Lecture 34 Flashcards
Minerals
1
Q
minerals
A
- macrominerals: Ca, P, Mg, Na, K, Cl, S
- microminerals: Fe, Zn, Cu, Se, Cr, I, Mn, Mo, F
- ultra trace minerals: As, B, Ni, Si, V, Co
- non-nutrient: Pb
pg 839
2
Q
mineral overview
A
- mineral balance tightly regulated -> GI tract does absorption from food based on needs, kidneys excrete excess or reabsorbs
- not destroyed by heat, acid, oxygen, or UV
- can leach into cooking water
- fluid/electrolyte and acid/base balance -> extracellular/intracellular
- bone and teeth formation
- cofactors in: antioxidant systems, energy production, muscle contraction, nerve transmission
- mineral deficiency and toxicity is rare
pg 842
3
Q
sodium and chloride
A
maintains water balance, osmotic equilibrium, acid-base balance and membrane potential (electrical gradient)
- primary extracellular electrolytes
- absorption of glucose, galactose and free AAs by Na+-linked transporters
- Cl- for HCl in stomach
- hypertension: where sodium goes, water follows; stimulates ADH (vasopressin) by pituitary -> increases water retention, blood volume, and vasoconstriction
- hyper- and hyponatremia: excess water loss (hyper) or decreased aability to excrete water (hypo)
pg 844
4
Q
sodium
A
- high sodium intake correlates with HTN, heart disease, and stroke
- DASH eating pattern aims to reduce sodium and increase potassium intakes
- higher Na intake is associated with higher Ca excretion
- sodium deficiency: muscle cramps, mental apathy, loss of appetite; hyponatremia during ultra-endurance athletic activities
- sodium - excessive intakes: edema and acute HTN, prolonged high intake associated with HTN
- processed foods and added table salts are primary sources
pg 844
5
Q
potassium
A
- nutrient of public health concern -> especially for people on dialysis
- major intracellular cation (intracellular electrolyte)
- concentration differential maintained by Na+/K+ ATPase
- narrow range of normal serum K+ (hyper- or hypokalemia can result in cardiac arrythmias and skeletal muscle weakness)
- thiazide and loop diuretics cause K loss
- K helps lower HTN -> causes kidneys to excrete excess Na
- helps buffer blood and preserve Ca and P in the bones
- increased risk of HTN, kidney stones, and loss of bone mass with moderately low dietary intake
- deficiency/excess: muscle weakness, lethargy, paralysis, cardiac arrhythmias
- rich sources: meat, milk, fruits, veggies, grains, legumes
pg 846
6
Q
calcium
A
- nutrient of public health concern
- ~98% of bone as hydroxyapaptite
- involved in: signaling, muscle contraction, blood clotting
- binds to and alters enzyme activity: calmodulin, phospholipase A2 and protein kinase C
- sources: dairy products, fortified foods (juices, cereals, some mineral waters), beet greens, bok choy, broccoli, kale
pg 848
7
Q
phosphorus
A
- important for people on dialysis
- ~85% in bone as hydroxyapatite (crystal form)
- intracellular organic compounds: phospholipids, nucleic acids, ATP, and creatine phosphate
- as ATP, transferred to kinase and as Pi to phosphorylase -> removal or addition of phosphorus regulate the enzyme activity
- sources: animal foods, protein, peas, phosphate additives
pg 848
8
Q
calcium regulation
A
- dietary deficiency does not change blood calcium -> it reduces bone calcium
- allows for homeostasis of serum levels
pg 849
9
Q
hypercalcemia
A
- over production of PTH (hyperparathyroidism)
- malignancy
- causes constipation and kidney stones
- treatment: limit calcium intake
pg 850
10
Q
hypocalcemia
A
- deficiency of PTH (hypoparathyroidism)
- hypocalcemic tetany
- vitamin D deficiency
- chronic low intake of calcium
- treatment: vit D and Ca supplements or foods high in both
pg 850
11
Q
hyperphosphatemia
A
- decreased PTH levels
- renal failure
- excess free phosphorus can combine with Ca2+ and form crystals -> deposit in soft tissue
- problem for dialysis patients
- treatment: limit P intake, P binders
pg 850
12
Q
hypophosphatemia
A
- hereditary (hereditary hypophosphatemia rickets -> early childhood)
- overuse of aluminum-containing antacids
- overuse of phosphate binders
- treatment: P supplements or foods high in P (processed foods), active vitamin D
pg 850
13
Q
calcium and phosphate
A
Ca2+/Pi ratio important for bone formation -> needs to be roughly 2/1
pg 850
14
Q
epidemiology - Rickets
A
- not a reportable disease in the USA (but still seen)
- nutritional rickets is the main type reported outside the US, followed by vitamin D-dependent, vitamin D-resistant, and renal rickets
- CDC says there are 5 cases per million children aged 6 mths to 5 yrs of age
- most affected children are African American
pg 851
15
Q
magnesium
A
- deficiencies are rare: weakness, confusion, convulsions, bizarre muscle movements of eye and face, hallucinations, difficulty swallowing, growth failure in children
- alcohol abuse, protein malnutrition, kidney disorders, prolonged vomiting and diarrhea
- insufficient Mg intake associated with T2D
- Mg protects against heart disease and HTN -> low magnesium restricts walls of arteries and capillaries
- Mg toxicity: symptoms from nonfood Mg are diarrhea, alkalosis, and dehydration
- sources: nuts, legumes, whole grains, dark green veggies, seafood, chocolate, cocoa
- too much magnesium from supplements can stop the heart (lead to cardiac arrest)
pg 853
16
Q
iron
A
- nutrient of public health concern
- hemoglobin, myoglobin
- component of catalytic (hydroxylase) and noncatalytic (ETC carrier proteins and heme prosthetic group) reactions
- free ion can be toxic because of ROS production
- iron is absorbed in Fe2+ form and stored (bound to ferritin) or transported (bound to transferrin) in Fe3+
- ferritin in healthy individuals is about 1/3 saturated
- ferroportin is regulated by hepatic peptide, hepcidin -> induces internalization and lysosomal degradation of ferroportin
- hepcidin expression is suppressed during Fe deficiency
pg 855
17
Q
iron absorption enhancers and inhibitors
A
Absorption-Enhancing Factors
- MFP factor enhances the absorption of non-heme iron
- when non-heme iron is consumed with vitamin C, absorption of iron increases
- citric acid and lactic acid from foods, HCl from the stomach, and sugars enhance non-heme iron absorption
Absorption-Inhibiting Factors
- phytates and fibers from legumes, grains, rice
- veggie proteins in soybeans, legumes, nuts
- calcium in milk
- tannic acid and other polyphenols in tea, coffee, grains, oregano, red wine
MFP factor unidentified component of meat, fish, and poultry that enhances the absorption of non-heme iron present in other foods eaten at the same time
pg 856
18
Q
sources of iron
A
- red meats, fish, poultry, shellfish
- eggs
- legumes
- enriched/fortified breads and cereals
- broccoli, parsley
pg 856
19
Q
iron deficiency and overload
A
- recycled iron meets 90% of body needs
- Fe deficiency: microcytic anemia -> decreased Hb synthesis, decreased RBC size
- Fe overload: hereditary hemochromatosis -> mutation of high iron (HFE) gene -> damage to the liver, pancreas and heart; hyperpigmentation with hyperglycemia (bronze diabetes); mutations to the proteins of Fe metabolism (lower levels of hepsidin)
pg 857
20
Q
iron deficiency anemia
A
- women, preterm infants, toddlers at higher risk -> children can develop irreversible intellectual impairment
- trauma (sudden large blood loss)
- symptoms: fatigue, pallor (pale), irritability, SOB, sore tongue, brittle nails, pica (craving non-food substances), frontal headache, blue tinge to whites of eyes, decreased appetite
- treatment: Fe supplements, take with orange juice or vitamin C source, avoid taking with milk or antacids
pg 858
21
Q
copper
A
- important for ferroxidases such as ceruloplasmin and hephaestin (several enzymes require copper)
- major food sources: legumes, whole grains, and seafood
pg 860
22
Q
Menkes disease
A
- X-linked, ATP7A gene, kinky hair disease
- efflux of dietary copper from enterocytes into portal circulation by copper transporting ATPase (ATPaseA) is impaired -> systemic copper deficiency
- progressive neurological degeneration and CT disorders
- urinary and serum free and ceruloplasmin bound copper are low
- treatment: subQ injections of Cu solution, treatment w/in 28 days of birth, low body temp (hypothermia) in newborn period, prolonged yellowing of skin in newborn
- considered a lethal condition
pg 861
23
Q
Wilson disease
A
- ATP7B gene, have at birth
- efflux of excess copper from liver by ATPaseB is impaired -> accumulates in liver, leaks into blood, deposited into brain, eyes, kidney and skin, hepatic dysfunction
- free copper is high in serum and urine
- symptoms: failure to thrive, menstrual period irregularities, increased risk of miscarriage and infertility, anemia, easy bruising and prolonged bleeding, kidney stones, early-onset arthritis, osteoporosis, mental health symptoms
- also, Kaiser-Fleischer rings (corneal deposits of copper)
- treatment: diet low in Cu, Cu chelators
pg 862
24
Q
iodine
A
- for synthesis of thyroid hormones, triiodothyronine (T3) and thyroxine (T4)
- thyroperoxidase does three things -> oxidation, iodination, and coupling to synthesize T3 or T4
- 90% of the secreted thyroid hormone is T4
- sources: iodized salt, seafood, seaweed, bread and dairy products -> plants grown in iodine-rich soils, animals that feed on plants grown in iodine-rich soils
- function: in target tissue (liver and developing brain) -> T4 converted to T3 by Se-containing deiodinases -> T3 binds to nuclear receptor -> binds to the thyroid response element in DNA
pg 864
25
Q
hypothyroidism
A
- under ingestion of iodine -> excessive stimulation of TSH
- fatigue, weight gain, decreased thermogenesis, and decreased metabolic rate
- congenital hypothyroidism: irreversible intellectual disability, short stature
- Hashimoto’s Thyroiditis: autoimmune destruction of thyroid peroxidase
- low salt diets
- goitrogen (glucosinolates in cabbage) overconsumption
pg 865
26
Q
hyperthyroidism
A
- overproduction of thyroid hormone
- Graves Disease: an antibody mimicking effects of TSH -> dysregulation of thyroid hormone production
- treatment: radioiodine therapy, antithyroid drugs, prednisone for eyes
pg 865
27
Q
zinc
A
- sources: shellfish, meats, poultry, milk, cheese, whole grains, legumes
- deficiency: may occur in pregnant women, young children, the elderly; GROWTH retardation; delayed sexual maturation; impaired immune function; hair loss, eye and skin lesions; altered taste, loss of appetite, and delayed wound healing
- toxicity: loss of appetite, impaired immunity, low HDL, copper and iron deficiencies, vomiting and diarrhea, exhaustion, headaches
pg 867
28
Q
selenium
A
- sources: seafood, meat, whole grains, veggies (dependent on soil content)
- antioxidant -> glutathione peroxidase (selenocysteine) -> basis for RDA
- thyroid hormones (deiodinases)
- deficiency: TPN, associated with heart disease and some cancers; Keshan disease -> endemic cardiomyopathy with high fatality rates, congestive heart failure, acute heart failure, and cardiac arrhythmia
- toxicity: loss and brittleness of hair and nails; skin rash, fatigue, irritability, and nervous system disorders; garlic breath odor
pg 868
29
Q
lead is NOT a nutrient
A
- no known requirement for lead in diet
- may: damage fertility, damage unborn child, cause harm to breast-fed children (effects on or via lactation)
- very toxic to aquatic life with long lasting effects
- cut off for children: 5 μg/dL in blood (10 μg/dL for pregnant women) -> biological exposure index (BEI) is 30 μg/dL; typically asymptomatic
- 100 mg/m3 in air is immediately dangerous to life or health (IDLH)
- lead based paint, dust, contaminated soil, lead plumbing, folk remedies (pay-loo-ah to treat fevers)
pg 870
