Nutrition - Minerals

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acrodermatitis enteropathica sx

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skin lesions, diarrhea, alopecia, failure to thrive/growth retard/sex matur delayed, increased infxn

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acrodermatitis enteropathica pathophys

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defect in GI absorption of Zn
acquired (assoc w/ malabsorption) or genetic (rare auto rec)

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acrodermatitis enteropathica tx

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oral Zn = rapid recovery

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adolescent Zn deficiency - pop'n affected

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first ID'd in mid east, males

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adolescent Zn deficiency - sx

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growth retard, hypogonadism, delayed sex characteristics/puberty; assoc w/ dietary phytate (phosphorous) & geophagia (eating soil, clay, etc.)

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maternal Zn deficiency

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common, reduced fetal & neonatal growth

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dz's assoc w/ Zn deficiency

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liver cirrhosis, nephrotic syndr, chronic ID, gastrectomy, malabsorption (Zn, Se, Cu def), hemolytic anemias, burns, chelating drugs, uremia, pneumonia, diarrhea, alcoholism (both increased urinary excretion & poor diet)

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does Zn improve cold sx?

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v. high does might reduce duration of common cold sx, but mixed results from several studies (zn lozenges sold in many pharmacies)

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Wilson's dz
(hepatolenticular degeneration)

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rare, autosomal recessive
plasma Cu & ceruloplasmin low
tissue Cu high

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wilson's dz sx

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brain & liver lesions

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wilson's dz - tx

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D-penicillamine*
high doses of Zn
low Cu diet

*sometimes causes Zn deficiency

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how can tx of lead poisoning cause Cu or Zn deficiency?

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use of chelating agents (EDTA, D-penicillamine). esp why they're not used prophylactically.

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does ingestion of pennies cause Cu deficiency?

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yes, b/c of their high Zn content

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how does hemodialysis affect mineral levels in patients?

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contaminated dialysis fluids may have high concentrations of trace elements like Cu, Al, Zn; elevated levels found in these pts

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What is Menkes' Syndrome?

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recessive, X-linked trait
defect in cellular Cu transport

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copper deficiency sx

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microcytic anemia, neutropenia, leukopenia, low serum Cu & ceruloplasmin; myelopathy & peripheral neuropathy resembling B12 deficiency (may coexist w/ Cu def)

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copper deficiency myelopathy - tx

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Cu supplementation fixes anemia & neutropenia, but doesn't reverse myelopathy

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Menkes' syndrome - sx

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1) ↓ plasma Cu & ceruloplasmin
2) early death
3) ↑ infxns
3) kinky hair
4) tortuosity of abdominal and intercostal vessels
5) progressive cerebral degeneration w/ freq seizures

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Cu deficiency- pts at risk

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malabsorption/PUD/bariatric surgery
Zn at high doses

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chromium deficiency - sx

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impaired glucose tolerance may be associated; in a small % of cases, may respond to Cr, but not definite

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Cr supplements

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widely used to increase muscle mass during wt training. no good evidence.

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Menkes' syndrome - tx

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parental Cu administration is not effective!!

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Keshan dz

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cardiomyopathy assoc w/ Se deficiency (widespread, pediatric, endemic in China, eradicated by Se fortification)

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Se & Cancers

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anti-oxidant, assoc w/ lower incidence of lung, colorectal, prostate ca. Currently: SELECT trial for prostate ca w/ Se and/or vit E

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Mo deficiency- common settings

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TPN pts

generally v well absorbed in GI tract, homeostasis maintained by urinary excretion

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fluoride excess

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mottling of teeth in children
skeletal fluorosis and bone fx in adults

topical/oral = decreased caries

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Mn toxicity - settings

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pts w/ liver dz --> reduced Mn excretion in bile

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Mn excess - sx

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neurologic dysfxn (sx similar to Parkinson's), increased blood levels.

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most prevalent deficiency in the world

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Fe

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hereditary hemochromatosis - pathophys

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excessive GI absorption of iron

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hereditary hemochromatosis - sx

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lethargy, abd pain --> liver cirrhosis, ca; cardiomyopathy

increased transferrin saturation, serum ferritin

dx: liver biopsy for Fe concentration

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hereditary hemochromatosis - tx

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periodic phlebotomy

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2nd most common deficiency in the world

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Iodine

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iodine deficiency - sx

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decreased thyroid hormones
impaired growth, mental retardation, goiter (enlarged thyroid)

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Kashin-Beck osteoarthropathy

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prob due to iodine deficiency
endemic in Tibet, Siberia, NKorea

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interactions among metals (6 examples)

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1) Cu deficiency, anemia w/ ↑ Zn
2) Se = ↓ toxicity of Hg, Cd
3) ↑ Ca, Mg = ↓ absorption Pb
4) Mo & S = ↓ Cu retention
6) small amts Cd = protective against larger doses Cd, Hg (induces liver & kidney to synth metallothiens - w/ S atoms which can bind to subsequent doses)

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2 examples of dose-response effects

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1) Zn: inadequate intake = deficiency; excess = anemia & death

2) Cd = small amts necessary for growth in rats; larger amts = v. toxic to kidneys

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why are metals biologically impt?

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affect fxn or structure of enzymes (metalloenzymes for Zn & Cu; 'Zn finger' proteins)

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chelating agents
1) mechanism
2) 4 drugs

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1) bind transition metals, form 5-6 member ring (v stable)
2) ethambutol, INH; EDTA, penicillamine

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Hodgins dz & pregnancy alter metabolism of which metals?

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Hodgins: Cu
Pregnancy: Cu & Zn

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What kinds of foods are trace elements normally found in?

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High protein foods, b/c trace elements are usually bound to S, O, N atoms of proteins.

Exceptions: tea & Mn

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Does adequate intake of a trace element guarantee bioavailability?

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No - e.g., high dietary phytate ↓ absorption of Zn

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What are some tx for dz's that might cause trace element deficiencies?

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1) TPN
2) ethambutol -> ↓ Zn -> ↓ visual acuity
3) INH

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pharmacologic effects of moderate to high doses of trace elements:

2 examples

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1) ↑ niacin: ↓ serum cholesterol
2) ↑ Zn: tx Wilson's dz, maybe common cold sx

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GI absorption
1) poorly absorbed (2)
2) well absorbed (4)
3) variable (3)

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1) Cr, Mn
2) F, I, Mo, Se
3) Cu, Fe, Zn

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Major excretory routes
1) urine
2) GI tract (bile vs. pancreas)
3) menstrual, bleeding

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1) Cr, F, I, Mo, Se
2) bile: Cu, Mn; pancreas: Zn
3) Fe

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Deficiencies caused by several weeks of TPN

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Most common: Cu, Zn
Hypochromic, microcytic anemia
AE-like sx: impaired wound healing

Modern TPN fluids have trace elements, but caution in pts w/ liver/kidney dz: excess Mn can cause severe neuro dz (1° excretion thru bile)

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3 Frequently fortified foods:

element (food)

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1) I (salt)
2) Fe (cereals)
3) Zn (cereals)

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Lab tests available for evaluating trace elements excess/deficiencies

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1) blood
2) urine
3) hair: for excess As, Cr, Hg
4) ↓ AP assoc w/ ↓Zn
5) ceruloplasmin to dx Wilson's Dz & Menkes Syndr

Caution:
acute ID may produce ↑ in Cu, masking deficiency

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At-risk groups (trace elements toxicities/deficiencies)

Name examples w/ respect to diet, diseases, environment.

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Diet:
1) low calorie diets, unusual diets
2) users of megadose supplements (interactions)
3) TPN (deficiency, toxicity)

Other medical conditions:
1) medication side effects
2) Other diseases: HIV, cardiomyopathy, malapsorption, GI surgery, anorexia, drug abuse/alcoholism

Environmental
1) environmental exposures (Fe ↓ w/ Pb poisoning)
2) residents of poor countries

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Why are premature infants susceptible to Cu deficiency?

What are the sx?

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1) they have inadequate Cu liver stores

2) ↓ plasma Cu & ceruloplasmin; neutropenia/leukopenia; bone demineralization; failure of erythropoeisis; death