Minerals Flashcards
What is a mineral? List minerals in order of most to least importance (according to those covered int he lecture)
solid, inorganic substance of natural occurrence. • Iron • Copper • Zinc • Selenium • Iodine • Fluoride • Chromium • Cobalt
What are the macrominerals (minerals you need more than 1g of daily)
- Calcium (bones)
- Phosphorous (ATP)
- Potassium (Na/K pump)
- SULFUR
- Sodium (Na/K pump)
- Chloride
- MAGNESIUM
What are the microminerals (minerals you need less than 1g of daily)
- IRON
- Zinc
- Copper
- Iodide
How much Fe is needed daily male/female from 9-13 years old? 19-30 years old?
- 8/8 mg/day
- 8/18 mg/day
Increased for woman because woman lose their endometrium every month in reproductive years, so they need mroe Fe.
Where do you find Fe?
Heme Fe (animal product form) • Lamb • Chicken liver • Eggs • Oysters, Clams, shrimp • Beef liver • Turkey leg Non-Heme Fe (plants) • Beans • Tofu • Lentils • Spinach • Brown rice • Raisins
Why is Heme-Fe (animal based) better absorbed in the body?
Found with MPF peptide, which increases its bioavailability and absorption
Describe Fe absorption process.
- Fe3+ (FERRIC) enters (will NOT enter as Fe2+ (FERROUS)) into small intestine, mainly in duodenum and jejunum
- Fe3+ contacts brush border, which converts it to Fe2+, allowing for entry into enterocyte
- if body needs Fe2+, it passes to basolateral side, runs through Ferroportin transporter, GET S CONVERTED BACK TO FERRIC (F3) FORM, and enters blood to get to liver. It uses Transferrin transporter (this is why it needs to be F3. won’t work otherwise…thank cereloplasmin for conversion) in order to survive in blood until it reaches liver.
- if body’s Fe levels are A1, Hepcidin molecule inhibits Ferroportin. The Fe2 would then be stuck in enterocyte, bound to Ferritin and stored until needed. When the enterocyte is shed (this happens regularly) into the lumen, it is excreted in feces. There is no formal mech to excrete Fe. only 1 mg is lost daily through luminal shedding, so our body just tends to conserve it.
How do you measure Fe?
Total iron binding capacity (TIBC) and transferrin saturation
What increases Fe’s presence in the body?
INCreased in presensce of:
- vitamin c
- MPF peptide (Heme iron found in animals)
- acids (citiric and lactic)
* most girls are iron deficient. so they take supplemental iron with Orange juice
What decreases Fe’s presence in the body?
Oxalates- Spinach, Kale, Beets, Nuts, Rhubarb. (sucks since all the things you are supposed to eat are bound to oxalates.)
• Phytates- whole grains, legumes, nuts, seeds
• Polyphenols-blueberries, onions, spinach, wheat, coffee, tea
• Fiber
• ↑ in gastric pH (antacids = bad). makes scene since it likes citric and lactic acids. proton pump inhibitors = bad
• Calcium, Zinc, and Magnesium (minerals in the presense of other minerals similar in size and charge enforces competition, which reduces bioavailabooility…effectiveness.)
WHere deos Fe2 go after it reaches th eblood?
- bone marror to bind to heme
- liver
- myoglobine production for O2 for muscles and other tissues
what are the 2 storage forms of iron? which one readily releases iron when needed?
- Ferritin (eneterocyte form + other cells in body). smaller molecule, so easier to release iron
- hemosiderin (macrophage form, as well as hepatocytes). this one does NOT readily release iron when needed since it’s a large molecule and bound to other lipids and proteins.
Where is FE2 found in ETC? Note that lack in Fe = screw up atp production
complexs 1 and 3
what causes Fe deficiency?
- decrease fe intake/absorption (malnourished, vegitarians/vegans (since their source of iron is plant based, which isn’t as well absorbed since they are lacking mpf protein), or mal-absorption (CELIAC DISSEASE…impacts proximal small intestine, which is where Fe is absorbed))
- Increased Fe loss (menstrual cycles (some women have fibroids, leading to heavy cycles each month), or bleeding-hemmorroids (older men), peptic ulcer disease)
symptoms of Fe deficiency. what is koilonychia?
- fatigue (decreased amount of hemoglobin and myoglobin)
- PICA- the craving of non-nutritional items such as uncooked rice, ice
chips, chalk - Plumer-Vinson syndrome- Triad (Step 1 emphasizes this) of esophageal webs…fbrious tissue in esophagus leading to difficulty swallowing…, glossitis (inflammed tongue), and iron deficiency anemia
- koilonychia - pitting of fingernails
what would the iron studies show in iron deficiency anemia?
MCV = mean corposule volume (size of the blood cell)
Total iron binding CAPACITY (TIBC = amount of tansferrin molecule in the body)
A) ↑ MCV, ↑ ferritin, ↓ transferrin saturation, ↑ TIBC
B) ↑ MCV, ↓ ferritin, ↑ transferrin saturation, ↓ TIBC
C) ↓ MCV, ↑ ferritin, ↑ transferrin saturation, ↑ TIBC
D) ↓ MCV, ↓ ferritin, ↓ transferrin saturation, ↑ TIBC
D) ↓ MCV, ↓ ferritin, ↓ transferrin saturation, ↑ TIBC
low size of robc molecule since oyu lack heme
low size of ferritin since it is the heme stroage molecule and there is no heme.
decreased transferrin saturation since, again, there is no heme.
increased total iron binding capacity since there is a reduced amount of heme binding to transferrin, again, becasue there is no heme.
what type of anemia is iron deficiency anemia how would it look on a blood smear?
microcytic anemia (MCV less than 80…referring to rbc size). blood smear shows hypochromic (no color), microcytic (small) rbcs. hyperchromic part stems from bone marrow lacking heme, so can’put as much in the formed rbcs
what causes iron toxicity?
Note: ROS = reactive oxygen species
1. Increased transfusions (remember, there is no formal way to ditch iron from body, so when you transfuse, you get more iron, but you can’t ditch it)-
Sickle Cell Disease, Thalassemia
2. Hereditary Hemochromatosis- autosomal recessive gene mutation in HFE (STEP 1) which ↑ iron absorption by enterocytes and dumps it in our blood
–Liver in these hemochromatosis patients- Increased iron storage in liver (liver = major fe storage, and still no way to ditch Fe) ↑ ROS (caused by increased Fe presence)
–Diabetes- ROS damage to pancreas beta islaet cells, decreasing insulin release
—-“Bronze diabetes” as a result (these patients develop jaundice…yellow hue..as result)
5. Increased risk of cancer- ROS damage to cells
6. Sexual dysfunction
7. Arthritis
how could kiddies suffer fe toxicity? what does x ray show?
kiddie eating mother’s prenatal vitamins. x ray shows opaque (white). expect to be asked this on Peds shelf.
where do you find copper
- Oysters
- Kale
- Mushrooms
- Sesame seeds
- Cashews
- Chickpeas
- Chocolate
- Avocados
- Goat cheese
how do you absorb copper?
- similar to Fe absorption (proximal intestin). takes in 30-40% of ingested copper
- Cu2+ is how it enters. MUST BE REDUCED (again, like iron) to Cu+ to be used. in fact, the molecule that reduces Fe also reduces Cu (Fe/Cu reductase!).
- Transported into enterocyte (Ctr1) and stored in cell as metallothioneine (TGN) OR sent through to basolateral side
Cu+ blood transport molecule? where’s it headed? what does liver use to transport Cu+ to other tissues?
enterocyte-albumin, headed to
Liver
hepatocyte: ceruloplasmin
how do you excrete cu?
bile (liver does this)
what increases Cu+ bioavailability?
acidic environment (like Fe)
what decreases Cu+ bioavailability?
- Phytates
- Fiber
- Calcium (similar size and charge)
- Zinc (similar size and charge)
- Iron- due to DMT1 (fe/cu reductase) and ceruloplasmin (same enzymes used for reduction and transport (respectively), so there is competition)
job of ceruloplasmin, besides Cu+ liver to body tissue transport?
oxidizes Fe2 to Fe3 so that it can bind to trasnferrin
storage forms of Cu+
- liver (go-to)
2. cell (metallothionein)
job of copper in body
- component for lysyl oxidase (used for collagen formation)
- cofactor for superoxide dismutase (which converts O2- to H2O2 and O2 (molecular O2))
- cofactor for monoamine oxidase (which inactivates neurotrasnmitters seratonin, melatonin, norepi, and dopeamine)
causes for Cu deficiency
• ↓ intake • Menke’s disease: X-linked recessive disorder caused by mutations in ATP7A needed to transport copper across cell membranes
symptoms of Cu deficiency (Menke’s disease)
- Wiry silvery hair
- ↓ growth
- Hypotonia
Causes of Cu toxicity? symptoms of assocaited disease?
Wilson’s disease (STEP 1): autosomal
recessive mutation in ATP7B
gene responsible for copper
transport (excretion) in the BILE and
incorporation into ceruloplasmin (too much accumulation).
symptoms: rigdi movement, RINGS AROUND EYES (Cu accumulation in descement’s membrane of eyes cornea, leading to kayser-fleischer rings). you’ll also see liver cirrosis due to cu buildup. can also buildup in basal ganglia, leading to parkinson’s disease and psychosis
Are ceruloplasmin levels high or low in patients with
Wilson’s disease? Why?
LOW
Reason: ATP7B is mutated in Wilson’s disease. Cu is loaded onto apoceruloplasim to make ceruloplasim, and this only happens if ATP7B is functioning. If its not, can’t load Cu, so that Cu just stays in hepatocyte, and that backflows (entering enterohepatic circulation instead, binding to albumin) into circulation and leads to accumulation (descemets membrane in eye cornea)
where do you find zinc?
- Shellfish
- Cashews
- Garbanzo beans
- Yogurt
- Meat
describe absorption, storage of zinc.
absorbed as ZIP4. if body needs it, runs through basolateral side. Binds to albumin to get to other tissues. is not needed, stored as metellathionene in enterocyte
what decreases zinc bioavaliability?
interactions with Fe and Cu (increaes these 2 guys = screw up Zn further)
• Which of the following diseases has Zinc supplementation been used to decrease symptoms? • A) Iron deficiency anemia • B) Hemophilia • C) Porphyria • D) Wilson’s disease
• D) Wilson’s disease (reason: it fights against fe and Cu!)
function of zinc
Cofactor for digestive enzymes needed to break down carbohydrates, fats, and protein (lipases, amylases, proteases)
• Involved in the synthesis of Heme ALA dehydratase
• Involved in synthesis of DNA and RNA
• Involved in gene expression
• Immune function
• Sexual maturation
• MEDIATES SENSE OF SMELL AND TASTE
• Treatment of Wilson’s disease- Zn is FDA approved for the treatment of Pediatric and Adult Wilson’s disease in
presymptomatic and symptomatic individuals
what leads to zn deficiency?
1. ↓ intake • Vegetarians • Mal-absorption disorders 2. ↑ copper • Wilson’s disease 3. ↑ loss • Alcoholics • Lactating • Heavy smokers
Acrodermatitis Enteropathica
another cause for Zn deficiency.
1. Autosomal recessive gene mutation in a zinc
membrane transport protein within enterocytes in
the duodenum and jejunum
2. Symptoms
• Peri-orificial and acral dermatitis (around mouth and lips and anus/gentilia)
• Alopecia (random bald spots)
• Diarrhea
t/f. quantity of selenium in plant-based food depends on amount of selenium in soil that it is grown in
True
where do you find selenium?
- Seafood
- Meat
- Grain
- Brazil Nuts
how do you store selenium? active form of selenium?
selenomethionine in liver, pancreas, muscles, kidneys, thyroid.
active form: selenocysteine (active, organic form is 19% more effective than inorganic form in terms of absorption)
what are jobs of selenium?
1. Component of 25 proteins. Antioxidants enzymes such as • Glutathione Peroxidase • Thioridexin reductase • Selenoprotein P • Prevents lipid peroxidation and cell membrane damage 2. Essential for normal THYROID (T4 needs to be converted to T3 (active form). selenium facilitates this conversion) function 3. Essential for normal IMMUNE FUNCTION
cause and symptoms of selenium deficiency?
cause: low selenium in soil
symptoms. canalso be casued by TPN (total parenternal nutrition…receiving nutritoon through veins, but some nutrients, vitamins, and minerals…this it no longer an issue. but selecnium has since been added to it): Keshan’s disease (china disease…they have low selenium). manifests as dialated cardiomyopathy, loss of appetite, and nausia
what happen upon increased selenium intake? (toxicity)
- Garlic breath
- Hair loss
- Nail discolorations
where do you find iodine?
- Saltwater
- Seafood
- Seaweed
- Iodized salt
Iodine function?
needed for T3, T4 synth in thyroid
what decreases iodine bioavailability?
things that disrupt T4/T3 production by interfering with Iodine intake (goitrogens): • Cassava • Sweet potato • Cabbage • Cauliflower • Broccoli
what causes iodine deficiency symptoms? what are said symptoms?
- ↓ intake
- Goitrogens
Symptoms: 1. Goiter, hypothyroidism 2. Cretinism seen in babies: • Bloated belly • Pale • Umbilical hernia • Protuberant tongue • Poor brain development. remedy with increased Iodine intake
what causes iodin toxicity?
- ↑ intake
- Amiodarone (drug that increases iodine intake). this is an antiarryhthmic med.
- Iodine used as contrast agent for X-ray and
CT scan
Symptoms
• Hyperthyroidism (patient started with low amount of iodin and is now on this amiodarone drug and get this boost): Jod-Basedow effect
• Hypothyroidism (patient already had a lot of iodine, so thyroid shunts excess iodine from amidarone….thyroid shuts off to stop excess iodine..present with fatigue, constipation, hair loss): Wolff-Chaikoff reaction
Where is fluoride found?
- Fluoridated water
- Tea
- Seafood
- Seaweed
- Non-dietaryà toothpaste
how is fluoride absorbed? bioavailability? cicrculation? function?
Fluoride is topical and is therefore NOT absorbed and metabolized! Function: • ↑ enamel mineralization • ↑ tooth density • ↓ dental caries (cavities)
fluoride deficiency cause? symptoms?
cause: decreased fluoride exposure
symtpoms:
dental caries (cavities)
enamel erosion
what happens in terms of excess fluorid? cause of excess fluoride?
cause: increase fluoride exposure
symptoms:
• Mottled teeth
• Discoloration of teeth and pitting of enamel
Chromium source, function, deficeitney symptoms?
source: egg, whole grain, nuts, muschrooms
function: enhances insulin action
deficiency: blood glucose levels stay high after meals
cobalt source, function, deficiency symptoms?
source: animal food containing B12
function: constituent of Vitamin B12
deficiency: B12 deficiency symptoms
