Nutritional Deficiencies Flashcards
Lack of consistent access to enough food for a
household to live healthy is defined as
Food insecurity
Health outcomes when malnourished
● Poor wound healing
● Immunocompromising
● Impaired organ function
● Increased length of hospital stays
● Increased mortality
● Inflammation acute or chronic can lead to malnutrition
Sources of caloric malnutrition
● Famine and starvation
● Disease
● Surgery
● Injury
● Socioeconomic factors
steatorrhea
- increased fat in the stool
Causes of vitamin insufficiency
● Food insecurity, hunger, poverty
● Abuse and neglect
● Insufficient diets
● Behavioral
● Medical problems, absorption
Thiamin defined and its solubility
Vitamin B1
■ Also spelled thiamine
■ Water-soluble
Functions of Thiamin
– Production of energy from food (Think Krebs Cycle and the Pentose Phosphate Cycle)
– DNA synthesis
– Conduction of nerve impulses
Dietary sources of Thiamin
– Yeast
– Pork
– Beef
– Whole grains
– Organ meat
– Legumes
– Nuts
In the US, processed flour must be enriched with ______
thiamin, riboflavin, niacin, folic acid, and iron
When healthy individuals are deprived of
thiamine, thiamine stores are depleted
within ______
1 month
However, within a week after thiamine
intake stops, healthy people develop
- Anorexia
- Resting tachycardia
- Weakness
- Decreased deep tendon reflexes
- Peripheral neuropathy
Thiamin Primary deficiency
- 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
Thiamin Secondary deficiency
Increased demand
– Hyperthyroidism, pregnancy, lactation, strenuous exercise, fever
Impaired absorption
– Prolonged diarrhea, bariatric surgery
Medications
- eg. diuretics and ↑ urine excretion
Impaired metabolism
– Hepatic insufficiency
Alcoholics & Thiamin
Multiple mechanisms- Low intake, and lower absorption
Dry beriberi
- 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
Wernicke-Korsakoff Syndrome
– Occurs in alcoholics who do not consume food
fortified with thiamin. Can occur in
nonalcoholics. Combination of two syndromes
– Often underrecognized
Wernickeʼs encephalopathy
Triad of: Confusion, ataxia, nystagmus
■ Psychomotor slowing, nystagmus, ataxia,
ophthalmoplegia, impaired consciousness
Korsakoffʼs Syndrome
■ Mental confusion, dysphonia, confabulation
■ Impaired memory of recent events
■ If left untreated, coma and death ensue
Wet beriberi
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
Infantile beriberi
– Usually occurs by age 3-4 weeks
– Babies who are breastfed by
thiamin-deficient mothers
– Heart failure (sudden)
– Aphonia
– Absent deep tendon reflexes
Thiamin Diagnosis
– Usually based on response to treatment with
thiamin
■ Labs
– B vitamins
– Erythrocyte transketolase activity
– 24-h urinary thiamine excretion
– CMP
Treatment for Dry beriberi
Oral thiamin
Treatment for Wet beriberi
IV Thiamin
Treatment for Wernicke-Korsakoff syndrome
IM or IV Thiamin followed
by oral thiamin
Riboflavin and its solubility
■ Vitamin B2
■ Water-soluble
Riboflavin functions
– Convert carbohydrates into glucose
– Neutralize free radicals
– Convert vitamins B6 and B9 into active forms
Riboflavin dietary sources
– Milk and dairy
– Cheese
– Eggs
Riboflavin primary deficiency
– Inadequate intake
Riboflavin Secondary deficiency
– Chronic diarrhea
– Liver disorders
– Hemodialysis
– Peritoneal dialysis
– Long-term barbiturates
– Chronic alcoholism
Riboflavin deficiency clinical manifestations
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
Riboflavin diagnosis
– Characteristic signs and
other B vitamin deficiencies
– B vitamins
– Urinary excretion of riboflavin
Niacin and solubility
■ Vitamin B3
■ Water-soluble
Niacin Functions
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)
Niacin effects for cholesterol
– Supplements in high doses
– Lowers LDL
– Lowers triglyceride levels
– Increases HDL
Side effects of niacin supplementation
■ Flushing
■ Hepatotoxicity
■ Atherosclerosis?
■ Possible relationship to hardening of
arteries
– Increases levels of homocysteine
Niacin dietary sources
– Meat
– Red fish
– Poultry
– Milk
– Yeast
Niacin primary deficiency
– 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
Niacin Secondary deficiency
– Alcoholism
– Cirrhosis
– Diarrhea
– Carcinoid syndrome
– Hartnup Disease
Niacin mild deficiency symptoms
– Loss of appetite
– Weakness/ Fatigue
– Irritability
– Depression
– Indigestion
– Burning sensation in the mouth
– GI symptoms
Niacin - Pellagra
Severe deficiency
The 4 Dʼs
1. Diarrhea
2. Dermatitis
3. Dementia
4. Death
Pellagra skin effects
● Bilateral, symmetric lesions
● Pressure points of sun-exposed skin
● Pellagrous glove
● Pellagrous boots
● Sunlight may cause butterfly-shaped lesions on the face
Niacin deficiency diagnosis
– May be straightforward if dermatitis,
diarrhea, and dementia occur
simultaneously
– Presentation often not very specific
■ Labs
– B vitamins
– Urinary excretion
Niacin deficiency treatment
– Often occurs with other B vitamin deficiencies
– Balanced diet
– Nicotinamide
■ 100- 200 mg/day PO divided doses 3 times per day
Vitamin A
Group of fat soluble retinoids
● Retinol
Provitamin A carotenoids (metabolized to Vit A)
● Beta-carotene
90% of vitamin __ stored in the liver
A
Vitamin A functions
● Night vision- Rod cells of the retina
● Proper development of the embryo in the womb
● Epithelial Cellular Integrity
Vitamin A dietary sources
– Yellow
– Red
– Green
– Carrots
– Spinach
– Tomatoes
– Peppers
– Cooking enhances uptake
– Apricots
– Liver, eggs
Vitamin A primary deficiency
● Prolonged dietary
deprivation
● Southern and eastern Asia
● Xerophthalmia
Xerophthalmia
○ Common cause of
blindness among
young children in
developing countries
○ Pathognomonic
○ Vitamin A deficiency in
breastfeeding
mothers
Vitamin A secondary deficiency
● 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
Vitamin A Clinical Manifestations
Xerophthalmia
– Night Blindness
– Bitotʼs spots
Superficial foamy patches
– Keratomalacia
Cornea becomes hazy, erosions
Vitamin A diagnosis & Labs
● 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
Vitamin A Deficiency prevention
– Diet
– Carotenoids are absorbed better when
consumed with some dietary fat
– In developing countries vitamin A is
advised for children
Vitamin A Deficiency treatment
– 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
Vitamin A Toxicity - Hypervitaminosis 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
Vitamin C and its solubility
Ascorbic acid
● Water-soluble
● 6-8% of adult in the US
Vitamin C functions
● Collagen production
● Wound healing
● Synthesize neurotransmitters
● Block damage caused by free radicals
● Plant based- Iron Absorption
Need for vitamin C increased by:
● Febrile illness
● Inflammatory disorders
● Diarrheal disorders
● Achlorhydria- lack of hydrochloric acid in gastric secretions
● Smoking
● Thyrotoxicosis
● Iron deficiency
● Cold or heat stress
● Surgery
● Burns
Scurvy
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
Scurvy diagnosis & labs
– 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
Vitamin C deficiency prevention
● Smokers should consume an additional 35
mg/day
● 5 servings of most fruits and vegetables
provide > 200 mg of vitamin C
Vitamin C deficiency treatment
● 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
Vitamin C Toxicity
Upper limit (UL) is 2000 mg/day
Vitamin D solubility
■ Fat-soluble
Vitamin D functions
– 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
Vitamin D deficiency
■ 8% of US adults
■ Inadequate exposure/intake
■ Reduced absorption
■ Obesity
■ Abnormal metabolism
■ X-linked hypophosphatemia
Vitamin D deficiency clinical manifestations
– Muscle aches
– Muscle weakness
– Bone pain at any age
Vitamin D - Rickets in infants
– Softening of entire skull
■ Older infants
– Delayed sitting, crawling, fontanel
closure
– Rachitic rosary
Vitamin D - rickets in children
■ 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)
Vitamin D - Tetany
– Caused by hypocalcemia
– May cause paresthesias of the
lips, tongue, and fingers
– Carpopedal
– Facial spasm
– If very severe → seizures
Vitamin D - Osteomalacia
– Softening of the bones
– Predisposes to fracture
Vitamin D deficiency prevention
– 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
Vitamin D Treatment
– 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.
X-linked hypophosphatemia (XLH)
Vitamin D
■ Does not respond to the doses usually
effective for rickets due to inadequate
intake → Tx was oral phosphate,
calcitriol, osteotomy
Treatment for X-linked hypophosphatemia (XLH)
■ 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
Vitamin D Supplements
Thought to be a bit of a wonder supplement with possible:
● Reduction in cancer
● Cardiovascular risk
● Depression
● Multiple Sclerosis
● Type 2 Diabetes
Vitamin D Toxicity
Upper Limit is 4,000 IU/d
Excessive Vit D causes ____
Increases in calcium (hypercalcemia)
Vitamin K solubility
Fat soluble
Vitamin K types
■ Occurs naturally in 2 forms
– K1 (phylloquinone) found in plantsGreen Leafy stuff
– K2 (menaquinones)- bacterial origin
found in the human gut, fermented
foods
Vitamin K functions
– Blood clotting (Coenzyme for Vitamin
K-dependent carboxylase)
– Maintain bone health
– Proper blood vessel function
Vitamin K dificiency in nursing infants
– 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
Vitamin K clinical manifestations
■ Easy bruising
■ Mucosal bleeding
– Epistaxis
– Menorrhagia
■ Hemorrhagic disease of
the newborn
– Cutaneous, GI,
intrathoracic, intracranial
bleeding
Vitamin K diagnosis
■ PT prolonged- Really the only clinical indicator of Vitamin K activity.
■ PTT normal
■ Platelet count normal
■ D-dimer normal
■ Fibrinogen normal
Vitamin K treatment
Phytonadione 0.5-1 mg IM
– Recommended for all neonates
within 6 h of birth
■ Phytonadione PO
■ Phytonadione IV
The most common mineral in the human
body
Calcium
More than ____% of total body calcium
stored in bones and teeth
99
Calcium functions
– Maintain healthy bones
– Mediate blood vessel function and nerve
impulse transmission
– Absorb and use other micronutrients
Hypocalcemia
■ Total serum calcium < 8.5
■ Acute, severe hypocalcemia is a
medical emergency
– Seizures
■ Most commonly occurs with
chronic renal failure and
hypoparathyroidism
Calcium clinical manifestations
– Chronic hypocalcemia may be
asymptomatic
– Muscle cramps
– Perioral and peripheral paresthesias
– Carpopedal spasm or tetany
– Confusion
– Irritability
– Spontaneous or latent tetany
Chvostekʼs sign
Calcium deficiency
Percussion of the ipsilateral facial
muscle anterior to the ear causes
facial muscle contraction
Trousseauʼs sign
Calcium deficiency
– Carpal spasm after 3 min of
occlusion with a blood pressure
cuff
– Quite uncomfortable and rarely
used in clinical practice
Treatment
Chronic hypocalcemia
– Calcitriol
– Calcium supplementation
Treatment Acute hypocalcemia
– One ampule of 10% calcium
chloride or gluconate intravenous
injections over 10-15 min OR
– Calcium chloride 10% intravenous
injection
Marasmus
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
Kwashiorkor
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
What may this child have?
Marasmus - PEM
What do these children likely have?
Kwashiorkor - Wet form PEM
Secondary PEM causes
■ 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
Marasmus clinical manifestations
■ Hunger
■ Weight loss
■ Growth retardation
■ Wasting of subcutaneous fat and
muscle
■ Ribs and facial bones appear
prominent
■ Loose, thin skin hangs in folds
Kwashiorkor clinical manifestations
● 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
Alternating episodes of under-nutrition and adequate nutrition may cause a “striped flag” appearance with
Kwashiorkor clinical manifestations
PEM diagnosis
■ 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
Protein Energy Malnutrition Treatment worldwide
– Reduce poverty
– Improve nutritional education
– Public health measures
Treatment for mild/moderate PEM
– 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
Treatment for severe PEM
– 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
