HYPERTHYROIDISM

- Increased serum levels of thyroid hormones,

- Surgical correction is frequently appropriate

NORMAL THYROID FUNCTIONThe 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:

- increase the metabolic rate,

- increase the O2 consumption,

- increase glycogenolysis,

- enhance the actions of catecholamines

The result is:Increase in the PR, CO. Nervousness,

irritability, muscular tremor, muscle wasting

These effects can be blocked by the use of beta-blockers

HORMONAL ACTIONThe 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 GLANDCLINICAL EXAMINATION

HyperthyroidismSymptoms: 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

INVESTIGATIONSTSH- raised in primary hypothyroidism and

after treatment of thyrotoxicosis by surgery or radioiodine, - reduced in hyperthyroidism

Free T3, T4- radioimmunoassays,Radioiodine uptake,Thyroid isotope scanningUltrasonography, CT, MRIFine needle aspiration cytologyThyroid autoantibodies (ab.to thyroglobulin)

Thyroid scintigramAutonomous 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.

GOITERENLARGEMENT OF THE THYROID GLANDSimple goiter - diffuse hyperplastic goitre,

- nodular goitreToxic 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

HYPERTHYROIDISMRare causes: - metastatic thyroid carcinoma, - pituitary tumour secreting TSH

GRAVE’S DISEASE

The most common cause of hyperthyroidismIt is an immunological disordersThyroid stimulating antibodies (IgG type)

bind to the TSH receptor of the thyroid cells- excess of the thyroid hormones

The thyroid gland hypertrophiesDiffuse enlargement

GRAVE’S DISEASEClinical Diagnosis

Symptoms and signs of thyrotoxicosis result from excess thyroid hormones:Cardio vascular Neurological Metabolic ExophtalmosDiffuse enlargement of the thyroid

GRAVE’S DISEASEOphthalmopathy- 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

HYPERTHYROIDISMPREOPERATIVE PREPARATION

Surgery must be done in the euthyroid state ATD for a period then discontinueBetablockers to control cardiac symptomsLugol’s solution, 10 days, will diminish the

peroperative hemorrhagic risk

GRAVES’ DISEASETREATMENT

To restore the euthyroid state:Antithyroid drugs + beta-blockersRadioactive iodine - distroys overactive tissue

Surgery - bilateral subtotal/total thyroidectomy

Grave’s diseaseMultiple nodules and hypervascularity

Grave’s diseasePressure 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 GOITREMANAGEMENT

Hyperthyroid- iodine scanLarge- ATD & surgerySmall- iodine therapy

EuthyroidNo dominant nodule-observeDominant nodule-FNAC

Benign, no sy-observeMalignant- surgerySuspicious- surgeryInadequate- repeat FNACRetrosternal- surgeryCosmetic- surgery

SOLITARY THYROID NODULEMANAGEMENT

Hyperthyroid- FNAC & isotope scanGreater than 3 cm.- surgeryLess than 3 cm.- iodine therapy

Euthyroid- FNACBenign-no pressure sy.-observe, repeat FNAC in 6

monthsBenign- with pressure sy.- surgeryThyoiditis- T4 treatmentSuspicious- surgeryMalignant- surgeryInadequate FNAC- repeatCystic benign- observe, review in 6 weeksCystic malignant- surgery

TOXIC SOLITARY NODULETREATMENT

This condition is caused by a single autonomous thyroid nodule

Best option- surgery- unilateral thyroid lobectomy

Toxic compressive goiter

POSTOPERATIVE COMPLICATIONS

1. Postoperative bleeding2.Postoperative thyrotoxic crisis3.Postoperative voice changes4. Hypoparathyroidism5. Hypothyroidism

POSTOPERATIVE BLEEDINGPostoperative 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 veinsCompressive hematoma- respiratory

embarrasment- evacuation is mandatory

POSTOPERATIVETHYROTOXIC CRISISSerious 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 HYPOPARATHYROIDISMHypocalcemia- 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