00:01
If that was
hyperaldosteronism,
we will then move on
to hypoaldosteronism.
00:06
You did the same thing.
Quickly tell me
Sodium levels,
decrease
potassium levels,
elevated hydrogens increase
does pH is decreased.
00:13
Can you do it that quickly?
Yes, you can.
00:15
Listen to me again,
you'll get it.
00:18
Results in, results from
type 4 renal tubular acidosis
or could result in
What do you mean?
I just told you,
if you didn't have
enough aldosterone,
your hydrogen concentration
increases in your plasma.
00:31
What happens to pH?
Oh, renal tubular acidosis.
00:36
When you say
renal tubular acidosis,
what does that acidosis
actually referring to?
Not in the urine, right?
It's in the plasma.
00:44
Type 4, type 4, type 4.
00:45
Remember, RTA you want to know,
one, two, and four.
00:53
However,
the biggest difference between
this type of RTA in any other
if you don't have aldosterone,
take your time,
aldosterone and potassium,
If you don't have aldosterone,
you're not getting
rid of a potassium,
you're retaining it
resulting in hyperkalemia.
01:12
That is dangerous.
01:13
That hyperkalemia is dangerous,
especially for the heart.
01:16
You're then causing,
as you remember,
depolarization of the
resting membrane potential,
and that is not a good thing,
is it?
Hypoaldosteronism. Hyporeninemic.
How is this occurring?
Common in chronic kidney disease.
01:34
So if the kidney starts
decreasing in function,
then you know that
you don't have enough renin.
01:38
If you don't have enough renin,
then what then happens
to your aldosterone level?
Decreases.
01:43
This is called
hypoeninemic hypoaldosteronism.
01:47
So that three times fast.
01:49
Language, language,
language.
01:51
Apart from maybe a
little bit of memorization,
but really understand
what this is saying.
01:56
Also seen with NSAIDs
cyclosporine, and HIV.
02:01
It could potentially have
hyporeninemic hypoaldosteronism.
02:07
Hyperreninemic hypoaldosteronism.
02:11
How is this even possible?
What if you give an ACE inhibitor?
If you give an ACE inhibitor,
you've inhibited the conversion of
angiotensin I into angiotensin II.
02:21
Stop there.
02:24
So if you don't even have
angiotensin II,
how in the world
are you going to stimulate
that enzyme called
aldosterone synthase?
You can't.
02:32
Resulting in, what's my topic?
Good.
02:35
Hypoaldosteronism.
02:36
But if you blocked that enzyme,
all substrates
approximately will...
02:41
increase.
02:42
You put a block such as
an ACE inhibitor, a pro drug
Renin increases.
Hyperreninemic hypoaldosteronism.
02:52
Heparin,
primary adrenal insufficiency,
and Addison's disease.
02:57
In Addison's disease,
how much of your cortex
is destroyed?
All of it.
03:02
From henceforth,
if you want to think of Addison's,
primary adrenal insufficiency,
you need to add hormones
to your patient,
because all hormones
are deficient.
03:15
That's Addison's.
03:18
And now we're getting
really interesting,
Conn's syndrome,
Cushing, Addison's.
03:24
Students get this confused
all the time.
03:27
Keep replaying this,
replaying this, replaying this.
03:31
So this is firmly
etched in your head.
03:33
You must know the difference
between Conn, Cushing, and Addison.
03:38
So in Addison, aka
primary adrenal insufficiency
entire cortex is dead,
aldosterone is decreased.
03:46
What's my feedback
for aldosterone?
Renin.
I told you clinically,
that's what you're paying
attention to
hyperreninemic
hypoaldosteronism.
03:55
Potassium sparing drugs,
congenital adrenal hyperplasia,
What's this one?
The most important
enzyme deficiency
in congenital adrenal hyperplasia.
04:05
21 beta hydroxylase.
04:07
If that is deficient,
no mineralocorticoid
hypoaldosteronism hyperreninemic.
04:14
Are we clear now?
You should be able to go through
each one of these differentials
and understand why your patient
has hypoaldosterone.
04:23
And what kind of concentration
of renin do you actually find?
after patient upright
for three hours.
04:31
Check for plasma renin activity,
serum aldosterone,
and serum cortisol.
04:37
After patient upright
for three hours.
04:39
And see as to
whether or not you,
what kind of levels do you find
of your plasma and renin?
What about aldosterone?
And so on and so forth.
04:48
PRA and aldosterone
will be low
in hyporeninemic hypoaldosteronism
straightforward.
04:53
Give me an example there please.
04:55
If you're hyperreninemic
it means that maybe
you have chronic kidney injury.
No renin.
05:02
Plasma renin activity
will be high in
adrenal insufficiency
AI stands for
adrenal insufficiency.
05:09
That's your Addison's.
05:13
Topic, hypoaldosteronism
no aldosterone
plasma renin activity,
increased.
05:18
Whereas, serum aldosterone
of course, that will be low. Right?
in Addison's insufficiency
or adrenal insufficiency.
05:27
Tell me about this area
in Addison's,
tell me about this area
around the mouth.
05:32
Hyperpigmented.
05:33
Good.
05:34
Mineralocorticoid replacement
will addressed to hyperkalemia.
05:37
But it's not advisable for many
patients with hyporeninemic
hypoaldosteronism
due to potential for
worsening of hypertension,
and fluid overload.
05:48
Keep that in mind.
05:50
So, if you have fluid overload,
and you're thinking about giving me
a corticoid
aren't you making matters worse?
If you have a patient a CHF,
or if you have a patient that is in
a state of increased volume,
and then you give aldosterone,
you're making things worse.
06:07
In the setting low potassium diet,
and if needed,
a loop or thiazide diuretic would be
much much, much more advisable
to control the hyperkalemia.
06:17
Spend a minute here
on this paragraph
so that you understand how,
what your next step
of management would be
if your patient is suffering from
hyporeninemic hypoaldosteronism.
06:29
That's your primary focus
in this paragraph.
06:33
And your focus here
would be more symptoms
trying to get rid of the fluid
through proper management.