iron Flashcards
where is iron found
center of hemoglobin in ferrous 2+ state
iron can REVERSIBLY bind with
oxygen
heme binds with _________ in lungs and carries to tissues
oxygen
oxidized iron in ferric state
methemoglobin (doesn’t carry oxygen)
how much do humans have of iron (all forms)
3-5 grams
how much iron is transported to bone marrow for heme molecules
80%
if you can’t get iron
iron deficiency anemia (IDA)
what is the center of myoglobin (muscles)
iron
massive breakdown of muscle=
lots of free iron released (toxic to the body)
iron storage places
bone marrow, liver, and spleen
2 forms of iron storage
ferritin and hemosiderin
how does iron get into RBC?
via transferrin receptors
where does iron go
depending on the needs of the cell
-shuttle for storage
-mitochondria for hemoglobin
how is iron regulated
absorption in intestine
how can absorption be disrupted
gasteric bypass surgery
chrone’s disease
if lining of intestine disrupted- absorption disrupted
what state of iron does absorption occur in
ferrous 2+
what state is iron after absorption
ferric 3+ bu gut mucosa
normal serum iron levels
60-170 mg/dL
body iron distribution
1) functional iron– needed for metabolic processes
2) Transport iron finish
body iron distribution
1) functional iron
2) transport iron
3) storage iron
functional iron
needed for metabolic processes (ex. Hgb)
transport iron
transferrin helps iron
-serves as way to get iron where needed
-prevents toxicity
-keeps iron soluble
storage iron
ferritan– 800 mg in the body
where is ferritin found
liver
spleen
bone marrow
macrophages
what moves to beta region on electrophoresis
transferrin
where is transferrin secreted?
apoferritin molecule (shell helps transport ferritan)
how many molecules of ferric iron does transferrin bind
2
what is the saturation rate of transferrin with iron
30%
in IDA saturation rate ____ because no iron to bind to
decreases
in IDA serum levels _______ because un bound transferrin
increased
what is saturation in iron overload
increased
in iron overload serum transferrin _______ because bound
decreased
main iron storage form
ferritan
most diagnostic indicator of IDA
ferritan
DO NOT look at serum iron as indicator of IDA because
serum levels remain normal because pulling from storage so look at ferritan
main iron storage site
liver
if there is liver damage
can’t hang onto iron
-release ferritin
-increase in serum iron
end stage hepatitis = iron toxicity
liver lets go of iron and dumped everywhere
APR acute phase reactant
ferritin
how is ferritin an acute phase reactant
increased in inflammation, malignancy, infection
COVID people have increased ferritin levels
ferritin woman levels
10-120
men ferritin levels
20-250
2nd form of storage iron
hemosideran
how is hemosiderin released from the body
slowly
granules in liver and macrophage help diagnose with prussian blue stain
hemosiderin granules
anemia has decreased
iron granules
protein made only in liver
hepcidin
what is main iron regulatory hormone
hepcidin (nothing to do with iron)
changes of mutations lead to IDA or iron overload
where is hepcidin found
serum or urine
function of hepcidin
control amount of extracellular iron that gets into body
how does hepcidin regulate
1) decrease or increase dietary iron absorption
2) control amount of iron released, enterocytes, gut cells, and macrophages
3) either destroying or not destroying ferroportin
ferroportin channels
in order iron inside cells to outside goes through ferroportin tube to extracellular
hepcidin can break down ferro protein to
decrease release
iron deficient in serum:
hepcidin levels decrease because need fetoprotein tubes are needed
iron overload in serum:
hepcidin increases because break down ferroportin so iron can’t exit
_______ follows iron levels
hepcidin
another APR
hepcidin
when hepcidin increased due to inflammation
will decrease serum iron levels
appear iron anemic but not
anemia of chronic inflammation
don’t give more iron! need to decrease inflammation
all cells have _______ receptors on them
transferrin
(bind transferrin and iron complex)– receptors turn inward release and turn back outward
once iron released
cleaved by enzymes and become soluble in serum
increase receptor
go along with decrease in available iron (wants every molecule it can find to attach to transferrin)
increase in iron= decrease in receptors
don’t need to go out and looks for them, it comes to them
NOT APR
soluble transferrin receptors
advantage because won’t increase in inflammation only in relation to iron status
look at chart in book
average iron balance in male
4 grams of body iron
average iron body woman
2.5 grams – lower RBC count
daily requirement of iron depends on
age, infant, toddlers, puberty, gender
lose 2 mg of iron everyday through
stool
urine
cells - dying
where does iron regulation – absorption occur
intestine
body uses what it needs and get rids of rest
major factors of iron abs
rate of RBC production
rate of myoglobin production
iron stored
what vitamin stored in combo with iron
vitamin C– helps with absorption
alcohol also increases absorption
interfering sources of absorption
dairy foods
tea
iron and calcium taken at same time
certain antibiotics
leading cause of anemia
iron deficiency
1 reason for IDA
nutrition
other reasons for IDA
-lead poisoning
-gastric bypass
-crohn’s disease
-celiac disease
-parasitic infection
how does IDA develop
serum iron first lowered
don’t see because call on ferritin to pull out reserve
-no symptoms until serum iron levels are low upon testing (ferritin also low)
test levels full blown IDA
decreased MCV, MCH, MCHC
increased transferrin, total binding iron capacity
decreased percent saturation
increased soluble transferrin receptors
decrease hepcidin– no inflam.
what happens in body during IDA
-lack of energy(oxygen not getting around)
-decrease mental capacity in child
-decrease growth
-large tongues
-sores in mouth
impairment of GI tract
main reason for iron overload
MAIN: hereditary hemochromatosis
hereditary hemochromatosis
not everyone homozygous- show expression later in life
men 5x to display symptoms because aren’t getting rid of iron like women
can absorb more iron than body needs
hereditary hemochromatosis symptoms
tan
liver problems
diabetes
if not dealt with how much iron can be in body
20 g
look at lab test for hereditary hemochromatosis
lots of patients get liver biopsy
prussian blue stain for hemosiderin
treatment for hereditary hemochromatosis
therapeutic phlebotomies
-chelation therapy
what occurs in celation therapy
deferoxamine
other reason for Iron overload
hemosiderosis
hemosiderosis
iron over load due to repeated blood transfusions
ex. sickle cell
have to monitor for diabetes, liver disease (pancreas destroyed bc iron overload)
use celation?
specimen for iron testing
serum tube and heparin
no oxalate, citrate, or EDTA : binds iron
combine detection … color metric
dissociation ferric iron from transferrin through addition of acid
ferric– ferrous= chromagin + ferrus = color proportional to amount of serum iron
serum iron levels
60-170
amount of iron that transferrin can bind if all binding sites saturated
TIBC
TIBC reflects
unsaturated transferrin (UIBC)
total iron binding capcity=
unsaturated iron binding capacity + serum iron
TIBC procedure?
1) saturate serum with per determined amount of iron that will saturate all transferrin sites
2) add agent that complex will all unbound iron
normal TIBC
250-425
amount of transferrin saturated with iron at any given moment
% saturation
% saturation equation
serum iron/ TIBC. x 100
normal % sat
20-50 %
below 20= IDA
above 50 = iron overload
