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Graves disease is an autoimmune disorder
that can affect the thyroid the eyes and
the skin it is the most common cause of
hypothyroidism in the United States
stimulation of autonomous production of
t4 and t3 is through antibodies against
TSH receptors these receptors can be
checked in the serum as a TSI or thyroid
stimulating him in a goblin or thyroid
releasing antibody a positive family
history is always a frequent
accompaniment a new diagnosis of Graves
disease one would start by checking
carrot stimulating immunoglobulins which
are there to stimulate TSH receptors
present on the thyroid gland which in
turn increase the activity of the gland
with consequent increased production of
thyroid hormones usually t4 and
occasionally t3 thyroid function tests
revealed the classic features of low TSH
high t4 and / t3 let's go through some
of the clinical signs of Graves disease
patients may have an elevated blood
pressure on physical exam they may also
have a widening of their pulse pressure
a widening of the pulse pressure
manifests when the systolic blood
pressure is much higher than the
diastolic blood pressure this is the
hallmark hallmark of thyroid hormone
effect on the heart where increased
cardiac output and increased pumping of
the myocardium occurs that's widening
the pulse pressure patients also
manifest clinically with tachycardias
these tachycardias may be regular or
irregular if they're irregular they're
called atrial fibrillation there's also
a diffusely enlarged thyroid and
occasionally a thyroid bruit which is
the abnormal sound that the blood
vessels of the thyroid make as blood
flows through them rapidly patients may
also manifest pretibial myxedema which
we'll will describe in subsequent slides
and they have the characteristic eye
signs these eye signs can include lid
retraction or
Lag proptosis which looks like bulging
of the eye in the orbits scleral
injection where the sclera of the eye
appears red and finally periorbital
edema where the entire orbit seems to be
swollen in the right image you see many
of the features of classic destroyed eye
disease the diagnosis of Graves disease
is made clinically in most cases the
first lab to tech to check after TSH and
free t4 would be the thyroid stimulating
antibodies radioactive iodine uptake and
scan will show increased uptake with
diffuse activity on the scan image the
treatment of Graves disease is a
stepwise approach usually starting with
theá-- ami drugs
followed by beta blockers to control
heart rates if the thyrotoxicosis recurs
or if there any compressive symptoms of
the thyroid gland surgery is considered
in the absence of a response to
medications one can also consider ride
radioactive iodine ablation therapy
fionna my drugs can be used
consecutively for up to two years
methimazole one of the first-line agents
has a higher intro thorough oil
retention rate and therefore is more
effective typically once daily dosing
also makes this drug quite convenient
and it has a reduced side-effect profile
one important thing to be aware of is
that it is a first-trimester teratogen
causing a condition called aplasia
acutest
in the fetus this should be taken into
account especially when prescribing with
them as all 2 women of reproductive age
another drug is called profile theour
uracil or PTU which has limitations
based on its side effects it can
increase a minor transferase levels and
affect the liver and in very rare cases
lead to fatal hepatotoxicity second-line
treatment for Graves disease includes
radioactive iodine ablation which will
in most cases render the patient
completely hyper thyroid as a
consequence they then would require
lifelong thyroid replacement finally
surgery is considered in patients in
whom control cannot be achieved with
drugs and who are not comfortable
radioiodine therapy other lab patterns
of thyroid disease worth mentioning when
you see a normal TSH but an elevated t4
and or t3 consider the rare condition of
secondary hypothyroidism that is caused
by a TSH secreting pituitary adenomas
where the TSH is low plus a normal free
t4 but in elevated t3 this is the
condition we described earlier known as
t3 toxicosis and then finally if the TSH
is low with a normal t4 and t3
considered the condition of subclinical
hypothyroidism typical causes of which
include pregnancy and other non thyroid
'el illness
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