THYROID LECTURE DR OCAMPO (1) (Autosaved)

THYROID &
PARATHYROID
OBJECTIVES
At the end of the lecture, the students should be able

to:
 Explain the anatomy, physiology and pathology of thyroid and
parathyroid
 Discuss how to evaluate patients with thyroid and parathyroid

disease
 Explain the management of common thyroid and parathyroid

diseases
THYROID
THYROID GLAND
THYROID
 Shield-shaped gland in the
anterior neck
 Greek word “thyreoides”
 19th century
 Thyroid physiology
byBillroth and Kocher
THYROID GLAND
EMBRYOLOGY
 Outpouching of the
primitive foregut (3rd week
of gestation)
 Origin: base of the tongue

at the foramen caecum
 Endoderm cells in the floor

of the pharyngeal anlage
 thicken to form the medial
thyroid anlage
THYROID GLAND
 EMBRYOLOGY
 During its descent, the anlage
remains connected to the
foramen caecum
(thyroglossal duct )
 THYROGLOSSAL DUCT
 Usually reabsorbed after 6
weeks of age
 Remnant becomes the
Pyramidal lobe in adult
 Epithelial cells of anlage gives

rise to the thyroid follicular
cells
THYROID GLAND
EMBRYOLOGY
 4th branchial pouch –
origin of the two lateral
anlage
 fuse with the median anlage
(5th week of gestation)
 Lateral anlage
 Neuroectodermal in origin
 Provides calcitonin
producing parafollicular or C
cells
 Lie in the superoposterior
region of the gland
THYROID GLAND
EMBRYOLOGY
 8th week AOG
 Formation of thyroid follicles
 11th week AOG

 Start of colloid formation
THYROID GLAND
DEVELOPMENTAL ABNORMALITIES
 Thyroglossal Duct Cyst
 Thyroglossal duct should obliterate by 8th week of gestation
 Most common cervical congenital anomaly
 80% are found in juxtaposition of the hyoid bone, midline mass
 Usually asymptomatic
 Problem: infection
 Thyroglossal Duct Sinus

 Results from infection of the cyst or inflammation from surgical
drainage of the cyst
THYROID GLAND
 Diagnosis:
 Midline structure in the neck that moves with protrusion of the
tongue and deglutition too
 Sistrunk operation
 Treatment of choice
 Includes removal of the cyst and excision of the central hyoid

bone
THYROID GLAND
 Lingual Thyroid
 Failure of the median anlage to descend normally
 Symptoms: choking, dysphagia, airway obstruction and

hemorrhage
 Treatment: Thyroid suppression or RAI ablation
 Surgery: rarely needed, make sure that the lingual thyroid is NOT
the only thyroid tissue present
THYROID GLAND
DEVELOPMENTAL
ABNORMALITIES
 Ectopic Thyroid
 Esophagus, trachea,
anterior mediastinum
 Pyramidal Lobe
 50% of individuals
 Distal end of the atrophied
thyroglossal duct persists
 Projecting up from the
isthmus
THYROID GLAND ANATOMY
LOCATION:
 Bilobed structure lies next
to the thyroid cartilage
 Posterior to the strap

muscles
 Anterior and lateral to the

junction of the larynx and
trachea
LOCATION:
 Lobes are adjacent to the
thyroid cartilage
 Connected to the midline

by the isthmus
Normal weight: 20 gms

LOCATION:
 Enveloped by a loose
connecting fascia formed
from the deep cervical
fascia
 Berry’s ligament or
posterior suspensory
ligament
 Thickening of the thyroid
capsule near the cricoid
cartilage and the trachea
BLOOD SUPPLY
 Superior thyroid artery
 Inferior thyroid artery
 Thyroid ima artery (1-4%)
 Superior thyroid vein

 Middle thyroid vein
 Inferior thyroid vein
RECURRENT
LARYNGEAL NERVE
 Lateral to the ligament of
Berry as they enter the
larynx (25% contained in
the ligament)
 Innervates all intrinssic

muscles except
cricothyroid
RECURRENT
LARYNGEAL NERVE
 LEFT - loops around
ligamentum arteriosum or
arch of the aorta
 RIGHT – right subclavian

artery
 ~1cm lateral to or within
the tracheoesophageal
groove
 0.5-1% nonrecurrent R
laryngeal nerve
RECURRENT
LARYNGEAL NERVE
 Passes anterior or
posterior to the artery
 INJURY can lead to

paralysis of the ipsilateral
vocal cord
 Hoarseness
 Airway obstruction if
bilateral
SUPERIOR LARYNGEAL
NERVE
 Arises from the vagus nerve
 External branch descends

along inferior pharyngeal
constrictor muscle along the
superior thyroid vessels
SUPERIOR LARYNGEAL
NERVE
 Injury leads to:
 inability to tense the vocal
cord (cricothyroid muscles)
 Difficulty hitting high notes,

voice fatigue during
prolonged speech
LYMPHATIC DRAINAGE
 Pretracheal, paratracheal ,
perithyroidal, RLN, superior
mediastinal, retropharyngeal,
esophageal, upper middle
and lower jugular chain
nodes
 Central compartment
 Nodes between the two
carotid sheath
THYROID PHYSIOLOGY
THYROID AS ENDOCRINE GLAND

 Weighs 10-20gms
 Responsible for the production of

 Thyroxine (T4)
 Triiodothyronine (T3)
 Calcitonin (Calcium regulating)
 Thyroid follicle
 Single layer of cuboidal follicular cells
 Central depository of colloid filled with thyroglobulin (Tg)
THYROID PHYSIOLOGY
IODINE METABOLISM
 Iodide is actively transported to the thyroid follicular cells
 Thyroid is the storage unit of 90% of body’s iodine content

THYROID PHYSIOLOGY
THYROID HORMONE
SYNTHESIS
1. Iodide trapping
2. Oxidation of iodide to
iodine, iodination of
tyrosine residues forming
MIT and DIT (mono and
diiodotyrosines)
THYROID PHYSIOLOGY
THYROID HORMONE
SYNTHESIS
3. Coupling of 2 DIT to form
thyroxine (T4), 1 MIT and 1
DIT to form T3 (T3 and T4
are bound by Thyroglobulin
TG)
4. Release of free T3 and T4

upon TSH stimulation
5. Deiodination of MIT and

DIT
THYROID PHYSIOLOGY
THYROID HORMONE SYNTHESIS

 T3 vs T4
 T3 is more potent
 T3 has lower circulating plasma level
 T3 is less tightly bound to protein (more readily available)
 Only 20% of T3 is produced by the thyroid, the other 80% is

produced via peripheral iodination (100% for T4)
 Preferential synthesis of T3 rather than T4 during low iodine

intake
THYROID PHYSIOLOGY
THYROID HORMONE
SYNTHESIS
 Hypothalamic-pituitary-
THYROID axis (HPT)
 TRH TSH T3/T4
 Negative feedback
mechanism
THYROID PHYSIOLOGY
THYROID HORMONE FUNCTION

 Fetal brain development and skeletal maturation
 Increases oxygen consumption, basal metabolic rate and heat
production
 Positive inotropic and chronotropic effects on the heart
 Responsible for maintaining the normal hypoxic and
hypercapnic drive in the respiratory center
 Increase GI motility
 Increase bone and protein turnover, muscle contraction and
relaxation
 Increase glycogenolysis, hepatic gluconeogenesis, intestinal
glucose absorption, cholesterol synthesis and degradation
EVALUATION OF PATIENTS WITH
THYROID DISEASES
TSH (N: 0.5-5µU/mL) Calcitonin
Total T4 (55-150  Marker for MTC
nmol/L) Radionuclide Imaging
Total T3 (1.5-3.5 nmol/L)  Hot and cold nodule
Free T4 (12-28 pmol/L) Ultrasound
Free T3 (3-9 pmol/L) CT/MRI
Thyroid antibodies
Tg
 Normally not released into
the system
 Monitoring of thyroid CA
BENIGN THYROID DISORDERS
HYPERTHYROIDISM
 Excessive circulating
thyroid hormone
 Grave’s Disease, solitary

toxic nodular goiter, toxic
multinodular goiter are
most relevant to surgeons
DIFFUSE TOXIC GOITER
GRAVES’ DISEASE/DIFFUSE TOXIC GOITER

 Robert Graves 1825
 Most common cause of hyperthyroidism (60-80%)
 F: M ratio is 5:1
 Peak incidence: 40 and 60 years of age

DIFFUSE TOXIC GOITER GRAVES
ETIOLOGY:
 Autoimmune, but with unknown exact etiology of the
initiation of autoimmune process
 TRIGGERS: bacterial and viral infections, postpartum state,

iodine excess, lithium therapy
 GENETIC FACTORS: associated with certain Human

leukocyte antigen (HLA-B8, HLA-DR3, HLA DQA1) and
cytotoxic T lymphocyte antigen (CTLA-4)
GRAVES
PATHOGENESIS:
 Initiation of autoimmune process causes T-helper lymphocytes
to stimulate B lymphocytes
 Produces antibodies directed at thyroid hormone receptor
 Thyroid – stimulating antibodies stimulate thyrocytes to grow

and synthesize excess thyroid hormone
GRAVES
SIGNS AND SYMPTOMS:

 Generally related to hyperthyroidism
 Palpitations, heat intolerance, weight loss, nervousness, increased

sweating and thirst, tremors, amenorrhea
 Tachycardia, fine finger tremors, hyperactive tendon reflexes
Faciculations of tounge
SIGNS AND SYMPTOMS:

 Specific to Graves’ disease
 Ophthalmopathy (50% of patients)
 Von Graefe’s sign: lid lag pen test
 Dalrymple’s sign: spasm of up per eyelid

revealing sclera
 Prominent stare
 Periorbital edema, conjunctival swelling, proptosis, limitation of
upward and lateral gaze, keratits and blindness
 Dermopathy (1-2%)
 Thickened skin in pretibial and dorsum of the foot aka
PERTIBIAL MYXEDEMA and
DIAGNOSTIC TESTS:
 Suppressed TSH, elevated free T3 and T4
 Thyroid UTZ: Diffuse enlargement of the thyroid
 Increased RAI uptake

TREAMENT
 Antithyroid drugs (PTU 100-300mg tid, methimazole 10-
30mg tid)
 May relapse after drug discontinuation (1-2 years)
 Propanolol 20-40mg QID
 Thyroid ablation with 131I (8-12 mCi)
 Surgery: Thyroidectomy
THYROIDECTOMY
 Recommended only if RAI is contraindicated:
 Confirmed cancer or suspicious thyroid nodule
 Young patients
 Desire to conceive soon (<6 months after treatment)
 Severe reactions to antithyroid medications
 Large goiters (>80 gms) causing compressive symptoms
 Reluctant to undergo RAI
 Total or near total thyroidectomy (ATA Guidelines and

AACE recommendation)
TOXIC MULTINODULAR GOITER
Usually occur in older indivisuals, often with prior

history of nontoxic multinodular goiter
Hyperthyroid signs and symptoms, without

extrathyroidal features of Graves’ disease
Surgical Management:
 Total or Near Total Thyroidectomy
TOXIC ADENOMA
Hyperthyroidism from a single hyperfunctioning

nodule
Occurs in younger patients
Characterized by somatic mutations in the TSH-R
gene
“hot” nodule on RAI scan, rarely malignant
TREATMENT:
 Small nodules – antithyroid and RAI
 Larger nodules – lobectomy with isthmusectomy (subtotal
thyroidectomy)
THYROID STORM
Condition of hyperthyroidism accompanied by fever,

CNS agitation or depression, cardiovascular and GI
dysfunction including hepatic failure
TRIGGERS:
 Abrupt cessation of antithyroid
 Infections
 Trauma
 Surgery
THYROID STORM
TREATMENT:
 β blockers
 PTU
 Corticosteroids
HYPOTHYROIDISM
 Deficiency in circulating thyroid hormone
 CRETINISM: found in neonates
HYPOTHYROIDISM
 CLINICAL FEATURES
(Neonates):
 Cretin Fascie similar to

Down’s syndrome and
dwarfism
 Failure to thrive and

severe mental retardation
HYPOTHYROIDISM
 CLINICAL FEATURES
(Childhood and adults):
 Tiredness, weight gain, cold
intolerance, constipation and
menorrhagia
 MYXEDEMA
 severe hypothyroidism
 facial and periorbital

puffiness, loss of outer 2/3
of the eyebrows, hairloss,
enlarged tongue,
bradycardia.
HYPOTHYROIDISM
 Low circulating levels of T3 and T4 and elevated TSH
 TREATMENT:
 T4 (Thyroxine)
 20-200µg/day
 Titrate to achieve euthyroid

THYROIDITIS
Acute, sub-acute, chronic thyroiditis
ACUTE SUPPURATIVE THYROIDITIS

 Hematogenous route
 Direct spread (from thyroglossal duct cysts or pyriform fistula)
 Trauma
 Immunosuppression
 In children: URTI or otitis media
 70% caused by Streptococcus and anaerobes

THYROIDITIS
ACUTE SUPPURATIVE THYROIDITIS

 Severe neck pain radiating to the jaw or ear
 Fever
 Chills
 Odynophagia
 Dysphonia
 Complications: sepsis, tracheal or esophagel rupture, jugular
vein thrombosis, laryngeal chondritis, sympathetic trunk
paralysis
 Treatment:
 Antibiotics and drainage of abscesses
THYROIDITIS
SUBACUTE THYROIDITIS
 Painful thyroiditis is viral or post viral in origin
 Painless thyroiditis is usually post-partum
 4 Stages:
 Initial hyperthyroid state
 Euthyroid state
 Hypothyroidism
 Return to euthyroid state
 Treatment
 Pain medications, thyroid hormone replacement, β blockers
THYROIDITIS
CHRONIC THYROIDITIS
 Hashimoto’s thyroiditis
 Riedel’s thyroiditis
HASHIMOTO’S THYROIDITIS
1912 by Hashimoto:
Lymphocytic thyroiditis
Struma lymphomatosa
 Transformation of thyroid tissue to
lymphoid tissue
 Leading cause of hypothyroidism

Autoimmune process
 Initiated by activation of CD4+ T
helper lymphocytes specific for
thyroid antigens
 Recruitment of the cytotoxic CD8+T

cells to the thyroid and autoantibodies
(directed against Tg (60%), TSH-R
(60%), TPO (95%)
 Destruction of thyrocytes leading to

hypothyroidism
Associated with:
 Increased iodine intake
 Interferon alpha, lithium and amiodarone intake
 Can also be GENETIC
M:F is 1: 10-20, between ages 30 and 50 yo

Painless anterior neck mass, hypothyroidism
Diagnostics:
 Elevated TSH and presence of thyroid antibodies
 Thyroid lymphoma may arise from chronic
thyroiditis
TREATMENT:
 Thyroid hormone replacement therapy (levothyroxine)
 Surgery:
 Only if with suspected malignancy
 Compressive symptoms
 Cosmetic Deformity
RIEDEL’S THYROIDITIS
Rare variant
Riedel’s struma or invasive fibrous thyroiditis
Painless hard anterior neck mass; produces

symptoms of compression
Surgery is mainstay treatment

NONTOXIC GOITERS
Goiter is any enlargement
of the thyroid gland
Most common cause:

inadequate thyroid
hormone synthesis
 Induce diffuse thyroid
hyperplasia resulting to
nodules that may or may
not concentrate iodine
(colloid nodules)
NONTOXIC GOITERS
CLINICAL FEATURES:
 Usually asymptomatic: complains of anterior neck mass
 Pressure sensation in the neck
 Compressive symptoms: dyspnea and dysphagia
 P.E.: soft, diffusely enlarged gland or nodules of various size
and consistency
DIAGNOSTICS:
 TSH, T3, T4
 UTZ
 FNAB to rule out malignancy (5-10% of Multinodular goiter
has malignancy)
NONTOXIC GOITERS
TREATMENT
 Medical treatment:
 Thyroid hormone replacement
 Iodine administration for endemic goiters
 Surgical Management (Total or Near Total

Thyroidectomy) is reserved for:
 Continued enlargement of nodule
 Compressive symptoms
 Substernal extension
 With proven malignancy (FNAB)
 Cosmetically unacceptable
SOLITARY THYROID NODULES
MALIGNANT THYROID DISEASE
THYROID CANCER
 <1% of all malignancies
 Thyroid tumorigenesis:
 RET proto-oncogene at chromosome 10 and encodes tyrosine
kinase receptor (binds to growth factors)
 p53 tumor suppressor gene
 Risk factors:
 young age - MEDULLARY (LC)
 radiation exposure- PAPILLARY (MC)
 family history- MEDULLARY
MALIGNANT THYROID DISEASE
SPECIFIC TUMOR
TYPES:
Differentiated Thyroid
CA:
Papillary CA (80%)
Follicular CA (10%)
Hurtle Cell CA (3%)
Medullary Thyroid CA (5%)

Anaplastic Thyroid CA (1%)
Lymphoma (<1%)
THYROID CANCER
Signs and symptoms:

 Anterior neck mass
Diagnostics:
 FNAB
 Thyroid UTZ
 TSH, T3,T4 levels
 CT scan of the neck
THYROID CANCER
Primary treatment: SURGICAL
Other Treatment Modalities:

RAI, EBRT, Thyroid
suppression
PAPILLARY THYROID CA
Most common (80%)
M:F ratio is 1:2, age 30-40 y.o.
LN metastases are common in children and young adults
Metastasis (20%) to regional LN, lungs, bone, liver and

brain
Histologic characteristic: psammoma bodies and

orphan Annie nuclei
Multifocal (up to 85%)
Rarely locally invasive to adjacent

structures
Prognosis: >95% 10 year survival rate
Good prognostic factors:

 Age <45
 Small tumors, well differentiated
 No extrathyroidal spread
Minimal/occult/microcarcinoma
 Tumors of 1cm or less in size
 No evidence of local invasiveness
through thyroid capsule or
angioinvasion
 Not associated with LN metastases
 2-36% of thyroids removed from

autopsy
 Associated with better prognosis
 25% have associated occult LN
metastases
Surgical Treatment:
 Total or Near Total Thyroidectomy
 Lobectomy for small tumors <1cm
 Lobectomy for tumors 1-2 cm has 24% risk of recurrence and

49% risk of thyroid cancer mortality
 LN dissection
 Central node dissection (level VI)
 Level II, III, IV dissection if indicated (for T3-T4 tumors)
FOLLICULAR THYROID CA
10% of thyroid cancers

M:F - 1:3
Mean age: 50 y.o.
Usual presentation:
 Solitary thyroid nodule with rapid size increase and long
standing goiter
 5% presents with cervical LN at initial presentation
Diagnosis:
 FNAB is UNABLE to distinguish a
benign follicular lessions vs
carcinoma
 >4cm follicular tumors in older men
are more likely to be malignant
Histology:
 Solitary Lesions surrounded by a
capsule
 Malignancy is defined by presence of
capsular and vascular invasion
Surgical Treatment:
 Lobectomy for small lesions (80% are follicular adenomas)
 Total thyroidectomy for tumors >4cm (50% risk of CA)( T3 T4
)
 Lobectomy with FS
 Debate on Completion Thyroidectomy because of the good

prognosis of the disease (except for frankly invasive disease)
Prognosis:
 15% mortality (10 years), 30% at 20 years
 Poor prognosis: >4 cm, 50 years old, higher tumor grade,
marked vascular and extrathyroidal invasion, metastasis
HURTLE CELL CA
3% of all thyroid malignancies
Subtype of Follicular thyroid CA
Difference:
 usually multifocal and bilateral (~30%)
 5% do not take up RAI
 More likely to metastasize to local nodes (25%) and distant
sites
 Higher mortality (~20% in 10 years)
DIFFERENTIATED THYROID CA
Post-op Management
 RAI therapy Indications (ATA guidelines):
 Known distant metastasis
 Gross extrathyroidal tumor extension
 Tumors >4cm, tumors 1-4 cm but with LN metastases
 High risk patient
 EBRT and chemotherapy

 For unresectable , locally invasive or recurrent disease
 Treatment of metastases (esp in bone)
 Thyroid Hormone Replacement
 Suppress TSH reduce growth stimulus for residual thyroid
 Maintain TSH
 <0.1 mU/mL for patients with persistent disease
 0.3 – 2 mU/mL for patients who are clinically and
biochemically free of disease, low risk
 0.1-0.5 mU/mL for high risk patients
 Follow-up: Thyroglobulin Measurement
 Tg and anti-Tg antibody levels
 6 month interval
 Disease Free: Tg level of <0.5ng/mL
 Recurrent Disease: Tg level of >2ng/mL
 Cervical UTZ
 6 and 12 months post op
 Annually for 3-5 years
 Thyroid scanning (RAI)

 Ablation of residual tumors
MEDULLARY THYROID CA
Arises from the parafollicular or C cells of the

thyroid (calcitonin)
Concentrated superolaterally
5% of thyroid cancers

M:F is 1: 1.5
50 and 60 years old
25% presents as familial/inherited syndromes (e.g.

familial MTC, MEN2B)
Presentation:
 Anterior neck mass associated with cervical LN (15-20%)
 Pain and compressive symptoms (dysphagia, dyspnea,

dysphonia) from local invasion
 F:M 1.5:1, between 50-60 years old, younger age for familial
MTC
 2-4% develop Cushing’s syndrome due to ectopic production of

ACTH
Pathology:
 80% are unilateral for sporadic disease
 90% are bilateral for familial disease
 C-cell hyperplasia is a premalignant lesion
 Presence of amyloid is diagnostic finding
 Positive for CEA and calcitonin gene-ralated peptide
 High incidence of multicentricity
Diagnosis:
 FNAB
 Elevated calcitonin
 Family history is important
 Calcitonin levels
(monitoring)
 CEA (for prognostication)
 Neck UTZ
 RET protooncogene
mutation testing
 Total Thyroidectomy + central node dissection
 RAI not effective
 Lateral Neck dissection (levels IIA, III, IV and V) if with

clinically positive LN or if tumor is ≥ 1.5cm (controversial)
 Tumor debulking for locally recurrent or widely metastatic

(palliation for pain, flushing and diarrhea)
Other forms of Management:

 EBRT for unresectable or recurrent tumors
 Chemotherapy is NOT effective
 Targeted Therapies: multikinase inhibitors

 Sorafenib
 Sunitinib
 Lenvatinib
 Canbozantib
 Ventatinib (USA-FDA approved for advanced and progressive
MTC)
PROPHYLACTIC TOTAL THYROIDECTOMY

 Indicated in RET mutation carriers
 If less aggressive mutations, surgery may be delayed for >5
years
 Children with mutations at codon 634 are advised to undergo
thyroidectomy at age <5 years of age
 Those with MEN2B-related mutations should undergo
procedure before age 1
 Mutation + neck UTZ + increased calcitonin: prophylactic

central node dissection is indicated
Follow-up:
 Annual CEA and calcitonin levels
 Hx and PE
 UTZ/CT/MRI/PET
Prognosis:
 80% 10 year survival for local disease
 45% 10 year survival for those with LN involvement
 35% 10 year survival for MEN2B
ANAPLASTIC THYROID CA
1% of thyroid malignancies

Majority presents at 7th and 8th decade of life
Most aggressive thyroid tumors
Presentation:
 Long standing neck mass that rapidly enlarges, fixed to
surrounding structures
 Painful, dysphagia, dyspnea, dysphonia are common
 Palpable LN
 Evidence of metastasis
Diagnostics:
 FNAB: giant and multinucleated cells
 Pre-op assessment is highly important to assess resectability
(laryngoscopy, ct scan, UTZ)
 Total or near thyroidectomy with LN dissection
 Tracheostomy if with airway compromise
Radiation and Chemotherapy

 Combination of Taxane, anthracycline and platinum
Prognosis:
 Poor
 Few patients surviving 6 months beyond diagnosis
 Disappointing forms of treatment
LYMPHOMAS
< 1% of thyroid malignancies
Most are Non-Hodgkin’s B cell type
Develop in patients with chronic lymphocytic

thyroiditis
Symptoms usually similar to those with anaplastic

CA but painless
LYMPHOMAS
TREATMENT:
 CHEMOTHERAPY
 CHOP: cyclophosphamide, doxorubicin, vincristine and
prednisone
 Combined RT + chemotherapy is recommended
 SURGERY:
 Thyroidectomy + nodal dissection
 To alleviate airway obstruction
THYROID SURGERY
Thyroidectomy
 Kocher’s incision
Minimally Invasive
Approach
 Laparoscopic
 Robotics
Complications:
 Injury (RLN, parathyroid,
external branch of the SLN
and surrounding structures)
 Hypocalcemia
 Bleeding and hematoma
 Infections
THYROID SURGERY
NECK DISSECTION
 Central compartment
(medial to the carotid
sheath)
 Usually involved in
papillary, medullary and
Hurtle cell CA
 MRND
 Clinically palpable nodes
 Prophylactic for MTC
 Levels II, III , IV and V
 Preserve IJ, spinal
accessory, SCM, cervical
sensory nerves
PARATHYROID
PARATHYROID
Embryology
 Superior parathyroids
from 4th branchial pouch
(thyroid)
 Inferior parathyroids from

3rd branchial pouch
(thymus)
PARATHYROID
Location
 Superior parathyroids are
more consistent (80%
near the posterior aspect
of the upper and middle
thyroid lobes, at the level
of cricothyroid)
 Inferior parathyroids
within 1cm from the entry
of the inferior thyroid
artery and RLN
PARATHYROID
Anatomy/Physiology:
 Most have 4 parathyroid
gland, may have ectopic PT
 Yellow to light brown in color
(adults)
 7mm in size and weighs ~40-
50 mg each
 Blood supply derived from
superior and inferior thyroid
arteries
 Secretion of PTH important
for calcium homeostasis
 Targets bone, kidney and the
gut
HYPERPARATHYROIDISM
Hyperfunctioning of the parathyroid glands
PRIMARY HYPERPARATHYROIDISM
 Parathyroid adenomas
 Incidence: 0.1 to 0.3% of the general population
 More common in women (1: 500)
 Characterized by increased parathyroid cell proliferation and
PTH secretion independent of the Ca levels
 Etiology: Unknown
 Risk factors: radiation, diet, familial disposition (MEN1,
MEN2A, familial HPT)
HYPERPARATHYROIDISM
Signs and Symptoms:

 Classic “Pentad”: kidney stones, painful bones, abdominal
groans, psychic moans, fatigue
 Non-specific: Weakness, polydipsia, polyuria, nocturia, bone
and joint pain, constipation, nausea, heartburn, decreased
appetite, depression and memory loss
 On PE: usually nonpalpable parathyroids
Complications:
 Renal disease (kidney stones, nephrocalcinosis leading to
Renal failure
 Bone disease (osteopenia, osteoporosis, osteitis fibrosa cystica)
HYPERPARATHYROIDISM
Complications:
 Gastrointestinal disease (peptic ulcer, cholelithiasis,
pancreatitis)
 Neuropsychiatric disease (psychosis, depression, anxiety,
coma)
Diagnostics:
 Elevated calcium, with normal PTH, elevated 24 hr urinary Ca
concentrations
HYPERPARATHYROIDISM
Management:
 Medical
 For asymptomatic HPT
 Biphosphonates
(pamidronate) , hormone
replacement therapy and
selective estrogen
modulators (raloxifene)
HYPERPARATHYROIDISM
Management:
 Surgical
(Parathyroidectomy)
 Indicated for symptomatic
HPT with complications
 Asymptomatic but with
disease progression
 Results in resolution of
osteotitis fibrosa cystica
and kidney stones
 Decreased risk in fracture
 Pre-op localization tests

PARATHYROIDECTOMY
Sestamibi scan is widely
used for pre-op detection of
parathyroid adenomas
Neck ultrasound +
sestamibi scan can isolate
the tumor in 95% of the
time
MRI and CT scan for

esophageal or mediastinal
locations
PARATHYROIDECTOMY
Unilateral/focused parathyroid
exploration/Minimally invsive parathyroidectomy
Double adenomas (0-10%) incidence

Multiple adenomas is more common in familial
HPT, MEN syndromes and elderly
Thank you!

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THYROID &

At the end of the lecture, the students should be able

 Discuss how to evaluate patients with thyroid and parathyroid

 Explain the management of common thyroid and parathyroid

 Greek word “thyreoides”

 Origin: base of the tongue

 Endoderm cells in the floor

 Epithelial cells of anlage gives

 11th week AOG

 Thyroglossal Duct Sinus

 Includes removal of the cyst and excision of the central hyoid

 Symptoms: choking, dysphagia, airway obstruction and

 Treatment: Thyroid suppression or RAI ablation

 Posterior to the strap

 Anterior and lateral to the

 Connected to the midline

Normal weight: 20 gms

 Superior thyroid vein

 Innervates all intrinssic

 RIGHT – right subclavian

 INJURY can lead to

 External branch descends

 Difficulty hitting high notes,

THYROID AS ENDOCRINE GLAND

 Responsible for the production of

 Iodide is actively transported to the thyroid follicular cells

 Thyroid is the storage unit of 90% of body’s iodine content

4. Release of free T3 and T4

5. Deiodination of MIT and

THYROID HORMONE SYNTHESIS

 T3 has lower circulating plasma level

 T3 is less tightly bound to protein (more readily available)

 Only 20% of T3 is produced by the thyroid, the other 80% is

 Preferential synthesis of T3 rather than T4 during low iodine

 TRH TSH T3/T4

THYROID HORMONE FUNCTION

 Grave’s Disease, solitary

GRAVES’ DISEASE/DIFFUSE TOXIC GOITER

 Most common cause of hyperthyroidism (60-80%)

 Peak incidence: 40 and 60 years of age

 TRIGGERS: bacterial and viral infections, postpartum state,

 GENETIC FACTORS: associated with certain Human

 Produces antibodies directed at thyroid hormone receptor

 Thyroid – stimulating antibodies stimulate thyrocytes to grow

SIGNS AND SYMPTOMS:

 Palpitations, heat intolerance, weight loss, nervousness, increased

 Tachycardia, fine finger tremors, hyperactive tendon reflexes

SIGNS AND SYMPTOMS:

 Dalrymple’s sign: spasm of up per eyelid

 Thyroid UTZ: Diffuse enlargement of the thyroid

 Increased RAI uptake

 Thyroid ablation with 131I (8-12 mCi)

 Total or near total thyroidectomy (ATA Guidelines and

Usually occur in older indivisuals, often with prior

Hyperthyroid signs and symptoms, without

Hyperthyroidism from a single hyperfunctioning

Condition of hyperthyroidism accompanied by fever,

 Cretin Fascie similar to

 Failure to thrive and

 facial and periorbital

 Titrate to achieve euthyroid

Acute, sub-acute, chronic thyroiditis

ACUTE SUPPURATIVE THYROIDITIS