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THYROID DISEASES
By
Dr. Abdul Qadeer
MBBS; FCPS; FICS
Assistant Professor in General Surgery
King Faisal University College of Medicine
Kingdom of Saudi Arabia
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
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
DISEASES OF EMBRYOLOGICAL MALDEVELOPMENT
 Ectopic thyroid
 Ectopic parathyroid
 Thyroglossal cyst
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
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)
RELATIONS OF THYROID GLAND
 Recurrent laryngeal nerves
 Superior laryngeal nerves
 Thyroid arteries: superior & inferior
 Thyroid veins: superior, middle & inferior
 IJVs
 Carotid arteries
 Parathyroid glands
 Thymus
 Lymph nodes
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
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)
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
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
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
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
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
CLINICAL FEATURES OF CRETINISM
 Hoarse cry
 Macroglossia
 Umbilical hernia
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
ADULT HYPOTHYROIDISM
 SIGNS:
1. Bradycardia
2. Cold extremities
3. Dry skin & hair
4. Periorbital puffiness
5. Hoarse voice
6. Bradykinesis, slow
movements
7. Delayed relaxation
phase of ankle jerk
 SYMPTOMS:
1. Tiredness
2. Mental lethargy
3. Cold intolerance
4. Weight gain
5. Constipation
6. Menstrual disturbance
7. Carpal tunnel
syndrome
 Myxoedema = Severe
thyroid failure
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
MYXOEDEMA
 Severe hypothyroidism
 S/S:
1. Typical facial appearance
2. Supraclavicular puffiness
3. Malar flush
4. Yellow tinge of the skin
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
PRIMARY OR ATROPHIC MYXOEDEMA
 An autoimmune disease like Hoshimoto’s
thyroiditis, but without goitre formation
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
5. GOITER & SOLITARY THYROID NODULE &
MANAGEMENT
 Generalized enlargement of the thyroid gland
 Discrete swelling (nodule) in one lobe or
 Dominant swelling
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
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
GOITROGENS
 Vegetables e.g. cabbage, kale, rape, which
contain thiocyanate
 Drugs e.g. para-aminosalicylic acid (PAS),
anti-thyroid drugs
 Large quantities of iodides
INVESTIGATIONS
 Thyroid function tests
 X-ray thoracic inlet & chest
 USS
 CT scan
 FNAC
COMPLICATIONS
 Tracheal compression = acute respiratory
obstruction
 Secondary thyrotoxicosis
 Carcinoma
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
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
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
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
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
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)
FNAC
Classification of FNAC reports
Non-diagnosticThy 1
Non-diagnostic cysticThy 1c
Non-neoplasticThy 2
FollicularThy 3
Suspicious of malignancyThy 4
MalignantThy 5
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
CORE BIOPSY NEEDLE
HYPERTHYROIDISM / THYROTOXICOSIS
 Clinical types are:
1) Diffuse toxic goiter (Graves’ disease)
2) Toxic nodular goiter
3) Toxic nodule
4) Hyperthyroidism due to rare causes
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
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
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
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
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
TREATMENT OF THYROTOXICOSIS
A. Antithyroid drugs
B. Surgery
C. Radioiodine
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
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
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
POSTHYROIDECTOMY COMPLICATIONS
 Hemorrhage
i. Tension hematoma
ii. Subcutaneous hematoma
 Respiratory obstruction (Tracheomalacia)
 RL nerve paralysis & voice change
 Thyroid insufficiency
 Parathyroid insufficiency
 Toxic crisis (storm)
 Wound infection
 Hypertrophic or keloid scar
 Stitch granuloma
6. THYROID MALIGNANCY & MANAGEMENT
 Tumors of thyroid may be benign or
malignant
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
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)
HISTOLOGY OF PAPILLARY CARCINOMA
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
FOLLICULAR CARCINOMA (VASCULAR INVASION)
HURTHLE CELL TUMOR
 Variant of follicular carcinoma
 Contain Hurthle/Askanazy cells histologically
 Poor prognosis
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
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
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
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
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
TREATMENT OF MEDULLARY CARCINOMA
 Total thyroidectomy
 Prophylactic or therapeutic resection of
cervical lymph nodes
 Preoperatively, pheochromocytoma must be
excluded by measuring urinary
catecholamines
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
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
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
MULTIPLE ENDOCRINE NEOPLASIA TYPE 2
 Three subtypes
1. Familial medullary thyroid carcinoma
(FMTC)
2. MEN-2a and
3. MEN-2b
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
REFERENCE
 Bailey & Love’s short practice of surgery, 26th
edition, chapter 51: pages 741-777
The end

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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
  • 5. DISEASES OF EMBRYOLOGICAL MALDEVELOPMENT  Ectopic thyroid  Ectopic parathyroid  Thyroglossal cyst
  • 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)
  • 9. RELATIONS OF THYROID GLAND  Recurrent laryngeal nerves  Superior laryngeal nerves  Thyroid arteries: superior & inferior  Thyroid veins: superior, middle & inferior  IJVs  Carotid arteries  Parathyroid glands  Thymus  Lymph nodes
  • 10.
  • 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
  • 19. CLINICAL FEATURES OF CRETINISM  Hoarse cry  Macroglossia  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
  • 21. ADULT HYPOTHYROIDISM  SIGNS: 1. Bradycardia 2. Cold extremities 3. Dry skin & hair 4. Periorbital puffiness 5. Hoarse voice 6. Bradykinesis, slow movements 7. Delayed relaxation phase of ankle jerk  SYMPTOMS: 1. Tiredness 2. Mental lethargy 3. Cold intolerance 4. Weight gain 5. Constipation 6. Menstrual disturbance 7. Carpal tunnel syndrome  Myxoedema = Severe thyroid failure
  • 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
  • 32. INVESTIGATIONS  Thyroid function tests  X-ray thoracic inlet & chest  USS  CT scan  FNAC
  • 33. COMPLICATIONS  Tracheal compression = acute respiratory obstruction  Secondary thyrotoxicosis  Carcinoma
  • 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)
  • 40. FNAC
  • 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
  • 44. HYPERTHYROIDISM / THYROTOXICOSIS  Clinical types are: 1) Diffuse toxic goiter (Graves’ disease) 2) Toxic nodular goiter 3) Toxic nodule 4) Hyperthyroidism due to rare causes
  • 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
  • 50. TREATMENT OF THYROTOXICOSIS A. Antithyroid drugs B. Surgery C. Radioiodine
  • 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
  • 54. POSTHYROIDECTOMY COMPLICATIONS  Hemorrhage i. Tension hematoma ii. Subcutaneous hematoma  Respiratory obstruction (Tracheomalacia)  RL nerve paralysis & voice change  Thyroid insufficiency  Parathyroid insufficiency  Toxic crisis (storm)  Wound infection  Hypertrophic or keloid scar  Stitch granuloma
  • 55. 6. THYROID MALIGNANCY & MANAGEMENT  Tumors of thyroid may be benign or malignant
  • 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
  • 61. HURTHLE CELL TUMOR  Variant of follicular carcinoma  Contain Hurthle/Askanazy cells histologically  Poor prognosis
  • 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