1. Nutrient Deficiencies
N323

2. Vitamins
FAT-SOLUBLE:
 A, D, E & K
 Are absorbed with fat.
 Transported by protein lipids (LDL)
 Excessive amounts are stored.
 Not necessary to eat every day but toxic
amounts can accumulate.
 Found in fat or oil portion of foods.

3. Vitamins
WATER-SOLUBLE:
 C & B (thiamine, riboflavin, niacin, folate,
B6, B12, biotin & pantothenic acid)
 Are absorbed with water.
 Transported free floating in blood.
 Excessive amounts are excreted.
 Necessary to eat every day; toxic amounts
unlikely to accumulate.
 Found in water portion of foods.

4. Requirements
Recommended Daily Allowance: (RDA): Average
daily intake sufficient to meet nutrient
requirements for a healthy individual.
Dietary Reference Intake (DRI): New set of 4
values to set dietary goals: RDA plus:
 Estimated Average Requirement (EAR): Amt.
of nutrient sufficient to meet the needs of
50% of individuals.

5. Requirements
 Adequate Intake (AI): Recommended daily
intake when actual amt. is unproven.
 Tolerable Upper Intake Level (UL): Highest
level of daily nutrient intake that is not apt to
cause harm.

6. Sources
BREAD, CEREAL, RICE FOOD GROUP
 B vitamins (thiamine, riboflavin, niacin,
folate, B6), Vitamin E
 Fortified cereals contain almost all
vitamins.
VEGETABLE GROUP:
 Beta-carotene, C, K, & folate
FRUIT GROUP:
 Beta-carotene & vitamin C

7. Sources
MILK, YOGURT & CHEESE GROUP
 Vitamin A, D, B6, B12, riboflavin
MEAT, POULTY, FISH, BEANS, EGGS & NUTS
 B vitamins (B6, B12, niacin, riboflavin)
 Vitamin A (fish)
FATS & OILS GROUP
 Vitamin E

8. Vitamin A
ACTION:
 Promotes night vision
 Integrity of mucus membrane & skin
 Bone growth
SOURCES:
 Preformed A: animal fats; No-fat milk and
cereals are fortified.
 Beta-carotene (precursor to vitamin A): yellow
& orange vegetables and fruits, dark green
leafy vegetables

9. Vitamin A
TOXICITY:
 Unlikely except by supplements.
 Teratogenic during pregnancy so excess
supplements are not recommended
(Accutane is vitamin A).
 Beta-carotene, if excessive is not converted
to vitamin A, but stored in body fat. Can
turn skin yellow-orange
(hypercarotenemia)

10. Vitamin A
DEFICIENCY:
 Tender gums, sores at corners of mouth.
 A major cause of blindness worldwide
Xerophthalmia = dry, lusterless conjunctiva.
Keratomalacia = necrosis of cornea with
perforation and loss of ocular fluid
 “Smart” rice is A-fortified to prevent this.

11. Vitamin A
PEOPLE AT RISK:
 Eat no vegetables
 Constant dieters
 “Statin” drug users
 poor absorption of fat

12. Vitamin D
ACTION:
 Necessary for calcium absorption from GI
tract; incorporation of calcium into bone.
SOURCE:
 Ultraviolet sunlight & a precursor to
cholesterol is synthesized by liver;
activated by kidney.
 Liver, fatty fish & egg yolks only natural
food sources.
 Milk is fortified to supply vitamin D.

13. Vitamin D
TOXICITY:
 Vitamin most apt to cause toxicity.
 Increases GI calcium absorption = kidney
stones, hypercalcemia.
DEFICIENCY:
 Osteomalacia in adults (weakened bones)
 Rickets in children (curved bones)
 Tetany (from hypocalcemia)

14. Vitamin D
PEOPLE AT RISK:
 Elderly (receive less sunlight; kidneys don’t
function as well)
 People living in heavy smog, pollution areas.
 Children who don’t drink milk.

15. Rickets
 Weakened bone formation from lack of calcium
ASSESSMENT:
 Craniotabes
 Delayed tooth development
 Rachitic rosary & epiphysis swelling
 Late closure of fontanelles
 Bow legs; Kyphosis
 Pelvic contraction
 Confirmed by x-ray examination

16. Rickets
NURSING DIAGNOSIS:
 Immobility related to poor bone formation.
THERAPY/INTERVENTIONS:
 Vitamin D, calcium & sun exposure
EXPECTED OUTCOME:
 Child ingests adequate intake.
 Bone changes stop with treatment but are not
irreversible.

17. Vitamin E
ACTION:
 Potent antioxidant (keeps polyunsaturated
fats from being destroyed; protects against
atherosclerosis, cell wall damage)
 Important for immune function.
SOURCES:
 Found in almost all plants.

18. Vitamin E
TOXICITY:
 Large amts. interfere with vitamin K so can
lead to hemorrhage.
DEFICIENCY:
 Rare because sources are so abundant.
 Premature infants develop anemia from
oxidization of red blood cells.
RISKS:
Low-birth weight infants; poor fat absorption.

19. Vitamin K
ACTION:
 Important for blood clotting (synthesis of
prothrombin).
SOURCES:
 Green, leafy vegetables, liver, milk
 Manufactured in intestines by bacteria.

20. Vitamin K
TOXICITY:
 Rare
DEFICIENCY:
 Not a lot is stored so deficiency can occur.
 Hemorrhagic Disease of the newborn
RISKS:
 Newborns for 1st 24 hours (why vitamin K
is routinely administered).
 Coumadin users (blocks vitamin K action)
 Intestinal surgery with antibiotics

21. Thiamine (B1)
ACTION:
 Necessary for glucose metabolism & nervous
system health.
SOURCES:
 Meat & grains
 Alcohol impairs absorption

22. Thiamine (B1)
TOXICITY:
 Rare
DEFICIENCY:
 Beriberi
RISK:
 Alcoholics
 Poor protein intake in developing countries

23. Beriberi
 Thiamine (B1) deficiency (found in people who
eat polished rice as dietary staple (B1 is found
in hull of rice)
ASSESSMENT:
 Tingling/numbness of extremities; edema,
heart palpitation; exhaustion & dyspnea
 Diarrhea/vomiting
 Infants dry without sound (aphonia) Edema &
convulsions
THERAPY/INTERVENTIONS:
 Thiamine

24. Riboflavin (B2)
 Necessary for glucose metabolism
 Either toxicity or deficiency rare

25. Niacin (B3)
ACTION:
 Necessary for glucose & fat metabolism.
 Lowers cholesterol.
SOURCE:
 Whole grains and protein rich foods.
TOXICITY:
 Causes severe flushing from vasodilatation
 Hypotension from vasodilatation.

26. Niacin (B3)
DEFICIENCY:
 Rare as body can convert an amino acid to
niacin.
 Pellagra
RISKS:
 People who use corn as dietary staple.
 Reduces cholesterol

27. Pellagra
 Niacin deficiency (found in people who eat
corn as main dietary staple)
ASSESSMENT:
 4 Ds:
 Dermatitis: looks like sunburn at first, then dry
and cracked; tone is sore and raw-looking.
 Dementia: loss of memory; general irritability
 Diarrhea:
 Death:

28. Pellegra
THERAPY/INTERVENTIONS:
 Niacin administration.
 Caution that severe flushing will occur.

29. Pyridoxine (B6)
ACTION:
 Necessary for amino acid & fat metabolism.
 Produciton of heme; myelin sheaths. Converts
tryptophan to niacin.
SOURCES:
 Meat, fish, grains
TOXICITY:
 Rare

30. Pyridoxine (B6)
DEFICIENCY:
 May be associated with convulsion in infants.
 May be associated with premenstrual
syndrome.
 Pain, numbness of extremities; muscle
weakness
RISKS:
 Alcoholics
 People on INH

31. Folate (Folic Acid)
 ACTION:
 Necessary for synthesis of DNA (new cell
growth)
 Necessary to activate B12.
 SOURCES:
 Green leafy vegetables

32. Folate (Folic Acid)
TOXICITY:
 Rare
DEFICIENCY:
 Neural tube defects during pregnancy.
 Megaloblastic anemia
RISKS:
 Rapid growth periods
 Hemolytic anemias

33. Cobalamin (B12)
ACTION:
 Necessary to activate folate.
 Fat metabolism; myelin sheaths.
SOURCES:
 Animal sources
 Intrinsic factor necessary for absorption

34. Cobalamin (B12)
TOXICITY:
 Rare
DEFICIENCY:
 Pernicious anemia
RISKS:
 Elderly; gastric surgery;  gastric secretions

35. Vitamin C
ACTION:
 Necessary for collagen formation.
 Poor muscle, bone, blood vessel formation.
 Inc. iron absorption.
 Strengthens immune system.
SOURCES:
 Citrus fruits; vegetables

36. Vitamin C
TOXICITY:
 No specific effects
DEFICIENCY:
 Scurvy
RISKS:
 Elderly (fruit spoils easily)

37. Scurvy
 Vitamin C deficiency interferes with collagen
formation
ASSESSMENT:
 Infants 2 to 12 months of age.
 Walls of capillaries become fragile; petecchial
hemorrhage from vessels occurs.
 Gums are swollen & bleed easily
 Extreme muscle tenderness (cry when
handled)
 Can be suspect for child abuse.

38. Scurvy
THERAPY/INTERVENTIONS:
 Vitamin C (why English sailors are called
limeys)

39. Protein
 Major nutrient necessary for building cells.
 Necessary for immune system function.
 If not enough carbohydrate present, is used
for energy (carbohydrates are protein sparing)
 Composed of carbon, hydrogen, oxygen plus
nitrogen. Excess nitrogen is excreted as urea =
excessive load for kidneys.
 Protein is broken down into amino acids and
then used to construct 22 amino acids (8 are
essential in adults; 9 in children)

40. Protein
 Use of protein is all or none concept: if all
ingredients for essential amino acids are not
present, they are not made. Excess is excreted.
 Complete protein: animal sources.
 Incomplete: plant sources.
 Complementary proteins: two incomplete that
make a complete protein

41. Essential Amino Acids
 Tryptophan (TRIP-toe-fane)
 Valine (VAY-leen)
 Threonine (THREE-o-neen)
 Isoleucone (I-so-LOO-seen)
 Lysine (LYE-seen)
 Leucine (LOO-seen)
 Phenylalanine (fee-nul-AL-uh-neen)
 Methionine (meh-THIGH-o-neen)
 In infants: Histidine (HISS-tuh-deen)
 TV TILL PM

42. Kwashiorkor
 Protein deficiency
ASSESSMENT:
 1-3 years of age
 Developing countries
 Growth failure; extensive edema and ascites;
muscle wasting.
 “Zebra” hair , anorexia
 Concurrent iron-deficient anemia

43. Kwashiorkor
THERAPY/INTERVENTIONS:
 Protein
 May have long-term cognitive effects.

44. Marasmus
 Deficient food intake
ASSESSMENT:
 Seen in developing countries or poor parenting
 Under 1 year of age
 Wasted muscles, diarrhea, growth failure.
 Hungry
THERAPY/INTERVENTIONS:
 Feed

45. Maple Syrup Urine Disease
 Unable to convert leucine and valine into
breakdown products.
 Raw amino acids built up in blood stream.
 Toxic to brain cells.
 Severe cognitive impairment
 Can be recognized in utero by amniocentesis
 Urine smells like maple syrup
 Placed on low Leucine & Valine diet
 Almost impossible to maintain so outcome is
limited

46. Phenylketonuria (PKU)
H p
H HH Hp
p PH pp
 Inborn error or
metabolism
 Unable to use an
essential amino acid
 Autosomal Recessive
• H = Healthy gene
• p = PKU gene

47. Phenylketonuria
 Lack liver enzyme (phenylalanine hydroxylase)
that converts phenylalanine into tyrosine.
 Tyrosine is responsible for formation of
• epinephrine
• thyroxine
• melanin

48. Phenylketonuria
 Without ability to convert phenylalanine to
tyrosine,
• high levels of phenylalanine build up in
blood stream
• Cross blood-brain barrier
• Toxic to brain cells leading to cognitive
impairment
• Excess is excreted in urine as phenylpyruvic
acid.

49. Phenylketonuria
ASSESSMENT:
Urine has a musty odor compared to mouse
urine
Without ability to produce tyrosine
• Short stature
• Light skinned, blonde haired
• Eczema or atopic dermatitis

50. Phenylketonuria
Diagnosed by:
 All newborns in U.S. are tested by a Guthrie
Test at birth
 Must have 24 to 48 hours of milk intake b/4
test
 Parents must return newborn for test if
discharged b/4 24 hours.
 Can not be diagnosed by amniocentesis as
mother clears excess phenylalanine

51. PKU
THERAPY:
Low phenylalanine diet
• Protein foods contain highest levels of amino
acids so diet is very low in protein
• Lofenalac is a synthetic milk almost devoid of
phenylalanine.
• A little regular milk or breast milk is added to
supply some phenylalanine

52. PKU
NURSING INTERVENTIONS:
 Teach parents to perform regular Guthrie
Tests.
 Educate parents about diet.
 Breakfast: Lofenalac 6 oz. 1 serving puffed rice
cereal; 1 serving applesauce
 Lunch: Lofenalac, 6 oz. Orange and pear slices
 Dinner: Lofenalac, 6 oz. 1 serving mashed
potatoes; 1 serving carrots

53. PKU
EXPECTED OUTCOMES:
 Child demonstrates normal G&D
 Diet looks so deficient, unlicensed hospital
personnel may assume something is missing
and add: meat or milk
 Educate children not to trade lunches in school
 How to select lunches from school lunch menu
or take lunch.

54. PKU
 Caution that Holidays are often most difficult
times:
• Birthday cake
• Turkey
• Hotdogs on 4th of July
• Must remain on diet until past 5 years
(brain growth is 90%)
• Many advocate for always following diet.

55. PKU
 Women who intend to be pregnant must
return to diet 3 months b/4 conceiving
 Otherwise fetus grows in a high phenylalanine
environment. Cognitive impairment will occur.