Important renal tubular acidoses that you
want to know further and really this kind
summarizes the two that you need to know down
the collecting duct. So lets keep it simple.
You need to know about one, two and four.
Remember two? You do. How many lines you need
to form an X? One. Two. What part of the nephron
requires an X? Proximal convoluted tubule,
Are we clear now? What was my problem with
proximal convoluted tubule RTA type II? There
might have been an issue with your carbonic
anhydrase. Remember that discussion that
we had quite extensively. Let us now jump
over and skip down to the distal convoluted
tubule, please. In the distal convoluted tubule,
we will first take a look at type I. Now it
can be in the collecting duct distal region.
Do not get hung up for the exact location.
That is going to be at this point not the
best use of your time. The best use of your
time at this point is that you know that you
are not in the proximal convoluted tubule.
So what is going with type I? Now the
details as far as how this occurs is a little
theoretical, but all we know for sure is this
first bullet point for type I RTA, distal.
Impaired excretion of hydrogen. When you say
renal tubular acidosis couple of things automatically
come to mind. That acidosis is referring to
your pH in your blood, blood, blood. Not
your urine. And your blood being decreased.
Number 1. How did this occur? In the distal convoluted
tubule, you would not able to properly
get rid of your hydrogen, hydrogen, hydrogen,
therefore, remains within the blood. What
happens to your pH? Drops. Next, as I said
unclear in terms of its etiology, hydrogen
remains back in your blood results in severe
non-anion gap, metabolic acidosis. What does
that mean to you? Let sync together. When you
do metabolic acidosis, you are going to do
anion gap. Always. So metabolic acidosis anion
gap that should be next step in terms
of diagnosis. What is anion gap mean to you?
It is your cations minus the anions. The cation
is the sodium. The anions are your chloride
and bicarb. When you do that formula, you
end up getting a normal anion gap between
8 and 12 clinically we call this a non-anion
gap. Okay. Severe though severe.
Now the causes include the following. These
are things which you are looking for underlying
with type I, maybe it's do re mi fa so la. What am I
talking about? What is this? This is ro and
you have heard of la. In other words Ssa and
Ssb. Really. Remember clinical practice all
jokes aside. Clinical practice Ssa and Ssb
is huge for you to diagnose Sjogren. Ssa is
going to ro. Ssb is going to la. Okay. If
you want, you may want to use lab, la is Ssb.
Ro is Ssa. What is my diagnosis? Autoimmune
disease called Sjogren. Type I RTA. Tell me
about Sjogren. No tears. Xerophthalmia. The lacrimal
gland has been knocked out. Autoimmune disease.
What about your mouth? No saliva. You can’t
protect the teeth maybe dental caries causes
xerostomia. Sjogren. Number 1. Distinguishing feature
dryness. Autoimmune diseases, Sjogren, children, hereditary
transport defect, of what? Hydrogen. That is
type I. So type II proximal convoluted tubule.
You cannot reabsorb bicarb. Welcome to RTA
type II. RTA type I distal...
hydrogen, is it going to be type IV? Type
IV renal tubular acidosis, hypoaldosteronism.
If you don't have sufficient amount of aldosterone,
hence the time that we have spent on truly
understanding aldosterone and at some point
maybe even got bored, which is a good thing,
which means that you know aldosterone in and
out. So based on that you tell me what just happened.
If for whatever reason aldosterone is not present
or inadequately present, then your sodium
is not being properly reabsorbed. Look for
decreased sodium. Okay fine. Next what about
potassium? You can't properly get rid of this so
it may result in hyperkalemia. Okay fine.
I understand the electrolytes Dr.Raj get
to the point. Renal tubular acidosis. This
is the only one in which you would have hyperkalemia
and you can’t get rid of the hydrogen. What
happens to your pH, please? Here you go. Acidosis.
So type IV renal tubular acidosis is a simple
as understanding that there is either aldosterone
inadequacy or there is resistance to that
aldosterone resulting in acidosis with prominent
hyperkalemia. Did we see such a thing with
type II RTA? No, we did not see hyperkalemia
in type II. What about type I? We did not
see hyperkalemia in type I. In type I the
hydrogen for unclear etiology know that, you
are not able to properly secrete your hydrogen.
In type II, one more time maybe it's issues
with your carbonic anhydrase and just to be
technical in the proximal convoluted tubule
with type II may be you are not able to get
rid of that hydrogen. So therefore resulting
in RTA I, II and IV. This would be a good
time for you to review all of the three major
renal tubular acidoses, metabolic acidosis
non-anion gap type of issues. What about type
III, Dr. Raj? Let it go. Please, can you do that for me?
TypeI, II and IV is what you pay attention to. Period.
Medical findings of Addison's. You will find
this to be interesting. In Addison's disease,
lets stop here. What does that mean? I want
to take the ADD in Addison's, what does that
spell? Add. So you are adding hormones to
this disease. There you have it. So what ends
up happening primarily is that the adrenal
gland is primarily destroyed so that adrenal
gland is gone. It is destroyed. What do you
need to do? You need to add hormones. Is that
clear? So what is this called when adrenal
gland is dead and you don't have, number 1: aldosterone.
Number 2: it's a fasciculata. Cortisol, you don't
have that either. And those are two that you
want to pay attention to, because that will then
give you a diagnosis of Addison's for right
now since we are doing nephrology lets stick
with the aldosterone, shall we? Thank you.
So this is primary adrenal insufficiency aka
Addison's. Okay. If you don't have your glomerulosa
working properly, you don't have aldosterone,
can you then walk me through and may result
in what kind of renal tubular acidosis? Type IV,
good. Hyponatremia, hypokalemia. You get that.
I am not going to cover that again. We have done
that plenty. Due to inhibition of sodium reabsorption
and potassium excretion, hypertonic loss of
sodium in the urine. It is a salt wasting
disease. Salt wasting disease, what kind of
question are going to get here in physio?
Walk you through this. You are losing fluid.
What happens to ECF? You are losing fluid.
What is the first compartment that you always
pay attention to? Work with me here. Look
at me. What is the first compartment you pay
attention to? It is always a plasma compartment.
Where is the plasma compartment in the ECF?
Are we good? You are losing fluid. Plasma
compartment contracts. ECF compartment contracts.
Stop there. In Addison's disease, you are
losing a lot of, look at what that says. Hypertonic
loss of sodium. So you are losing fluid, granted
but you are losing a lot of solutes. So
ECF osmolarity decreases. ECF volume decreases.
Number 3, If your ECF osmolarity decreases, where
are you going to go? Into the ICF. Are we clear?
If you go into the ICF, what happens to ICF
volume? Expansion, good. If water goes into
the ICF, what happens to ICF osmolarity? Decreases.
Do you see how simple this is when you understand
the physio, you can bring in the clinical
application? You don't have to sit there and
memorize. But if you go through that order
every single time, you are in good shape.
ECF volume, ECF osmolarity, ICF volume, ICF
osmolarity in that order . Next, retention
of hydrogen. What does it cause?
RTA type IV.