HYPERTHYROID

1. Anxiety
2. Emotional lability
3. Weakness
4. Tremor
5. Palpitations
6. Heat intolerance
7. Increased perspiration
8. Weight loss despite a normal or increased appetite
9. Some patients gain weight, due to excessive appetite
stimulation
10. Hyperdefecation
11. Urinary frequency
12. Oligomenorrhea or amenorrhea
13. Gynecomastia
14. Erectile dysfunction
Physical examination
Hyperactivity and rapid speech.
Lid retraction and lid lag (sympathetic hyperactivity)
Warm and moist skin
Thin and fine hair
Tachycardia
Systolic hypertension
Hyperdynamic precordium
Tremor
Proximal muscle weakness
Hyperreflexia

Exophthalmos
Periorbital and conjunctival edema
Gravess Disease
Limitation of eye movement
Infiltrative dermopathy
Goiter :
Thyroid enlargement ranges from minimal
to massive in patients with Graves' disease
or toxic multinodular goiter.

A nonpalpable thyroid occurs commonly in elderly

patients with Graves' disease..

Patients with subacute lymphocytic (painless)

thyroiditis may have no, minimal, or modest
thyroid enlargement.

The absence of any thyroid enlargement should

also suggest exogenous hyperthyroidism or struma ovarii.

A single palpable nodule raises the possibility of

an autonomously functioning thyroid adenoma.
THYROID FUNCTION IN
HYPERTHYROIDISM
Excess thyroid hormone in the circulation.
Elevated circulating levels of free T4, and/or T3.
Subnormal serum TSH concentrations

Overt hyperthyroidism :

Low serum TSH and high free T4 and T3.

Subclinical hyperthyroidism :

Low serum TSH and normal free T4 and T3.

Have no or minimal symptoms of thyroid
hormone excess.
I. Overt hyperthyroidism
A. Low serum TSH and high free T4 and T3.

B. T3-toxicosis : Low serum TSH and high T3

(and free T3) but normal free
T4 concentrations
-. Most caused by Graves' disease or nodular goiter
-. Disproportionate increase in thyroidal T3 secretion
-. Increased extrathyroidal conversion of T4 to T3

C. T4-toxicosis : Low serum TSH, high free T4, and

normal T3 concentrations
Hyperthyroidism plus a concurrent nonthyroidal
illness that decreases extrathyroidal conversion
of T4 to T3. (Amiodarone, Exogenous thyroxine)
D. TSH-induced hyperthyroidism
a. TSH-secreting pituitary adenoma
b. Partial resistance to the feedback effect of
T4 and T3 on TSH secretion.
c. Normal or high serum TSH
d. Pituitary mass is present
or genetic abnormalities in the T3 receptor.

II. Subclinical hyperthyroidism :

Low serum TSH and normal free T4 and T3.

Have no or minimal symptoms of thyroid
hormone excess.
Some patients have a goiter
 Subclinical hyperthyroidism

A. Central hypothyroidism

B. Nonthyroidal illness
Those receiving high-dose glucocorticoids
or dopamine.

C. Recovery from hyperthyroidism

Serum TSH concentrations may remain
low for up to several months after
normalization of serum T4 and T3
DIAGNOSTIC TESTS

I. Serum TSH
Serum free T4

II. Normal value of TSH, the patient is

very unlikely to have hyperthyroidism.

III. Hyperthyroidism with a normal or elevated

serum TSH value.
Serum free T4 and T3 should be measured.
If both serum free T4 and T3 are elevated,
serum alpha subunit and a pituitary MRI
should be obtained.
IV. Low serum TSH concentrations
without hyperthyroidism

Central hypothyroidism
Serum free T4 and T3 concentrations
are low or low-normal.
Nonthyroidal illness
Serum free T4 is normal, low-normal, or low,
while serum T3 is low-normal or low.
Recovery from hyperthyroidism
Low serum TSH concentrations may persist for
months after treatment despite normal or low
serum free T4 and T3 concentrations.
 THE CAUSES OF HYPERTHYROIDISM

Hyperthyroidism results from two different mechanisms :

1. High radioiodine uptake indicates

de novo synthesis of hormone.
These disorders can be treated with a thionamide,
such as methimazole.

2. Low radioiodine uptake indicates either inflammation

and destruction of thyroid tissue with release of
preformed hormone into the circulation, or an
extrathyroidal source of thyroid hormone.
Thionamide therapy is not useful in these disorders.
HYPERTHYROIDISM WITH A
HIGH RADIOIODINE UPTAKE

1. Graves' disease
An autoimmune disorder resulting from thyrotropin
(TSH)-receptor antibodies (thyroid-stimulating
immunoglobulins)
Additional manifestations are Ophthalmopathy
and pretibial myxedema.

2. "Hashitoxicosis

3. Toxic adenoma and toxic multinodular goiter

Focal and/or diffuse hyperplasia of thyroid
follicular cells whose functional capacity is
independent of regulation by TSH.
4. Iodine-induced hyperthyroidism
Administration of contrast agents used for
angiography or CT
Iodine-rich drugs such as amiodarone

5. Trophoblastic disease and germ cell tumors

Hyperthyroidism can occur in women with
a hydatidiform mole or choriocarcinoma or in men
with testicular germ cell tumors via
direct stimulation of the TSH receptor.

6. TSH-mediated hyperthyroidism
Neoplastic and non-neoplastic
HYPERTHYROIDISM WITH
A LOW RADIOIODINE UPTAKE
1. Subacute thyroiditis

-. Subacute granulomatous thyroiditis

(de Quervain's thyroiditis),
-. Direct chemical toxicity with inflammation (amiodarone)
-. Radiation thyroiditis, from external radiation or after
radioiodine therapy.
-. Drugs that interfere with the immune system such as
interferon alfa.
-. Palpation thyroiditis occurring, for example,
during parathyroid surgery.

2. Exogenous and ectopic hyperthyroidism

Resulting from excess thyroid hormone originating
from outside the thyroid gland
Treatment of hyperthyroidism

Thionamide
I. The thionamides

1. Propylthiouracil (PTU)
2. Methimazole (MMI)

a. Inhibit both the organification of iodine

to tyrosine residues in thyroglobulin and
the coupling of iodotyrosines
b. Inhibit thyroid hormone secretion
c. Have immunomodulatory activity upon the
underlying autoimmune disease
II. Beta blockers

Atenolol (25 to 50 mg/day) ameliorate the symptoms

that are caused by increased beta-adrenergic tone
(palpitations, tachycardia, tremulousness, anxiety,
and heat intolerance).

III. Iodinated contrast agents and iodine

-. Severe hyperthyroidism
-. Allergic to thionamides.

The oral radiocontrast agents sodium ipodate

and iopanoic acid are potent inhibitors of the
peripheral conversion of T4 to T3.
IV. Other medications
1. Glucocorticoids inhibit peripheral T4 to T3
conversion and reduce thyroid secretion.
2. Lithium blocks thyroid hormone release.
3. Cholestyramine
4. Carnitine is a naturally occurring peripheral
antagonist
of thyroid hormone action.

V. Radioiodine ablation

As an oral solution of sodium 131I, resulting

in ablation of the thyroid within 6 to 18 weeks.
VI. Surgery

-. Obstructive goiter or a very large goiter.

-. Coexisting thyroid nodule.
-. Patients who want rapid restoration of euthyroidism.
-. Had an adverse effect with thionamide drugs.