Nutritional Deficiencies Flashcards

1
Q

Lack of consistent access to enough food for a
household to live healthy is defined as

A

Food insecurity

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2
Q

Health outcomes when malnourished

A

● Poor wound healing
● Immunocompromising
● Impaired organ function
● Increased length of hospital stays
● Increased mortality
● Inflammation acute or chronic can lead to malnutrition

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3
Q

Sources of caloric malnutrition

A

● Famine and starvation
● Disease
● Surgery
● Injury
● Socioeconomic factors

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4
Q

steatorrhea

A
  • increased fat in the stool
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5
Q

Causes of vitamin insufficiency

A

● Food insecurity, hunger, poverty
● Abuse and neglect
● Insufficient diets
● Behavioral
● Medical problems, absorption

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6
Q

Thiamin defined and its solubility

A

Vitamin B1
■ Also spelled thiamine
■ Water-soluble

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7
Q

Functions of Thiamin

A

– Production of energy from food (Think Krebs Cycle and the Pentose Phosphate Cycle)
– DNA synthesis
– Conduction of nerve impulses

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8
Q

Dietary sources of Thiamin

A

– Yeast
– Pork
– Beef

– Whole grains
– Organ meat
– Legumes
– Nuts

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9
Q

In the US, processed flour must be enriched with ______

A

thiamin, riboflavin, niacin, folic acid, and iron

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10
Q

When healthy individuals are deprived of
thiamine, thiamine stores are depleted
within ______

A

1 month

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11
Q

However, within a week after thiamine
intake stops, healthy people develop

A
  • Anorexia
  • Resting tachycardia
  • Weakness
  • Decreased deep tendon reflexes
  • Peripheral neuropathy
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12
Q

Thiamin Primary deficiency

A
  • Caused by inadequate intake
  • Common due to diet of highly refined carbohydrates eg. milled rice
    and grain. Common in cultures who rely on these.
  • Occurs with mixed B vitamin deficiencies
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13
Q

Thiamin Secondary deficiency

A

Increased demand
– Hyperthyroidism, pregnancy, lactation, strenuous exercise, fever
Impaired absorption
– Prolonged diarrhea, bariatric surgery
Medications
- eg. diuretics and ↑ urine excretion
Impaired metabolism
– Hepatic insufficiency

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14
Q

Alcoholics & Thiamin

A

Multiple mechanisms- Low intake, and lower absorption

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15
Q

Dry beriberi

A
  • Neurologic Findings
    – Peripheral neurologic deficits
    – Bilateral and roughly symmetric
    – Occurs in stocking-glove distribution
    – Paresthesia in the toes, burning in the
    feet (particularly severe at
    night),muscle cramps in the calves,
    pains in the legs, and plantar
    dysesthesias
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16
Q

Wernicke-Korsakoff Syndrome

A

– Occurs in alcoholics who do not consume food
fortified with thiamin. Can occur in
nonalcoholics. Combination of two syndromes
– Often underrecognized

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17
Q

Wernickeʼs encephalopathy

A

Triad of: Confusion, ataxia, nystagmus
■ Psychomotor slowing, nystagmus, ataxia,
ophthalmoplegia, impaired consciousness

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18
Q

Korsakoffʼs Syndrome

A

■ Mental confusion, dysphonia, confabulation
■ Impaired memory of recent events
■ If left untreated, coma and death ensue

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19
Q

Wet beriberi

A

Cardiovascular Involvement, although overlaps with dry beriberi
Myocardial disease
■ Vasodilation → High Cardiac Output
■ Tachycardia
■ Wide pulse pressure
■ Sweating, warm skin
■ Lactic acidosis
Later stages
■ Heart failure
– Pulmonary and peripheral edema
■ Vasodilation → Shock

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20
Q

Infantile beriberi

A

– Usually occurs by age 3-4 weeks
– Babies who are breastfed by
thiamin-deficient mothers
– Heart failure (sudden)
– Aphonia
– Absent deep tendon reflexes

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21
Q

Thiamin Diagnosis

A

– Usually based on response to treatment with
thiamin
■ Labs
– B vitamins
– Erythrocyte transketolase activity
– 24-h urinary thiamine excretion
– CMP

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22
Q

Treatment for Dry beriberi

A

Oral thiamin

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23
Q

Treatment for Wet beriberi

A

IV Thiamin

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24
Q

Treatment for Wernicke-Korsakoff syndrome

A

IM or IV Thiamin followed
by oral thiamin

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25
Q

Riboflavin and its solubility

A

■ Vitamin B2
■ Water-soluble

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26
Q

Riboflavin functions

A

– Convert carbohydrates into glucose
– Neutralize free radicals
– Convert vitamins B6 and B9 into active forms

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27
Q

Riboflavin dietary sources

A

– Milk and dairy
– Cheese
– Eggs

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28
Q

Riboflavin primary deficiency

A

– Inadequate intake

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29
Q

Riboflavin Secondary deficiency

A

– Chronic diarrhea
– Liver disorders
– Hemodialysis
– Peritoneal dialysis
– Long-term barbiturates
– Chronic alcoholism

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30
Q

Riboflavin deficiency clinical manifestations

A

Angular stomatitis (or Cheilosis)
– Can become infected by Candida
albicans
– Causes grayish/white lesions
– Tongue may appear magenta- glossitis
– Sore throat
– Dermatitis
– Anemia and corneal vascularization
when severe

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31
Q

Riboflavin diagnosis

A

– Characteristic signs and
other B vitamin deficiencies
– B vitamins
– Urinary excretion of riboflavin

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32
Q

Niacin and solubility

A

■ Vitamin B3
■ Water-soluble

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33
Q

Niacin Functions

A

Functions mainly in active form as a coenzyme nicotinamide adenine dinucleotide (NAD) and NADP – cellular respiration
– Aids in releasing energy from carbohydrates, fats, alcohol, and proteins
– Essential for DNA synthesis and repair
– Necessary for healthy skin, nerves, and digestive system
– Production of steroid hormones in the adrenal glands- (Role of NADP)

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34
Q

Niacin effects for cholesterol

A

– Supplements in high doses
– Lowers LDL
– Lowers triglyceride levels
– Increases HDL

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35
Q

Side effects of niacin supplementation

A

■ Flushing
■ Hepatotoxicity
■ Atherosclerosis?
■ Possible relationship to hardening of
arteries
– Increases levels of homocysteine

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36
Q

Niacin dietary sources

A

– Meat
– Red fish
– Poultry
– Milk
– Yeast

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37
Q

Niacin primary deficiency

A

– Inadequate intake of niacin
and tryptophan
– Occurs in areas where corn is
the primary dietary staple

Deficiency
– Rare in the US
– more in Developing countries

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38
Q

Niacin Secondary deficiency

A

– Alcoholism
– Cirrhosis
– Diarrhea
– Carcinoid syndrome
– Hartnup Disease

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39
Q

Niacin mild deficiency symptoms

A

– Loss of appetite
– Weakness/ Fatigue
– Irritability
– Depression
– Indigestion
– Burning sensation in the mouth
– GI symptoms

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40
Q

Niacin - Pellagra

A

Severe deficiency
The 4 Dʼs
1. Diarrhea
2. Dermatitis
3. Dementia
4. Death

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41
Q

Pellagra skin effects

A

● Bilateral, symmetric lesions
● Pressure points of sun-exposed skin
● Pellagrous glove
● Pellagrous boots
● Sunlight may cause butterfly-shaped lesions on the face

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42
Q

Niacin deficiency diagnosis

A

– May be straightforward if dermatitis,
diarrhea, and dementia occur
simultaneously
– Presentation often not very specific
■ Labs
– B vitamins
– Urinary excretion

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43
Q

Niacin deficiency treatment

A

– Often occurs with other B vitamin deficiencies
– Balanced diet
– Nicotinamide
■ 100- 200 mg/day PO divided doses 3 times per day

44
Q

Vitamin A

A

Group of fat soluble retinoids
● Retinol
Provitamin A carotenoids (metabolized to Vit A)
● Beta-carotene

45
Q

90% of vitamin __ stored in the liver

A

A

46
Q

Vitamin A functions

A

● Night vision- Rod cells of the retina
● Proper development of the embryo in the womb
● Epithelial Cellular Integrity

47
Q

Vitamin A dietary sources

A

– Yellow
– Red
– Green

– Carrots
– Spinach
– Tomatoes
– Peppers
– Cooking enhances uptake
– Apricots
– Liver, eggs

48
Q

Vitamin A primary deficiency

A

● Prolonged dietary
deprivation
● Southern and eastern Asia
● Xerophthalmia

49
Q

Xerophthalmia

A

○ Common cause of
blindness among
young children in
developing countries
○ Pathognomonic
○ Vitamin A deficiency in
breastfeeding
mothers

50
Q

Vitamin A secondary deficiency

A

● Decreased bioavailability
● Interference with absorption
○ Sprue, giardiasis, duodenal
bypass, chronic diarrhea,
○ Cystic fibrosis- 2nd to
pancreatic insufficiency
● Pro-longed protein malnutrition
○ Storage and transport
defective

51
Q

Vitamin A Clinical Manifestations

A

Xerophthalmia
– Night Blindness
– Bitotʼs spots
Superficial foamy patches
– Keratomalacia
Cornea becomes hazy, erosions

52
Q

Vitamin A diagnosis & Labs

A

● Suggested by ocular findings
● Impaired dark adaptation
Labs
● Vitamin A level (serum retinol)
○ Only decreases if deficiency is
advanced
○ Liver contains large stores
○ Can get falsely low numbers
during inflammatory states

53
Q

Vitamin A Deficiency prevention

A

– Diet
– Carotenoids are absorbed better when
consumed with some dietary fat
– In developing countries vitamin A is
advised for children

54
Q

Vitamin A Deficiency treatment

A

– Vitamin A supplements
– Prolonged daily administration of large
doses must be avoided
– For pregnant or lactating women,
prophylactic or therapeutic doses
should not exceed 10,000 IU/day

55
Q

Vitamin A Toxicity - Hypervitaminosis A

A

Acute (> 150 mg x 1 dose)
○ Nausea and vomiting
○ Vertigo and seziures
○ Confusion, headaches, coma, death
Chronic Adult (> 15 mg/day for months)
○ Changes in skin, hair, nails
(beta-carotene)
○ Alopecia, seborrhea, cheilosis,
peeling palms & soles
○ Abnormal ALT, AST

56
Q

Vitamin C and its solubility

A

Ascorbic acid
● Water-soluble
● 6-8% of adult in the US

57
Q

Vitamin C functions

A

● Collagen production
● Wound healing
● Synthesize neurotransmitters
● Block damage caused by free radicals
● Plant based- Iron Absorption

58
Q

Need for vitamin C increased by:

A

● Febrile illness
● Inflammatory disorders
● Diarrheal disorders
● Achlorhydria- lack of hydrochloric acid in gastric secretions
● Smoking
● Thyrotoxicosis
● Iron deficiency
● Cold or heat stress
● Surgery
● Burns

59
Q

Scurvy

A

Vitamin C disorder
■ Early stages: Weakness, irritability, malaise,
weight loss, myalgias, arthralgias,
■ Later stages: Follicular hyperkeratosis,
perifollicular hemorrhages
– Gums may become swollen,
purple, spongy, and friable
– Teeth become loose and avulsed
– Wounds heal poorly and tear
easily; spontaneous hemorrhages
may occur

60
Q

Scurvy diagnosis & labs

A

– Usually made clinically in patients
with skin and/or gum disease
Labs
– CBC→ Anemia common
– Coag studies and bleeding times
normal
Imaging
– Altered bone formation→ defect in
spongiosa of metaphysis at growth
plate
– “Ground-glass” osteopenia
– Line of Frankel

61
Q

Vitamin C deficiency prevention

A

● Smokers should consume an additional 35
mg/day
● 5 servings of most fruits and vegetables
provide > 200 mg of vitamin C

62
Q

Vitamin C deficiency treatment

A

● Ascorbic acid 100-500 mg PO TID is given for 1-2 weeks until signs disappear and followed by a nutritious diet supplying 1-2 x the recommended dose
● Symptoms and signs usually disappear over 1-2 weeks
● Chronic gingivitis with extensive
subcutaneous hemorrhage persists longer

63
Q

Vitamin C Toxicity

A

Upper limit (UL) is 2000 mg/day

64
Q

Vitamin D solubility

A

■ Fat-soluble

65
Q

Vitamin D functions

A

– Maintain healthy blood levels of calcium
and phosphorus, increase calcium
absorption in the GI tract.
– Bone growth and remodeling
– Used with calcium supp. in adults
(Prevent and improve Osteoporosis)
– Control cell division and specialization
– Modulate the immune system
– Inhibits parathyroid hormone secretion

66
Q

Vitamin D deficiency

A

■ 8% of US adults
■ Inadequate exposure/intake
■ Reduced absorption
■ Obesity
■ Abnormal metabolism
■ X-linked hypophosphatemia

67
Q

Vitamin D deficiency clinical manifestations

A

– Muscle aches
– Muscle weakness
– Bone pain at any age

68
Q

Vitamin D - Rickets in infants

A

– Softening of entire skull
■ Older infants
– Delayed sitting, crawling, fontanel
closure
– Rachitic rosary

69
Q

Vitamin D - rickets in children

A

■ Children 1-4 years
– Epiphyseal cartilage at the lower ends of
the radius, ulna, tibia, fibula enlarge
– Kyphoscoliosis, delayed walking
■ Older children/adolescents
– Walking painful
– Deformities (genu varum- younger, genu
valgum- older children)

70
Q

Vitamin D - Tetany

A

– Caused by hypocalcemia
– May cause paresthesias of the
lips, tongue, and fingers
– Carpopedal
– Facial spasm
– If very severe → seizures

71
Q

Vitamin D - Osteomalacia

A

– Softening of the bones
– Predisposes to fracture

72
Q

Vitamin D deficiency prevention

A

– 5-15 min to arms and legs or face,
arms, and hands at least 3 times/week is recommended
– Recommends that healthy older adults consume 600- 800 IU/day

73
Q

Vitamin D Treatment

A

– As long as Ca and P intake is
adequate, adults with osteomalacia
and children with uncomplicated
rickets can be cured by giving vitamin
D - Dosed to appropriate age.

74
Q

X-linked hypophosphatemia (XLH)

A

Vitamin D
■ Does not respond to the doses usually
effective for rickets due to inadequate
intake → Tx was oral phosphate,
calcitriol, osteotomy

75
Q

Treatment for X-linked hypophosphatemia (XLH)

A

■ New Drug -Burosumab (Crysvita) 2018
- FGF23 production is increased in XLH,
and this causes inhibition of renal
phosphate reabsorption.
- Burosumab is a Anti-FGF23
Monoclonal Antibody

76
Q

Vitamin D Supplements
Thought to be a bit of a wonder supplement with possible:

A

● Reduction in cancer
● Cardiovascular risk
● Depression
● Multiple Sclerosis
● Type 2 Diabetes

77
Q

Vitamin D Toxicity

A

Upper Limit is 4,000 IU/d

78
Q

Excessive Vit D causes ____

A

Increases in calcium (hypercalcemia)

79
Q

Vitamin K solubility

A

Fat soluble

80
Q

Vitamin K types

A

■ Occurs naturally in 2 forms
– K1 (phylloquinone) found in plantsGreen Leafy stuff
– K2 (menaquinones)- bacterial origin
found in the human gut, fermented
foods

81
Q

Vitamin K functions

A

– Blood clotting (Coenzyme for Vitamin
K-dependent carboxylase)
– Maintain bone health
– Proper blood vessel function

82
Q

Vitamin K dificiency in nursing infants

A

– Placenta transmits lipids and vitamin K
relatively poorly
– Neonatal liver is immature with respect to
prothrombin synthesis
– Breast milk is low in vitamin K, containing
about 2.5 micrograms/liter (cowʼs milk
contains 5000 micrograms/liter)
– Poor fat stores

83
Q

Vitamin K clinical manifestations

A

■ Easy bruising
■ Mucosal bleeding
– Epistaxis
– Menorrhagia
■ Hemorrhagic disease of
the newborn
– Cutaneous, GI,
intrathoracic, intracranial
bleeding

84
Q

Vitamin K diagnosis

A

■ PT prolonged- Really the only clinical indicator of Vitamin K activity.
■ PTT normal
■ Platelet count normal
■ D-dimer normal
■ Fibrinogen normal

85
Q

Vitamin K treatment

A

Phytonadione 0.5-1 mg IM
– Recommended for all neonates
within 6 h of birth
■ Phytonadione PO
■ Phytonadione IV

86
Q

The most common mineral in the human
body

A

Calcium

87
Q

More than ____% of total body calcium
stored in bones and teeth

A

99

88
Q

Calcium functions

A

– Maintain healthy bones
– Mediate blood vessel function and nerve
impulse transmission
– Absorb and use other micronutrients

89
Q

Hypocalcemia

A

■ Total serum calcium < 8.5
■ Acute, severe hypocalcemia is a
medical emergency
– Seizures
■ Most commonly occurs with
chronic renal failure and
hypoparathyroidism

90
Q

Calcium clinical manifestations

A

– Chronic hypocalcemia may be
asymptomatic
– Muscle cramps
– Perioral and peripheral paresthesias
– Carpopedal spasm or tetany
– Confusion
– Irritability
– Spontaneous or latent tetany

91
Q

Chvostekʼs sign

A

Calcium deficiency
Percussion of the ipsilateral facial
muscle anterior to the ear causes
facial muscle contraction

92
Q

Trousseauʼs sign

A

Calcium deficiency
– Carpal spasm after 3 min of
occlusion with a blood pressure
cuff
– Quite uncomfortable and rarely
used in clinical practice

93
Q

Treatment
Chronic hypocalcemia

A

– Calcitriol
– Calcium supplementation

94
Q

Treatment Acute hypocalcemia

A

– One ampule of 10% calcium
chloride or gluconate intravenous
injections over 10-15 min OR
– Calcium chloride 10% intravenous
injection

95
Q

Marasmus

A

Protein Energy Malnutrition
■ Dry form of PEM
■ Weight loss and depletion of
fat and muscle
■ Most common form of PEM in
children in developing
countries

96
Q

Kwashiorkor

A

Protein Energy Malnutrition
■ Wet form of PEM
– Cell membranes leak, causing extravasation of
intravascular fluid and protein resulting in peripheral
edema
■ Associated with premature abandonment of
breastfeeding
■ Acute GI illness in a child who already has PEU
■ Less common
■ Rural Africa, Caribbean, and Pacific islands
■ Staple foods (e.g., yams cassavas, sweet potatoes,
green bananas) are low in protein and high in
carbohydrates

97
Q

What may this child have?

A

Marasmus - PEM

98
Q

What do these children likely have?

A

Kwashiorkor - Wet form PEM

99
Q

Secondary PEM causes

A

■ Disorders that affect GI function: Interfere with digestion, absorption, lymphatic
transport
■ Wasting disorders: AIDS, cancer, end-stage heart failure
■ Conditions that increase metabolic demands
– Infection
– Hyperthyroidism
– Burns

100
Q

Marasmus clinical manifestations

A

■ Hunger
■ Weight loss
■ Growth retardation
■ Wasting of subcutaneous fat and
muscle
■ Ribs and facial bones appear
prominent
■ Loose, thin skin hangs in folds

101
Q

Kwashiorkor clinical manifestations

A

● Peripheral and periorbital edema
● Abdomen protrudes because abdominal muscles are weakened,
intestine is distended, liver enlarges, ascites
● Skin
- Dry, thin, wrinkled
- Hyperpigmented and fissured; later hypopigmented, friable,
atrophic
● Hair
- Thin, reddish brown or gray
- Scalp hair falls out easily, becomes sparse

102
Q

Alternating episodes of under-nutrition and adequate nutrition may cause a “striped flag” appearance with

A

Kwashiorkor clinical manifestations

103
Q

PEM diagnosis

A

■ Based on history
■ To determine severity
– BMI, plasma albumin, total lymphocyte count, CD4+ count, serum
transferrin
■ To diagnose complications
– CBC, electrolytes, BUN, glucose, Ca, Mg, phosphate

104
Q

Protein Energy Malnutrition Treatment worldwide

A

– Reduce poverty
– Improve nutritional education
– Public health measures

105
Q

Treatment for mild/moderate PEM

A

– Balanced diet, preferably orally
– Liquid oral food supplements can be used when
solid food cannot be adequately ingested
– Diarrhea often complicates oral feeding
– If persistent (suggesting lactose intolerance)
yogurt-based rather than milk-based formulas are
given
– Multivitamin supplements

106
Q

Treatment for severe PEM

A

– Controlled diet in hospital
– First priority is to correct fluid and electrolyte
abnormalities and treat infections
– Next priority is to supply macronutrients orally
or, if necessary (e.g., when swallowing is
difficult), through a feeding tube, an NG tube or
a gastrostomy (G) tube
– Parenteral nutrition is indicated if malabsorption
is severe
– Pt should take micronutrients at about twice
RDA until recovery is complete