In this discussion, we will take a look at
Generally speaking, a patient walking through
the door will have decreased basal metabolic
rate, tired fatigued, constipated, gaining
weight without necessarily consumption of
too much food.
Hypothyroidism defined by insufficient circulating
thyroid hormone levels for normal cellular
functioning, extremely common especially in
women due to Hashimoto, a chronic lymphocytic
type of thyroiditis.
At this juncture, you should be able to integrate
your complete picture of Hashimoto to the
point where initially you may have in a female
is experience-is experiencing Hashitoxicosis.
Some point in time, with that lymphocytic
infiltration may result in hypothyroidism
Your patient with hypothyroidism will have
puffy face, puffy hands; eye, periorbital
region will be puffy.
Differentiate this from Graves’ disease.
This is not exophthalmos; mixed edema in all
parts of the body.
There is no pathognomonic sign or symptoms
Typical patient is lethargic, fatigued, multi…
mild constipation, cold intolerance, dry skin,
dulled facial expression, puffiness of the
face, around the eyes, coarse hair.
The complexion is going to be yellow because
of decreased conversion or decreased metabolism
Do not confuse this with jaundice; this is
vitamin A that is not being properly metabolized
due-due to decreased T3, T4.
Loss of lateral eyebrows and that’s an interesting
symptom, isn’t it?
There will be delayed DTR or delayed relaxation
of deep tendon reflexes, growth failure in
children because of lack of long bone growth,
think of that child; it may have cretinism,
yellowing of the skin, why?
Because of increased carotene accumulation,
short stature, extreme, extremely low IQ,
galactorrhea, a decrease in T… a decrease
in T3, T4 result in increase in TRH and TSH,
thus resulting in hyperprolactinemia and galactorrhea.
Hypercholesterolemia, especially LDL, type
2 hyperlipidemia, why?
Because if you have decreased T3, T4, the
LDL receptors aren’t working properly.
By definition, what is type 2 hyperlipidemia?
It is the fact that the LDL receptors aren’t
working properly and one that you are also
familiar with is the familial type autosomal
dominant where the LDL receptors aren’t
working or it could the acquired type, right?
Your T3, T4 plays a pivotal role in receptor
Hoarseness, hypoventilation, dyspnea, sleep
apnea, pleural effusion all seen with hypothyroidism.
Everything is slowed down, there is going
to be ileus, the tongue is going to be enlarged
Once again, think of that cretin who is going
to then have an enlarged tongue in that child.
Myalgias, arthralgias, non pitting edemas,
depression, psychosis, carpal tunnel syndrome.
Bunch, a bunch of symptoms and signs that
you can expect with hypothyroidism, cannot
With hypothyroidism, there might be
amenorrhea, anemia, platelet defects, dry skin,
and once again,
accumulation of carotene.
This is not jaundice, delayed puberty
Continue discussion of signs and symptoms
You would expect there to find increased systemic
Remember that if you did have thyroid hormones
normally then as far as your cardiovascular
system is concerned, everything is working
in sync and you would have the normal effects
of the catecholamines.
The beta 2 receptors normally located on your
blood vessels would then cause dilation.
However, in hypothyroidism, due to lack of
your norepinephrine working upon your beta
2 receptors may result in increased systemic
This is then confirmed by diastolic hypertension.
Because the receptors aren’t working properly,
you can expect your beta 1 receptors to be
Therefore, there will be decreased anatropy
and decreased cardiac output, therefore you
would find there to be decreased systolic
Any time there is decreased systolic function,
eventually you will also find decreased diastolic
function because you cannot properly fill
up your heart and that’s a huge physiologic
concept, isn’t it?
If the receptors aren’t working properly,
beta 1 in the heart, your heart rate here
would be decreased, bradycardia, and there
is a possibility of accumulating fluid in
the pericardial cavity, pericardial effusion.
Let us now talk about hypothyroidism and the
The most common is the one that we should
Chronic lymphocytic infiltration of a thyroid
gland known as Hashimoto.
We have silent thyroiditis, there is quite
a bit of overlap that will be taking place
between a hyper and hypothyroidism in these
topics, especially when dealing with thyroiditis
and the reason for that is initially you could
find hyperthyroid symptoms, may slowly start
dropping the T3, T4 into euthyroid phase and
then eventually getting into your hypothyroid
Some may result in permanent hypothyroid or
there is a possibility that if it is a viral
or your bacterial that we talked about earlier
that there might be a recovery phase.
Hashimoto permanent hypothyroidism.
The subacute thyroiditis, the reason that
we have the term transient is because with
subacute, let’s say that is a granulomatous
and the viral infection preceded by an upper
respiratory tract infection, initially hyperthyroid,
exactly the spectrum that I had walked you
through just a few minutes ago.
Acquired causes of hypothyroidism.
The patient came in with Graves’ disease,
the Graves’ disease was then dealt with
by radiation therapy.
There might have been excess thyroid destruction
or excess thyroid removal.
When there is excess destruction of your thyroid
gland, this may then result in acquired hypothyroidism,
the patient is now placed on thyroid replacement
or thyroid hormone replacements.
Following head and neck radiation therapy
and iodine deficiency, much less seen in developed
countries, maybe perhaps a patient coming
from a developing country where iodine excess
might be limited, therefore resulting in acquired
type of hypothyroidism.
Drugs that may cause hypothyroidism include
Lithium, Amiodarone, anti-thyroid drugs such
as Propylthiouracil, Methimazole or centrally
acting such as Sunitinib and Bexarotene.
Secondary, tertiary, what does that mean?
It means that now you are not looking at a
problem within the thyroid gland, you might
be looking at problems elsewhere.
When you say secondary, you are referring
to the pituitary for saying or referring to
tertiary then you are thinking of the hypothalamus.
If it is secondary then you do not have enough
TSH for whatever reason, why?
Or maybe infarction of the pituitary, Sheehan’s,
we talked about, pituitary apoplexy, maybe
a non functioning type of adenoma or an empty
sella, you get the point.
The pituitary is not present or there is a
head injury when the hypothalamus is not releasing
TRH secondary and tertiary respectively.
Central hypothyroidism; central resistant
to thyroid hormone, rare, rare, but nonetheless
Congenital, biosynthetic enzyme deficiency,
the most famous of them all being peroxidase.
Congenital absence of thyroid gland known
as thyroid aplasia all may result in hypothyroidism.
At this point, you broaden your differentials
for hypothyroidism beyond Hashimoto’s and
we are looking at drugs and secondary, tertiary