Lecture 13: Iron Defiency Anemia Flashcards
——- is the most common form of anemia world wide
iron deficiney anemia
iron difiency anemia is te most common cause of a —
microcytic hypochromic anemia
etiology (——-) of IDA:
origin or cause of a disease/
1)Inadequate intake of iron, which may result from a diet low in iron or from the
INABILITY TO ABSORB IRON.
2)Increased demand for iron such as pregnancy, rapid growth (infants, children)…
3)Excessive loss of iron, for ex, due to acute or chronic hemorrhage.
in humans, iron is a major component of:
1) hemoglobin (Hb contains 2/3 of the body’s iron)
2) myoglobin in muscle cells
3)most cells of the body because they have enzymes that contain iron (cytochromes, peroxidases, catalase)
pararaph page 1 (end)
Iron daily utilized by the body for Hb synthesis is obtained almost entirely from ——-and iron taken in the food is only used to —–
the stores/replace iron lost from the body
iron circulates in plasma bound to—-
the glycoprotein transferrin which has two high affinity binding sites for Fe (III).
tranferrin binding maintains iron in a —and serves as —
soluble form (=dissolved form)/ major vehicle for iron delivery into cells via the transferrin receptor TfR1 so byeje l transferrin be3ale2 3al TfR1 w the iron can enter the cell.
In humans, plasma transferrin is normally about —-saturated with iron./ a tranferrin sturation of less than 16% indicates —whereas more than 45%—
30% / iron deficinecy/ is a sign of iron overload
iron is also released into the cicrulation from –
duodenal enterocytes (duodenum= part of small intestine) which absorb 1-2 mg of dietary iron per day and from macrophhages which internally recycle 20-25 mg of iron senescent erythrocytes.
Hepatocytes play a dual role in systemic iron metabolism:
1) they’re the major sites of iron storage
2)they secrete the regulatory hormone hepcidine
what does hepcidin do?
hepcidin orchestrates systemic iron fluxes —-go to page 2
circulating of iron in the human body is bound to– and then delivered to tissues/
what’s the difference between trasnferrin and holo-Tf?
transferrin (holo-Tf)/
trasnferrin=iron binding protein while holo-Tf is the iron loaded protein
Holo-Tf is primarily
replenished by —-but also by—. under conditions of iron defienciy,
iron recycled from tissue macrophages/dietary iron
absorbed by duodenal enterocytes / iron
stored in hepatocytes can also be mobilized
iron efflux to the blood stream is inhibited by —-
liver-derived peptide hormone hepcidin, which binds to the iron exporter
ferroportin (FPN) and promotes its degradation.
It is important to pinpoint that there are two kinds of iron in the diet —-/ each has its own
non heme iron and heme iron/method of absorption and and own reaction to dietary intercation
the most active sites of iron absorption are:—-/ iron is absorbed either as —
deudenom and upper jejunum/ ferrous iron or as heme/
after the reduction of Fe 3+ –
(present in Non
Heme Iron) Fe++, Fe++ comes to the duodenum and enters the lining cells of the
duodenum where there are receptors for iron on these cells.
check out pic page 3
The entry of Fe++ in the duodenal cell lining is increased in the presence of——-
high EPO therefore excess EPO = excess iron absorption (EPO is a hromone for RBC production so high EPO =high Fe absorption =high Hb production)
what happens to the heme in the intestinal cell?
it’s split in the intestinal cell and its iron is released as Fe2+ to join the Fe++ taken up
as such by the mucosal cell.
the iron absorbed by the intestinal cells may have one of 2 fates:
1) If the body needs iron more than normal (EPO is high ), then the iron passes from the
intestinal cell to the blood stream. This occurs in the growing state, during
pregnancy and Fe deficiency.
2) If the body does not need much iron and has excess iron, the absorbed iron is
caught in the cell lining of the duodenum by a protein called ferritin and is
deposited there as such. And because there is daily loss of intestinal mucosa, Fe is
lost with the intestinal mucosa and goes with the stool.
if that iron is not shed,—–
our body becomes poisoned by excess iron. People who
inherit a deficiency in this mechanism go on absorbing iron, that goes to the blood
stream and gets deposited in vital organs such the heart, kidney, liver and
pancreas leading to their damage. This condition is known as hemochromatosis.
The iron that is absorbed into the blood stream from the intestine does not ——
travel free, instread it’s bound to a transport protein called transferrin (i think it’s safe to say eno it’s always bound to some kind of transport proteun)
transferrin is synethsized by–/ 1 molecule of transferrin binds–
liver cells/ 2 molecules of iron
note that in the plasma, Fe 2+ is reduced to —
Fe 3+ the moment it’s absorbed
The iron bound to transferrin is transported to certain specific cells in the body —-/ these cells include:
cells with receptors to transferrin/
1The erythroid series including the reticulocytes
2)Muscle cells to form myoglobin
3)Placental cells in pregnant women
4)Histiocytes in the B.M.
5)Hepatic cells
What happens when transferrin carries the iron to the erythroblasts found in the
B.M?
Transferrin comes and sticks to the cell membrane receptor and then the whole complex
is taken and iron is liberated in the cell; it is first changed to Fe++, and then it enters the
mitochondria in which a series of enzyme controlled reactions occurs the result of which
is a substance called heme. Then the heme leaves the mitochondria and comes to the
cytoplasm to meet the globins synthesized on the ribosomes. Some iron is not changed
into heme, but remains stored in the RBC as ferritin.
iron stores (ferritin) are found in—-
the liver, BM and spleen, however, the majority of the stores are found in the liver.
When the erythroblast matures, it becomes smaller; its nucleus becomes smaller
pyknotic. Finally, it is extruded, and ——
and this extruded nucleus is taken up by the
histiocyte of the B.M. With this nucleus, there is a thin rim of Hb, which is also
taken up by the histiocyte. This Hb is broken down to release iron, so that with
time, this histiocyte becomes loaded with iron this iron is stored in the
histiocyte. When so many RBC(s) have matured, a great amount of Hb is wasted
and stored as iron in the histiocytes of the B.M.
if tere is a high rate of death around the histiocyte—
(ineffective erythropoiesis), then the amount of Hb wasted is much higher the histiocytes become loaded
with Fe.
Any rigid RBC or any defective RBC on the other hand,——-/in a nomral person, ——
will not be able to pass
through the sinusoidal lining safely it is caught there and phagocytized by the
endothelial lining. /as much as 5% of the RBC(s)
produced daily are defective and are therefore phagocytized by the endothelial
lining.
so the first iron store is in the — while the second one is in the—
liver /sinosoids of the BM
FINALLY, the normal RBC goes into cocrylation where it stays there for —
100-120 days, after which it’s taken by the spleen its Hb is broken down to release iron that
is stored in the macrophages of the spleen.
iron is stored in one of 2 forms:
1) ferritin (fe 3+) which is water soluble
2) hemosiderin which is water insoluble
difference between ferritin and apoferritin
ferritin =apoferritin + stored iron
