Nutritional Deficiencies Flashcards

(106 cards)

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
Riboflavin and its solubility
■ Vitamin B2 ■ Water-soluble
26
Riboflavin functions
– Convert carbohydrates into glucose – Neutralize free radicals – Convert vitamins B6 and B9 into active forms
27
Riboflavin dietary sources
– Milk and dairy – Cheese – Eggs
28
Riboflavin primary deficiency
– Inadequate intake
29
Riboflavin Secondary deficiency
– Chronic diarrhea – Liver disorders – Hemodialysis – Peritoneal dialysis – Long-term barbiturates – Chronic alcoholism
30
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
31
Riboflavin diagnosis
– Characteristic signs and other B vitamin deficiencies – B vitamins – Urinary excretion of riboflavin
32
Niacin and solubility
■ Vitamin B3 ■ Water-soluble
33
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)
34
Niacin effects for cholesterol
– Supplements in high doses – Lowers LDL – Lowers triglyceride levels – Increases HDL
35
Side effects of niacin supplementation
■ Flushing ■ Hepatotoxicity ■ Atherosclerosis? ■ Possible relationship to hardening of arteries – Increases levels of homocysteine
36
Niacin dietary sources
– Meat – Red fish – Poultry – Milk – Yeast
37
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
38
Niacin Secondary deficiency
– Alcoholism – Cirrhosis – Diarrhea – Carcinoid syndrome – Hartnup Disease
39
Niacin mild deficiency symptoms
– Loss of appetite – Weakness/ Fatigue – Irritability – Depression – Indigestion – Burning sensation in the mouth – GI symptoms
40
Niacin - Pellagra
Severe deficiency The 4 Dʼs 1. Diarrhea 2. Dermatitis 3. Dementia 4. Death
41
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
42
Niacin deficiency diagnosis
– May be straightforward if dermatitis, diarrhea, and dementia occur simultaneously – Presentation often not very specific ■ Labs – B vitamins – Urinary excretion
43
Niacin deficiency treatment
– Often occurs with other B vitamin deficiencies – Balanced diet – Nicotinamide ■ 100- 200 mg/day PO divided doses 3 times per day
44
Vitamin A
Group of fat soluble retinoids ● Retinol Provitamin A carotenoids (metabolized to Vit A) ● Beta-carotene
45
90% of vitamin __ stored in the liver
A
46
Vitamin A functions
● Night vision- Rod cells of the retina ● Proper development of the embryo in the womb ● Epithelial Cellular Integrity
47
Vitamin A dietary sources
– Yellow – Red – Green – Carrots – Spinach – Tomatoes – Peppers – Cooking enhances uptake – Apricots – Liver, eggs
48
Vitamin A primary deficiency
● Prolonged dietary deprivation ● Southern and eastern Asia ● Xerophthalmia
49
Xerophthalmia
○ Common cause of blindness among young children in developing countries ○ Pathognomonic ○ Vitamin A deficiency in breastfeeding mothers
50
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
51
Vitamin A Clinical Manifestations
Xerophthalmia – Night Blindness – Bitotʼs spots Superficial foamy patches – Keratomalacia Cornea becomes hazy, erosions
52
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
53
Vitamin A Deficiency prevention
– Diet – Carotenoids are absorbed better when consumed with some dietary fat – In developing countries vitamin A is advised for children
54
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
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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
56
Vitamin C and its solubility
Ascorbic acid ● Water-soluble ● 6-8% of adult in the US
57
Vitamin C functions
● Collagen production ● Wound healing ● Synthesize neurotransmitters ● Block damage caused by free radicals ● Plant based- Iron Absorption
58
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
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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
60
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
61
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
62
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
63
Vitamin C Toxicity
Upper limit (UL) is 2000 mg/day
64
Vitamin D solubility
■ Fat-soluble
65
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
66
Vitamin D deficiency
■ 8% of US adults ■ Inadequate exposure/intake ■ Reduced absorption ■ Obesity ■ Abnormal metabolism ■ X-linked hypophosphatemia
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Vitamin D deficiency clinical manifestations
– Muscle aches – Muscle weakness – Bone pain at any age
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Vitamin D - Rickets in infants
– Softening of entire skull ■ Older infants – Delayed sitting, crawling, fontanel closure – Rachitic rosary
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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)
70
Vitamin D - Tetany
– Caused by hypocalcemia – May cause paresthesias of the lips, tongue, and fingers – Carpopedal – Facial spasm – If very severe → seizures
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Vitamin D - Osteomalacia
– Softening of the bones – Predisposes to fracture
72
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
73
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.
74
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
75
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
76
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
77
Vitamin D Toxicity
Upper Limit is 4,000 IU/d
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Excessive Vit D causes ____
Increases in calcium (hypercalcemia)
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Vitamin K solubility
Fat soluble
80
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
81
Vitamin K functions
– Blood clotting (Coenzyme for Vitamin K-dependent carboxylase) – Maintain bone health – Proper blood vessel function
82
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
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Vitamin K clinical manifestations
■ Easy bruising ■ Mucosal bleeding – Epistaxis – Menorrhagia ■ Hemorrhagic disease of the newborn – Cutaneous, GI, intrathoracic, intracranial bleeding
84
Vitamin K diagnosis
■ PT prolonged- Really the only clinical indicator of Vitamin K activity. ■ PTT normal ■ Platelet count normal ■ D-dimer normal ■ Fibrinogen normal
85
Vitamin K treatment
Phytonadione 0.5-1 mg IM – Recommended for all neonates within 6 h of birth ■ Phytonadione PO ■ Phytonadione IV
86
The most common mineral in the human body
Calcium
87
More than ____% of total body calcium stored in bones and teeth
99
88
Calcium functions
– Maintain healthy bones – Mediate blood vessel function and nerve impulse transmission – Absorb and use other micronutrients
89
Hypocalcemia
■ Total serum calcium < 8.5 ■ Acute, severe hypocalcemia is a medical emergency – Seizures ■ Most commonly occurs with chronic renal failure and hypoparathyroidism
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Calcium clinical manifestations
– Chronic hypocalcemia may be asymptomatic – Muscle cramps – Perioral and peripheral paresthesias – Carpopedal spasm or tetany – Confusion – Irritability – Spontaneous or latent tetany
91
Chvostekʼs sign
Calcium deficiency Percussion of the ipsilateral facial muscle anterior to the ear causes facial muscle contraction
92
Trousseauʼs sign
Calcium deficiency – Carpal spasm after 3 min of occlusion with a blood pressure cuff – Quite uncomfortable and rarely used in clinical practice
93
Treatment Chronic hypocalcemia
– Calcitriol – Calcium supplementation
94
Treatment Acute hypocalcemia
– One ampule of 10% calcium chloride or gluconate intravenous injections over 10-15 min OR – Calcium chloride 10% intravenous injection
95
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
96
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
97
What may this child have?
Marasmus - PEM
98
What do these children likely have?
Kwashiorkor - Wet form PEM
99
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
100
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
101
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
102
Alternating episodes of under-nutrition and adequate nutrition may cause a “striped flag” appearance with
Kwashiorkor clinical manifestations
103
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
104
Protein Energy Malnutrition Treatment worldwide
– Reduce poverty – Improve nutritional education – Public health measures
105
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
106
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