w/out tissue damage)

90
Q

What is primary idiopathic haemochromatosis?

A
  • Hereditary disorder of iron metabolism
  • Failure of iron absorption control mechanism at intestinal level
  • abnormally high iron absorption
91
Q

What can high deposits of iron in liver and heart lead to?

A
  • cirrhosis
  • hepatocellular cancer
  • congestive heart failure
  • death
92
Q

What preventive measures can be done for primary idiopathic haemochromatosis patients?

A
  • early detection
  • genetic screening
  • regular blood removal
93
Q

How much zinc is in human body in g?

A

1.5-3g (in all organs, tissues, body fluids)

94
Q

What happens in the inborn error of zinc metabolism?

A
  • acrodermatitis enteropathica in gene coding Zip4 transporter
  • dermatitis
  • dwafism
  • diarrhoeal disease
  • poor immune function
95
Q

In what way is zinc involved in nucleic synthesis?

A
  • protein digestion/synthesis
  • bone metabolism
  • oxygen transport
  • protection against free radical formation
96
Q

What does bound zinc stabilise?

A
  • RNA and DNA structures = zinc finger motifs (neuromodulator?)
97
Q

What are zinc fingers?

A
  • proteins with secondary structure or shape, due to presence of zinc atom linked through cysteinyl/histidyl residues in protein
  • found within many transcription factors which bind to metal response/regulatory elements in the promoter regions of genes to enhance/inhibit transcription
98
Q

Explain the functions of metallothionein (MT) when it binds to excess Zn:

A
  • it has low molecular weight (7kDa)
  • high cys content
  • increased synthesis
  • binds to other heavy metals (cadmium, mercury)
  • part of body’s defence mechanism to toxic metals
99
Q

What are the 2 systemic symptoms of zinc excess?

A
  • copper deficiency and sequelae

- altered lymphocyte function

100
Q

What are the 2 systemic symptoms of zinc deficiency?

A
  • growth retardation

- immune dysfunction and interaction

101
Q

Explain how Zn status is accessed:

A
  • difficult to access accurately
  • measuring circulating levels in plasma
  • affected by infection or high protein diet
  • indices, Zn in WBC (very laborious), hair (seasonal changes)
  • physiological functions: taste acuity/dark adaptation
  • RBC metallothionine (decreased in deficiency, increased in loading)
102
Q

What is the recommended intake of iodine in men and women?

A 
men = 243 μg/d
women = 176 μg/d
103
Q

What is the recommended intake of iodine in pregnant/breastfeeding women?

A

250 mcg

104
Q

What is the maximum iodine intake per day?

A

600 mcg

105
Q

What are the 2 thyroid hormones that iodine partly forms?

A
  • T3 (thyroxine)

- T4 (triiodothyronine)

106
Q

What are the metabolic functions of iodine?

A
  • regulates BMR and cellular metabolism

- nervous system development in foetus = important in pregnancy

107
Q

What enzyme catalyses the step of converting T4 to T3?

A

Selenium-dependent deiodinase enzyme

108
Q

What are the physiological effects of thyroid hormones?

A
  • enhances lipolysis @ adipose tissue
  • enhances contraction @ muscles
  • promotes anabolism (growth, development) @ bone
  • increase heart rate
  • stimulates nutrient digestion/absorption
  • stimulate metabolic rate and cellular oxygen consumption in metabolically active tissues
109
Q

How many individuals affected worldwide by iodine deficiency?

A

2 billion

110
Q

Particularly where in the world are individuals affected by iodine deficiency?

A
  • South asia

- Sub-saharan africa

111
Q

Is iodine the most common cause of preventable mental impairment worldwide?

A

Yes

112
Q

What are the direct causes of iodine deficiency disorders (IDD)?

A
  1. Low dietary iodine
  2. Low salt diet
  3. Stress - affects function of thyroid
  4. Endocrine disruptors - pesticides/heavy metals compete with iodine receptors = affecting the absorption of iodine from thyroid
113
Q

What are the indirect causes of iodine deficiency disorders (IDD)?

A
  • high levels estrogen - block iodine absorp. into thyroid + increase need for Iodine
  • pregnancy cause thyroid issues
  • hormone replacement therapy
  • estrogenic food consumption (unfermented soy)
  • fibroids
114
Q

Can liver damage cause IDD?

A

Yes. There’s lack of conversion of iodine to its active form

115
Q

What are the consequences of IDD?

A
  1. Fetal development
  2. Severe iodine deficiency during pregnancy
  3. Goitre is a classic sign of iodine deficiency
  4. Growth retardation, impaired mental function
  5. Lethargic, apathetic and lack initiative
  6. Poor psychomotor function
116
Q

What is goitre?

A

hypertrophy of thyroid gland

117
Q

What happens in cretinism?

A
  • mental retardation
  • dwafism
  • deaf mute
  • squint
  • motor spasticity
118
Q

What are some future perspectives for minerals and trace elements?

A
  1. Greater understanding of molecular/cellular processes in intestinal absorption/tissue uptake
  2. Identify functional biomarkers
  3. Evaluate further health risks associated with marginal deficiencies
  4. Define adverse effects of acute and chronic high intakes
  5. Elucidate impact of single nucleotide polymorphisms

Malnourishment and Obesity (21 decks)

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