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Course: Health and medicine > Unit 6
Lesson 6: Iron deficiency anemia and anemia of chronic diseaseAnemia of chronic disease
Created by Nauroz Syed.
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Is it not splenic macrophages that are the main target for hepcidin rather than hepatic macrophages?(4 votes)
I think you are correct because the degradation of RBCs mostly occurs in the machrophages of the spleen(4 votes)
- Hepcidin doesn't block ferroportin. It induces it's internalization and degradation in the enterocytes.(3 votes)
- Is "anemia of chronic disease" the same as chronic anemia due to chronic kidney disease? Or is this different? Thanks.(1 vote)
They are different. Strictly Speaking, "Anemia of chronic disease" would be referring to anemia in the setting of prolonged inflammation in the body, where the inflammatory cytokines stimulate hepcidin production to supress circulating iron stores and induce an iron deficiency anemia. Saying "Chronic kidney disease anemia" would be more referring to anemia caused by a failure of the kidneys to secrete erythropoetin (EPO). Without EPO, the signal for the bone marrow to produce more red blood cells is lost and anemia results. In real life, these categories do become a little blurred because often people with chronic renal disease also have iron deficiency. Also, if you had a chronic inflammatory process in your body such as Lupus, you might get renal failure anemia as well as anemia of chronic disease, so it would be tough to determine how much each problem is contributing to the overall anemia.(4 votes)
Do anemia of chronic diseases occur in children?(1 vote)
Of course. Some anemias are acquired but a lot are also just conditions that children are born with or that they inherited from their parents. Same goes for chronic disease (which is a VERY broad term; if you want to know about a specific chronic disease feel free to ask :) )(2 votes)
It is incorrect to state that hepcidin blocks the degradation of RBCs. Rather, it blocks the release of the iron sequestered in ferritin in the macrophages that have broken down the RBCs (mostly in the spleen). Therefore the iron is not available for production of new hemoglobin. So it interferes with the production of new normal RBCs, but does not prevent degradation of old RBCs.(1 vote)- I keep getting questions about total iron binding capacity in anemia of chronic disease. I always thing TIBC should be increased because there isnt much iron available. Nothing else makes sense, but apparently that's wrong, according to kaplan's qbank. I was hoping this video would mention it. =(
Are there other videos that explain this?(1 vote) - How does body stop autoimmune diseases by decreasing serum iron?(1 vote)
Video transcript
- [Voiceover] So anemia of
chronic disease is the second most common cause of anemia
in hospitalized patients and it's a type of microcytic anemia, microcytic anemia. So, that tells us that
anemia of chronic disease is somehow due to a problem, a problem in producing hemoglobin because we know that
all microcytic anemia's result from a problem
in producing hemoglobin. The second thing that's really
important about this disease is that it's always, always,
always, always related to some inflammatory condition. So that's to say that
there must be some source of inflammation in the body
for this disease to result. Now, anemia of chronic disease
has absolutely everything to do with the molecule, hepcidin which is a polypeptide,
is just a fancy term for a chain of amino acids
that's produced by the liver that serves as the bodies
major iron regulator. And by regulator, I mean that when the serum iron levels are low, when the bodies iron
levels are running low, there's a low production of hepcidin. But, when the bodies iron
storage are running high or when there is excessive
amount of iron in the body, the liver increases
it's hepcidin production and it does this because the hepcidin then turns around and
it decreases serum iron, decreases serum iron. And it does this, it decreases serum iron in a couple of different ways. And to understand how it decreases it, I guess we'd have to go
back for a couple seconds to understand iron physiology. So, we talked about how iron
is absorbed it the duodenum, but something we didn't mention is that at the base of these cells in duodenum is this channel called ferroportin and ferroportin is what allows the iron to go across these cells in the duodenum and be absorbed into the bloodstream. Now hepcidin comes in and it blocks the ferroportin channels and by doing so, it inhibits the absorption
of the iron from the gut. So, that's the first way
in which hepcidin acts to decrease serum iron levels. Now, I'm going to scroll down, scroll down just a little, okay, so secondly, let's
take a look at the liver, and here's a blood vessel
that has blood in it and we know that blood has
lots of red blood cells in it. And every 120 days or so, each
one of these red blood cells is taken out of commision, it's retired and it's degraded by cells in
the liver called macrophages. So, these red blood
cells are broken down by the macrophages and
inside the red blood cells we know we have lots of hemoglobin and the hemoglobin has iron in its center, and the iron that is
released from the degradation of the red blood cells
isn't just thrown away, instead it's saved and it's recycled to be used later on to
make new red blood cells. So, what hepcidin does in this scenario is it comes in and it
inhibits the degradation, it prevents a degradation
of these red blood cells, and it does so to prevent this iron from being saved and
being recycled later on. So this is the second
way in which hepcidin acts to decrease serum iron. So, moving to the side just a little, so just to quickly
summarize what hepcidin does is it decreases serum iron by decreasing the absorption of iron from the gut and decreasing recycling by inhibiting the degradation of red blood cells. And, in normal people,
hepcidin is released in response to an increase
in serum iron, right? So it's essentially the
bodies compensatory mechanism to deal with too much iron. Now, in the case of
anemia of chronic disease, hepcidin is released in response to any inflammatory condition, so any condition in which
there's inflammation. So firstly, what do I mean
by inflammatory condition? Well, I mean things such as infection, because we know our body
mounts an inflammatory response to protect us from infections. Now I also mean things like cancer, who's malignancies a pretty
inflammatory condition and also autoimmune diseases,
autoimmune diseases, and usually what comes to
mind with autoimmune diseases is things like rheumatoid
arthritis or lupus but really any autoimmune condition can do the same thing. So these are just three
of the most common causes of inflammation but really
there's several other disorders that could lead to the same response. Now, when there's any source
of inflammation in the body, the body releases cytokines or small signalling molecules. And these cytokines cause an increase in hepcidin production. The hepcidin then decreases
the absorption and recycling of iron to lead to a
decrease in serum iron. That much we've already established. Now this decrease in serum iron then leads to a decrease
in hemoglobin production, and that decrease in hemoglobin production is what leads to the anemia. And that's how an inflammatory condition or a chronic disease leads to anemia. Now, I guess something that we haven't really addressed very well, is why would you want
there to be a decrease in serum iron in response to
an inflammatory condition, why does this pathway even occur? And the response to that
is really important. So, in conditions such as, for example, such as infection, bacteria
thrive off of iron. They use it as an
essential nutrient to grow. So really what the body
does is quite smart, it essentially plays
keep-away with the iron. So it releases hepcidin
to keep away the iron so that the bacteria can't use it to grow. And really, this same thing occurs in cancer and in autoimmune condition in which these cells use iron
as an essential nutrient. So that is essentially the background and the pathophysiology of
anemia of chronic disease.