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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
ī Follicular cells: Thyroglossal duct as
median bud in the pharynx
ī Foramen cecum: at the base of tongue is its
remnant
ī Parafollicular (C) cells: from
ultimobronchial body (neural crest)
ī Inferior parathyroid: from 3rd pharyngeal
pouch
ī Superior parathyroid: from 4th pharyngeal
pouch
ī Thymus: from 3rd pharyngeal pouch
6. 2. SURGICAL ANATOMY OF THYROID
ī Normal weight = 20-25 g
ī Lobule: is the functional unit supplied by
single arteriole
ī Lobule is made up of 24-40 follicles with
cuboidal epithelium
ī Follicle contains colloid material in which
thyroglobulin is stored
ī Blood supply: rich supply by superior &
inferior thyroid arteries + tracheal &
esophageal arteries
7.
8. SURGICAL ANATOMY OF THYROID
ī 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
ī Tri-iodothyronine (T3) and Thyroxine (T4) are
formed by:
ī Iodide trapping
ī Oxidation of iodide to iodine
ī Binding of iodine to tyrosine =
monoiodotyrosine
ī MIT + MIT = DIT
ī MIT + DIT = T3
ī DIT + DIT = T4
12. SERUM TRANSPORT PROTEINS
1. Albumin
2. Thyroxine-binding globulin (TBG)
3. Thyroxine-binding prealbumin (TBPA)
ī Small amounts of free (unbound) hormones
are biologically active
ī Free T4 = 0.03% of total circulating
hormone
ī Free T3 = 0.3% of total circulating hormone
ī T3 (& RT3) is quick acting (within few hours)
ī T4 is slow acting (4-14 days)
13. PARATHYROID HORMONE (PTH)
ī Secreted by parathyroid glands
ī Released in response to low serum calcium
or high serum magnesium level
ī 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
ī Thyrotrophin releasing hormone (TRH) is
secreted by hypothalamus. It stimulates TSH
ī Thyroid stimulating hormone (TSH) is
secreted by anterior pituitary, depends upon
the circulating level of thyroid hormones
ī TSH is controlled by negative feedback
mechanism
15.
16. TREATMENT BY THYROID HORMONES
ī T4 replacement dose = 0.15 mg OD
ī T4 suppressive dose = 0.2 mg OD
ī T3 suppressive dose = 20Âĩg TDS
ī TSH (recombinant human) is used to
maximize radioactive iodine uptake as an
alternative to thyroid hormone withdrawal
17. 4. BENIGN THYROID DISORDERS & THEIR
MANAGEMENT
ī Benign thyroid disorders include:
1. Hypothyroidism: Infantile (cretinism) and
adult (myxedema and dyshormonogenesis)
2. Goitre (Thyroid enlargement)
3. Hyperthyroidism
18. FETAL/INFANTILE HYPOTHYROIDISM
(CRETINISM)
ī 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
19. CLINICAL FEATURES OF CRETINISM
ī Hoarse cry
ī Macroglossia
ī Umbilical hernia
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
ī Low T3 & T4 levels
ī High TSH level
ī High serum level of TPO antibodies:
autoimmune disease
ī Oral thyroxine 0.10 â 0.20 mg /day is
curative
ī 0.05 mg / day replacement dose
ī T3 20 Âĩg three times a day for rapid
response
25. MYXOEDEMA COMA
ī Characterized by:
a) Altered mental state
b) Hypothermia
c) Precipitating medical condition e.g. cardiac
failure or infection
d) High mortality
ī Treatment:
ī Bolus of 0.50 mg of T4 or 10 Âĩg of T3 i/v or
orally every 4-6 hours
ī Slow warming of the patient
ī Antibiotics
ī Hydrocortisone
26. PRIMARY OR ATROPHIC MYXOEDEMA
ī An autoimmune disease like Hoshimotoâs
thyroiditis, but without goitre formation
27. DYSHORMONOGENESIS
ī Genetic deficiencies in the enzymes
controlling the synthesis of the thyroid
hormones e.g. TPO
ī Usually autosomal recessive pattern
ī 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
ī Generalized enlargement of the thyroid gland
ī Discrete swelling (nodule) in one lobe or
ī Dominant swelling
29. CLASSIFICATION OF THYROID SWELLINGS
No Simple
(Euthyroid)
Toxic Neoplastic Inflammatory
1 Diffuse
hyperplastic
i. Physiological
ii. Pubertal
iii. Pregnancy
Diffuse
(Gravesâ
disease)
Benign Autoimmune
a) Chronic lymphocytic
b) Hoshimotoâs disease
2 Multinodular Multinodula
r
Malignant Granulomatous i.e.
De Quervainâs thyroididtis
3 Toxic
adenoma
Fibrosing i.e.
Riedelâs thyroididtis
4 Infective i.e.
i. Acute (Bacterial, viral
ii. Subacute
iii. Chronic (TB,
Syphilis)
5 Other i.e. amyloid
30. SIMPLE GOITRE
ī 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 0.1â0.15 mg
iv. Defective hormone synthesis
ī Other factors include growth factors and
immunoglobulins
31. GOITROGENS
ī Vegetables e.g. cabbage, kale, rape, which
contain thiocyanate
ī Drugs e.g. para-aminosalicylic acid (PAS),
anti-thyroid drugs
ī Large quantities of iodides
34. RETROSTERNAL GOITRE
ī It may remain
symptomless
ī 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
ī Dietary iodized salt
ī Thyroxine 0.15-2.0 mg daily for few months
may regress the goiter
ī Surgery due to:
i. Cosmetic grounds
ii. Pressure symptoms
iii. Patient anxiety
iv. Retrostrenal goitre
36. SURGERY OF GOITRE
ī 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
ī Clinically discrete swelling may be:
i. Isolated or solitary (70%)
ii. Dominant (30%)
ī 15% of isolated swellings prove to be
malignant
ī 30-40% are follicular adenomas
ī Remaining are cysts, thyroididtis or colloid
degeneration
38. INVESTIGATIONS
ī TSH & free T3, T4
ī Autoantibodies
ī Isotope scan (if there is toxicity & nodularity). It
may show hot (overactive), warm (active) or
cold (inactive) areas
ī USS: shows subclinical nodularity & cysts
ī May show signs of neoplasia e.g.
i. Microcalcification
ii. Increased vascularity
iii. Macroscopic capsular breach
iv. Nodal involvement
39. FNAC
ī 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
ī Chest and thoracic inlet x-rays
ī CTS
ī MRI
ī PET, to localize disease which does not take
up radioiodine
ī Laryngoscopy: vocal cords (medicolegal)
ī Core biopsy: may cause pain, bleeding,
tracheal damage, RL nerve damage
ī Serum calcium estimation
45. HYPERTHYROIDISM / THYROTOXICOSIS
ī SYMPTOMS:
i. Tiredness
ii. Emotional lability
iii. Heat intolerance
iv. Weight loss
v. Excessive appetite
vi. Palpitations
ī SIGNS:
i. Tachycardia
ii. Hot, moist palms
iii. Exophthalmos
iv. Eyelid lag/retraction
v. Agitation
vi. Goitre with bruit
46. DIFFUSE TOXIC GOITER (GRAVESâ DISEASE)
ī Primary thyrotoxicosis
ī The goiter is diffuse &
vascular
ī Affects younger women
usually
ī Family history in 50%
cases
ī Autoimmune disease
ī Abnormal thyroid
stimulating antibodies
(TSH-RAb) that bind to
TSH receptor sites &
produce a disproportionate
47. TOXIC NODULAR GOITER & TOXIC ADENOMA
ī Secondary thyrotoxicosis
ī The goiter is nodular
ī A simple nodular goiter is present for a long
time before the hyperthyroidism
ī The nodules are inactive & the internodular
thyroid tissue is overactive
ī If a nodule becomes overactive, it is toxic
adenoma (autonomous)
ī Toxic adenoma hypertrophy and hyperplasia
is not due to TSH-Rab
48. SYMPTOMATOLOGY OF TOXIC GOITRE
ī Primary thyrotoxicosis:
i. Goitre diffuse &
vascular
ii. Onset is abrupt
iii. Associated signs
include orbital
proptosis,
ophthalmoplegia,
pretibial myxedema
ī 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
ī Normal gland:
acini lined with
flattened cuboidal
epithelium and filled
with homogeneous
colloid
ī Hyperthyroidism:
hyperplasia of acini,
lined by high
columnar epithelium
51. ANTITHYROID DRUGS
ī Carbimazole 10 mg TDS to QID
ī Propylthiouracil
ī β-adrenergic blockers e.g. propranolol (40
mg TDS), nadolol (160 mg OD)
ī Iodides
ī Advantages: No surgery, no radioactive
material
ī Disadvantages: prolonged treatment, 50%
failure rate, dangerous drug reactions e.g.
agranulocytosis or aplastic anemia
52. THYROID SURGERY
ī Advantages:
i. Goiter is removed
ii. Cure is rapid and high
ī Disadvantages:
i. Recurrent of thyrotoxicosis (5%) in subtotal
thyroidectomy
ii. Hypoparathyroidism
iii. Nerve injury
iv. Scar
v. Thyroid failure
53. RADIOIODINE THERAPY
ī Advantages:
i. No surgery
ii. No prolonged drug therapy
ī 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
ī Most common among the carcinomas of
thyroid
ī May be multifocal in one lobe or both
ī Lymphatic spread is common
ī Blood-borne spread unusual
ī May infiltrate to esophagus, trachea or
sternothyroid muscle
ī Orphan Annie-eyed nuclei: characteristic
pale, empty nuclei visible histologically as
papillary projections
ī Occult carcinoma (microcarcinoma)
59. FOLLICULAR CARCINOMA
ī Macroscopically encapsulated but
microscopically invades the capsule and the
vascular spaces
ī Rarely multifocal
ī Lymph node involvement is less common
ī Blood-borne metastasis is more common
ī Mortality rate is twice as compared with the
papillary carcinoma
62. TREATMENT OF DTC
ī Treatment of differentiated thyroid cancer (DTC)
depends upon:
I. Preoperative diagnosis or
II. After diagnostic lobectomy
1. Total thyroidectomy
2. ÂąNode 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
ī Very important in the follow-up and detection of
metastatic disease after surgery of DTC
ī Endogenous TSH production must be
suppressed by T4
ī Surgery or therapeutic radioiodine is then
indicated
ī Presence of antithyroglobulin antibodies
interferes with and invalidates thyroglobulin as
serum marker for recurrence
ī Careful clinical palpation of neck is important in
such cases
64. UNDIFFERENTIATED (ANAPLASTIC) CARCINOMA
ī Occurs mainly in elderly women
ī Local infiltration is early feature
ī Lymphatic & blood-borne spread is common
ī Extremely lethal tumor & survival is
calculated in months
ī Usually needs palliative treatment by surgery
or radiotherapy. Chemotherapy is ineffective
ī Surgery for complications e.g. tracheal
decompression
65. MEDULLARY CARCINOMA
ī Tumor of parafollicular (C cells)
ī 10-20 % are familial, (affects children &
young)
ī Resembling carcinoid tumor
ī Has characteristic amyloid stroma
ī Levels of calcitonin & CEA are usually high
66. MEDULLARY CARCINOMA
ī Diarrhea occurs (30% cases) due to 5-HT
and prostaglandins produced by the tumor
cells
ī May occur as part of MEN-2A or MEN-2B
ī Calcitonin is its tumor marker
ī Tumors are not TSH dependent, donât take
up radioiodine
67. TREATMENT OF MEDULLARY CARCINOMA
ī Total thyroidectomy
ī Prophylactic or therapeutic resection of
cervical lymph nodes
ī Preoperatively, pheochromocytoma must be
excluded by measuring urinary
catecholamines
68. LYMPHOMA OF THYROID
ī May be isolated tumor of thyroid or part of
widespread malignant lymphoma disease
ī May cause tracheal compression, managed
by isthmusectomy
ī Very good response to radiotherapy in local
disease
ī Worse prognosis as part of generalized
lymphoma disease
69. 7. MEN-1 AND MEN-2
ī Multiple endocrine neoplasia are inherited
syndromes
ī Characterized by a combination of benign &
malignant tumors in different endocrine
glands
ī Two types i.e. MEN-1 and MEN-2
70. MULTIPLE ENDOCRINE NEOPLASIA TYPE 1
ī Also called Wermerâs syndrome
ī 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
ī Three subtypes
1. Familial medullary thyroid carcinoma
(FMTC)
2. MEN-2a and
3. MEN-2b
72. MULTIPLE ENDOCRINE NEOPLASIA TYPE 2
ī MEN-2a (Sippleâs syndrome): characterized by
the combination of:
i. MTC
ii. pHPT
iii. Pheochromocytoma (Bilateral)
ī MEN-2b: characterized by
i. MTC,
ii. pHPT,
iii. Pheochromocytoma
iv. Neuromas of lips, tongue, eyelids
v. Marfanoid habitus
73. REFERENCE
ī Bailey & Loveâs short practice of surgery, 26th
edition, chapter 51: pages 741-777