We’ll continue our discussion of
dermatology by looking at angioedema.
Take a look at
these lovely lips.
Well, this was not implantation.
This was not a patient that went in for
cosmetic surgery and had it enhanced.
So, what do you think
Well, there are two ways in which your patient
may develop what’s known as angioedema.
To begin with, by definition,
when you have angioedema, it is the fact
that you have edema that’s taking place.
Obviously, it’s leaving, or should I say
the fluid is escaping from the angio,
which refers to
your blood vessels.
And when it does, in terms of
its location, most likely,
it would be deep into your skin,
so you’re thinking about dermis, and maybe
perhaps even, your subcutaneous tissue.
With that said, our
topic is angioedema.
It could be acquired
And with skin, the last time we
talked about this was, in fact,
a type 1 hypersensitivity in which
you would be releasing histamine,
and that would be a type
of acquired angioedema.
And at some point in time, we’ve also
discussed hereditary type of angioedema,
which from immunology,
will be more or less
considered to be a complement
type of pathology,
in which your patient is then
deficient of C1-inhibitor.
All those should come in mind, and we have
swelling of the lips, airways, or eyes
when dealing with angioedema
The causes include --
well, in order for you
to understand this,
it’s the concept that you
want to keep in mind.
The concept here is going
to be the fact that
you are not able to properly
control with hereditary.
Your complement system.
And by this, we mean, for example, we’ve
talked about a few complement pathologies,
in which you have unrestricted or
unopposed complement activity.
These include paroxysmal
These also include
your dense deposit
disease that we saw with
glomerulonephritis type 2.
And then here, normally,
you require a C1-inhibitor
so that you keep
things under control,
so that you do not have excessive
Let’s say that you’re
missing the inhibitor.
If you’re missing the
inhibitor of C1,
then you have unopposed
C1 esterase inhibitor deficiency,
and you would not consider
this to be hives.
So therefore, this is not
considered to be urticaria.
Patients will present with, well,
this is important, low C4 levels.
And the reason for that is
because, well, as I told you,
if you have unopposed
guess what you’re going to
do with your complement.
You’re activating it, or activating
them, and you’re also consuming them.
So therefore, you can expect your
complement levels to be decreased,
but this is a concept
we’ve seen earlier,
when in fact we did
Then we move on to acquired type.
Acquired type, obviously,
would be more common.
And with the acquired type,
what if there was a patient
who had hypertension,
and with hypertension, this patient
was then put on ACE inhibitor,
and all of a sudden,
started having dry cough?
In addition to dry cough, there was also
angioedema that was also developing.
Remember that with ACE,
it’s an enzyme that normally knocks
out or metabolizes bradykinin.
And so therefore, if
you inhibit the ACE,
then there could be increase
levels of bradykinin.
This bradykinin then brings
about, at this point,
the theory that you
want to take with you,
is a dry cough and the fact that the
patient may present with angioedema.
Do not confuse this
This is twice now that I’ve asked you
not to confuse this with urticaria.
Urticaria means hives, thinking
about wheal formation.
Urticaria would be a
type 1 hypersensitivity
in which that histamine is
then causing vasodilation.
This is either hereditary or
acquired type of angioedema,
and this is deep down beyond the skin
so you will not have urticarial hives.
Remember, edema, it’s taking place,
affecting the mucosal membrane.
Then the allergy acquired, which
we talked about extensively.
So, still under acquired
type of angioedema,
your patient has been,
perhaps, exposed to drugs
or maybe perhaps
associated with urticaria.
Keep the two separate, please.
By that, we mean urticaria would
be more superficial in nature.
And so therefore, it is the blood vessels
in the epidermis undergoing
wheal or hive formation.
Whereas here, we’re talking
about blood vessels
deeper down in perhaps
the subcutaneous tissue.
Well, epinephrine if
airway is compromised.
Remember, please, that if it
is in fact the acquired type,
there’s every possibility that you would
have severe involvement of your airways.
So therefore, epinephrine is something
that you want to keep in mind.
If it’s allergic that
you’re thinking about,
then obviously, antihistamine or
IV steroids so that you can remove
the effects of your constriction,
or in this case, vasodilation.
And if it’s hereditary,
well, in this case, you
want to try to replenish
some of that C1-inhibitor that
was deficient to begin with.
Another name for that C1-inihibitor is
technically called C1 esterase inhibitor,
and this then has to be replenished,
you’re thinking about FFP,
which stands for
fresh frozen plasma.
And then if it’s ACE inhibitor
obviously, remove the offending agent and
stop administering to ACE inhibitor.