Transcript hipertiroidii

HYPERTHYROIDISM
- Increased serum levels of thyroid hormones,
- Surgical correction is frequently appropriate
NORMAL THYROID FUNCTION
 The follicular cells- T3, T4
 T3, T4 bind with thyroglobulin, stored on the gland
until released onto the bloodstream
 Release is under the control of TSH and TRH
 A feed-back mechanism regulating T3, T4 release is
related to the level of circulating T3, T4.
HORMONAL ACTION
 The thyroid hormones:
 The result is:
 Increase in the PR, CO.
 Nervousness, irritability,
- increase the metabolic rate,
muscular tremor, muscle
- increase the O2
wasting
consumption,
- increase glycogenolysis,
- enhance the actions of
catecholamines
These effects can be blocked
by the use of beta-blockers
HORMONAL ACTION
 The parafollicular or C-cells- produce thyrocalcitonin
 Thyrocalcitonin action:
- to lower serum calcium and phosphate concentration,
- reduces bone resorption
- in the kidney accelerates calcium and phosphate
excretion:
THYROID GLAND
CLINICAL EXAMINATION
 Hyperthyroidism
 Symptoms: dyspnea on effort, palpitation,
tiredness, preferance for cold, sweating,
nervousness, weight loss, good appetite
 Signs: palpable thyroid, exophtalmos, lid lag,
hyperkinesis, finger tremor, hot and moist
hands, rapid PR
INVESTIGATIONS
 TSH- raised in primary hypothyroidism and after
treatment of thyrotoxicosis by surgery or radioiodine,
- reduced in hyperthyroidism
 Free T3, T4- radioimmunoassays,
 Radioiodine uptake,
 Thyroid isotope scanning
 Ultrasonography, CT, MRI
 Fine needle aspiration cytology
 Thyroid autoantibodies (ab.to thyroglobulin)
Thyroid scintigram
 Autonomous adenoma in the
right lobe of the struma.
 The test substance accumulates
almost exclusively in the range
of the autonomous adenoma.
 The other areas of the struma
show a considerable reduced
accumulation of activity.
GOITER
ENLARGEMENT OF THE THYROID GLAND
 Simple goiter - diffuse hyperplastic goitre,
- nodular goitre
 Toxic goiter - diffuse (Grave’s disease),
- toxic multinodular goitre,
- toxic solitary nodule
 Neoplastic goiter - benign,
- malignant
 Thyroiditis - subacute (de Quervain’s),
- autoimmune(Hashimoto’s),
- invasive fibrous thyroiditis (Riedel’s)
- acute suppurative
HYPERTHYROIDISM
 Common causes:
- diffuse toxic goitre (Graves’s disease),
- toxic multinodular goitre (Plummer’s disease),
- toxic solitary nodule,
- exogenous thyroid hormone excess,
- thyroiditis
HYPERTHYROIDISM
 Rare causes:
- metastatic thyroid carcinoma,
- pituitary tumour secreting TSH
GRAVE’S DISEASE
 The most common cause of hyperthyroidism
 It is an immunological disorders
 Thyroid stimulating antibodies (IgG type) bind to the
TSH receptor of the thyroid cells- excess of the thyroid
hormones
 The thyroid gland hypertrophies
 Diffuse enlargement
GRAVE’S DISEASE
Clinical Diagnosis
 Symptoms and signs of thyrotoxicosis result
from excess thyroid hormones:
 Cardio vascular
 Neurological
 Metabolic
 Exophtalmos
 Diffuse enlargement of the thyroid
GRAVE’S DISEASE
 Ophthalmopathy- two major components:
-Non-infiltrating ophthalmopathy-sympathetic activity:
- upper lid retraction,
- a stare,
- infrequent blinking
-Infiltrative ophthalmopathy- edema of the orbital
contents, lids, periorbital tissue, cellular infiltration
within the orbit
HYPERTHYROIDISM
PREOPERATIVE PREPARATION
 Surgery must be done in the euthyroid state
 ATD for a period then discontinue
 Betablockers to control cardiac symptoms
 Lugol’s solution, 10 days, will diminish the peroperative
hemorrhagic risk
GRAVES’ DISEASE
TREATMENT
 To restore the euthyroid state:
 Antithyroid drugs + beta-blockers
 Radioactive iodine - distroys overactive tissue
 Surgery - bilateral subtotal/total
thyroidectomy
Grave’s disease
Multiple nodules and hypervascularity
Grave’s disease
Pressure symptoms
Recurrent Grave’s disease after subtotal
thyroidectomy, nodule at the piramidal lobe
Right thyroid nodules after subtotal
thyroidectomy
Nodules with cystic degeneration after
subtotal thyroidectomy
Left upper nodule with cystic degeneration
MULTINODULAR GOITRE
MANAGEMENT
 Hyperthyroid- iodine scan
 Large- ATD & surgery
 Small- iodine therapy
 Euthyroid
 No dominant nodule-observe
 Dominant nodule-FNAC
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Benign, no sy-observe
Malignant- surgery
Suspicious- surgery
Inadequate- repeat FNAC
Retrosternal- surgery
Cosmetic- surgery
SOLITARY THYROID NODULE
MANAGEMENT
 Hyperthyroid- FNAC & isotope scan
 Greater than 3 cm.- surgery
 Less than 3 cm.- iodine therapy
 Euthyroid- FNAC
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Benign-no pressure sy.-observe, repeat FNAC in 6 months
Benign- with pressure sy.- surgery
Thyoiditis- T4 treatment
Suspicious- surgery
Malignant- surgery
Inadequate FNAC- repeat
Cystic benign- observe, review in 6 weeks
Cystic malignant- surgery
TOXIC SOLITARY NODULE
TREATMENT
 This condition is caused by a single autonomous
thyroid nodule
 Best option- surgery- unilateral thyroid lobectomy
Toxic compressive goiter
POSTOPERATIVE COMPLICATIONS
 1. Postoperative bleeding
 2.Postoperative thyrotoxic crisis
 3.Postoperative voice changes
 4. Hypoparathyroidism
 5. Hypothyroidism
POSTOPERATIVE BLEEDING
 Postoperative bleeding
 there is always a risk of postop .bleeding,
 it is rare but sometimes dramatic
 The bleeding may occur in one of two sites,
- deep to the myofascial layer in relation to thyroid
vessels-evacuation must be done quickly
- deep to the skin flaps, from veins
 Compressive hematoma- respiratory
embarrasment- evacuation is mandatory
POSTOPERATIVE
THYROTOXIC CRISIS
 Serious complication-where there has not been
adequate preop.preparation
 It occurs within the first 24 hours of thyroidectomy
 Symptoms: confusion, hyperactive, fever, profuse
sweating, rapid PR.
 Treatment: beta-blockers, iv steroids, iodine
POSTOPERATIVE VOICE CHANGES
 Rare due to any damage to recurrent laryngeal nerves- this
occurs in less than 1%
 Probably minor changes in the muscles around the cricoid
and thyroid cartilages are the most important, inevitable
with the mobilization of the gland
 Trauma to external laryngeal nerve- cricothyroid muscle-
voice change- difficulty in achieving vocal cord tension
 Trauma t the internal laryngeal nerve can occur where
there is difficulty in mobilizing the superior pole
POSTOPERATIVE
HYPOPARATHYROIDISM
 Hypocalcemia- usually a consequance of a metabolic
changes- re-entry of calcium into bone demineralized
by hyperthyroidism (“hungry bones”)
 Parathyroids are small and are not always easy to
identify
 The incidence of hypoparathroidism after surgery
shoud be less than 1%
POSTOPERATIVE
HYPOTHYROIDISM
 All forms of treatment for thyrotoxicosis will produce a
population of patients prone to develop hypothyroidism
 Greatest risk after radioiodine therapy