2. INTRODUCTION
• It is a clinical state of inappropriately high
levels of circulating thyroid hormones (T3 and
T4) in the body from any cause .
• Predisposing factors include;being female,
Family history of thyroid disease, Autoimmune
diseases such as addison,s disease and people
of age above 60.
3. AETIOLOGY
• It is caused by:
Grave’s disease-Common cause
Toxic multinodular goitre
Toxic adenoma
Thyroiditis
TSH producing adenoma /Pituitary adenoma
Factitious hyperthyroidism
Excessive replacement therapy with levothyroxine
4. PATHOPHYSIOLOGY
• Thyroid hormone affects almost every tissue and organ system in
the body by increasing basal metabolic rate and tissue
thermogenesis by upregulating alpha-adrenergic receptors leading
to an increase in sympathetic activity. Thyroid hormone causes
increased expression of myocardial sarcoplasmic reticulum calcium-
dependent ATP, increasing heart rate and myocardial contractility
with the net effect of increased cardiac output. Decreased systemic
vascular resistance (SVR) and decreased afterload results from
arterial smooth muscle relaxation by metabolic end products, such
as lactic acid, produced with increased consumption of oxygen.
Decreased SVR leads to activation of the renin-angiotensin system,
increasing reabsorption of sodium and expanding blood volume to
increase preload. If left untreated, this may lead to left ventricular
hypertrophy and congestive heart failure.
5. • Graves’ disease is an autoimmune disease
comprised of antibodies that stimulate TSH
receptors to cause excess secretion of thyroid
hormones via a type II hypersensitivity reaction.
This results in hyperplasia of thyroid follicular
cells causing a diffuse goiter. The cause of Graves’
disease is not known, but genetic and
environmental factors, such as smoking, stress,
and dietary iodine play a role. The thyroid-
stimulating immunoglobulin (TSI) triggers the
hyperthyroidism.
6. thyroiditis, thyrotoxicosis is caused by the
release of preformed thyroid hormone into
the circulation as inflammation destroys
thyroid follicles. This causes transient
thyrotoxicosis that most often self-resolves.
Inflammation can be precipitated by a variety
of insults to the thyroid gland, including
autoimmune, infectious, chemical, or
mechanical insults.
7. • Gestational hyperthyroidism generally occurs
in the first trimester of pregnancy, due to
increased stimulation of the thyroid gland by
excess human chorionic gonadotropin (HCG),
which is similar in structure to TSH and binds
the TSH receptor.
8. • toxic multinodular goiter and toxic adenoma,
autonomously functioning nodules over-
secrete thyroid hormone independently
without stimulation from TSH. Rarely, these
Nnontoxic adenomas or goiter can convert to
toxic adenomas after exposure to iodinated
contrast, such as from a cardiac
catheterization or undergoing a CT study with
contrast
9. CLINICAL MANIFESTATION
• Weight loss with an increased appettite
• Heat intolerance with increased sweating.
• Palpitations
• Goitre
• Tremors
• Anxiety
• Proximal muscle weakness
• Alopecia
• Fatigability
• Men may present with gynaecomastia while ladies with
amenhorrhea.(RARE)
11. TREATMENT
• Anti-thyroid drugs; Methimazole and
propylthiouracil (PTU)- Block thyroid gland from
making hormones.
• Radioactive iodine-Causes thyroid to shrink by
damaging cells hence reducing thyroid hormone
production.
• Surgery ; thyroidectomy.
• Beta blockers; Propanolol- Control palpitations
and shakiness.
• Glucocorticoids.
12. COMPLICATIONS
• Heart issues such as heart failure.
• Osteoporosis
• Grave,s opthalmopathy
• Thyroid storm
• Hypothyroidism from treatment such as
radioactive iodine
13. PROGNOSIS
• The prognosis is always good except for some
have chances of developing hypothyroidism
due to treatment.
14. REFERENCES
• Bartalena L,Fatourechi V. Extrathyroidal
manifestation of graves disease.
• Robbins basic pathology by kumar, Abbas and
Aster.
• Master Medicine: General and systemic
pathology by paul Bass, Susan Burroghs,
Norman Carr and claire Way.
