Lecture 4: Micronutrient Malnutrition Flashcards

1
Q

Micronutrient Deficiencies focus on what?

AKA as what?

A

Focus: Iron, iodine, Vitamin A

AKA “hidden” malnutrition

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2
Q

Define anemia

A

Not having enough healthy RBCs/hemoglobin to carry oxygen to body’s tissues.

Causes tiredness, weakness, shortness of breath

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3
Q

____ part of many proteins involved in oxygen transport and energy metabolism reactions

A

Iron

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4
Q

Myoglobin

A

protein similar to hemoglobin found in cytoplasm of muscle cells

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5
Q

_____ and ____ in the energy metabolism pathway

A

Enzymes and electron carrie molecules

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6
Q

Regarding iron: ____ involved in frug metabolism, immune system, and protection against free radicals

A

protein

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7
Q

What needs iron to carry oxygen and for energy metabolic reactions?

A

Hemoglobin, myoglobin, enzyes/electron carrier molecules, proteins

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8
Q

When does iron deficiency occur?

A

When diet doesn’t provide enough to meet needs

“Absence of iron stores + signs of iron-deficient RBC production = insufficient supply of iron to various tissues”

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9
Q

Iron deficiency Anemia

A

Not enough hemoglobin produced due to lack of iron.

No more iron stores left ~12mg/dL

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10
Q

Causes of Iron Deficiency and Iron Deficiency Anemia

A

Insufficient intake (lack of iron in your
diet) to cover normal needs or to meet
the increased needs for

  1. Blood loss
    • Menses, GI bleeding, parasites (esp. hookworm)
  2. Growth
  3. Pregnancy
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11
Q

Other causes of anemia

A
  1. Malaria: destroys RBCs + reduces RBCs production
  2. Other parasites: feed on host blood OR causes damage -> loss
  3. Other Infections: inflammation -> change in immunity + how body use Iron
  4. Other nutrient deficiencies for blood production (A, B Vitamins, …)
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12
Q

Ideal levels of iron

A

2/3 functional: usable
1/3: stored

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13
Q

How can iron be stored?

A

Attached to protein “Ferritin” -> in mucosal clinic -> of intestine + liver

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14
Q

How is iron transported through blood?

A

attach to protein “Transferrin”

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15
Q

Stages of iron deficiency

A
  1. Decrease of ferritin (stores)
  2. Iron deficiency hematopoiesis
    - Iron stores depleted with insufficient absorption to counteract normal losses
    - Leads to decreased hemoglobin production
  3. Iron deficiency anemia
    - Hemoglobin falls below a set standard
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16
Q

A Negative Balance Leads to progressively more severe conditions: draw the graph

A
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17
Q

Know recommended intakes for iron

A

birth to 6mo: 0.27 mg

4-8 yrs: 10 mg

9-13 yrs: 8 mg

14-18 yrs: 11mg (male), 15mg (female)

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18
Q

Food sources of iron

A

Total cereal: passes RDA

Cooked spinach
Lentiis

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19
Q

_________ is part of hemoglobin and
myoglobin and is obtained from meat of all
types; about ___% absorbed

A

Heme iron, 25%

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20
Q

_______ iron is found in grains, leafy
green vegetables, legumes, and meat and
is absorbed at about half (or less) the rate
of heme iron.

A

Non-heme iron

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21
Q

____ iron can also leach out of iron cookware into food

A

non-heme

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22
Q

Iron deficiency anemia symptoms

A

Brittle/spoon shaped nails
Cold hands/feet
Headache

Fatigue
Weakness
Shortness breath

Pica
Pallor
Poor appetite

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23
Q

Plant foods are different regarding iron absorbability + #iron

  • Fiber, phytate, tannins, oxalate do what regarding iron?
  • Milk, calcium can do what?
A
  • bind iron and prevent absorption
  • decrease absorption
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24
Q

Concurrent intake of Vita can do what to non-heme iron?

A

enhance absorption

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25
Q

___ also increases absorption of non-heme and henna iron

A

“meat factor”

  • heme iron taken into cells more efficiently than non-heme iron
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26
Q

Possible interventions?

A

*Diet containing adequate amounts of bioavailable iron

*Oral iron supplements (women of child-bearing age)

*Malaria control; Deworming

*Fortification of wheat/maize flours, and rice

*Delayed cord clamping

*Early interventions targeting adolescent females

*Good hygiene reduces risk of infection

*Education on reproductive health, family planning services to encourage dialogue,
adequate birth spacing.

27
Q

Doninent Effects of lack of iron?

A
  1. Cognitive defects in kids
  2. Poor motor control
  3. Maternal deaths <- severe anemia
  4. Decreased productivity
28
Q

Problem results from iodine

29
Q

Iodine is needed for synthesis of what?

A

Thyroid hormones -> controls metabolic activity of all cells

30
Q

What regulates metabolic activities of all cells>

A

Thyroid hormones <- iodine

31
Q

Iodine availability depends on what?

Also abundant in what?

A

soil concentrations

also abundant in seawater making seafood and seaweed good sources

32
Q

Extremely high intakes of iodine also causes what?

A

Impaired thyroid function

33
Q

What plays key role in cell replication?

Most relevant for what?

A

iodine, especially relevant for brain

34
Q

Fetal iodine deficiency leads to what?

A

 Increased rates of spontaneous abortion
 Stillbirths
 Congenital anomalies
 Congenital hypothyroidism
 Psychomotor deficits
 Neonatal mortality

35
Q

Thyroid hormones contain ____ atoms of iodine

36
Q

Adult iodine deficiency leads to what

A

Goiter and its complications
Hypothyroidism
Impaired mental function

37
Q

Interventions and considerations for iodine deficiency

A
  • Salt iodization
     Law mandates
     Quality assurance standards
  • Target populations: Pregnant women, children under the age of 3
  • Soil testing
  • Iodine toxicity-not usually a concern
  • Too much salt? Hypertension, Heart Disease.
38
Q

______________ is the leading
cause of preventable blindness in children
and increases the risk of disease and death
from severe infections.

A

Vitamin A deficiency (VAD)

39
Q

A major role of vitamin A is as part of
the visual pigment ______

40
Q

Other responsibilities of Vitamin A

A

 Maintenance of epithelial tissue
(Skin, lungs, blood vessels, GI tract, etc.)

 Regulation of growth and
differentiation/specialization of cells (Including some cells of the immune
system)

41
Q

As part of rhodopsin, retinol
binds with the protein
opsin: Describe visual and light in terms of these

(?????)

A

 Rhodopsin absorbs light, which
signals visual cortex of brain
 Reconversion and replenishing of
rhodopsin must occur before it can
respond again to light
 When Vitamin A pool is low, dark
adaptation is slowed down
 When amt. of rhodopsin is limited,
difficult to see in dim light “night
blindness”

42
Q

Deficiency of ___ is // with decreased resistance to infection

A

VitA

plays important role in maintenance of epithelial cells

43
Q

Why is it crucial to maintain epithelial tissues and mucus production?

A

Act as barriers to invading pathogens

44
Q

___ is often accompanied by cell proliferatio: continuous development of cells in tissue formation

45
Q

____ is needed for production, structure and normal function of epithelial cells in lungs, trachea, skin GI tract, …

Essential for production fo mucous-forming cells in these organs

46
Q

Vit A is fat-soluble or non-fat? How is it transported?

A

Fat-soluble, via lipids

47
Q

Where is VitA stored>

48
Q

___ is also needed for Retinal binding protein (RBA): needed for storage/transport of VitA in body

49
Q

Several forms fo Via A

A

Retinoids, BEta-carotene, Antioxidant

50
Q

Describe retinoids

A

Common in animal tissues, can serve VitA functions directly

51
Q

Describe Beta-carotene

A

is a precursor of VitA founding plant tissues

converted/split by intestine into retinal and retinol

52
Q

What is pre-formed VitA?

A

from animal sources

53
Q

How much is pre-formed VitA (animal sources) absorbed?

54
Q

Describe Pro-vitamin A sources (carotenoids from plants)

A
  • Dependent on type of plant source and fat content of the meal
  • Absorption of beta-carotene about 1/3 of retinol and conversion to vitamin A about 1/2
55
Q

Good diet courses for VitA

A

 beef liver
 carrots (as beta-carotene)
 mustard greens (as beta-carotene)
 Egg yolk
 apricots (as beta-carotene)

56
Q

What is much less toxic
in higher doses than is the preformed
animal forms of vitamin A

A

BEta-carotene

57
Q

Symptoms of VitA deficiency

A

 Impaired immune function
 Night blindness (insufficient retinal
for rhodopsin formation)
 Dry, hard skin
 Dry cornea and eventual blindness
(Xerophthalmia)

58
Q

Steps in VitA Deficiency

A

 Body stores are depleted
leading to impairment of
physiologic functions

 1st integrity of the epithelial
barriers and then the immune
system is compromised

 Finally, the visual system is
impaired

59
Q

Xeropthalmia –Sequence of
Events

A

 Night blindness is a common early symptom of low levels of Vitamin A

 Mucus forming cells deteriorate and are no longer able to synthesize the mucus that
lubricates the body

 The eye especially needs mucus to keep the surface moist and to wash away dirt and other particles that settle on the eye

 Deterioration of the eye results from
bacterial invasion
- Role of A in resistance to infection

 Conjunctival xerosis (abnormal dryness
of the lining of the eyelids and the outer
surface of the eyeball) and Bitot’s spots
(drying out of the eye and appearance of
hardened epithelial cells) appear as VAD
worsens

 Finally, corneal ulcerations and
keratomalacia (softening of the
cornea) results in scarring
- Can see effects from barely
detectable to blindness

60
Q

Other problems with VitA Deficiency

A

 Keratinized cells in the outer layer of skin
replace the normal epithelial cells in the
underlying skin layers
 Hair follicles become plugged with keratin
 Skin has a bumpy appearance and rough
texture and is very dry
 Deficiency also causes a decrease in appetite
and poor growth
 Mortality and severity of measles worsened with vitamin A deficiency

61
Q

Treating VitA Deficiency

A

 15,000 to 60,000 micrograms of Vitamin A
every 6 months can prevent deficiency in
children

 Common dose is 200,000 IUs periodically

 Improving the Vitamin A status of young
children reduces mortality rates by about 20% in populations where there is vitamin A
deficiency

62
Q

What are the major source of pro-VitA in kids where animal products are limited?

63
Q

Can you have too much VitA?

A

 Toxic levels can be reached by excess
consumption of liver and supplements of
preformed vitamin A (not beta-carotene)

  • recorded instances of toxicity involve excess consumption of polar bear liver by Arctic explorers and supplement use
64
Q

Symptoms of VitA toxicity include:

A

 Nausea, vomiting
 Headache, blurred vision
 Lack of muscular coordination