Thyroid Disorders Seminar
Thyroid Disorders Seminar
Thyroid Disorders Seminar
MWANGA
SURGICAL ANATOMY
Thyroid gland = shield like
site lower part of the anterior and lateral
sides of the neck.
Gland contains right and left lobe joined by
Isthmus.
Vertebral level C5,6,7,T1.
Each lobe extends from middle of thyroid
cartilage to the 4th or 5th tracheal ring.
Isthmus2nd and 3rd tracheal ring.
Contd
Dimensions lobe -5cms x 2.5cm x2.5cm.
Isthmus 1.5cm x1.5cms.
Weight 20 to 25 grams in adults.
Functional unit is lobule.
Each lobule is supplied by an arteriole.
2 capsules True capsule.
False capsule.
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.)
BLOOD SUPPLY
1. Superior thyroid artery first anterior branch of
the external carotid artery.its in close relation
with external laryngeal nerve. It divides in to
anterior and posterior branches. Supplies
upper 1/3rd of lobe and upper of isthamus.
2. Inferior thyroid artery branch of thyrocervical
trunck.its terminal part is in close relation with
recurrent laryngeal nerve.supplies lower 2/3rd
of lobe and lower of isthamus.
Venous drainage
Superior thyroid vein drains in to internal
jugular vein or common facial vein.
Middle thyroid vein into internal jugular
vein .
Inferior thyroid vein Lt brachiocephalic
vein.
Thyroid vein of kocher in to internal
jugular vein.
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.
PHYSIOLOGY
THYROID HORMONES
Iodine & tyrosine form both T3 & T4
under TSH stimulation. However, 10%
of T4 production is autonomous and is
present in patients with central
hypothyroidism.
When released into circulation T4
binds to:
Globulin TBG
75%
Prealbumin TBPA
20%
SYMBOL
NORMAL RANGE
Total serum
thyroxine
T4
55 150 nmol/I
Total tri
iodothyronine
Free thyroxine
T3
t4
8 26 pmol/I
Free triiodothyronine
t3
3 9 pmol/I
INVIVO TESTS
1. Radio iodine active uptake test.
2. Thyroid scan.
Thyroid disorders.
1.
2.
3.
4.
5.
Hypothyroidism
Goitres
Hyperthyroidism
Neoplasams of the thyroid .
Thyroiditis .
HYPOTHYROIDISM
ETIOLOGY AND CLASSIFICATION
1. Failure of thyroid development
a. complete- sporadic cretinism.
b.Partial
2.Endemic cretinism
3.Iatrogenic a. After thyroidectomy
b.after radio iodine therapy
c.After pituitary ablation
d.Drug induced eg PAS, Iodide
Contd
4 .Auto immune thyroiditis
a.Non- goitrous[ primary
myxedema ]
b. Goitrous [Hashimoto goitre]
5. Dyshormonogenesis
6.Goitrogens
7.Vascular damage to anterior pituitary.
CRETINISM
MYXOEDEMA
A very advanced form of adult hypothyroidism.
CLINICAL FEATURES
SYMPTOMS 1.Tiredness
2.mental lethargy
3.cold intolerence
4.increase in weight
5.constipation
6. menstrual disturbances
Contd
1.
2.
3.
4.
5.
6.
7.
8.
9.
Signs:
Carpal tunnel syndrome
Slow pulse rate
Dry skin
Dry hair
Cold extremeties
Periorbital puffiness
Hoarse voice
Slow movements
Sluggish ankle jerk
Cont.
1.
2.
3.
Investigations:
Serum T4 levels below 55 nmol/l
Free T4 8 pmol/l
Radioiodine studies shows reduced
thyroid uptake and increased renal
excretion- less than 12% at 24 hours is
diagnostic
4. ECG T wave flattened or inverted
5. TSH raised
Treatment:
L-thyroxine is curative
A dose of 0.15 -0.2 mg/day
In elderly patients with Myocardial
insufficiency 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
GOITRE
ENLARGED THYROID GLAND
Classifications of goitre
1. SIMPLE GOITRE (EUTHYROID)
Diffuse hyperplastic goitre
Nodular goitre
Colloid goitre
Iron deficiency goitre
Multinodular goitre
Cont.
2. TOXIC GOITRE
Diffuse toxic goitre (Graves disease)
Toxic nodular goitre
Toxic nodule
Secondary thyrotoxicosis in MNG
3. NEOPLASTIC GOITRE (BENIGN &
MALIGNANT)
FOLLICULAR ADENOMA
NEOPLASMS
MALIGNANT
METASTATIC
(BLOOD BORNE)
SECONDARY
LOCAL INFILTRATION
PRIMARY
CARCINOMA
DIFFERRENTIATED
PAPILLARY
MALIGNANT LYMPHOMA
UNDIFFERENTIATED
(ANAPLASTIC)
FOLLICULAR
MEDULLARY CA
4. INFLAMMATORY GOITRE
Autoimmune
Chronic lymphocytic thyroiditis
Hashimotos disease
Granulomatous
De- Quervains thyroiditis
Fibrosing
Riedels thyroiditis
Infective
Acute
Chronic
Others
Amyloid
SIMPLE GOITRE
-Due to hyper stimulation of thyroid gland by anterior
pitutary
1.
Aeitiology
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
2.
3.
4.
5.
TREATMENT
L-thyroxine is given in maximum doses
0.2mg/day for several months and then
very slowly tail off to 0.1mg/day which
should be continued for many years
Surgery indicated for cosmetic reasons,
pressure symptoms and no response for
medical treatment
Prevention fortified salt
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
PUBERTY
GENETIC FACTORS
GOITROGENS
IODINE DEFICIENCY
DIFFUSED HYPERPLASIA
MIXED PATTERN
NECROSED FOLLICLES
MULTINODULAR GOITRE
After a few years
MALIGNANCY
Investigations
Thyroid profile
X-ray of the neck
-
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 of
Graves disease
c) Cold nodule-nodules doesnt take up isotope
Ultrasound scan
FNAC
PEMBERTONS SIGN
TOXIC GOITRE
(thyrotoxicosis)
DEFINITION:
Its a complex disorders which occurs due
to increased levels of thyroid hormones
and manifests clinically with various signs
and symptoms involving many body
systems.
CLINICAL TYPES
Diffuse toxic goitre - Graves diseaseprimary thyrotoxicosis
Toxic nodular goitre- secondary
thyrotoxicosis
Toxic nodule
others
GRAVES DISEASE
1.
2.
3.
4.
5.
PATHOLOGY
As a result of continous stimulation acinar
hypertrophy and hyperplasia takes place.
Acinar cells which are usually flat
becomes tall columnar. The normal colloid
disappears and the cells are empty
however, rich vascularity is seen.
Thus, small follicles with hyperplastic columnar
epithelium is characteristic.
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
Cont.
Fine tremors
Excitability
Excessive sweating
Oligomenorrhoea free steroid hormones
level decrease in graves disease, this
results in decreased effective estrogen at
the cellular level which in turn causes
oligomenorrhoea
GRAVES DISEASE
SIGNS
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 signs:
Pulse rate is always raised and rapid
indicating tachycardia
Depending upon the pulse rate
thyrotoxicosis is classified as follows:
Mild- 90 100/ min
Moderate 100 110/min
Severe - >110/min
Palpitations and extra systoles
Fibrillations and cardiac failure are rare
EYE SIGNS:
Prominent eyeballs-proptosis and lid retraction
result in exophthalmos
Lid spasms
Classical stare
Sclera is visible beyond limbus
Typically seen in Graves disease
Rare in secondary thyrotoxicosis
In late stages optic nerve damage and blindness
can occur
THYROTOXIC MYOPATHY
Mild weakness of proximal limb muscles in
common difficulty in climbing steps do
occur
Weakness of extraocular muscles results
in double vision (Diplopia)
Myopathy responds to antithyroid
treatment
Features suggestive of myasthenia gravis
and periodic paralysis can be found
SKIN CHANGES
INVESTIGATIONS
Routine inv- CCP, RBG,FBG, postprandial 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
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
DOSE
Carbimazole
10 mg 6 hrly
*M-10mg 2-3/day
Propranolol
10-20 mg BD / TDS
CCF,Bronchial asthma
Lugols iodine
Potassium
perchlorate
200 mg TDS
* M 200-400 mg OD
PLEASE NOTE
Iodine containing anti-arrhythmic drug
AMIODARONE may worsen
thyrotoxicosis.
Propyl thiouracil is safe in pregnancy with
Graves disease.
Role of Lugols iodine is doubtful.
TO MINIMISE COMPLICATIONS
Good pre-op preparation
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
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)
surgery
1.
2.
3.
4.
5.
6.
Hemi thyroidectomy
Total thyroidectomy
Near total thyroidectomy
Subtotal thyroidectomy
Lobectomy
Isthumusectomy
complications
1.
2.
3.
4.
5.
6.
7.
8.
9.
Haemorrage
Respiratory obstruction
Recurrent laryngeal nerve paralysis
Thyroid insufficiency
Parathyroid insuficiency
Throtoxic storm
Wound infection
Keloid scar
Stitch granuloma
Post op follow up
1.indirect laryngoscopy
Serum calcitonin at 6 wks
Observation every 6 months for
recurrence
RADIO IODINE
ADVANTAGE:
No surgery
no prolonged drug therapy
DISADVANTAGE:
unavailability
thyroid insufficiency-70-80% after 10yrs
an indefinite follow up is essential
CHOICE OF THERAPY
Diffused toxic goitre
over 45yrs-radioiodine
under 45 yrs surgery for large goitre
drugs for small goitre
Toxic nodular goitre surgery
Toxic nodule surgery is mainstay radioiodine
for >45yrs
Recurrent thyrotoxicosis after adequate surgery:
> 45 yrsradioiodine, <45 yrs drugs
Failure of previous Rx with antithyroid drug or
radio iodine surgery or thyroid ablation
FOLLICULAR ADENOMA
NEOPLASMS
MALIGNANT
METASTATIC
(BLOOD BORNE)
SECONDARY
LOCAL INFILTRATION
PRIMARY
CARCINOMA
DIFFERRENTIATED
PAPILLARY
MALIGNANT LYMPHOMA
UNDIFFERENTIATED
(ANAPLASTIC)
FOLLICULAR
MEDULLARY CA
PAPILLARY
FOLLICULAR
ANAPLASTIC
MEDULLARY
Etiology
Irradiation
Endemic goitre
Unknown
Sporadic or
familial
Incidence
60%
17%
13%
6%
Age
20-40
30-50
>50
Middle age
Dx
Thyroid
swelling, local
fixity, stridor
Difficult to Dx
clinically
Angioinvasion,
capsular invasion
Poorly
differentiated
cells
Amyloid
stroma-like
carcinoid
Spread
Blood
Local
infiltration
Lymphatic,
blood
Lymphatic
PAPILLARY
FOLLICULAR
ANAPLASTIC
MEDULLARY
Invx
FNAC
FROZEN
SECTION
FNAC,
BIOPSY
FNAC,
CALCITONIN
Rx of
1O
TOTAL
THYROIDECTO
MY
Rx of
mets
PALLIATIVE
EXT. RT
RADICAL
BLOCK
DISSECTION
TSH
YES
depende
nce
YES
NO
NO
VERY RARE
NO
CALCITONIN,
5-HT, ACTH
Px
GOOD
WORST
BAD
EXCELLENT
FOLLICULAR NEOPLASM
PAPILLARY CARCINOMA
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 total 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 total THYROIDECTOMY
+Lymphnode excision of central nodes
+Modified radical neck dissection
LOW RISK
1.8% Mortality Rate
PROGNOSIS
HIGH RISK
46% Mortality Rate