Unit 6 - Vitamins and Minerals Flashcards
what are the optimal amounts of vitamins?
occur in a range, from toxicity symptoms»_space; nutrient-nutrient or nutrient-drug interactions > average dietary intake > biochemical parameters of deficiency (detectable, but mild)»_space; deficiency symptoms
how is the RDA fixed?
RDA is set 2 standard deviations above normal, to meet the needs of 97-98% of the population
how do deficiencies arise?
- poor nutrition
- increased demand
- problem with absorption of 1+ vitamins
- interactions with medications
how do the fat and water soluble vitamins differ in terms of deficiency VS toxicity?
fat: stored more efficiently (resemble lipids), so deficiencies «< toxicities
water: not stored (hydrophilic), so deficiencies»_space;> toxicities
functions of vit A
- visual cycle (carotenoids are precursors for rhodopsin and cone opsins)
- synthesis of certain glycoPRO and mucopolysaccharides
- retinoic acid acts as a hormone
- antioxidant
vit A deficiency VS toxicity
deficiency: night blindness (early), xeropthalemia (advanced); follicular hyperkeratosis; anemia (although normal Fe); poor child growth; increased infection/cancer
toxicity: accumulates in liver for nausea, diarrhea, bone pain, scaly/orange skin
what are susceptible groups for vit A deficiency?
poor, malnourished, or premature babies
what form of vit A do plants have?
carotenoids (pro-vitamin A); require further processing for biological activity in humans
progression of vit A deficiency
extreme dryness and thickening of conjunctiva mucus membrane lining inner surface of eyelid and exposed eyeball (xerophthalmia), that progresses to corneal ulceration, perforation, and destruction of eye (keratomalacia)
functions of vit D
- maintains bone
- Ca++ homeostasis
- acts as hormone; receptors in many tissues, but full range of activity unknown
vit D deficiency VS toxicity
deficiency: rickets (children), osteomalacia (adults), increased susceptibility to breast and other cancers, metabolic syndrome/diabetes, infection
toxicity: rare, but causes hypercalcemia and bone loss
what are susceptible groups to vit D deficiency?
poor, elderly, alcoholics
relationship of vit D and cancer
low serum vit D in post-menopausal women are correlated with increased risk of breast cancer
-some correlation between polymorphisms in vit D receptor and certain cancers
function of vit K
- localization of enzymes for blood clotting
- helps catalyze addition of gamma-carboxyglutamate to clotting enzymes (GLA modification)
vit K deficiency and susceptible gruops
easy bruising, bleeding, hemorrhage
- newborns: lack intestinal bacteria that makes vit K, so need supplementation
- adults: long-term antibiotics kill intestinal bacteria that make vit K
- patients with poor fat absorption are also insufficient
structure of vit K and its forms (K1/2)
quinone ring
K1 = phylloquinone in plants (esp. green vegetables)
K2 = menaquinone from intestinal bacteria
vit E functions
antioxidants (scavenge free radicals)
- protect membranes from damage
- prevent LDL oxidation
deficiency of vit E
cardiovascular disease and neurological symptoms
what are susceptible groups to vit E deficiency?
patients with severe, prolonged defects in absorption (celical) or genetic defects
what are the overall vit E structures and what is the major form in plasma?
called tocopherols and tocotrienols
-major forms are alpha and gamma
how does vit E exert its protective effect?
vit E is located in all cell and organelle membranes
-alpha-tocopherol in membrane will intercept ROS and other FR to prevent chain reaction of lipid destruction of especially unsaturated lipids
functions of vit C
- cofactor for oxidases in collagen formation
- -hydroxylation of pro, lys, and epinephrine
- required for synthesis of steroids in stress response (trauma will decrease vit C)
- aids Fe absorption
- antioxidant activity
mild VS severe cit C deficiency
mild: bruising, immunocompromised
severe: scurvy (decreased wound healing, osteoporosis, pinpoint hemorrhage, anemia, fatigue, corkscrew hairs, severe peridontal disease)
who are susceptible groups for vit C deficiency?
people with poor diet (Widower’s scurvy); smokers; long-term treatment of aspirin, oral contraceptives, and corticosteroids (esp. Devlin); severe stress/trauma
how much vit C is absorbed from food?
almost all of it (readibly absorbed)
what are common deficiencies for energy-releasing B vitamins?
symptoms show up in rapidly growing tissues (dermatitis, glossitis, diarrhea), then affect nervous system (peripheral neuropathy, depression, confusion, lack of coordination, malaise)
what are B1 functions?
required cofactor for enzymes in cellular energy metabolism as TPP)
-particularly critical in nervous system
what are 3 enzymes that involve thiamine pyrophosphate (TPP)?
- transketolase/transaldolase (pentose phosphate shunt)
- pyruvate dehydrogenase (TCA)
- a-KG dehydrogenase (TCA)
what are mild, moderate, and severe B1 deficiency symptoms, and their susceptible groups?
mild: GI symptoms, depression, fatigue (poor, elderly)
moderate: Wernicke-Korsakoff syndrome (alcoholics; may get CHF)
severe: beriberi (sometimes alcoholics, mostly if only polished rice)
dry VS wet beriberi
both have extreme muscle weakness, poly neuropathy, and CHF, but only wet has pitting edema
functions of riboflavin
precursor of FAD and FMN for REDOX energy reactions
what does deficiency of B2 cause? susceptible group?
ariboflavinosis - rash around nose, inflammation of mouth and tongue, burning/itchy eyes, and light sensitivity
-in alcoholics, but deficiency is usually uncommon
functions of niacin
precursor of NAD and NADP for REDOX energy reactions
what kinds of patients are given niacin for treatment?
patients with hypercholesterolemia or hypertriglyceridemia
-also given if have deficiency (along with tryptophan)
what groups are susceptible to niacin deficiency?
people with corn or millet based diets (deficient in tryptophan)
function of biotin
coenzyme for several carboxylases
biotin deficiency
rare, but caused by eating raw eggs with avidin (binds biotin tightly)
-biotin in many food sources, and made by intestinal bacteria, so deficiencies are rare
function of pantothenic acid (B5)
required for synthesis of CoA, and TCA cycle, metabolism of all fats and PRO
deficiency of B5 (pantothenic acid) and susceptible groups
very rare, but if present, have typical symptoms of B vit deficiency
-usually in patients taking isoniazid
pyridoxine (B6) function?
precursor of pyridoxal phosphate (PLP) cofactor required for glycogen breakdown and GABA/heme synthesis
mild and severe B6 (pyridoxine) deficiency?
mild: irritability, nervousness, depression
severe: peripheral neuropathy, convulsions, decreased glucose tol`erance, hyper-homocysteinemia (CVD risk), anemia
E-releasing VS hematopoietic B vitamins
E-releasing: B1-6 + biotin
hematopoietic: folate + cobalamin
folate function
precursor of THF coenzyme in making precursors for DNA and PRO synthesis
folate deficiency
- NTDs if deficient mothers,
- macrocytic anemia
- hyperhomocysteinemia (CVD risk)
susceptible groups to folate deficiency
pregnant women, elderly, alcoholics, pts with long-term drug treatments, or people with genetic polymorphisms in folate metabolism
why does folate deficiency inhibit DNA synthesis?
decreases availability of purines and dTMP
what makes cobalamin unique as a water-soluble vitamin?
it can be stored in the liver (up to 6-year supply)
cobalamin function
- methionine synthesis
- mmCoA –> SCoA conversion
- needed in folate metabolism
what does B12 deficiency cause?
pernicious (megaloblastic) anemia with demyelination
-usually due to lack of IF
susceptible groups to cobalamin deficiency
elderly, malabsorptive diseases, and long-term vegetarians (although debate b/c have stores)
how is B12 released and absorbed?
released from PRO by acid hydrolysis in stomach, then bound to IF to be absorbed in ileum
what element does cobalamin contain?
cobalt
what makes it macrocytic VS microcytic anemia?
macro (megaloblastic): from folate or B12 (specifically pernicious) deficiency
- large RBC due to deficiency in nucleotides, so decreased DNA and RNA synthesis
- cells increase in size w/o division, and large immature RBCs can’t carry enough O2
micro: from Fe deficiency (as well as vit C and Cu)
- small, pale RBC b/c less hemoglobin made, so RBC undergo more cell divisions in bone marrow while waiting for hemoglobin
- fatigue, pallor, weakness, and dizziness
what is the general role of minerals?
enzyme cofactors, but also can play structural roles in PRO or on their own
functions of calcium
- major component of bone
- signaling
- coagulation
- muscle contraction
- neurotransmission
mild VS severe calcium deficiency and susceptible groups
mild: muscle cramps, osteoporisis
severe: rickets
in children, adult women, and elderly
what sources does calcium come from?
solely from diet, and distribution highly regulated
when is calcium intake important to prevent osteoporosis?
when bone is reaching max density (10-35 in women); even higher amounts needed to maintain bone mass in postmenopausal women (exercise can also maintain bone density)
functions of magnesium
essential chelator for many enzymes (F1Fo synthase, Na/K-ATPase, SERCA Ca++ pumps) that use MgATP or MgADP as substrate
-if Mg not complexed, many transporters fail to recognize ATP or ADP
what does deficiency of Mg cause? susceptible groups?
weakness, tremors, cardiac arrythmias
in alcoholics and patients taking diuretics, or severe vomit and diarrhea
phosphorus functions
mostly in phosphates, and major part of hydroxyapatite
- constituent of nucleic acids, membrane lipids
- required in all E-producing reactions
phosphorus deficiency
rare (since abundant in food supply), but causes rickets, muscle weakness/breakdown, and seizure
what is the most common nutrient deficiency worldwide? what is the most common mineral in humans?
deficiency: Fe
present in humans: Ca
Fe functions
- O2/CO2 transport in hemoglobin
- oxidative phosphorylation
- cofactor in several nonheme Fe proteins and cytochromes (REDOX properties important)
what does Fe deficiency cause? susceptible groups?
microcytic hypochromic anemia, decreased immunity
common in children, menstruating women, pregnant women (almost impossible to get from diet alone, so need supplements), elderly
how is Fe absorption and distribution tightly regulated?
- reduction from 3+ to 2+ promoted by vit C
- low pH in stomach releases 3+ from ligands to make bioavailable
- uptake via mucosal cells is regulated in response to Fe-deficient or overload states
- Fe is carefully “escorted” in circulation and cells b/c of potential REDOX damage
what are the 2 major barriers to Fe absorption?
- release of 3+ from food (usually tightly chelated, so need acidic stomach to release)
- need reducing agent (like vit C) to convert 3+ to 2+
what is hepcidin?
signals Fe sufficiency and prevents export of Fe++ from duodenal mucosal cell by downregulating exporter
what is MCV and what is it used for?
mean corpuscular volume
- provides measure of average RBC size
- what is reported in lab
long term VS chronic Fe toxicity
long term: hemochromatosis; Fe deposits in multiple tissues
- compromised liver, pancreas, and heart function
- ultimately compromises mitochondrial function causing lactic acidosis (due to oxidative damage)
acute: Fe overdose in kids
- most common cause of death due to toxicity in kids under 6 yo (b/c eat adult Fe supplements)
copper functions
- assists Fe absorption via ceruloplasmin
- cofactor for enzymes in collagen synthesis (lysyl oxidase needs Cu and vit C), FA metabolism, and elimination of reactive O2 species
copper deficiency? susceptible patients?
rare, but includes microcytic anemia, hypercholesterolemia, fragile large arteries, demineralization, demyelination
those with Menkes syndrome, or consuming excessive zinc
why does excess zinc cause copper deficiency?
they compete for the same transporter in initial uptake
Menkes disease VS Wilson’s disease
Menkes: mutations in Cu transporter ATP7A causes deficiency
-needed to transport Cu to Golgi for enzymes; if not attached to Cu, enzymes are secreted
Wilson: mutations in Cu transporter ATP7B causes overload
- Cu not sequestered properly, and accumulates in liver with severe liver and nervous system symptoms
- -causes liver failure/cancer due to REDOX damage
- -forms brown ring around iris if accumulated in brain
function of zinc
- cofactor for over 300 metalloenzymes
- plays structural role in many PRO as Zn finger domains
deficiency in zinc? susceptible groups?
poor wound healing, dermatitis, reduced taste acuity, poor growth, impaired sexual development in kids
in alcoholics, elderly, or people with malabsorptive or kidney disease
what is the earliest symptom of Zn deficiency?
scaly dermatitis
- early and easily detectable
- can be reversed before more severe
chromium functions? deficiency? susceptible groups?
- component of chromodulin that facilitates insulin binding to its receptor
- impaired glucose tolerance (from reduced insulin effectiveness)
- those with impaired glucose tolerance, but Cr+++ hasn’t been proven helpful in DM2
iodine function and deficiency
- incorporated into T3/4 to regulate BMR
- goiter enlarges thyroid gland (b/c low I- causes increased TSH), and either hyperthyroidism or hypothyroidism
selenium function and deficiency
- component of antioxidant enzymes (glutathione peroxidase) and deiodinase enzymes (T3/4 metabolism)
- Keshan disease (in areas with little Se in soil); cardiomyopathy and cretinism
manganese functions
in arginase, pyruvate carboxylase, superoxide dismutase
molybdenum functions
in xanthene oxidase
fuoride functions
incorporated into bones and teeth to strengthen
boron functions
involved in bone formation
sulfer functions
component of AA, used in post-translational modifications
what are the most common deficiencies in:
- children
- teens
- women
- elderly
- alcoholics
- Fe, Ca
- Ca, Mg, vit A/C/B6
- Fe, Ca, Mg, B6, B9
- B6, B12, D, Zn, Cr
- susceptible to many, but especially B1, B6, B9
most common reasons for vit/min deficiencies?
- drug-nutrient interactions
- compromised liver function
- poor absorption
