Enlargement of the Thyroid Gland

 Physiological - puberty / pregnancy

 Pathological

Embryology & Anatomy

Thyroid gland develops from 1st & 2nd pharyngeal pouches
● Derived from epithelial proliferation in the floor of the pharynx
● Migrates downwards in front of forgegut to lie anterior to trachea - during movement – remains
attached to floor of mouth by thyroglossal duct – which ultimately disappears
If the thyroglossal duct persists – results in: Thyroglossal sinus or Thyroglossal cyst
Hormone synthesis begins @ 10-12 wks gestation
Maternal hormones thus NB in 1st half of pregnancy
● When thyroid gland reaches position it occupies in adult, just below the cricoid cartilage → divides
into 2 lobes
● Isthmus → thin midline band of tissue – lies horizontally below the cricoid cartilage
● Normal thyroid weighs 15-25g & is attached to trachea by loose CT
Surgical Anatomy
Gland → invested by thick fibrous sheath (pretracheal fascia)
Sends septa into gland and binds it to larynx therefore → normal gland =
moves on swallowing
● Rich blood supply → superior & inferior thyroid arteries
↑’d BF in hyperthyroidism therefore → surgery = difficult
● Lymphatic drainage → via mid & lower deep jugular, pretracheal & mediastinal
LN’s
● Gland → laterally traversed by recurrent laryngeal nerve (RLN)
Injury → paralysis of vocal cords
● Close relationship to Parathyroid glands – thus during surgery may remove them
accidentally = hypoparathyroidism

Histo Physiology

Follicles (acini) Thyroid Gland produces 2 hormones

→ roughly spherical – diameter = 3mm
Lined with epithelial cells →
secrete thyroid hormones →
stored in colloid of follicle
Epithelial cells → cuboidal
cells – but become columnar
in response to TSH
C-cells = btwn follicles (also
Parafollicular cells) – make and
secrete Calcitonin
THYROXINE – regulates metabolic rate
IODINE TRAPPING → Iodine reduced to iodide in GIT→ absorbed from small bowel → actively trapped by follicular cells
ORGANIFICATION → Iodide → oxidized and bound to tyrosine in thyroglobulin → forms mono-iodotyrosine (MIT) & di-iodotyrosine (DIT) via
action of Thryoid Peroxidase
COUPLING → MIT & DIT - cleaved then coupled to form tri-iodotyrosine (T3) & thyroxine (T4) via action of Thryoid Peroxidase → stored in
follicles
TRH released from hypothalamus – causes release of TSH from anterior pituitary → TSH binds to receptors on thyroid gland → ↑ adenylyl
cyclase (AC) activity - ↑ cAMP (phosphoinositide pathway also stimulated – may stimulate thyroid growth)
In response to TSH → thyroglobulin hydrolysed → T3 & T4 secreted into plasma - bind to thyroxine-binding globulin (TBG) and albumin
T4 de-iodinated peripherally – form T3 (common site of conversion = liver)
Negative feedback – TSH & TRH ↓
CALCITONIN – calcium homeostasis
↓ calcium concentration in serum – via inhibition of osteoclast – therefore ↓ calcium absorption by bone & ↑ renal excretion of calcium
Approach to the Thyroid
Embryology & Anatomy
A. Dysfunction
B. Organic
C. Combination
1st Important Question for any growth: Is it malignant or benign?
Then: Take a History
 Behaviour of the growth
 Risk factors
- Personal (the patient)
- Family (history)
Then: Clinical Examination
 Signs of malignancy in any growth
Diagnosis of a thyroid growth in the neck:
1. Hx & Clinical
2. TSH blood test
3. Ultrasound
4. CT scan
5. Ionised iodine
 Hyperthyroidism
 Hypothyroidism
Mass growing in the neck
No dysfunction
- multinodular goiter
- solitary nodule
Growth + dysfunction
- Hashimoto’s
- Toxic multinodular goiter
- Solitary nodule
- Grave’s
tissue.
similarly to normal thyroid
tumours - behave very
Well-differentiated
Behaviour:
 Most commonly slow growth - Rapid growth seen only in Anaplastic & Medullary carcinoma
 Usually no weight loss
 Spread: Tracheal invasion
Radiation exposure to the head/neck Bone pain
Extremes of ages (very young/old) Headaches
Female sex (3:1) Odynophagia
Poorer prognosis (males) Dysphonia (hoarseness)
Hx of previous thyroid cancer
MEN II Examination of the growth (thyroid):
+ Family Hx for Ca other than MEN  Lesion fixed to surrounding tissues (hardly ever to the skin)
 Lymphadenopathy - unilateral
- isolated cervical
- immobile
- firm
 Hoarseness (dysphonia)
 Diffuse / Multinodular / Solitary
Investigating the Thyroid

Patient presents with suspicious Clinical & Blood = Hyperthyroidism Ultrasound NORMAL On U/S:
clinical history of thyroid a thyroid Diffuse goitre OR Non-palpable - no toxic adenoma - Solidary nodule
problem. … - Multinodular nodule
 Grave’s Disease Distinguishing between Grave’s and - Diffuse goitre
(overstimulated cells) Hashimoto’s
Step 1  Hashimoto’s Thyroididits Must check cellular architecture
(gland destroyed, thyroid
hormone release)
Benign vs.
 Toxic Adenoma
Malignant

TSH Ultrasound Auto-Antibodies FNA

 TSH Hyperthyroidism Must do ultrasounds Graves: Done under guidance

High T3 T4  Confirm clinical findings TSH antibodies 80% sensitive for malignancy
Radioisotope Scan
 TSH Hypothyroidism  Rule out small nodules (Toxic Hashimoto’s: Repeated 2x if negative
Low T3 T4 Adenoma) Anti-microsomal antibodies
Anti-thyroglobulin antibodies Can’t report X Follicular
 TSH Sub-Clin hyperthyroidism Can report Papillary Serves to map out dysfunction
U/S is the most sensitive test for
Normal T3 T4 98% Sensitivity Medullary through the entire gland - visual
nodules!
 TSH Sub-Clin hypothyroidism Anaplastic pattern of functionality.
Normal T3 T4
Info Gathered from U/S: Other distinguishing test:  Hot - active
TSH:T4 ratio >20 = Graves Usually normal gland
- cystic vs. solitary nodule
Done in pts not on hormone - features of malignancy  ESR = Hashimoto’s  Cold - decreased uptake
replacement therapy, with no other - find non-palpable nodules Hypoactive (e.g. Hashi)
influencing drugs. - confirm solitary nodule  Patchy
98% Sensitivity - solitary vs. multi-nodular Toxic multinodular goitre
- size of lesion (of either type) Hashimoto’s
- find scary lymphadenopathy  Isolated uptake (Focal Hot)
Toxic adenoma
 Diffuse dysfunction
Grave’s
Treating Thyroid Problems
Grave’s Disease
Or PLUMMER’S DISEASE
- toxic multinodular goitre
 Make the patient euthyroid

Anti-thyroid drugs
Protect target organs
B-Blockers
 Radioactive Ablation
Once patient is euthyroid
 Follow up - After 4 months -
should indicate success of
ablation (past peak, enter
euthyroid or hypothyroid
phase)
Ablation:
 95% cure rate with 1st dose
 should reach euthyroid state 12
weeks post-ablation
CI X for Ablation:
- pregnancy
- iodine allergy
- failed medical Rx
- pressure symptoms
(need surgery)
Hashimoto’s Thyroiditis
 Self-limiting disease
 Usually reaches euthyroid state
 Protect target organs
B-Blockers
 Rx hypothyroid state
Altroxin
Beta-Blockers
- Prevent’s T4 - T3 conversion
- Protects the heart
Toxic Adenoma
U/S showed solitary nodule
Toxic patient
 Do Isotope scan (see focal hot

spots)
Areas of good uptake - do
lobectomy & isthmectomy
 Totally suppressed gland - do
radical thyroidectomy
Cancer
Follicular Ca
 Won’t see on FNA report
 Can’t distinguish Follicular Ca /
Adenoma
 Do complete lobectomy
Best
 Follicular adenoma = leave
alone
Success
Medullary
 Total neck dissection
 Investigate for MEN
Papillary Ca
 Total thyroidectomy
Anaplastic
 Can Dx on FNA
 Very often presents in
advanced stage
 For METS: surgery for primary
first
 Ablation can follow surgery
(better uptake by metastatic
cells)
NB: Follicular / Papillry - TSH
dependent. Needs post-op ablation
& TSH suppression for 2 yrs .