But macrocytic what are we looking for?
decreased hemoglobin, increased MCV, more than 100.
Now, pay attention here because we will not
differentiate between folate and B12 deficiency.
If it's folate, you will have increased
homocysteinemia or hyperhomocysteinemia.
B12 (deficiency) - decreased serum B 12.
And what was that enzyme
that B12 was a cofactor there?
MethylmalonicCoA or methylmalonyl mutase, right.
And then if it was homocysteine,
you're dealing with methionine synthase.
Letter M stands for B12.
Signs and symptoms of anemia with macrocytic.
Now, under B12, I'm going to first walk
you throughthose neurologic symptoms
that I was referring to earlier when I was
referring to our attaxic gait, spinal, cerebellar.
If it's proprioception and positive Romberg,
that'd be posterior column or dorsal column.
And that corticospinal tract would
then give you a positive Babinski sign
referring to your premotor neuron lesion.
You're taking a tongue depressor, and in
an adult, you take the lateral aspect the foot
and you caress it as you do so.
As an adult, normally, we
should then flex your toes, okay.
However, if it's positive Babinski, in
an adult, where the toes then fan out
upon lateral caressing of the toe, or
excuse me lateral caressing of the foot.
Then this is going to be a sign
of upper motor neuron lesion.
And this is not good, this is not good.
Last little thing that I wish to
add in here and just stick with me,
and physiology aspects of
treatment of B12 deficiency.
And boards love asking questions
like this, so that they know that you know
that you have an understanding of B 12.
Earlier I said that if you find a substance
within your urine, upon consumption of it,
or that food or whatever it may be, then you
know that it had to have been reabsorbed first,
then filtered and gotten into urine.
Okay. Let me walk you through the following.
Your patient has all the signs
and symptoms of B12 deficiency.
There is a megaloblastic anemia and unfortunately,
there is neurologic deficit that's occurring.
And now the neurologic
deficit is going to be irreversible.
Now, you don't find any B12 in the urine,
because whatever that the patient is not consuming,
let's say now, there's diet deficiency, either
in a nursing home with an elderly patient,
or maybe maybe it's a vegan
that we talked about for years, years.
Well, now at this point, there's consumption
of it, and there's supplementation of B 12.
And there's no problem inside your body.
It's just lack of diet, right.
So therefore, after consuming it, you
can then expect to find B12 in your urine
because then it has been reabsorbed and
filtered and then taken up to liver and so forth.
Keep that in mind.
Now understand though, in a true
Schillings test, you would then have to saturate
all the receptors on the liver for B 12.
And that will not be asked
because that's radiolabeled.
But the concept here becomes important.
Next, well if your patient had B12
deficiency, and now at this point,
you're suspecting that is that is
something like Pernicious anemia?
Well, let's say that you give intrinsic factor.
And now you find that there's reabsorption
of B12 from the terminal ileum into the plasma,
and it's been
Well, let's say that you give intrinsic factor,
and you still do not find the B 12 in the urine
Your diagnosis cannot be Pernicious anemia.
So what's your next step?
Need to find out where it
is B12 deficiency occurring?
The diet doesn't help with
supplementation, intrinsic factor didn't help.
Let's go ahead and give this
patient and pancreatic enzyme.
Would you tell me physiologically
why you require a pancreatic enzyme?
To remove the R factor from a B 12.S
o that it then gets properly reabsorbed
in the terminal ileum with intrinsic factor.
So now you give pancreatic
enzyme and you find B 12 in the urine.
What's your diagnosis?
So now, let's say the diet didn't work with
supplementation, the intrinsic factor didn't work.
How do you know?
Because he ended up finding it the
B12 in the stool, and it wasn't in the urine.
Andpancreatic enzyme you
had given, that didn't work.
Next, maybe you give antibiotics, you
give antibiotics and you find B12 in the urine.
Theoretically, what happens here?
Well, your diagnosis should be?
Good. Back to overgrowth, right.
So back to overgrowth there, you
kill off the overgrowth with antibiotic.
The B12 is now properly
reabsorbed and ends up in the urine.
Do you understand the concept of how
there are certain attributes of the Schilling test
that you're going to use from head to toe so
that you can then properly diagnose the patient.
And how they will most likely work this with B12 is
going to be the fact that yo have cobalamin, okay?
C-O, Cobalamin, keep that in mind.
And whether or not you find that in the urine
and that table that I showed you with B12 ,
all the different methods by which
you can develop it is important.
aLst little thing that I wish
to bring to your attention,
Is it megaloblastic anemia that you only find?
meaning megaloblastic RBCs.
No, remember that the neutrophils also are not
properly developing because as pancytopenia,
you would expect to find, what can you think
of what a normal neutrophils should look like?
Okay, should they be segmented?
But what if you end to end
up finding 8 to 12 segments?
That's called a hypersegmented neutrophil.
And that to you should clue you in.
Oh, I must be suffering from or the
patient's suffering from megaloblastic anemia.
Last little bit that I wish to
bring to your attention is earlier,
when I set up the overview
for anemias I said that there was
megaloblastic and non-megaloblastic anemia.
Up until this point, your focus should
be strictly upon megaloblastic anemia.
And where's my problem with megaloblastic anemia?
It's effect in DNA, or in the bone
marrow, you don't have proper maturation,
maybe either due to lack of DNA synthesis,
or as we saw with diamond Blackfan anemia,
We have a problem with
aerythroid progenitor, right?
If it's non megaloblastic macrocytic, and
then you're thinking about alcohol, liver disease
or reticulocytosis, think about those:
Liver has nothing to do with the bone marrow.
Alcoholism has nothing to do with the bone marrow.
and reticulocytosis means a bone
marrow is producing too many reticulocyte
which is immature RBC into circulation.
Would you tell me the size of a cell that is always a
little bit immature or premature than the mature cell
The size, the size is always bigger.
So reticulocyte is always larger than an RBC.
And so therefore, you can have
non megaloblastic macrocytic anemia,
The big ones here, liver disease,
alcoholism, and reticulocytosis.
Keep those in mind and that gives
you big time high yield information
for all macrocytic anemias that you
have to be familiar with on your boards.