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Thyroid diseases
1. THYROID DISEASES
By
Dr. Abdul Qadeer
MBBS; FCPS; FICS
Assistant Professor in General Surgery
King Faisal University College of Medicine
Kingdom of Saudi Arabia
2.
3. OBJECTIVES
1. Embryology & related diseases
2. Anatomy of thyroid
3. Physiology of thyroid hormones
4. Benign thyroid disorders & their management
5. Goiter & Solitary thyroid nodule &
management
6. Thyroid malignancy & management
7. MEN 1 and MEN 2
4. 1. EMBRYOLOGY OF THYROID
Follicular cells: Thyroglossal duct as
median bud in the pharynx
Foramen cecum: at the base of tongue is its
remnant
Parafollicular (C) cells: from
ultimobronchial body (neural crest)
Inferior parathyroid: from 3rd pharyngeal
pouch
Superior parathyroid: from 4th pharyngeal
pouch
Thymus: from 3rd pharyngeal pouch
6. 2. SURGICAL ANATOMY OF THYROID
Normal weight = 20-25 g
Lobule: is the functional unit supplied by
single arteriole
Lobule is made up of 24-40 follicles with
cuboidal epithelium
Follicle contains colloid material in which
thyroglobulin is stored
Blood supply: rich supply by superior &
inferior thyroid arteries + tracheal &
esophageal arteries
7.
8. SURGICAL ANATOMY OF THYROID
Extensive lymphatic drainage by different
groups of lymph nodes i.e.
a. Subcapsular lymph nodes
b. Paratracheal nodes
c. Nodes on superior & inferior thyroid veins
(Level VI)
d. Deep cervical nodes (Level II, III, IV, V)
e. Mediastinal nodes (Level VII)
11. 3. PHYSIOLOGY OF THYROID HORMONES
Tri-iodothyronine (T3) and Thyroxine (T4) are
formed by:
Iodide trapping
Oxidation of iodide to iodine
Binding of iodine to tyrosine =
monoiodotyrosine
MIT + MIT = DIT
MIT + DIT = T3
DIT + DIT = T4
12. SERUM TRANSPORT PROTEINS
1. Albumin
2. Thyroxine-binding globulin (TBG)
3. Thyroxine-binding prealbumin (TBPA)
Small amounts of free (unbound) hormones
are biologically active
Free T4 = 0.03% of total circulating
hormone
Free T3 = 0.3% of total circulating hormone
T3 (& RT3) is quick acting (within few hours)
T4 is slow acting (4-14 days)
13. PARATHYROID HORMONE (PTH)
Secreted by parathyroid glands
Released in response to low serum calcium
or high serum magnesium level
Functions include:
1. Activates osteoclasts to reabsorb bone
2. Increases Ca++ reabsorption from urine
3. Renal activation of vitamin D
4. Increases gut absorption of Ca++
5. Increases renal excretion of phosphate
14. THE PITUITARY THYROID AXIS
Thyrotrophin releasing hormone (TRH) is
secreted by hypothalamus. It stimulates TSH
Thyroid stimulating hormone (TSH) is
secreted by anterior pituitary, depends upon
the circulating level of thyroid hormones
TSH is controlled by negative feedback
mechanism
15.
16. TREATMENT BY THYROID HORMONES
T4 replacement dose = 0.15 mg OD
T4 suppressive dose = 0.2 mg OD
T3 suppressive dose = 20µg TDS
TSH (recombinant human) is used to
maximize radioactive iodine uptake as an
alternative to thyroid hormone withdrawal
17. 4. BENIGN THYROID DISORDERS & THEIR
MANAGEMENT
Benign thyroid disorders include:
1. Hypothyroidism: Infantile (cretinism) and
adult (myxedema and dyshormonogenesis)
2. Goitre (Thyroid enlargement)
3. Hyperthyroidism
18. FETAL/INFANTILE HYPOTHYROIDISM
(CRETINISM)
Inadequate thyroid hormone production
during fetal & neonatal development
a. Endemic cretinism: due to dietary iodine
deficiency
b. Sporadic cretinism: may be due to (i). An
inborn error of thyroid metabolism (ii).
Complete or partial agenesis of the gland
20. MANAGEMENT OF CRETINISM
a. Immediate diagnosis &
treatment with thyroxine is must
to prevent physical & mental
under-development
b. Iodized salt in sporadic cases
c. Biochemical screening of
neonates using TSH & T4
assays on a heel-prick blood
sample
d. Monitoring of anti-thyroid drugs
in women under treatment
e. No radioactive iodine in
pregnancy
22. TREATMENT OF ADULT HYPOTHYROIDISM
Low T3 & T4 levels
High TSH level
High serum level of TPO antibodies:
autoimmune disease
Oral thyroxine 0.10 – 0.20 mg /day is
curative
0.05 mg / day replacement dose
T3 20 µg three times a day for rapid
response
23. MYXOEDEMA
Severe hypothyroidism
S/S:
1. Typical facial appearance
2. Supraclavicular puffiness
3. Malar flush
4. Yellow tinge of the skin
24.
25. MYXOEDEMA COMA
Characterized by:
a) Altered mental state
b) Hypothermia
c) Precipitating medical condition e.g. cardiac
failure or infection
d) High mortality
Treatment:
Bolus of 0.50 mg of T4 or 10 µg of T3 i/v or
orally every 4-6 hours
Slow warming of the patient
Antibiotics
Hydrocortisone
26. PRIMARY OR ATROPHIC MYXOEDEMA
An autoimmune disease like Hoshimoto’s
thyroiditis, but without goitre formation
27. DYSHORMONOGENESIS
Genetic deficiencies in the enzymes
controlling the synthesis of the thyroid
hormones e.g. TPO
Usually autosomal recessive pattern
Pendred syndrome:
a) TPO deficiency leads to goitre
b) associated with severe sensorineural
hearing impairment and
c) abnormality of bony labyrinth observed on
28. 5. GOITER & SOLITARY THYROID NODULE &
MANAGEMENT
Generalized enlargement of the thyroid gland
Discrete swelling (nodule) in one lobe or
Dominant swelling
29. CLASSIFICATION OF THYROID SWELLINGS
No Simple
(Euthyroid)
Toxic Neoplastic Inflammatory
1 Diffuse
hyperplastic
i. Physiological
ii. Pubertal
iii. Pregnancy
Diffuse
(Graves’
disease)
Benign Autoimmune
a) Chronic lymphocytic
b) Hoshimoto’s disease
2 Multinodular Multinodula
r
Malignant Granulomatous i.e.
De Quervain’s thyroididtis
3 Toxic
adenoma
Fibrosing i.e.
Riedel’s thyroididtis
4 Infective i.e.
i. Acute (Bacterial, viral
ii. Subacute
iii. Chronic (TB,
Syphilis)
5 Other i.e. amyloid
30. SIMPLE GOITRE
Simple goiter may develop by the stimulation
of thyroid gland by TSH. This stimulation may
be by:
i. Microadenoma in the anterior pituitary
ii. Chronically low circulating thyroid hormones
iii. Dietary deficiency of iodine (endemic). Daily
iodine requirement is 0.1–0.15 mg
iv. Defective hormone synthesis
Other factors include growth factors and
immunoglobulins
31. GOITROGENS
Vegetables e.g. cabbage, kale, rape, which
contain thiocyanate
Drugs e.g. para-aminosalicylic acid (PAS),
anti-thyroid drugs
Large quantities of iodides
34. RETROSTERNAL GOITRE
It may remain
symptomless
May lead to
complications e.g.
A. Dyspnea
B. Dysphagia
C. Engorgement of
facial, neck and
superficial chest wall
veins
D. RL nerve paralysis
35. PREVENTION & TREATMENT OF SIMPLE GOITRE
Dietary iodized salt
Thyroxine 0.15-2.0 mg daily for few months
may regress the goiter
Surgery due to:
i. Cosmetic grounds
ii. Pressure symptoms
iii. Patient anxiety
iv. Retrostrenal goitre
36. SURGERY OF GOITRE
The choice of surgical treatment in
multinodular goiter may be:
i. Total thyroidectomy
ii. Subtotal thyroidectomy leaving up to 8 g of
normal tissue
iii. Near-total thyroidectomy leaving up to 2 g
(Dunhill procedure)
iv. Lobectomy with isthmusectomy
37. MANAGEMENT OF CLINICALLY DISCRETE
SWELLING
Clinically discrete swelling may be:
i. Isolated or solitary (70%)
ii. Dominant (30%)
15% of isolated swellings prove to be
malignant
30-40% are follicular adenomas
Remaining are cysts, thyroididtis or colloid
degeneration
38. INVESTIGATIONS
TSH & free T3, T4
Autoantibodies
Isotope scan (if there is toxicity & nodularity). It
may show hot (overactive), warm (active) or
cold (inactive) areas
USS: shows subclinical nodularity & cysts
May show signs of neoplasia e.g.
i. Microcalcification
ii. Increased vascularity
iii. Macroscopic capsular breach
iv. Nodal involvement
39. FNAC
Following conditions can be diagnosed by
FNAC:
i. Colloid nodules
ii. Thyroiditis
iii. Papillary carcinoma
iv. Medullary carcinoma
v. Anaplastic carcinoma
vi. Lymphoma
Note: FNAC cannot distinguish between a benign
follicular adenoma & follicular carcinoma (i.e. by
capsular & vascular invasion)
41. Classification of FNAC reports
Non-diagnosticThy 1
Non-diagnostic cysticThy 1c
Non-neoplasticThy 2
FollicularThy 3
Suspicious of malignancyThy 4
MalignantThy 5
42. RADIOLOGY & OTHER
Chest and thoracic inlet x-rays
CTS
MRI
PET, to localize disease which does not take
up radioiodine
Laryngoscopy: vocal cords (medicolegal)
Core biopsy: may cause pain, bleeding,
tracheal damage, RL nerve damage
Serum calcium estimation
45. HYPERTHYROIDISM / THYROTOXICOSIS
SYMPTOMS:
i. Tiredness
ii. Emotional lability
iii. Heat intolerance
iv. Weight loss
v. Excessive appetite
vi. Palpitations
SIGNS:
i. Tachycardia
ii. Hot, moist palms
iii. Exophthalmos
iv. Eyelid lag/retraction
v. Agitation
vi. Goitre with bruit
46. DIFFUSE TOXIC GOITER (GRAVES’ DISEASE)
Primary thyrotoxicosis
The goiter is diffuse &
vascular
Affects younger women
usually
Family history in 50%
cases
Autoimmune disease
Abnormal thyroid
stimulating antibodies
(TSH-RAb) that bind to
TSH receptor sites &
produce a disproportionate
47. TOXIC NODULAR GOITER & TOXIC ADENOMA
Secondary thyrotoxicosis
The goiter is nodular
A simple nodular goiter is present for a long
time before the hyperthyroidism
The nodules are inactive & the internodular
thyroid tissue is overactive
If a nodule becomes overactive, it is toxic
adenoma (autonomous)
Toxic adenoma hypertrophy and hyperplasia
is not due to TSH-Rab
48. SYMPTOMATOLOGY OF TOXIC GOITRE
Primary thyrotoxicosis:
i. Goitre diffuse &
vascular
ii. Onset is abrupt
iii. Associated signs
include orbital
proptosis,
ophthalmoplegia,
pretibial myxedema
Secondary
thyrotoxicosis:
i. Goitre is nodular
ii. Onset is insidious
iii. Cardiac signs are
frequent e.g. cardiac
failure or atrial
fibrillations
A fast heart rate, which persists
during sleep is characteristic
49. HISTOLOGY OF NORMAL GLAND & TOXIC GOITRE
Normal gland:
acini lined with
flattened cuboidal
epithelium and filled
with homogeneous
colloid
Hyperthyroidism:
hyperplasia of acini,
lined by high
columnar epithelium
51. ANTITHYROID DRUGS
Carbimazole 10 mg TDS to QID
Propylthiouracil
β-adrenergic blockers e.g. propranolol (40
mg TDS), nadolol (160 mg OD)
Iodides
Advantages: No surgery, no radioactive
material
Disadvantages: prolonged treatment, 50%
failure rate, dangerous drug reactions e.g.
agranulocytosis or aplastic anemia
52. THYROID SURGERY
Advantages:
i. Goiter is removed
ii. Cure is rapid and high
Disadvantages:
i. Recurrent of thyrotoxicosis (5%) in subtotal
thyroidectomy
ii. Hypoparathyroidism
iii. Nerve injury
iv. Scar
v. Thyroid failure
53. RADIOIODINE THERAPY
Advantages:
i. No surgery
ii. No prolonged drug therapy
Disadvantages:
i. Availability of isotope facility
ii. Avoid pregnancy (Absolute
contraindication)
iii. Avoid close physical contact especially
children (Relative contraindication)
iv. Eye signs may be aggravated
56. CLASSIFICATION OF THYROID NEOPLASMS
Benign Malignant
Follicular
adenoma
Primary
i. Follicular (20%)
ii.Papillary (60%)
iii.Anaplastic (10%)
iv.Medullary (5%)
v.Lymphoma (5%)
Secondary
i. Metastatic
ii.Local infiltration
57. PAPILLARY CARCINOMA
Most common among the carcinomas of
thyroid
May be multifocal in one lobe or both
Lymphatic spread is common
Blood-borne spread unusual
May infiltrate to esophagus, trachea or
sternothyroid muscle
Orphan Annie-eyed nuclei: characteristic
pale, empty nuclei visible histologically as
papillary projections
Occult carcinoma (microcarcinoma)
59. FOLLICULAR CARCINOMA
Macroscopically encapsulated but
microscopically invades the capsule and the
vascular spaces
Rarely multifocal
Lymph node involvement is less common
Blood-borne metastasis is more common
Mortality rate is twice as compared with the
papillary carcinoma
62. TREATMENT OF DTC
Treatment of differentiated thyroid cancer (DTC)
depends upon:
I. Preoperative diagnosis or
II. After diagnostic lobectomy
1. Total thyroidectomy
2. ±Node dissection
3. Radioiodine to detect and ablate metastases
4. Thyroglobulin monitoring
5. Thyroxine 0.1-0.2 mg daily to suppress
endogenous TSH
63. THYROGLOBULIN AS TUMOR MARKER
Very important in the follow-up and detection of
metastatic disease after surgery of DTC
Endogenous TSH production must be
suppressed by T4
Surgery or therapeutic radioiodine is then
indicated
Presence of antithyroglobulin antibodies
interferes with and invalidates thyroglobulin as
serum marker for recurrence
Careful clinical palpation of neck is important in
such cases
64. UNDIFFERENTIATED (ANAPLASTIC) CARCINOMA
Occurs mainly in elderly women
Local infiltration is early feature
Lymphatic & blood-borne spread is common
Extremely lethal tumor & survival is
calculated in months
Usually needs palliative treatment by surgery
or radiotherapy. Chemotherapy is ineffective
Surgery for complications e.g. tracheal
decompression
65. MEDULLARY CARCINOMA
Tumor of parafollicular (C cells)
10-20 % are familial, (affects children &
young)
Resembling carcinoid tumor
Has characteristic amyloid stroma
Levels of calcitonin & CEA are usually high
66. MEDULLARY CARCINOMA
Diarrhea occurs (30% cases) due to 5-HT
and prostaglandins produced by the tumor
cells
May occur as part of MEN-2A or MEN-2B
Calcitonin is its tumor marker
Tumors are not TSH dependent, don’t take
up radioiodine
67. TREATMENT OF MEDULLARY CARCINOMA
Total thyroidectomy
Prophylactic or therapeutic resection of
cervical lymph nodes
Preoperatively, pheochromocytoma must be
excluded by measuring urinary
catecholamines
68. LYMPHOMA OF THYROID
May be isolated tumor of thyroid or part of
widespread malignant lymphoma disease
May cause tracheal compression, managed
by isthmusectomy
Very good response to radiotherapy in local
disease
Worse prognosis as part of generalized
lymphoma disease
69. 7. MEN-1 AND MEN-2
Multiple endocrine neoplasia are inherited
syndromes
Characterized by a combination of benign &
malignant tumors in different endocrine
glands
Two types i.e. MEN-1 and MEN-2
70. MULTIPLE ENDOCRINE NEOPLASIA TYPE 1
Also called Wermer’s syndrome
Characterized by triad of tumors
1. Tumor of anterior pituitary gland
(prolactinomas)
2. Hyperplasia of parathyroid causing primary
hyperparathyroidism (pHPT)
3. Pancreatico-duodenal endocrine tumors e.g.
gastrinoma, insulinoma, VIPoma,
glucagonoma, somatostatinoma
71. MULTIPLE ENDOCRINE NEOPLASIA TYPE 2
Three subtypes
1. Familial medullary thyroid carcinoma
(FMTC)
2. MEN-2a and
3. MEN-2b
72. MULTIPLE ENDOCRINE NEOPLASIA TYPE 2
MEN-2a (Sipple’s syndrome): characterized by
the combination of:
i. MTC
ii. pHPT
iii. Pheochromocytoma (Bilateral)
MEN-2b: characterized by
i. MTC,
ii. pHPT,
iii. Pheochromocytoma
iv. Neuromas of lips, tongue, eyelids
v. Marfanoid habitus
73. REFERENCE
Bailey & Love’s short practice of surgery, 26th
edition, chapter 51: pages 741-777