00:02
Let’s go into CLL.
00:05
This is chronic lymphocytic leukemia,
and you see that this is
then associated with SLL,
small lymphoblastic or
lymphocytic or lymphoma.
00:16
Why is CLL always associated
with SLL, always?
Diagnosis.
00:22
Basics.
00:23
Leukemia, the cancer began
in the bone marrow,
it then went into circulation, and
then it got into your lymph node.
00:33
You could no longer
call this CLL.
00:35
You will call this SLL.
00:37
From henceforth, you’ll never
see a CLL without SLL.
00:39
They are partners for life.
00:41
Partners for life.
00:42
In fact,
a very common cause of
non-Hodgkin's lymphoma is CLL/SLL.
00:50
Think about what I just said.
00:52
Are you ever going to find
Reed-Sternberg cell in a lymph node
in a patient who’s 70-some
years of age who has CLL/SLL?
Are you going to find
Reed-Sternberg cell?
Of course not.
01:04
Maybe you find smudge cell
or cracked chromatin,
but you will never find
a Reed-Sternberg cell.
01:09
If you don’t find a Reed-Sternberg
cell and you have a lymphoma,
you must call this a
non-Hodgkin lymphoma.
01:17
So now, you have diffuse
large B-cell lymphoma,
you have follicular lymphoma,
CLL/SLL, and multiple myeloma.
01:26
Eighty five percent of all of your
non-Hodgkin’s lymphoma will be those four.
01:32
What are they?
Diffuse large B-cell lymphoma,
follicular lymphoma,
this one, CLL/SLL,
and multiple myeloma.
01:42
Are you getting smart about
leukemias now, and lymphomas?
Yeah, you are.
01:46
Now, neoplasm of maturing
peripheral lymphocytes.
01:50
You only have two types,
T-cells and B-cells.
01:52
Don’t ever forget this.
01:54
You’ll always find
SLL attached to CLL.
01:58
They are partners for life.
02:00
The bone marrow is always involved, always.
02:02
That’s where the cancer
originated from.
02:05
Spleen and liver can also be involved.
02:07
How old is your patient?
Of all of the leukemias, all in general,
this is the most
common in the U.S.
02:14
So, this is the one you know --
you should know everything --
Actually, you know everything
about every leukemia.
02:19
But particularly, this one,
so this is by far the most
common leukemia overall,
older patient, older patient.
02:28
Now, specifically, the most common
leukemia in young children will be ALL.
02:32
I’ll give you that,
but overall, most common
leukemia is this one, CLL/SLL.
02:37
Let’s continue.
02:38
CLL disrupts your
normal immune function.
02:41
Why?
Well, if you knock out your bone marrow and
you don’t have proper B-cell production,
how in the world are you going to
then produce proper immunoglobulins?
You cannot.
02:49
You have hypogammaglobulinemia,
resulting in infections.
02:54
Also,
big time,
we talked about this
hematology with RBC pathology.
02:59
And we looked at autoimmune hemolytic
anemia, and I told you, I use a mnemonic.
03:04
It's cute.
03:05
I think warm in Georgia
and cold in Michigan.
03:08
Warm type of autoimmune
hemolytic anemia is IgG.
03:13
Could be associated, warm type
of autoimmune hemolytic anemia.
03:17
Do not forget that.
03:19
Also, associated with immune
thrombocytopenic purpura.
03:23
Immune thrombocytopenic purpura
is when you have autoantibodies
then attacking your glycoprotein IIb/IIIa,
or maybe perhaps your glycoprotein Ib.
03:33
Important, important associations with CLL,
you need to make sure you
know all of these, please,
before taking your boards and
walking on through your wards.
03:43
Some CLLs will transform
into a more aggressive form.
03:46
Stop here.
03:49
Blast crisis, is that what this is?
Nope.
03:52
Okay, now open your eyes again.
03:54
CLL.
03:56
CML went to blast crisis.
03:59
When CML goes onto blast
crisis, it may look like AML,
but you will know enough information,
you will know enough information
to identify the proper leukemia.
04:10
CLL, if it goes onto aggressive form,
if you remember correctly,
and I know you do,
that there are three ways in
which you can then develop
diffuse large B-cell lymphoma, three ways.
04:23
One was progression from
follicular lymphoma.
04:27
Two was the fact, de novo, BCL6.
04:31
Oh yeah, this one.
04:33
CLL may go onto?
Diffuse large B-cell lymphoma.
04:38
This is called Richter’s
transformation.
04:40
Prolymphocytic transformation,
known as a Richter,
transformation into diffuse
large B-cell lymphoma.
04:49
Third method of perhaps going
onto diffuse large B-cell.
04:53
All?
No, some.
04:58
With CLL, what are
you going to find?
Well, upon your morphology, you’ll find
something called cracked chromatin,
and you’ll find smudge cells as
you see in the picture here.
05:08
You’re not going to
find Reed-Sternberg.
05:11
Hence, if this enters a lymph
node, what do you call this?
Non-Hodgkin’s lymphoma.
05:17
Don’t forget that.
05:18
It is going to affect your lymph node,
quite commonly, in these patients,
so I keep bringing it up.
05:23
“Hey, doc”
“Hey, doc”
It’s just me
impersonating being old.
05:28
“Hey, doc. I have a
lump on my neck.”
“Does it hurt?”
“No, it doesn’t.”
Okay, this is concerning.
05:34
You'd find cracked chromatin
and smudge,
CLL.
05:39
Clinically, your patient,
median age of 60, oldest.
05:44
Take a look at the
WBC count, 100,000.
05:48
Remember that topic that we had for extreme
cases of neutrophilic leukocytosis,
extreme cases?
And at that time, I told you, what if
the appendicitis ruptured or sepsis?
Leukemoid reaction
was what that was.
06:02
Here, we'd find WBC count
greater than 100,000.
06:05
Insidious onset, once again.
06:07
Fatigue is going to be one
of your common symptoms.
06:10
I told you earlier, please
look for lymphadenopathy,
and also hepatosplenomegaly.
06:16
Older patient.
06:18
Progression is slow but my goodness,
if it transforms into what?
The more aggressive form known as
diffuse large B-cell lymphoma.
06:25
We have death within one year.