Thyroid Disorders Seminar

8/10/2019 Thyroid Disorders Seminar

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PRESENTER : DR. MWANGA


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SURGICAL ANATOMY

Thyroid gland = shield like

sitelower part of the anterior and lateral

sides of the neck.

Gland contains right and left lobe joined by

Isthmus.

Vertebral levelC5,6,7,T1.

Each lobe extends from middle of thyroidcartilage to the 4thor 5thtracheal ring.

Isthmus2ndand 3rdtracheal ring.


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Contd

Dimensionslobe -5cms x 2.5cm x2.5cm.

Isthmus 1.5cm x1.5cms.

Weight20 to 25 grams in adults. Functional unit is lobule.

Each lobule is supplied by an arteriole.

2 capsulesTrue capsule.False capsule.


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Normal anatomy of the recurrent laryngeal nerve. Note that on the right

side the recurrent laryngeal nerve hooks around behind the subclavian

artery, while on the left side this nerve passes around behind the aortic

arch before ascending in the neck.B) When there is a vascular anomaly of the right subclavian artery, the r

ecurrent laryngeal nerve no longer "recurs" around this artery but

proceeds from the vagus nerve in a more transverse direction to the

larynx. In such a situation, the nerve is much more likely to be damaged

during operation unless care is taken to visualize its course in the neck.

(From Skandalakis et al,:4 w ith permission.)


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BLOOD SUPPLY

1. Superior thyroid arteryfirst anterior branch of

the external carotid artery.its in close relation

with external laryngeal nerve. It divides in to

anterior and posterior branches. Suppliesupper 1/3rdof lobe and upper of isthamus.

2. Inferior thyroid arterybranch of thyrocervical

trunck.its terminal part is in close relation with

recurrent laryngeal nerve.supplies lower 2/3rdof lobe and lower of isthamus.


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Venous drainage

Superior thyroid vein drains in to internal

jugular vein or common facial vein.

Middle thyroid veininto internal jugular

vein .

Inferior thyroid veinLt brachiocephalic

vein.

Thyroid vein of kocherin to internal

jugular vein.


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Lymphatic drainage

Upper deep cervical lymph nodes .

Lower deep cervical lymph nodes.

NERVE SUPPLY:mainly by middle cervical ganglion and

partly from superior and inferior cervical

ganglia.


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PHYSIOLOGY

The hormones T3 and T4 are bound to

thyroglobulin within the colloid.

Synthesis within thyroglobulin complex is

controlled by several enzymes in

different steps1. Trapping

2.oxidation

3.coupling

4.Release


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THYROID HORMONES

Iodine & tyrosine form both T3 & T4under TSH stimulation. However, 10%

of T4 production is autonomous and ispresent in patients with centralhypothyroidism.

When released into circulation T4binds to:

Globulin TBG 75%

Prealbumin TBPA 20%


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THYROID HORMONES (2)

Less than 1% of T4 & T3 is free inplasma.

T4 is deiodinated in the tissues to

either T3 (active) or reverse T3(inactive).

At birth T4 level approximates

maternal level but increases rapidlyduring the first week of life.

High TSH in the first 5 days of life cangive false positive neonatal screening


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THYROID HORMONES IN SERUM

NAME SYMBOL NORMAL RANGE

Total serum

thyroxine

T4 55150 nmol/I

Total tri

iodothyronine

T3 1.23.1 nmol/I

Free thyroxine t4 826 pmol/I

Free tri-

iodothyronine

t3 39 pmol/I


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THYRIOD FUNCTION TEST

1. serum T3, T4.

2. Serum TSH

3. Serum creatinine

4. Serum cholesterol

5. Serum calcitonin

6. Thyroid autoantibody levels.

7. Thyroid scintigraphy .

8. TRH


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INVIVO TESTS

1. Radio iodine active uptake test.

2. Thyroid scan.


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Thyroid disorders.

1. Hypothyroidism

2. Goitres

3. Hyperthyroidism4. Neoplasams of the thyroid .

5. Thyroiditis .


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HYPOTHYROIDISM

ETIOLOGY AND CLASSIFICATION

1. Failure of thyroid development

a. complete- sporadic cretinism.

b.Partial2.Endemic cretinism

3.Iatrogenic a. After thyroidectomy

b.after radio iodine therapy

c.After pituitary ablation

d.Drug induced eg PAS, Iodide


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19/86CRETINISM


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MYXOEDEMA

A very advanced form of adult hypothyroidism.

CLINICAL FEATURES

SYMPTOMS1.Tiredness

2.mental lethargy

3.cold intolerence

4.increase in weight

5.constipation

6. menstrual disturbances


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Contd

Signs:

1. Carpal tunnel syndrome

2. Slow pulse rate

3. Dry skin4. Dry hair

5. Cold extremeties

6. Periorbital puffiness

7. Hoarse voice8. Slow movements

9. Sluggish ankle jerk


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Cont.

Investigations:

1. Serum T4 levels below 55 nmol/l

2. Free T4 8 pmol/l

3. Radioiodine studies shows reducedthyroid uptake and increased renalexcretion- less than 12% at 24 hours is

diagnostic4. ECGT wave flattened or inverted

5. TSH raised


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Treatment:

L-thyroxine is curative

A dose of 0.15 -0.2 mg/day

In elderly patients with Myocardialinsufficiency the initial dose should be as

low as 0.05 mg per day.

If rapid or short lived response is essential,then triiodothyronine is used


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GOITREENLARGED THYROID GLAND

Classifications of goitre

1. SIMPLE GOITRE (EUTHYROID)

Diffuse hyperplastic goitre Nodular goitre

Colloid goitre

Iron deficiency goitre Multinodular goitre


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Cont.

2. TOXIC GOITRE

Diffuse toxic goitre (Graves disease)

Toxic nodular goitre Toxic nodule

Secondary thyrotoxicosis in MNG

3. NEOPLASTIC GOITRE (BENIGN &MALIGNANT)


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CLASSIFICATION OF THYROID NEOPLASM

MALIGNANT

BENIGN

NEOPLASMS

FOLLICULAR ADENOMA

SECONDARY

METASTATIC

(BLOOD BORNE)

LOCAL INFILTRATION

PRIMARY

MALIGNANT LYMPHOMACARCINOMA MEDULLARY CA

DIFFERRENTIATED UNDIFFERENTIATED(ANAPLASTIC)

PAPILLARY FOLLICULAR


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4. INFLAMMATORY GOITRE

AutoimmuneChronic lymphocytic thyroiditis

Hashimotos disease

GranulomatousDe- Quervains thyroiditis

Fibrosing

Riedels thyroiditis

InfectiveAcute

Chronic Others

Amyloid


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SIMPLE GOITRE-Due to hyper stimulation of thyroid gland by anterior

pitutary

Aeitiology

1. Iodine deficiency

-daily iodine requirement is 100-125 mcg-low iodine areas

-goitrogenic area

-failure of intestinal absorption

2. Defects in synthesis of thyroid hormone

-enzyme deficiency within thyroid gland

-goitrogens:- vegetables of brassica family e.g.cabbage, kale, rap


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STAGES IN GOITRE FORMATION

1. Due to fluctuating TSH level a mixed pattern develops(active and inactive lobules)

2. Active lobules become more vascular and hyperplasticuntil haemorrhage occurs causing central necrosis andleaving only a surrounding ring of active follicles

3. Necrotic lobules coalesce to form nodules.4. Persistent TSH stimulation causes diffuse hyperplasia

and it is reversible if TSH stimulation ceases

5. Continual repetition of this process results in nodulargoitre

Apart from TSH Growth stimulating immunoglobulin is alsoresponsible for this process


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COLLOID GOITRE-SMOOTH SURFACE AND ROUND BORDERS


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DIFFUSE HYPERPLASTIC GOITRE

Children are affected in endemic areas

Sporadic cases in puberty where

metabolic demands are high

Stress and pregnancy

If TSH stimulation ceases the goitre may regress


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Multinodular goitre

Is the end stage result of diffuse

hyperplastic goitre

Aetiopathogenesis

-Puberty goitre

-Pregnancy goitre

-Iodine deficiency goitre All these 3 types of goitres if left untreatred

will change into multinodular goitre


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PUBERTY IODINE DEFICIENCY GOITROGENS

GENETIC FACTORS LOW LEVELS OF T3 AND

T4

TSH STIMULATION

MIXED PATTERN NECROSED FOLLICLESDIFFUSED HYPERPLASIA

MULTINODULAR GOITRE

MALIGNANCY TOXIC MULTINODULAR GOITRE

Feed back mechanism

After a few years


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Clinical features and diagnosis

Common in females Female : male ratio is 10:1

Age group is 20-40

Long duration of swelling in front of the neck

Dyspnoea, dysphagia

Gland is nodular, firm

Hard areas- calcification; soft areas- necrosis

Sudden increase in size with pain-haemorrhageThe most common site of a nodule is at the junction of

isthmus with one lobe


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Investigations Thyroid profile

X-ray of the neck- AP and lateral view- Calcifications

- Deviation of trachea

- To rule out retrosternal extension-soft tissue

Isotope scan- can demonstrate 3 patterns:

a) Hot nodule- glands no uptake, nodule takes

b) Warm nodule- entire gland takes up isotope e.g typical ofGraves disease

c) Cold nodule-nodules doesnt take up isotope Only 10% of the cold nodules are malignant

Ultrasound scan

FNAC


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PEMBERTONS SIGN


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TOXIC GOITRE

(thyrotoxicosis)

DEFINITION:

Its a complex disorders which occurs dueto increased levels of thyroid hormones

and manifests clinically with various signs

and symptoms involving many body

systems.


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CLINICAL TYPES

Diffuse toxic goitre - Graves disease-

primary thyrotoxicosis

Toxic nodular goitre- secondary

thyrotoxicosis

Toxic nodule

others


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GRAVES DISEASE

The exact aetiopathogenesis is not known but

some positive aetiological factors

1. Autoimmune disorder-abnormal thyroid

stimulating antibodies2. Familial

3. Thyroid stimulating immuoglobulins and long

acting thyroid stimulators

4. Exopthalmos- opthalmopathy

5. Female, emotions, stress, young age


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CLINICAL FEATURES

Primary thyrotoxicosis is more common in

females than males

Age: 15- 25 yrs

Loss of weight inspite of good apetite

Diarrhoea occurs due to smooth muscle

activity of small intestine

Intolerance to heat

Preference to cold


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Cont. Fine tremors

Excitability

Excessive sweating

Oligomenorrhoeafree steroid hormoneslevel decrease in graves disease, this

results in decreased effective estrogen at

the cellular level which in turn causes

oligomenorrhoea


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GRAVES DISEASE


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Cont. CNS signs

tremors of the tongue and the tongue is

within the oral cavity

- tremors of the outstretched hand- extensors are weak compared to flexors

- always a moist warm hand (shake hand

and see)

CVS i


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CVS signs:

Pulse rate is always raised and rapid

indicating tachycardia

Depending upon the pulse rate

thyrotoxicosis is classified as follows:

Mild- 90100/ min

Moderate100110/min

Severe - >110/min

Palpitations and extra systoles

Fibrillations and cardiac failure are rare


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SEVERE GRAVES OPTHALMOPATHY


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THYROTOXIC MYOPATHY

Mild weakness of proximal limb muscles incommondifficulty in climbing steps do

occur

Weakness of extraocular muscles resultsin double vision (Diplopia)

Myopathy responds to antithyroid

treatment Features suggestive of myasthenia gravis

and periodic paralysis can be found


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SKIN CHANGES

Pretibial myxoedema- non pitting

Pruritis

Palmar erythema

Thinning of hair

Skin is dry and course

Thyroid acropachy


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INVESTIGATIONS

Routine inv- CCP, RBG,FBG, post-

prandial Blood sugar, urinalysis, CXR,

neck xray, indirect laryngoscopy

Serum T3, T4 are high and TSH is low

Thyroid antibodies are elevated

Sleeping PR remains high

Thyroid scan will show warm gland


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OF PRIMARY THYROTOXICOSIS

AIMS OF TREATMENT

1. To reduce the functioning thyroid mass

to a very critical level (about 6-8 gms of

thyroid tissues)

2. To minimize complications

To restore the patient to euthyroid state:


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To restore the patient to euthyroid state:

DRUGS DOSE PRECAUTION & SIDE

EFFECT

Carbimazole 10 mg 6 hrly

*M-10mg 2-3/day

Takes 2-3 wks for its

action

Propranolol 10-20 mg BD / TDS CCF,Bronchial asthma

Lugols iodine 10-20 drops TDS 10

days before surgery

Bitter taste, to be used

with orange juice

Potassiumperchlorate

200 mg TDS* M 200-400 mg OD

Propyl thiouracil 200 mg TDS

*M- maintanance


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PLEASE NOTE

Iodine containing anti-arrhythmic drug

AMIODARONEmay worsen

thyrotoxicosis.

Propyl thiouracilis safe in pregnancy withGraves disease.

Role of Lugols iodineis doubtful.

TO REDUCE THE FUNCTIONING


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TO REDUCE THE FUNCTIONING

THYROID MASS

Subtotal thyroidectomy

Radio iodine therapy

TO MINIMISE COMPLICATIONS

Good pre-op preparation


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ANTITHYROID DRUGS

ADVANTAGES:

No surgery

No radio active materials

DISADVANTAGES:Treatment is prolonged

failure rate is 50%

Some goitres become vascular and

enlarge

rarely dangerous drug reactions


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SURGERY

ADVANTAGES

Goitre is removed

cure is rapid

cure rate is high with adequate surgery DISADVANTAGES

Recurrence of thyrotoxicosis in < 5%

Post op thyroid insufficiency in 20 -45%

parathyroid insufficiency < 0.5%

nerve injury (ELN , RLN)


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surgery

1. Hemi thyroidectomy

2. Total thyroidectomy

3. Near total thyroidectomy

4. Subtotal thyroidectomy

5. Lobectomy

6. Isthumusectomy


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complications

1. Haemorrage

2. Respiratory obstruction

3. Recurrent laryngeal nerve paralysis

4. Thyroid insufficiency5. Parathyroid insuficiency

6. Throtoxic storm

7. Wound infection

8. Keloid scar

9. Stitch granuloma


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Post op follow up

1.indirect laryngoscopy

Serum calcitonin at 6 wks

Observation every 6 months for

recurrence


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RADIO IODINE

ADVANTAGE:

No surgery

no prolonged drug therapy

DISADVANTAGE:

unavailability

thyroid insufficiency-70-80% after 10yrsan indefinite follow up is essential

CHOICE OF THERAPY


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CHOICE OF THERAPY Diffused toxic goitre

over 45yrs-radioiodine

under 45 yrssurgery for large goitre

drugs for small goitre

Toxic nodular goitresurgery Toxic nodulesurgery is mainstay radioiodine

for >45yrs

Recurrent thyrotoxicosis after adequate surgery:

> 45 yrsradioiodine,


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CLASSIFICATION OF THYROID NEOPLASM

MALIGNANT

BENIGN

NEOPLASMS

FOLLICULAR ADENOMA

SECONDARY

METASTATIC

(BLOOD BORNE)

LOCAL INFILTRATIONPRIMARY

MALIGNANT LYMPHOMACARCINOMA MEDULLARY CA

DIFFERRENTIATED UNDIFFERENTIATED(ANAPLASTIC)

PAPILLARY FOLLICULAR

SUMMARY OF MALIGNANT TUMOUR OF THYROID GLAND


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SUMMARY OF MALIGNANT TUMOUR OF THYROID GLAND

PAPILLARY FOLLICULAR ANAPLASTIC MEDULLARY

Etiology Irradiation Endemic goitre Unknown Sporadic orfamilial

Incidence 60% 17% 13% 6%

Age 20-40 30-50 >50 Middle age

Dx Thyroid swelling

with LN

Thyroid swelling

with metastasis-

bone

Thyroid

swelling, local

fixity, stridor

Difficult to Dx

clinically

Microscop

ic

Orphan Annie-

eyed nuclei,psammoma

bodies

Angioinvasion,

capsular invasion

Poorly

differentiatedcells

Amyloid

stroma-likecarcinoid

Spread Lymphatic Blood Local

infiltration

Lymphatic,

blood

PAPILLARY FOLLICULAR ANAPLASTIC MEDULLARY


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Invx FNAC FROZEN

SECTION

FNAC,

BIOPSY

FNAC,

CALCITONIN

Rx of

1ONEAR TOTAL

THYROIDECT

OMY

NEAR TOTAL

THYROIDECTO

MY

ISTHMUSECT

OMY,EXT. RT

TOTAL

THYROIDECTO

MY

Rx of

mets

FUNCTIONAL

BLOCKDISSECTION

I 131OR EXT RT PALLIATIVE

EXT. RT

RADICAL

BLOCKDISSECTION

TSH

depende

nce

YES YES NO NO

Hormonal prod

VERY RARE VERY RARE NO CALCITONIN,

5-HT, ACTH

Px EXCELLENT GOOD WORST BAD


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FOLLICULAR NEOPLASM


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PAPILLARY CA PRESENTING AS SOLITARY NODULE


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PAPILLARY CARCINOMA


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ULCERATED SECONDARIES IN THE SCALP BONE FROMFOLLICULAR CARCINOMA THYROID


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SECONDARY DEPOSIT IN THE STERNUM IN A

PATIENT WHO UNDERWENT NEAR TOTAL

THYROIDECTOMY FOR FOLLICULAR CARCINOMA 5

YEARS AGO

Based on BIOLOGICAL AGGRESIVENESS 2 RISK group s:


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Based on BIOLOGICAL AGGRESIVENESS, 2 RISK group s:

Low Risk:

(F) < 50, (M) < 40 years

Papillary Ca, Follicular Ca (cytologically suspicious)Tumour < 1.5 -2 cm, confined to one lobe, no metastases

SURGERY: LOBECTOMY

? Near to tal THYROIDECTOMY

Prognosis: Lobectomy ? Higher recurrence

No significant advantage in survival compared to TT

High Risk:Age: (F) > 50, (M) > 40 years

Larger, bilateral tumours or metastases

Papillary Ca (extrathyroidal)

Follicular Ca (widely invasive)

Medullary Ca

SURGERY: TOTAL THYROIDECTOMY

? Near tot al THYROIDECTOMY

+Lymphno de excis ion o f centra l nod es

+Modif ied radical neck dissect io n

LOW RISK

1.8% Mortality Rate

HIGH RISK

46% Mortality Rate


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Men under 41 and Women under 51

without distant metastasesAll patients with distant metastases

All men over 41 and women over 51 with:

Intra-thyroidal papillarycancer (papillary cancer confined

present only within the thyroid gland) OR follicular

cancer tumor with minor capsular involvement

(the tumor slightly extends into the capsule which

surrounds it) AND

Primary tumor less than 5 cm in diameter AND

No distant metastases

All men over 41 and women over 51 with:

Extra-thyroidalpapillarycancer (extends beyond the

thyroid gland) OR follicular cancer tumor with

major capsular involvement (the tumor extends

significantly into the capsule which surrounds it)

AND/OR

Primary cancer is 5 cm in diameter or larger, regardless

of the extent of the disease

PROGNOSIS

Documents

Thyroid Disorders Seminar