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hello
and welcome back to the nephrology
curriculum today we're going to be
talking about
secondary hypertension so interestingly
hypertension is actually the most common
disease specific reason
for office visits of adults to
physicians in the u.s
now when we think about the definition
of hypertension it really depends
on who's defining it so by the joint
national committee
which guidelines were produced in 2014
it's really based upon the average of
two or more properly measured readings
of each
of two or more visits of an initial
screen
normal blood pressure is considered a
systolic of less than
millimeters of mercury a diastolic of
less than 80.
pre-hypertension is considered a
systolic pressure
of between 120 and 139 and a diastolic
between
80 and 89 millimeters of mercury and
finally hypertension
is staged in two stages stage 1 is
considered a systolic blood pressure
of 140 to 159 with a diastolic between
90 and 99
and stage 2 is a systolic greater than
160
and a diastolic greater than or equal to
100.
now over the last couple of years we've
had some interesting randomized
controlled trials
and therefore the american college of
cardiology and the american heart
association
really have provided newer targets based
on the most recent evidence
a normal blood pressure according to the
acc and aha
is considered again less than 120 over
80.
but an elevated blood pressure now is
considered a systolic between 120 and
129
with a diastolic of less than 80. stage
1 hypertension
is now considered a systolic between 130
and 139
and a diastolic of 80 to 89. stage 2
by the acc and aha is considered a
systolic greater than or equal to 140
and a diastolic greater than or equal to
90.
now these are updated targets and i want
you to stay tuned because as new data
comes in
these might be moving targets for you
so when we think about hypertension the
majority of physician visits for
hypertension are due to what we used to
term essential
or primary hypertension but about 10
percent of those cases
are actually due to secondary
hypertension
when we think about the pathogenesis of
primary hypertension
it's really multifactorial and the
purpose of this slide is not to have you
memorize it
but to really understand that there's so
many different things that go
into primary hypertension we have things
like an increase in sympathetic nervous
tone
we have activation of ras that will
increase cardiac output
we also have local and circulating
regulators
that will ultimately increase peripheral
vascular resistance that
ultimately will manifest into primary
hypertension
this is in contrast to the pathogenesis
of secondary hypertension
where the pathogenesis is related to the
underlying condition
this is due to things like renal
vascular disease a functioning adrenal
adenoma
sleep disorder breathing medications
either iatrogenic or illicit substances
things like black licorice typically
european
and then finally coarctation of the
aorta
so when you have that patient sitting in
front of you it's very difficult
sometimes to distinguish between primary
and secondary hypertension
but there are a few clinical clues that
can suggest the presence of a secondary
cause
this includes things like young age of
onset typically before the third decade
a sudden onset of hypertension in
somebody who normally
was normotensive or uncontrolled or
refractory
hypertension we can also see things like
hypokalemia in association with
metabolic alkalosis
oftentimes without the use of diuretics
can also see a patient who perhaps has
features of a recognized underlying
cause
for example new onset of hyperglycemia
in the setting of weight gain
characterized by truncal obesity
immune faces very suggestive of
cushing's syndrome
so when we think about the causes of
secondary hypertension it's easiest to
group them into different categories
so we can group them into renal
categories
these are things like renal vascular
hypertension and renal parenchymal
hypertension
endocrine causes or endocrinopathies
these are things like primary
hyperaldosteronism
cushing's syndrome or cushing's disease
via chromocytoma
hyporeninism and hypothyroidism
we can also have cardiovascular causes
like sleep disordered breathing with
obstructive sleep apnea
and coachtation of the aorta now i want
you to notice that i've bolded a couple
of these topics and that's because we're
going to be going through those today
it's also because that's what you're
going to encounter most often in the
clinical scenario
and that's what you're going to be
responsible for on your boards
there's a couple of other causes to
think about in terms of secondary
hypertension
inherited causes these are a little bit
more obscure
but you should be aware of what they are
there are things like glucocorticoid
remediable aldosteronism
it's quite a mouthful but essentially
what that is is acth dependent
aldosterone production
so people have mineral corticoid excess
there's also something called syndrome
of apparent mineral or corticoid excess
another mouthful
but this is something that actually
causes excess cortisol levels that
activate mineral
mineralocorticoid receptors there's
little syndrome
which we'll be talking about in our
potassium lecture this is a gain of
function mutation at the epithelial
sodium channel
gordon syndrome which is essentially
like a gain of function
in the sodium chloride co-transporter in
the distal convoluted tubule
and then congenital adrenal hyperplasia
the 11 beta-hydroxylase variant which
again is going to cause
mineralocorticoid activation
now there's some medications and
supplements that you should be aware of
that can cause hypertension as well
things like glucocorticoids
non-steroidal anti-inflammatory drugs
combined oral contraceptives calcineurin
inhibitors these are medications we give
to our organ transplant recipients
pseudoephedrine caffeine which i think
many of us probably drink
and licorice and when i talk about
licorice i'm talking about typically
black licorice that
is not the typical kind that we get in
the united states but typically abroad
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you