HYPERTHYROIDISM

Increased serum levels of thyroid hormones, Surgical correction is frequently appropriate

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

GRAVES’S DISEASE
The most common cause of hyperthyroidism It is an immunological disorders Thyroid stimulating antibodies (Ig G type)

bind to the TSH receptor of the thyroid cellsexcess of the thyroid hormones The thyroid gland hypertrophies Diffuse enlargement

GRAVES’ DISEASE Clinical Diagnosis
Symptoms and signs of thyrotoxicosis result

from excess thyroid hormones:
Cardio vascular Neurological Metabolic Exophtalmos Diffuse enlargement of the thyroid

GRAVES’ DISEASE
Ophthalmopathy- two major components: -Non-infiltrating ophthalmopathy -sympathetic activity - upper lid retraction, - a stare, - infrequent blinking -Infiltrating ophthalmopathy- edema of the orbital contents, lids, periorbital tissue, cellular infiltration within the orbit

Surgical specimen

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

GRAVES’ DISEASE INVESTIGATIONS
Laryngoscopy- mobility of vocal cords CXR, ECG Measurement of free T3, T4, TSH Isotope scanning not essential but necessary

in the assessment of toxic solitary and multinodular goitre- the site of nodular overactivity Radioactive iodine uptake- increased uptake in the thyroid gland

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

TOXIC MULTINODULAR GOITRE TREATMENT

ATD- waste of time Radioactive iodine- not indicated Surgery- total thyroidectomy appropriate

TOXIC SOLITARY NODULE TREATMENT
This condition is caused by a single

autonomous thyroid nodule
Best option- Surgery- unilateral thyroid

lobectomy

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.

Toxic compressive goiter

Toxic nodular goiter
Thyroid USS:
 LTL-vol. 86,98 ml., RTL- vol. 5,54 ml.

TSH=0,1 mcg/ml (0,4-7) CT- expansive solid nodule LTL ENT exam.- laryngoscopy- left recurent nerve palsy AP- nodular goiter with cystic degeneration and areas of hyperfunction

HYPERTHYROIDY 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

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%

Hipoparathyroidism and hypocalcemia
Transient or definitive- 1%-15% Manipulation of the PT glands- neck dissection Single vs. 3 glands preserved for normal PT

fct. Non-capsular dissection technique- risk of injury Incidental removal with thyroid gland PT- reimplant into the SCM muscle Identification of PT- avoid injury risk

Hypoparathyroidism

THYROID CANCER
Tumors of thyroid follicular epithelium Papillary carcinoma Follicular carcinoma Anaplastic carcinoma Tumors of parafollicular cells
Medullary carcinoma

Tumors of lymphoid cells Lymphoma

PAPILLARY CARCINOMA
The commonest thyroid tumor Previous neck irradiation-risk factor-thy.ca. Hard whitish nodule Lymphatic spread Three types based on tu. size and extent: Minimal lesion<1cm Intrathyroid lesion>1cm.within the thyroid Extrathyroid lesion-locally advanced

FOLLICULAR CARCINOMA
Encapsulated, solitary nodule Usually firm, but soft when intratumor hg. Spread via the boodstream Two main types after histopathology: Minimally invasive-slight capsular or vascular invasion Frankly invasive-venous extension into thyroid and jugular veins

The TNM stages of thyroid cancer
 “TNM” stands for Tumour, Node, Metastasis.  T1 - the tumour is entirely inside the thyroid and is less than 2cm

across in any direction  T2 - The tumour is entirely inside the thyroid and is more than 2cm but no more than 4cm across in any direction  T3 - The tumour is entirely inside the thyroid and is more than 4cm across in any direction  T4a - The cancer has grown outside the thyroid gland into the surrounding tissue.  T4b - The cancer has grown outside the thyroid gland into the area surrounding the bones of the spine, or one of the main blood vessels nearby.

TNM staging
 N0- no lymph nodes contain cancer cells  N1a - there are lymph nodes containing cancer cells on one

side of the neck only (on the same side as the cancer)  N1b - there are lymph nodes containing cancer cells anywhere else (usually the other side of the neck or in the chest)
 M0- no distant MTS  M1 - present distant MTS

TNM staging Differentiated thyroid cancer: papillary and folicular thyroid cancer
Under 45years of age: Stage 1 - cancer is only inside the thyroid, or the thyroid and the lymph glands
Stage 2 - cancer has spread presenting

metastases

TNM staging for differentiated thyroid cancer, over 45 years of age
Stage 1 - cancer is only inside the thyroid and is

less than 2cm across Stage 2 - cancer is any size, but is only inside the thyroid Stage 3 - cancer has grown beyond the thyroid capsule, or there are cancer cells in the lymph nodes Stage 4 - cancer has spread to other parts of the body, such as lungs or bones

TREATMENT OF DIFFERENTIATED THYROID CANCER
Thyroidectomy is the treatment of choice Objectives- to eradicate primary tumor

- to reduce the incidence of recurrence Papillary cancer-multifocality-total thyroidectomy is the best option plus clearance of cervical lymph nodes Follicular cancer- if minimal-lobectomy - If invasive-total thyroidectomy

POSTOPERATIVE TREATMENT
Thyroxine after total thyroidectomy Thyroglobuline measurement-sensitive

indicator of residual or recurrent differentiated thyroid cancer after total thyroidectomy Radioactive iodine is a useful means of detecting metastatic disease after total thyroidectomy

ANAPLASTIC CARCINOMA
Highly aggressive tumor, affects the elderly Rapidly infiltrates local structures Metastases via bloodstream, lymphatics Long history of goitre that suddenly starts

to grow rapidly Voice change, dysphagia, dyspnea Resection is rarely possible Survival within six months

Staging for anaplastic thyroid cancer
There is no number staging system for anaplastic thyroid cancer. This is because there is a high risk of the cancer spreading. If the cancer is only in the neck - complete removal If the patient is fit enough - surgery or radiotherapy

MEDULLARY CARCINOMA
Incidence-8% of thyroid malignancies Solid non-follicular carcinoma Arises from the parafollicular cells, C-cells

which secretes calcitonin- hypocalcemia In the upper 2/3rds, multicentric, bilateral Spreads by lymphatics to regional nodes Spreads via bloodstream to liver, lungs, bones

MEDULLARY CARCINOMA
This tumor produces calcitonin- tu.marker CEA- another tu.marker This tu. can secrete a range of hormones and

peptides: prostaglandins, 5hydroxitryptamine, ACTH. Diagnosis- FNAC, serum calcitonin Association with pheochromocytoma- urinary VAM and metanephrines

MEDULLARY CARCINOMA TREATMENT
Total thyroidectomy is the best option Central and paratracheal lymph nodes

clearance, Carotid sheath nodes removed, if involved with tu.- modified radical neck dissection, preserving IJV, SCM, spinal accessory nerve. Bilateral lymph nodes clearance is advised

Medullary thyroid cancer
There are 4 number stages for medullary thyroid cancer. These are: Stage 1 - cancer is less than 2cm across Stage 2 - cancer is between 2cm and 4cm across Stage 3 - There is spread to cervical lymph nodes Stage 4 - The cancer cells have spread to another part of the body  

MEDULLARY CARCINOMA FOLLOW-UP
Follow-up: calcitonin, CEA If raised- persistent or recurrent disease Ultrasonography, CT, MRI,scintigraphy External irradiation- last chance Chemotherapy is disapointing Present lymph nodes metastases-survival rate

is 45% at 10 years

THYROIDITIS
Subacute thyroiditis Autoimmune thyroiditis Riedel’s thyroiditis Acute suppurative thyroiditis

SUBACUTE THYROIDITIS
Granulomatous or de Quervain’s thyroiditis Probably viral origin Painful swelling of one or both thyroid

lobes, malaise, fever Preceding history of sore throat or viral infection a week or two before the onset of thyroid symptoms Symptoms and signs of hyperthyroidism Thyroid hormone levels raised but low uptake of radioactive iodine, ESR is raised

SUBACUTE THYROIDITIS
The disease process is self-limiting with

resolution of local sy. and thy. dysfunction Few pts. pass through a mild hypothyroid phase Local sy.-aspirin, steroids Transient hyperthyroidism does not require antithyroid drugs

AUTOIMMUNE THYROIDITIS
Diffuse process throughout the thyroid gland-

Hashimoto’s disease Infiltration of thyroid by lymphocytes and plasma cells Immunological disorder- serum thyroid ab. Hypothyroidism- thyroxine, steroids Nodule present- FNAC to rule out lymphoma

RIEDEL’S THYROIDITIS
Invasive fibrous thyroiditis- dense fibrous

inflammatory infiltrate throughout the thyroid extended extracapsular Rare condition, can mimic malignancy Tamoxifen, or surgery for pressure sy.

ACUTE SUPPURATIVE THYROIDITIS

The thyroid can be infected by bacterial or

fungal agents Acute painfully inflammed gland Needle aspiration- dg. & bacteriology Appropriate antibiotics

PRIMARY HYPERPARATHYROIDISM
Symptoms: renal lithiasis, osteitis fibrosa

cystica, peptic ulcer, cholelithiasis, weakness, constipation Lab. tests: elevated serum calcium, serum PH high, decreased serum phosphorus, hyperphosphaturia Radiology: skull XR- ground-glass appearance Localization: USS, CT, MRI Surgery- removal of adenoma

DISORDERS OF THE PARATHYROID GLAND
PTH- regulator of calcium metabolism Acts in conjunction with calcitonin Serum Ca falls- PTH increases Serum Ca rises- PTH decreases Increased PTH secretion:
Hypercalcemia Hypocalciuria Hypophosphatemia hyperphosphaturia

PRIMARY HYPERPARATHYROIDISM
May occur as:

- part of a multiple endocrine adenomatosis syndrome, - familial hyperparathyroidism, - ectopic tumor 90% due to a solitary adenoma 10% due to four-gland hyperplasia 1%- due to parathyroid carcinoma

Osteita fibrosa cystica- parathyroid adenoma

Left parathyroid adenoma

Left parathyroid adenoma

Right parathyroid adenoma

Right parathyroid adenoma

Parathyroid adenoma

Surgical specimen

What is abnormal at this face??

Myasthenia gravis

Motor end-plate in MG

Which organ is involved in the patholopgy of MG??

Where the thymus is located??

Pneumomediastinography

A.Gh. 65 years old, 3 w. of severe myasthenia, Oss.III CT-calcified thymoma adherent to the left mediastinal pleura, op. 2003, histology- type A, medullary thymoma without capsular invasion, chemotherapy CP+PDN, obvious improvement

CT, 60 years old, thymoma+MG, Oss.IV, op. 2002, Lymphocitic thymoma (type I malignant thymoma)Masaoka II ( well encapsulated but microscopic capsular invasion), adhesions to left M. pleura which was resected

Radiotherapy 44 Gy, chemotherapy, 1 year CP+PDN Pericarditis and mixedema at 1 year postRxT Remission of MG for 5 years, 2008- AChE

Different approaches to the thymus

Position of the patient for thymectomy

Sterile field

Median complete sternotomy

Dissection

Intradermic suture

OP.IAN.2009

Longitudinal incision

Sternotomy

Sternal retracter

Dissection

Dissection

Dissection

Dissection

Dissection

Dissection

Left innominate vein

Mediastinal aspect after tumor resection+pleurectomy

Sternoraphy- 3 metalic wires

Specimen

CT-2009

Presternal fascial closure

Skin sutured

Right eye ptosis

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