1.
Dr .Befekadu Lemu

2.
Definition of goiter
Classification
MULTINODULAR GOITER
Aetiopathogenesis of MNG
Diagnosis of MNG
Treatment of MNG
HYPERTHYROIDISM
Definition
Classification
Primary hyperthyroidism
Aetiopathogenesis
Diagnosis
treatment

3.
GOITER
 Definition : is a diffuse enlargement of the thyroid
gland.
 Classification:
 Simple
 Toxic
 Neoplastic
 Inflammatory(thyroiditis)
 Others (Amyloid)

4.
Simple goiter
1. Puberty goiter
2. Colloid “
3. Iodine deficiency “
4. MNG
5. Pregnancy goiter

5.
Toxic goiter
1. Graves’ disease (Primary thyrotoxicosis)
2. Secondary thyrotoxicosis in MNG
3. Solitary nodule

6.
Neoplastic Goiter
1) Benign (adenoma)
2) Malignant tumors :
 Primary tumors :
• Papillary
• Follicular
• Anaplastic
• Medullary
• Malignant lymphoma
 Secondary tumors (mets. through blood spread
from melanoma, renal ca. breast ca. etc.

7.
Inflammatory (Thyroiditis)goiter
1) Autoimmune (ch. Lymphocytic, Hashimoto)
2) Granulomatous (de QUERVAIN’S)
3) Fibrous (Riedel’s)
4) Acute infection (bacterial, viral)
5) Ch. Thyroiditis (Tb. Syphilis)
OTHERS (Amyloid)

8.
MULTINODULAR GOITER (MNG)
Is the end stage result of a diffuse hyperplastic goiter
Is due to excessive metab. demand and continuous
stimulation of the gland by TSH.
Is common in women.
Aetiopathogenesis:
1. Puberty goiter
2. Pregnancy goiter
3. Iodine deficiency goiter
4. Goiterogenous substances (cabbage, PAS,sulfonamides)
which prevent oxidation of iodide to iodine.

9.
cont. etiopatogenesis
 All the 1st. 3 types of goiter, if left untreated, will be
changed to MNG. Following 3 stages:
I. Stage : diffuse hypertrophy &
hyperplasia
II. Stage : overstimulation & conversion of
some areas of the gland into active
follicles due to fluctuating levels of TSH
(pregn.,lactation, menstruation)
III. Stage :nodules formation stage

10.
DIAGNOSIS
 Is done by:
 Clinical features
 investigations

11.
Clinical features of MNG
 Common in female of 20-40 yrs.(10:1)
 Long standing neck’s swelling
 The swelling moves freely and is painless
 Both lobes enlarged ,nodular and firm
 Can have hard areas (calcifications) or soft
areas (necrosis)
 Can have dyspnea/dyphagia

12.
INVESTIGATIONS FOR THYROID DISEASES
1. Routine examinations
2. X-ray of the neck and chest
3. Isotope scan(radio-iodine):
 Hot nodule (autonomous)
 Warm nodule (graves’ disease)
 Cold nodule (haemorrhage,ca. Thyroiditis)
4. TFT(thyroid function test)
5. Indirect laryngoscopy
6. FNAC(fine needle aspiration cytology)
7. U/S
8. Autoantibody titers
9. Other scans (CT-scan, MRI)

13.
Treatment of MNG
PREVENTIVE Rx.:
 Rx. Of puberty goiter (thyroxin 0.1-o.2mg/day)
 Rx. Of iodine deficiency goiter (iodized salt, sea
foods, milk eggs etc.)
 Avoiding Goiterogenous substances (cabbage,
drugs)
CURATIVE:
 Subtotal thyroidectomy
 Postop. Rx. With thyroxin 0.2mg/day for 2-5 yrs.
to suppress the TSH stimulation

14.
Complications of MNG
1. Pressure symptoms
2. Sudden intraglandular hemorrhage
3. Secondary thyrotoxicosis with CVS
impairment (10-20%)
4. Malignancy (follicular ca.)

15.
HYPERTHYROIDISM
 Definition : is a complex disorder which
occurs due to increased level of thyroid
hormones and manifests clinically with
different signs and symptoms which
involve multiple body systems.

16.
Classification of hyperthyroidism
1. PRIMARY HYPERTHYROIDISM (Graves’
disease,exophtalmic goiter)
2. Secondary hyperthyroidism in MNG
3. Tertiary hyperthyroidism (solitary toxic nodule)
4. Hyperthyroidism of other causes:
 thyrotoxicosis facticia(due to over dosage of thyroxin in the Rx.
Of juvenile goiter)
 Jod –Bassedow thyrotoxicosis ( iodine induced thyrotoxicosis in
Rx. hyperplastic endemic goiter
 Thyroiditis in initial stage
 Neonatal thyrotoxicosis in babies of thyrotoxic mothers
 Toxic ca.

17.
PRIMARY HYPERTHYROIDISM
 AETIOPATOGENESIS:
 Autoimmune disorder (TsAb)
 Familial
 Thyroid stimulating immunoglobulin (TSI)
 Long acting thyroid stimulator (LATS)
 Exophthalmos producing substance (EPS)
 Others:
 Female sex(male : female =1:8)
 Young age (15-25yrs.)
 Emotions / stress

18.
Diagnosis of primary
thyrotoxicosis
 Is done based on :
1) Clinical features
1) investigations

19.
Clinical features of primary
hyperthyroidism
1) Signs on thyroid gland
2) CNS signs
3) Eye signs
4) CVS signs
5) GIT signs
6) MSS signs(musculoskeletal system signs)
7) Other signs (menstrual disturbances)

20.
Signs of prim. Hyperthyroidism
on the thyroid gland
Uniformly enlarged mild goiter
Smooth (no nodule)
Soft / firm
Warm (due to hypervascularization)
Bruit can be auscultated

21.
CNS signs of hyperthyroidism
Tremors (tongue / hand )
Sweating (hands)
Hyperkinetic
Intolerance to heat
Preference to cold
Excitability / irritability
restlessness

22.
Eye signs of prim hyperthyroidism
 Exophthalmoses
 Eye lid spasm
 Proptosis (protrusion of eye ball seen on
observation from behind)
 Classical staring
 Loss of eye ball conversion
 Infrequent blinking
 Lid lags behind when asked to look up and down
with speed of finger’s movement.
 Keratitis
 Corneal ulcers
 conjunctivitis /blindness

23.
CVS SIGNS OF PRIM.
HYPERTHYROIDISM
 Despite the predominance of CVS signs in secondary
hyperthyroidism, in primary hyperthyroidism there
are :
 Tachycardia
 Palpitations
 extracystoles

24.
GIT signs of prim. hyperthyroidism
Polyphagia
Diarrhea
Weight loss (despite good appetite)

25.
MSS & OTHER signs of prim.
hyperthyroidism
o Mild weakness of proximal limb
o Weakness of muscles (difficulty to climb steps)
o Menstrual disturbances etc.

26.
Treatment of primary hyperthyroidism
 Is based on 3 modalities :
1. Antithyroid drugs
2. Surgery (subtotal thyroidectomy)
3. Radio-iodine therapy
And it has 3 aims :
1. To restore the pt. to euthyroid state
2. To reduce the functioning thyroid mass to a
very critical level
3. To reduce complications

27.
Antithyroid drugs & others for the Rx. Of prim.
hyperthyroidism
 Are used to restore the pts. to euthyroid state. It takes 8-12
weeks or more.
 The usually used are :
 Antithyroid such as :
 PTU (200mg or more 8hrly..
 Carbimazole 10-15mg 6 or 8hrly
 Metimazole 10mg 6 or 8hrly
 Beta adrenergic blockers such as :
 Propranolol 10-20mg 8hrly (40mg tid in sever cases
 Nadolol 160mg./day
 Lugol’s iodine (10-12 drops po 8hrly for 14 days before surgery

28.
Minimizing the gland’s mass in the Rx.of prim.
hyperthyroidism
 Is achieved by :
I. Surgery (subtotal thyroidectomy) in :
 Young pts. (25-35yrs)
 Large toxic goiter
 Retrosternal goiter
 Sever toxicosis with pregnancy in 2nd. Trimester
 Reaction to Antithyroid drugs
II. Radio-iodine therapy in :
 Pts. > 40yrs.
 Recurrent hyperthyroidism after operation
 Prim. Hyperthyroidism with cardiac symptoms

29.
To reduce surgical complications in the
Rx of prim. hyperthyroidism
 Is achieved by :
 Good preop. Preparation
 Good anesthesia technique
 Good surgical tech.

30.
Post. Op. complication of thyroid surgery
1. Hemorrhage
2. Resp. obstruction due to laryngeal edema
3. Recurrent laryngeal nerve palsy/paralysis
4. Hypothyroidism
5. Hypoparathyroidism
6. Thyrotoxic crisis (storm)
7. Wound infection
8. Keloid scar
9. Stitch granuloma

31.
Advantages & disadvantages of each modality
of Rx. In prim. hyperthyroidism
 Medical RX.:
 Advantages :
 Avoids surgery
 No risk to life
 Is economical
 Disadvantages :
 Long duration of Rx.(1-2yrs.)
 Agranulocytosis
 Missed doses
 relapses

32.
Advantages & disadvantages of each
modality of prim. Hyperthyroid.
SURGICAL Rx.. RADIOIODINE Rx.
 ADVANTAGES
Permanent cure is
high
 DISADVANTAGES
Carries morbidity &
mortality
Postop side effects
Can recur
 ADVANTAGES
no surgery
No drugs
easy
 DISADVANTAGES
No in pregnancy
No in young girls
Permanent
hypothyroidism

33.
Carcinomas of the thyroid
gland(primaries)
 Thyroid gland is the only endocrine gland where :
 Malignant tumors are easily accessible for
clinical examination
 Malignant tumors occur in all ages and sex
 Malignant tumors spread by all routs (local,
lymphatic and blood)
The malignant tumors of this gland have a
good prognosis if diagnosed and treated
early.

34.
Classification of primary
thyroid tumors
I. Well differentiated
 Papillary
 follicular
II. Moderately differentiated
 Medullary Ca.
III. Poorly differentiated
 anaplastic
IV. Malignant lymphomas(from lymphatic tissue)

35.
Incidence of malign. Thyroid
tumors
 Papillary 60-65%
 Follicular 15-20%
 Anaplastic10-12%
 Medullary 5-10%
 Others 10%

36.
Clinical criterion for the diagnosis of thyroid Ca.
Can be suspected even with only 1 feature
1. Rapidly growing thyroid’s swelling
2. Thyroid swelling with cervical L/nodes
3. Hard gland fixed to trachea
4. Thyroid swelling with hoarseness of the voice
5. Thyroid swelling with Berry sign positive
(impalpable carotid pulsation in anaplastic Ca.)
6. Kocher’s test (+) due to tracheal
infiltration(stridor)

37.
Investigations
 As in all thyroid diseases + calcitonin dosification in
case of med. Ca.

38.
Etiology
1) Papillary
 Accidental radiation to the neck
 Post Hashimoto’s Thyroiditis
2) Follicular
 MNG(endemic goiter)
3) Anaplastic (unknown)
4) Medullary
 Familial / sporadic
5) Lymphoma (Hashimoto is the possibility)

39.
Clinical features of thyroid Ca.s
 Papillary
 Freq. In young female(20-40yrs)
 Solitary nodule
 Thyroid swelling with L/nodes
 Is TSH dependant
 Follicular
 Freq. In 40 yrs. Of age(30-50yrs.)with solitary nodule
 Can be presented in long standing MNG with rapid
growth
 Thyroid swelling with mets. in flat bones
 Is also TSH dependant

40.
Contin. Of clinical features of
thyroid Ca.s
 Anaplastic
Common in 60-70
Rapidly growing thyroid swelling with local fixicity
and stridor
Berry sign (+)
Is not TSH dependant
 Medullary
 Is difficult to diagnose clinically
 Is not TSH dependant

41.
Spread of thyroid Ca.s
 Papillary -------lymphatic
 Follicular ------blood
 Anaplastic------local infiltration
 Medullary-------lymphatic & blood

42.
Management of thyroid Ca.s
 In all thyroid Ca.s , Rx. is done with 3 targets:
1) Rx. Of the primary tumor
2) Rx. Of the secondaries in the L/nodes
3) Suppression of the TSH.

43.
Rx. Of thyroid Ca.s cont.
Rx.of prim .Rx.of L/ns. TSH
1) Papillary NTT dissection thyroxin
2) Follicular NTT Rt/radioiod thyroxin
3) Anaplastic isthmusectomy pal.Rt. No
4) Medullary NTT/TT dissection no
5) Lymphoma isthmus(if compress) Rt./chemo no
Rt./chemotherapy

44.
Prognosis of thyroid Ca.s
 Papillary---------excellent
 Follicular--------good
 Anaplastic-------worst
 Medullary--------bad

45.
BIBLIOGRAPHY
Bailey & LOVES :SHORT PRACTICE
OF SURGERY, 22nd. Edition, 1995
Manipal : Manual of surgery, 1st.
Edition, 2000
Text book of surgery : David C.
Sabiston, 1997

46.
THANK U VERY
MUCH