Unit 6 - Vitamins and Minerals Flashcards Preview

Molecular and Cellular Princples of Medicine > Unit 6 - Vitamins and Minerals > Flashcards

Flashcards in Unit 6 - Vitamins and Minerals Deck (87):

what are the optimal amounts of vitamins?

occur in a range, from toxicity symptoms >> nutrient-nutrient or nutrient-drug interactions > average dietary intake > biochemical parameters of deficiency (detectable, but mild) >> 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?

1. poor nutrition
2. increased demand
3. problem with absorption of 1+ vitamins
4. 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 >>> 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


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)?

1. transketolase/transaldolase (pentose phosphate shunt)
2. pyruvate dehydrogenase (TCA)
3. 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

1. methionine synthesis
2. mmCoA --> SCoA conversion
3. 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?



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
-muscle contraction


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

1. O2/CO2 transport in hemoglobin
2. oxidative phosphorylation
3. 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?

1. release of 3+ from food (usually tightly chelated, so need acidic stomach to release)
2. 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:

1. Fe, Ca
2. Ca, Mg, vit A/C/B6
3. Fe, Ca, Mg, B6, B9
4. B6, B12, D, Zn, Cr
5. susceptible to many, but especially B1, B6, B9


most common reasons for vit/min deficiencies?

-drug-nutrient interactions
-compromised liver function
-poor absorption