HYPERTHYROIDISM

Sudiarto, MN
 DEFINITION
 Hyperthyroidism (or "overactive
thyroid gland") is the clinical
syndrome caused by an excess of
circulating free thyroxine (T4) or free
triiodothyronine (T3), or both.
 CAUSES
 Hyperthyroidism is the result of excess
thyroid hormone production, causing an
overactive metabolism and increased
speed of all the body's processes.
 Thyroid hormone generally controls the
pace of all of the processes in the body.
This pace is called one's metabolism.
 If there is too much thyroid hormone,
every function of the body tends to speed
up. The thyroid gland regulates the body
temperature by secreting two hormones
that control how quickly the body burns
calories and energy
 CAUSES
 The exact cause is still not known
 It is described as an autoimmune process
of impaired immunoregulation that results
from an as yet unidentified viral trigger.
 The incidence is significantly associated
with the occurrence of other autoimmune
disorders, particularly pernicious anemia,
insulin dependent diabetes mellitus
myasthenia gravis, and Addison’s disease
 The onset commonly associated with an
episode of physical illness or significant
physical or emotional stress.
 CAUSES
Major causes are:
 Graves' disease (the most common etiology with
70-80%)
 Toxic thyroid adenoma
 Toxic multinodular goitre

Other causes of hyperthyroxinemia (high blood

levels of thyroid hormones) are not to be
confused with true hyperthyroidism and include
subacute and other forms of thyroiditis
(inflammation) and struma ovarii (a teratoma).
Thyrotoxicosis (symptoms caused by
hyperthyroxinemia) can occur in both
hyperthyroidism and thyroiditis. When it causes
acutely increased metabolism, it is sometimes
called "thyroid storm", a life-threatening event
characterized by tachycardia, hypertension, and
fever.
 EPIDEMIOLOGY
 Affect women 5 times as often as men,
and although it can occur in any age, the
peak incidence is between the ages of 20
– 40.
 There is a strong familial predisposition to
Graves’ Disease (GD)
 Estimated that 15 % of patient with GD
have a close relative with the disease, and
50 % of the biological relatives of these
patient have thyroid antibodies in their
blood.
 GRAVE’S DISEASE
(DIFFUSE TOXIC GOITER)
 The far most common form of
hyperthyroidism and accounts for 60-70 %
of all clinical causes.
 Classic Grave’s Disease involves four
separate components:
1. Thyrotoxicosis
2. Thyroid enlargement (goiter)
3. Ophthalmopathy
4. Dermopathy
 Not every patient exhibits every component
 PATHOPHYSIOLOGY
 The T lymphocytes become sensitized to
antigens within the thyroid gland and
stimulate the B lymphocyte to synthesize
antibodies Thyroid Stimulating
Immunoglobins (TSI).
 These antibodies attack themselves to the
thyroid stimulating hormones (TSH)
receptor sites on the thyroid cell
membrane and stimulate the cells to
increase in size and activity
 TSH is therefore displaced from its normal
regulator role.
 PATHOPHYSIOLOGY
 Thyroid hormone production increase ten times,
but the synthesis of triiodothyronine (T3) is
increased proportionally more than thyroxine (T4)
 T3 metabolically up to 4 times more potent than
T4.
 Plasma cell and lymphocyte are also present in
various amount throughout the thyroid gland 
contributing to the classic clinical sign of thyroid
enlargement or Goiter.
 Infiltration of lymphocytes and plasma cell plus the
accumulation of glycosamino  contribute to the
thickening of the skin and subcutaneous tissue
particularly over the lower tibia  Graves’
dermopathy
 PATHOPHYSIOLOGY
 Although still not understood, this
infiltration also plays a part in the
development of the classic opthalmopathy
 Muscle weakness and loss of mucscle
mass can be severe systemic effect of GD
 myositis
 Metabolism of carbohydrate, fats, and
proteins is also altered by hormone
excess. Glucogenesis increased  risk of
DM.
 CLINICAL MANIFESTATIONS
 Over 95 % of patient with Graves’ disease
have palpable thyroid enlargement or
goiter  generally diffuse and
symmetrical, but may be assymetric or
nodular (rare).
 Gastrointestinal  weight loss despite
hyperphagia, abdominal pain or cramping,
increased number of stools or diarhea
 Skin and hair  heat intolerance,
diaphoresis, thin, brittle hair, Graves’
dermopathy
 CLINICAL MANIFESTATIONS
 Neuromuscular  easy fatigability, muscle
weakness, fine tremors, particularly pelvis and
shoulder girdle.
 Cardiovascular  tachycardia, palpitations,
systolic hypertension, dyspnea.
 Psychological  anxiety and nervousness,
insomnia and early awakening, difficulty
concentrating, reduced tolerance to stress.
 Reproductive  oligomennorrhea or amenorrhea,
decreased libido.
 Ocular  proptosis (forward displacement of the
eye, upper lid retraction, periorbital edema,
diplopia, redness of conjunctiva, visual loss.
Exopthalmus (optalmopathy)
 DIAGNOSTIC TESTS RESULTS
 Elevated serum T4
 Elevated serum T3 and T3 resin
uptake
 Elevated thyroid radio active iodine
uptake
 Presence of thyroid autoantibodies

 Decreased TSH levels (the job of TSH

taken over by thyroid-stimulating
immunoglobulin [TSI]
 THERAPEUTIC MANAGEMENT
Temporary medical therapy
 Thyrostatics
Thyrostatics are drugs that inhibit the production of
thyroid hormones, such as carbimazole (used in UK) and
methimazole (used in US), or where these not tolerated
then propylthiouracil. Thyrostatics are believed to work
by inhibiting the iodination of thyroglobulin by
thyroperoxidase.
If too high a dose is used in pharmacological treatment,
patients can develop symptoms of hypothyroidism.
 Beta-blockers
Beta-blockers do not treat, but rather mask, common
symptoms of hyperthyroidism such as palpitations,
trembling, and anxiety. Propranolol in the UK, and
Metoprolol in the US, are most frequently used to
augment treatment for hyperthyroid patients.
 THERAPEUTIC MANAGEMENT
Permanent treatments
 Surgery
Surgery (to remove the whole thyroid or a part of it) is not
extensively used because most common forms of
hyperthyroidism are quite effectively treated by the
radioactive iodine method. However, some Graves' disease
patients who cannot tolerate medicines for one reason or
another, patients who are allergic to iodine, or patients who
refuse radioiodine opt for surgical intervention. Also, some
surgeons believe that radioiodine treatment is unsafe in
patients with unusually large gland, or those whose eyes
have begun to bulge from their sockets, claiming that the
massive dose of iodine needed will only exacerbate the
patient's symptoms. The procedure is quite safe - some
surgeons even perform partial thyroidectomies on an out-
patient basis.
 THERAPEUTIC MANAGEMENT
Permanent treatments
 Radioiodine
In Iodine-131 (Radioiodine) Radioisotope Therapy,
radioactive iodine is given orally (either by pill or liquid) on
a one-time basis to destroy the function of a hyperactive
gland. The iodine given for ablative treatment is different
from the iodine used in a scan. Radioactive iodine is given
after a routine iodine scan, and uptake of the iodine is
determined to confirm hyperthyroidism. The radioactive
iodine is picked up by the active cells in the thyroid and
destroys them. Since iodine is only picked up by thyroid
cells (and picked up more readily by over-active thyroid
cells), the destruction is local, and there are no widespread
side effects with this therapy. Radioactive iodine ablation
has been safely used for over 50 years, and the only major
reasons for not using it are pregnancy and breast-feeding.
 NURSING MANAGEMENT
ASSESSMENT
 Assess specific patient symptoms
 Assess family hystory of goiter, hyperthyroidism
or hypothyroidism or any auto immune diseases.
 Assess the enlargement of the gland by
inspecting or palpating
 Assess recent body weight, appetite or bowel
function  abdominal complaint usually occur in
older patients
 Asses dermal blood flow and perspiration
 Assess Grave’s dermopathy signs
 ASSESSMENT

 Assess Grave’s opthalmopathy assess patient’s

eyelid closure, diplopia, and patient complaints of
eye muscle weakness or dry.
 Assess tachycardia, systolic hypertension
 Assess signs of thyrotoxic myopathy 
generalised fatigue, weakness, and dyspnea on
exertion
 Assess psychological status
 NURSING DIAGNOSIS
 Altered nutrition: less than body requirement r/t an intake
less than metabolic need 2nddary to excessive metabolic
rate
 Diarrhea r/t increased peristaltic
 Activity intolerance r/t muscle fatigue
 Sleep pattern disturbance r/t difficulty falling asleep or
early morning awakening
 Knowledge deficit r/t Grave’s disease and its treatment
 High risk for injury; corneal damage r/t inability to properly
close eye lids 2nddary to proptosis
 Anxiety r/t perceived threat to self concept and loss control
 PLANNIG
 Patient ingest sufficient balanced nutritients to
achieve or maintain a desired body weight
 Patients reestablish and maintains a normal
pattern of bowel elimination
 Patient is able to participate in normal activities
of daily living
 Patient obtain sufficient rest and sleep to meet
perceived need
 Patient is knowledgeable about the disease
process and treatment regiment
 Patient employ measures to protect the eyes and
does not exhibit corneal damage.
 Patient can verbalize an understanding of is
behavior and does not exhibit signs of harmful
anxiety
 IMPLEMENTATION
 Eye care  restrict sodium intake
and trendelenburg positioning to
relieve periorbital edema
 Drug therapy

 Sodium 131I (Iodide 131) therapy

 Preoperative care

 Postopartive care