at. It is pretty much to kidney. We know vascular
Our topic continues with secondary hypertension.
Here, however, we are in the concept or in
the topic of endocrine. What does that mean?
Well, remember hypertension crosses all borders.
At this point, we have completed secondary
hypertension when dealing with the renals,
when we went through those important differentials.
Here under endocrinology, when we are referring
to Cushing’s syndrome, now right off the
bat, close your eyes and think about all the
different sources in which Cushing's could
take place. As soon as you hear about Cushing's,
take the scene Cushing's please and you know
that you have excess cortisol. Excess cortisol.
Whatever form that maybe, glucocorticoids,
prednisone. So here we have Cushing’s syndrome.
What are the four different causes? As you
go through them, tell me as to what is the
most important or what is the most common
cause of Cushing's? It is actually not even
from our body. It is exogenous sources. What
is that called, please? Called factitious.
It is called iotrogenic. It is exogenous.
Do you understand anytime that you see those
three words, what are they again? Iotrogenic, exogenous
or factitious. That to you should mean, that particular drug hormone
whatever it maybe is coming from an outside
source, is that clear? I hope so. So that
is the most common, isn't it? Think about
prednisone. All the different reasons as to
why patient might be taking prednisone.
I am going to give you secondary hypertension.
Let us move into this. This is Cushing’s
syndrome. Where am I? Not in the anterior pituitary.
How do you know? Because anterior pituitary, would you call
this Cushings syndrome? Good. No, you wouldn't.
You'd call this Cushing’s disease if it was
anterior pituitary. "So Dr. Raj what in the
heck that you are getting at?" If you had a
tumor in the adrenal cortex that is producing
cortisol, are you only producing cortisol?
No, you might also be producing aldosterone.
Now you are getting to my point. What is my
topic? Secondary hypertension. Remember, please.
In this case, the pathology, the end game is
the fact that you are going to develop increased
blood pressure. And that increased blood pressure
is coming from aldosterone in Cushing’s
syndrome. Take a look at the patient here.
The face, moon facies. What are we looking
at in this patient's torso? It is the fact
that there is truncal obesity and we have
striae. What else might you find in the back
of the neck perhaps? You are looking at buffalo
hump, right? So that your patient in general
with Cushing's because of excess corticoid
from whatever source. Just to be complete, the
other sources included the anterior pituitary
and then also your lung. And from the lung,
you should be thinking about most commonly,
small cell lung cancer. Now my point is this.
If you produce too much aldosterone at some
point in time, what may happen? You may then
cause increase in blood pressure resulting
secondary hypertension. Cushing. Now be very
careful because our next differential here
for secondary hypertension. Take a look. We
have removed our patient because this is Conn's
syndrome. Conn's sydnrome was not going to
have moon facies, buffalo hump and so on and
so forth as we just saw. Conn's syndrome is
a primary, listen to what I am saying? It is all
about verbiage. It is all about terminology
and if you are not careful about terminology
when you are reading something, it is quite
easy for you to miss a question, might be quite
easy for you to misintepret your patient.
You do not want to do that. So it is primary hyperaldosteronism.
What does primary mean to you?
It means that that particular problem
or pathology is actually taking place from
that organ. Aldosterone comes from where?
Adrenal cortex. What layer? Glomerulosa,
the most superficial layer. You have a tumor
there that is producing too much aldosterone.
This is called Conn's syndrome. This is primary
hyperaldosternoism causing what kind of hypertension?
You said primary. I am sorry. As much as you
want to, please note that this is not primary.
It is secondary hypertension. How common is
this? More common than what you think. Make
sure you know about Conn's. So in Conn's syndrome,
it is a primary hypoaldosteronism with a tumor
in your adrenal cortex producing too much
aldosterone resulting in what kind of hypertension?
Secondary hypertension. Is that clear? Now
give me the labs here because you are not
done. You are going to be given a sheet of
labs and you have to be able to interpret
as to your patient having Conn's. What happens
to sodium? Increase. What does that mean?
Greater than 145. What about potassium? You
are getting rid of it because you have too
much aldosterone. So my potassium is less
than 3.5. And then what about hydrogen? You
are getting rid of your hydrogen. So what
happens to your pH? Increases. Welcome to
alkalosis. Is that clear? Welcome to Conn's.
This is something we have looked at, we will
look at and we'll forever look at because it
comes up so many different times. Let us continue.
Endocrinology, now we have pheochromocytoma.
Where am I? Where are you? You are still in
adrenals, but what part please? The medulla.
In the medulla, you might have a tumor. You
have a tumor that does what? Produces too
much of your epinephrine. Remember normally
speaking, 80 percent of your epinephrine comes
from where? It comes from the adrenal medulla,
doesn't it? Eighty percent does. What about
epinephrine? Epinephrine works on many receptors,
catecholamine receptor, alpha-1, alpha-2,
beta-1, beta-2. At lower doses works on what?
Beta. At higher doses work on alpha. Works more
like an epinephrine. You know that from form,
I'll walk through that quickly. Right now let's just
focus upon the path. Inferior chromocytoma,
you have too much epinephrine and did you have
this epinephrine all the time? Is it constitutive?
No. It is episodic. You pay attention to the
term episodic hypertension. If you have too
much epinephrine, at some point in time might
you find its metabolites in the urine? Sure
you will. What is that called? VMA, vanillylmandelic
acid may be metanephrine so much so forth.
This episodic hypertension, headaches, diaphoresis,
what does that mean? Remember too much sympathetic
activity. Would you please tell me how you
sweat? It's a sympathetic or parasympathetic influence.
Sympathetic. Remember one of the big exceptions,
sympathetic muscarinic receptor, diaphoresis,
palpitations all the time. No, not
like Grave's disease. Is that clear? Give yourself a differential,
palpitation, Grave's. Here we have pheochromocytoma.
Let us continue. Adrenal mass. Where are you?
Adrenal medulla. What kind of tumor? It is
a benign tumor. What are you going to find?
Plasma free metanephrines, urine here it is,
VMA, vanillylmandelic acid. What does that
mean? It means that these are the metabolites
of your epinephrine being broken down. Rule of tens.
This is something that we discussed
in endocrinology. Ten percent of the time
it might be sporadic. Ten percent of the time
might be familial. Ten percent of the time might
be both kidneys are affected, so on and so
forth. What else may result in secondary hypertension
when dealing with endocrinology? How about the
thyroid gland? If it is hyperthroidism, it
might then increase your systolic blood pressure,
SBP. And if it is hypothyroidism, then it might
be something like increased diastolic blood
pressure. That is important for you to know
clinically, please. Hyper is the fact that
your patient's heart feels how? Oh! It is
palpating. And you have hypothyroidism, increased
diastole blood pressure, thyroid gland. Continue.
What about another endocrine pathology that
may result in secondary hypertension, but
this is hyperparathyroidism. What is this?
This is the fact that you are producing too
much what? PTH. Where? Your parathyroids.
Where am I? Right around the thyroids and
you have your parathyroid producing too much
PTH. What is that going to do? It is going
to run to the kidney. It is going to do what?
It is going to reabsorb the calcium. What
kind of effect does calcium have on your blood
vessels, please? Think about that. Your blood
vessel normally is what kind of muscle? Smooth.
What does smooth muscle mean to you? Think
about alpha-1. Are you there? Bring in some
biochem here. You've alpha-1 receptors, what
does it do? It stimulates your phospholipase.
What are you going to release? IP3, DAG. What
are you going to do next? Release calcium.
What does alpha-1 do to your blood vessel?
You know it causes vasoconstriction. So, therefore,
you have the calcium bind to calmodulin, so that
you do what? Vasoconstriction. What is that
going to do to your TPR and here we will go on
and call this PVR. It increases resistance.
Peripheral vascular resistance is going to
be increased. Is that going to increase your
blood pressure? Sure it will. What kind? Secondary.
Are you following me? Everything that we're
going to do here have an explanation, has
a story. You relate this to a patient, a presentation what-not,
you are in good shape. You cannot be fooled.
I don't care who you are. Understand your patient. You
won't miss a single question.
Next under cardiovascular, still secondary
hypertension, we have a condition called coarctation
of aorta. As soon as you have coarctation
of aorta, close your eyes, think of what please?
Think about this patient. Listen to what I
am saying. There is webbing of the neck. There
might be two cusps of the aortic valve. Interesting. If
it is a female, XO and if it is the ovaries
may result in something called dysgerminoma
ovaries. Who is my patient? Turner
syndrome. In this patient, you also noticed
that the blood pressure in the carotids might
be higher than the blood pressure in the extremities.
By extremities, I mean down by the feet. Think
about the dorsalis pedis. The blood pressure
in your upper extremity might be higher than
the blood pressure in your lower extremity.
How does that occur? Remember Turner is a
genetic problem with XO being the chromosome.
Next, what happened? I told you that there
was a webbing of the neck. What is that called?
It is called lymphangioma. Isn't it? It is
the fact that the lymph is becoming dilated
and you might actually be able to see this
in vitro with an ultrasound in which the back
of the neck you see being filled with fluid.
That is your "webbing of the neck". Make sure
that you know the full understanding of webbing.
Number 2, what else did I say? I said that the aortic
valve, which normally has now many cusps?
It has three cusps normally. But is it possible
that your patient might have congenital bicuspid
aortic valve? Sure they can because your patient
is Turner. And then what about the blood pressure?
The differential, coarctation. What is that
going to do? I want you to go back to physio
and I want you to think about a pipe and a
tube and you are going to add a resistor right
in the middle. You see that right there. You
added a resistor in the middle. When you added
a resistor in the middle, what then happen
to the pressure proximally? It increased.
What happened to the pressure distally? It
decreased. What did you do? You added your
resistor in a series. Where am I? The aorta
and you coarcted. What does coarcted mean? It
means constriction. So what happens to the
blood pressure in the upper extremity? You've
increased it. And what about the blood pressure
in the lower extremity? It is decreased. What
do you think happens to perfusion of the kidney?
Decrease. What kind of questions might they ask
you on physio? May I ask you about decreased
perfusion to kidney and coarctation, true
or false? True. So, therefore, what are you
going to release? Renin. When you go through
the same concept, secondary hypertension, coarctation.
Let us continue. Obstructive sleep apnea.
Now for this how
much do you think of. Maybe in older patient,
an obese patient perhaps and it is the fact
that there might be obstruction taking place
while breathing out. And so therefore around
the vocal cords, maybe there is the pharyngeal
folds and such and there might be excess muscle.
There might be excess "flap" and so, therefore,
makes it difficult for your patient to properly
breathe especially at night. Sleep apnea,
maybe for intervals of greater than 10 seconds,
there might be lack of proper breathing. That
is amazing. That is very scary, isn't it?
At some point in time, what is it going to
happen? This patient is not breathing properly.
So if there is improper ventilation taking
place, then what is the patient retaining?
Because the patient is not able to blow off,
what are you supposed to blow off normally?
Carbon dioxide. But that isn't a happening in
a patient with obstructive sleep apnea. You're literally
obstructing the ability to exhale your carbon
dioxide. Where is it remaining? Within your
blood. What does carbon dioxide mean to you in terms
of pH? Carbon dioxide equals acid, doesn't
it? Of course, it does. Think about the carbonic
anhydrase formula. So you're producing acid, so
what kind of acidisosis is this? Respiratory
acidosis, isn't it? And at some point in time
maybe with obstructive sleep apnea during
the day, you might find a little sleepy and
the patient might be feeling a little tired
and such, so obstructive sleep apnea.
So now what happens. Obesity, rapid weight
gain with snoring, neck size greater than
17.5cm. What kind of treatment measures are
you worried about in this patient? Well, you
need to make sure that you clear up that airway
ASAP. Think of CPAP, continous positive airway pressure.
What kind of drugs might you be thinking about
treating this patient's obstructive sleep apnea?
OCPs, NSAIDs, steroids, phenylephrine.
So think about this. This is no joke. Obstructive
sleep apnea once again is a huge issue and
so, therefore, those of you that are going
into family medicine and so on and so forth, you
are going to be involved in sleep studies
and that is going to be a huge part of your
practice because you are going to find a lot
of people coming in with such issues and would
have secondary hypertension. Keep that in
mind. Now with this table, we are going to quickly