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Gastrointestinal System > Trace Minerals - Abali 2/12/16 > Flashcards

Trace Minerals - Abali 2/12/16 Flashcards

1
Q

phytates

A
  • found in grains/beans, attach to trace minerals and reduce availability
  • can release the attachments by boiling/cooking
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2
Q

minerals

A

essential inorganic elements required for maintaining normal body fx

-roles in bone health, growth/devpt, blood formation/clotting, nerve impulses, as electrolytes, as antioxidants

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3
Q

micronutrients

A

vitamins and minerals

required in smaller amts [mg and microg]

  • not involved in supplying energy like macronutrients
  • play imp roles in maintaining body fx and health
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4
Q

microminerals

A
  • Fe, Zn, Cu, I, F, selenium - Cr, Co - Mn, Mb
  • grains, milk, meat/beans
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5
Q

major minerals

A

reqd in large amounts (>100mg daily)

  • Ca, P, K, S, Na, Cl, Mg
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6
Q

macronutrients

A

carbohydrates, proteins, lipids

required in GRAMS

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7
Q

Fe sources

A

meat, fish, poultry, eggs, dried peas beans, whole grains, fortified breads/cereals

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8
Q

Fe forms and storage

A

3-4 g in adult body

**free form is TOXIC, so it’s sequestered in several forms

  • circulation: bound to transferrin
  • 70% in RBC as heme in Hb
  • 5% in heart/sk muscle in myoglobin
  • 5% as cofactor in heme and nonheme enzymes
  • rest stored in ferritin in liver, spleen, bone marrow [converted to hemosiderin in cases of excess]
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9
Q

factors that increase bioavailability of a mineral

A
  • deficiency in a mineral = higher abs (reverse is also true)
  • cooking (in legumes, grains) [opposite for vitamins!]
  • vitamin C (increases abs of some, ex. Fe)
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10
Q

factors that decrease bioavailability of a mineral

A

-binders (ex. oxalate in spinach, binds to Ca - moves through int tract unabs)

  • phytates in grains
  • polyphenols in tea/coffee
  • supplementation (excess of one mineral can affect abs of competing minerals, ex. if abs occurs based on ionic state)
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11
Q

iron

  • forms
  • distribution in body
A

3-4 g of Fe in body; switches back and forth between ferrous and ferric states

  • bound to transport protein in circulation: transferrin
  • found in functional proteins
    • _​_hemoglobin (RBC, 70%), myoglobin (heart/sk muscle, 5%)
    • cofactor in redox rxns (5%)
    • electron carriers
  • found in storage proteins
    • ferritin (liver, spleen, bone marrow)
    • hemosiderin (liver, macrophages)
      • at high Fe conc, liver converts ferritin into hemosiderin to protect body from free Fe damage
      • found in macrophages, abundant following hemmorhage; formation might be related to phagocytosis of RBC and Hb)
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12
Q

hemosiderin

  • location, trigger, potential fx
A

at high Fe conc, liver converts ferritin into hemosiderin to protect body from free Fe damage

  • release of Fe from hemosiderin is sloooow, hence protection

found in macrophages, abundant following hemmorhage; formation might be related to phagocytosis of RBC and Hb)

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13
Q

forms of dietary iron in food and their sources/abs

A
  1. heme iron: 10% of daily Fe intake, well absorbed (25%), found in aminal pdts
  2. non-heme iron: 90% of daily intake, poorly absorbed (17%), found in plant pdts
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14
Q

factors that positively influence non-heme Fe abs

A

enhancing factors

  1. ​body need (pregnancy, weight training, etc)
  2. vitamin C: acidic environment = more abs bc will convert from ferric3 to ferrous2 (better for abs)
  3. animal tissues: MeatProteinFactor (peptide in meat/fish/poultry) and heme iron both improve non-heme Fe abs

sugars and acids too

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15
Q

factors that negatively influence non-heme Fe abs

A

inhibiting factors

  1. binding agents: oxalates, phytates, polyphenols, fiber
  2. low gastric acid (antacids, proton pump inhibitors)
  3. infection (body suppresses supply to keep Fe away from infection orgs)
  4. GI disease
  5. Ca, Zn, Mn
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16
Q

describe the roles of proteins in intestinal absorption of Fe in Fe-high and Fe-low conditions

A

body decreases absorption when Fe is high, increases absorption when Fe is low

ferritin: Fe storage protein in intestinal mucosal cells

transferrin: Fe transport protein in intestinal mucosal cells

  • high iron: low absorption
    • ​increased ferritin synthesis so as to absorb and hold Fe in mucosal cells
    • mucosal cells are sloughed off, excess iron is excreted
  • low iron: high absorption
    • ​decreased ferritin synth
    • more Fe bound to mucosal transferrin and handed off to other transferrin to get into circulation
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17
Q

where and how is Fe absorbed?

A

duodenum

  • heme Fe: transported across brush border
  • non-heme Fe: mostly ferric/oxidized/3, has to be converted to ferrous/reduced/2 before moving into cell

once inside cell…

  • stored: in ferritin, which can be lost as cells get sloughed off
  • mobilized, moved out of cell for incorp with transferrin: moved across basolateral membrane by action of ferroportin + ceruloplasmin [also imp in Cu abs]
    • ferroportin moves Fe+2 across basolateral membrane
    • ceruloplasmin converts back to Fe+3 for incorp into transferrin
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18
Q

how is iron recycled in the body

A

transferrin carries Fe in the blood, drops off at:

  • muscle: myoglobin
  • bone marrow: Hb of RBC, excess Fe in ferritin/hemosiderin
  • liver/spleen: dismantle RBCs and either package Fe in transferrin or stores excess Fe in ferritin/hemosiderin

losses: bleeding (blood), sweat, urine

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19
Q

Fe deficiency

A

most common deficiency nationwide

  • women in repro years: menstruating
  • pregnant women: high rate of growth
  • infants/children/adolescents: high rate of growth
  • abs disorders: Celiac disease

could be due to blood loss, inadequate intake (raw vegans - raw veggie Fe wont be released from binders!), Fe poor diet

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20
Q

Fe deficiency symptoms

A
  • Fe-deficiency anemia
    • fatigue, faintness, cold/abnormal sensation in extremeties, shortness of breath
    • low oxygenation bc of less Fe for Hb - energy metabolism affected
  • heme Fe used as prosthetic group in several antimicrobe enzymes
    • immunosuppression
  • altered neurotransmitter synth (Fe important for nt synth - serotonin, norepi, dopamine)
    • low IQ, learning problems
    • low motivation, energy, productivity
  • PICA - craving/consupmtion of nonfood substances (dirt, clay, ice)
    • ***can also be Zn deficiency
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21
Q

indicators of Fe deficiency (stages)

A

stages

  1. iron stores drop
  2. transport iron decreases (becomes more saturated)
  3. Hb production falls

early indicators:

  • serum ferritin (more being turned over to transferrin - instead of released to serum and excreted)
  • transferrin saturation (aka decrease in TIBC - total iron binding capacity)
  • protoporphyrin accumulation
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22
Q

blood cells in Fe deficiency anemia

A

hypochromic: pale

microcytic: small

**Fe defiency means Hb synthesis is impaired!

hyprochromic, microcytic anemia

  • impairs tissue oxygen delivery
    • weakness, fatigue, palpitations, light-headedness
    • nonuniform size RBCs
23
Q

epithelial changes from Fe deficiency

A
  • GI tract abnormalities
  • angular stomatitis: inflammation of mucosa at corners of ilps
  • glossitis: painful swelling of tongue
    • also smooth shiny tongue from flattened, atrophic lingual papillae
  • koilonychia: abnormality of nails producing concave deformity
    • long standing severe deficiency
24
Q

iron overload

A
  • causes
    • excess ingestion, transfusion
    • genetic hyperabsorption in spite of elevated liver stores: hemochromatosis
  • ​risks
    • ​high iron = risk of heart disease and cancer
    • older pts advised against taking Fe supplements unless deficient
25
Q

hemochromatosis symptoms

A
  • ​​affects pigmentation (bronze)
  • liver damage (cirrhosis)
  • pancreas damage (diabetes)
  • heart failure, athritis, sexual dysfunction
26
Q

zinc sources

A

seafood (oysters), meat/eggs, milk, legumes

bioavailability in plant sources ltd due to phytates, oxalate, Ca, Fe, Cu

27
Q

describe Zn absorption in high/low conditions

describe circulation/recycling after abs

A

metallothionein: Zn storage protein in intestinal mucosal cells

albumin: Zn transport protein (also transferrin, but more albumin)

  • high zinc: low absorption
    • ​Zn held in mucosal cells in stored form with metallothionein
    • mucosal cells are sloughed off, excess zinc is excreted
  • low zinc: high absorption
    • ​metallothionein releases zinc to albumin (or transferrin)

a lot of Zn is used by the pancreas to make digestive enzymes, which are secreted into the intestine

  • afterwards, dietary Zn and the Zn-containing pancreatic secretions can be reabs by the intestinal cell and move back to mucosal cell via enteropancreatic circulation of zinc
28
Q

Zn functions

A

found in tons of enzymes with varied fx

  • cofactor for enzymes in carb, fat, protein metabolism
  • heme/DNA/RNA synthesis
  • gene expression
    • Zn finger proteins
  • immune fx
  • sexual maturation
  • taste and smell

**stabilizies cell membrane proteins and receptor proteins for vitamin A, D, and thyroid hormone

29
Q

causes of Zn deficiency

A
  • malabsorption disorders (probs reabsorbing in enteropancreatic circ), chronic diarrhea
  • vegetarians (low efficiency of Zn abs from plant sources)
  • alcoholics (alcohol inhibits Zn absorption and promose Zn excretion)
  • lactating women (higher need for Zn: GROWTH)
  • chronic ulcer, bed sore pts
  • heavy smokers
  • acrodermatitis enteropathica (infl around limbs, issues with intestines - maybe diarrhea)
    • ​rare genetic disorder, develops after weaning: impaired intestinal Zn abs
30
Q

symptoms of Zn deficiency

A
  • poor appetite
  • reduced sensation/loss of taste and/or smell
  • hair loss, skin problems
  • poor wound healing, impaired immunity
  • delayed growth retardation and sexual maturation
31
Q

Zn deficiency historiy in Middle Eastern populations

A
  • noted that males pirmarily affected: growth retardation, hypogonadism, delayed onset puberty, failure of 2 sexual chars to develop
  • associated with high intake of unleavened bread and low Zn intake
    • unleavened bread = phytate heavy (yeast reduces effect of phytates)
32
Q

Zn toxicity

A
  • rare
  • diarrhea, nausea, vomiting (same as in deficiency!)
  • chronic toxicity
    • impairs Cu status - can cause Cu def
    • depresses immune fx
    • leats to urinary tract issues

bc Zn toxicity messes with Cu, Zn supplementation is used as a tx for Wilson disease (high Cu storage)

33
Q

Cu sources

A
  • liver, shellfish, nuts, seeds, lentils, soy products, DARK CHOC
  • dried fruits, whole grain, tap water

meat is a poor source, BUT might promote Cu abs (like it promotes nonheme abs)

34
Q

Cu absorption (location, relevant transport proteins, factors that increase/decrease abs)

A
  • abs in small intestine
    • transported from instestine to tissues bound to albumin
    • transported from liver to tissues bound to ceruloplasmin
  • increased
    • ​acidic medium
  • decreased
    • ​phytates, Ca, Zn, fiber
35
Q

Cu function

A
  • component of lysyl oxidase: key for elastin and collagen synthesis (skin, hair, conn tissue)
  • cofactor for superoxide dismutase: hey for protection of cells from ROS
  • cofactor for monoamine oxidase system involved in synth of neurotransmitters
    • also helps maintain myelin sheath and nervous system
  • component of ceruloplasmin (helps oxidize iron from ferrous to ferric before it can be bound to transferrin)
36
Q

ceruloplasmin

A

major Cu-containing protein in plasma

  • key in recycling Fe in macrophages
    • senescent erythrocytes are phagocytosed by macrophages
    • Hb degraded, Fe is released from heme and transported out of macrphage by ferroportin (Fp)
    • in plasma, ceruloplasmin oxidizes it from ferrous to ferric before it binds with transferrin
37
Q

Cu deficiency: causes and symptoms

[disease and symptoms]

A
  • rare
  • malnourished infants (only cows milk, low in Cu)
  • Menkes syndrome: poor Cu absorption
    • silvery hair, soft/lax skin, progressive conn tissue and neuro problems
    • often preterm, get to 6-8 weeks before symptoms seen. flattened nose bridge, unexpressive face
  • nutritional disorders (kwashiorkor, anemia, Celiac disease)

symptoms: anemia, connective tissue damage, clotting problems: excessive bleeding

38
Q

Cu toxicity

A
  • might occur via consumption of acidic beverages stored in Cu-containing containers
  • symptoms
    • abd pain, nausea, diarrhea, vomiting
    • anemia
    • death
  • Wilson’s disease: increased Cu deposits in brain, kidney, cornea, liver but low Cu blood levels​
    • Kayser-Fleischer rings: golden-brown, greenish-brown discoloration at top and bottom of cornea due to deposition
39
Q

Wilson’s disease

A

Cu toxicity

  • autosomal recessive disorder
  • defect in incorporation of Cu in hepatic lysosomes
    • faulty storage means Cu cant be excreted in bile, accumulates in liver cells, causes hepatocellular and biliary damage
    • liver is injured, Cu leaks out into blood
  • key symptom
    • Kayser Fleischer rings in 97% of patients with neuro manifestations
  • tx?
    • Zn supplementation! can reduce Cu intake
    • penicillamine: Cu chelator
40
Q

selenium sources

A

content in food varies based on SOIL

  • generally, nuts, whole grains, seafood, meat generally rich in selenium
  • Brazil nuts! super rich - shouldnt be eaten regularly due to tox risk
41
Q

selenium forms and absorption

A
  • forms​​: bound to proteins as…
    • selenocysteine: biologically active form (modified translation of UGA stop codon)
    • selenomethionine: storage form
  • absorption: v efficient; mostly regulated through urinary excretion
  • highest concentration in: liver, pancreas, muscle, kidneys, thyroid
42
Q

selenium fx

A
  • component of 25 selenoproteins
  • part of antioxidant enzymes that protect cells from free radical damage (protects lipic peroxidation/cell mem damage; works with vitamin E)
    • glutathione peroxidase
    • thioridexin reductase
    • selenoprotein P
  • thyroid metabolism: needed for proper deiodinase fx
    • conversion from T4 to T3
  • esential for normal immune fx
43
Q

selenium’s role in antioxidant network

A

glutathione peroxidase system (GPx): powerful antioxidant, esp in cell membranes and LDL cholesterol

  • degrades peroxides into water - prevents formation of free radicals and cell damage
  • supplements vitamin E (major ROS scavenger)
44
Q

selenium deficiency

A
  • total parenteral nutrition
  • GI problems: impaired abs
  • places with v poor selenium soil content (China, New Zealand, Venezuela): Keshan disease
    • enlarged heart, poor cardiac fx
45
Q

selenium toxicity

A

selenosis

  • rare
  • industrial accidents or accidental errors that give superdoses in supplements
  • symptoms
    • ​fatigue
    • upset GI
    • joint pain
    • hair loss
    • nail discoloration
46
Q

fluoride sources and fx

A

not essential, but important for bone/tooth strengthening

  • major sources: fluoridated water. tea, seafood, seaweed. fluoridated toothpaste.

no known metabolic fx

  • increases tooth mineralization, bone density
  • reduced dental caries
    • inhibits glycolysis in bacteria: inhibits enolase (req for survival)
  • promotes enamel remineralization
    • hydroxyfluoroapatite cystals
  • in circulation, contributes to saliva F
    • promotes remineralization and reduces net loss of minerals from tooth enamel
47
Q

fluoride deficiency and toxicity

A
  • deficiency
    • ​dental caries
  • toxicity
    • ​can occur if kids swallow toothpaste or F tabs
    • fluorosis: no real health risk. mottled teeth: discoloration and pitting of enamel
48
Q

iodine sources

A
  • sources: most foods have low iodine content
    • saltwater, seafood, seaweed, iodized salt.
    • dairy products (because of iodine added to feeds, processing methods).
    • vegetables, depending on I content of soil
    • breads and cereals made with I salt
49
Q

goitrogens

A

vegetables that decrease I absorption by enterocytes in gut

  • modulate I bioavailability
  • reduce thyroid fx (40% of I is in thyroid)
  • raw vegetables: turnips, cabbage, Brussel sprouts, cauliflower, broccoli, rutabagas, potatoes, peanuts, strawberries
50
Q

iodine fx

A
  • key for thyroid hormones, thyroid gland fx
    • energy metabolism: body temp, metabolic rate, growth
    • CNS function
    • reproduction
51
Q

iodine deficiency

adults vs children

risk factors

tx

A
  • TH production will drop (due to drop in I)
    • TSH secretion will rise to compensate, overstimulate thyroid, and you get hypertrophy : GOITER
  • ​symptoms
    • ​lethargy, dry skin, thick lips, enlarged tongue, low muscle/skeletal growth, mental retardation
  • deficiency during period of fetal growth/infancy: CRETINISM
  • symptoms
    • ​irreversible mental retardation/disability, short stature, muscle spasms
      • most common cause of preventable mental retardation/brain damage
  • risk factors: pregnancy, excessive tobacco/alcohol consumption, oral contraceptive use, high Ca intake, seletium deficiency
  • tx? iodized salt!!!
52
Q

iodine toxicity

A
  • negative feedback inhibits TH synthesis
    • can cause goiter too

*might see enlarged thyroid in iodine excess, iodine deficiency, and selenium deficiency

53
Q

chromium fx

A

enhances insulin action

54
Q

cobalt fx

A

part of vitamin B12 (aka cobalamin!)

Gastrointestinal System (35 decks)

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