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 C5 to T1 vertebrae.
 ensheathed by the

pretracheal layer of
deep cervical fascia
 lobes connected by

narrow, median
isthmus.
 weight - 25g

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 lobes are conical.
 Apices -At the level of the oblique

lines on the laminae of the thyroid


cartilage
 Bases- fourth or fifth tracheal

cartilages.
 5 cm long
 posteromedial aspects of the lobes

attached to the side of the cricoid


cartilage by lateral thyroid ligament.
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Isthmus
 connects the lower parts of the two

lobes.
 1.25 cm transversely and vertically
 anterior to the second and third

tracheal cartilages.

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Pyramidal lobe
 Conical
 Ascends towards the hyoid bone

from the isthmus or the adjacent


part of either lobe

 accessory thyroid glands


 Small detached masses of thyroid tissue
above the lobes or isthmus

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Tubercle of Zuckerkandl 
 pyramidal extension of the thyroid
gland
 posterior aspect of thyroid lobe
 RLN usually traverses the posterior

aspect of the tubercle.

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SURFACES AND RELATIONS
 Lateral (superficial)
surface
• sternothyroid.
 Anteriorly
• sternohyoid
• superior belly of
omohyoid
 inferiorly
• anterior border of
sternocleidomastoid

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medial surface
 Larynx and trachea
 Inferior pharyngeal constrictor
 Cricothyroid
 External laryngeal nerve.
 Recurrent laryngeal nerve and

oesophagus.

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Posterolateral surface
 close to the carotid
sheath
 Anterior border-
• anterior branch of the
superior thyroid artery.
 Posterior border-
• rounded
• Inferior thyroid artery
and its anastomosis with
the posterior branch of
the superior thyroid
artery.
 Parathyroid glands
 Thoracic duct.
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Isthmus
 covered by sternothyoid
 Superficially
• sternohyoid,
• anterior jugular veins,
• fascia and skin.
 superior thyroid arteries anastomose
along its upper border
 inferior thyroid veins leave the gland

at its lower border


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EMBRYOLOGY 
 third week of gestation.
 derived from the endoderm-
 ventral portion of the fourth pharyngeal
pouch form lateral thyroid lobes .
 The pyramidal lobe- migration of the
thyroglossal duct from the pharynx at the
foramen cecum
 The ultimobranchial bodies consist of neural
crest cells from the fourth and fifth branchial
pouches form parafollicular cells (C cells),
 Thyroid hormone synthesis begins at about
11 weeks' gestation.

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Blood supply
 Vessels lie between the fibrous capsule and the loose
fascial sheath.
 superior thyroid artery- first branches of the external
carotid
 Inferior thyroid artery –from thyrocervical trunks
 Thyroid ima- from the brachiocephalic trunk or aortic
arch
 Superior thyroid vein- emerges from the upper part of
the gland- drains into the internal jugular vein.
 Middle thyroid vein - emerges from the lateral surface
of the gland- drains into the internal jugular vein.
 Inferior thyroid vein - descends into brachiocephalic
vein.

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Lymphatic drainage
 prelaryngeal,pretracheal, and
paratracheal lymph nodes - Superior and
inferior deep cervical nodes-
brachiocephalic lymph nodes- Thoracic
duct.

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Nerve supply
 Superior, middle, and inferior cervical
sympathetic ganglia
 Cardiac and superior and inferior thyroid

periarterial plexuses
 Fibers are vasomotor, causing constriction

of blood vessels.
 Endocrine secretion from the thyroid gland

is hormonally regulated by the pituitary


gland

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Histology
 Thin capsule of
connective tissue,
which extends into the
parenchyma and
divides lobe into
lobules.
 functional units-
follicles
 spherical and cyst-like,
-0.02 and 0.9 mm in
diameter
 central colloid core
surrounded by a
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single-layered 15
 Colloid consists almost entirely of an
iodinated glycoprotein, iodothyroglobulin.
 Follicles are surrounded by a delicate

connective tissue stroma-plexuses of


fenestrated capillaries, lymphatic networks
and sympathetic nerve fibres

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physiology
 Thyroxine
 Triiodothyronine.
 Iodine-containing amino acids
 Reverse triiodothyronine -3,3',5'-

triiodothyronine, RT3
 Calcitonin an important hormone for

calcium metabolism

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Iodine Metabolism
 The minimum daily iodine intake is 150 µg
 Average dietary intake is 500 µg/d.
 The normal plasma I– level is 0.3 µg/dL
 principal organs that take up the I- thyroid

and kidneys
 About 120 µg/d enter the thyroid at normal

rates of thyroid hormone synthesis and


secretion.

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 (1) iodide (I-) trapping by the thyroid
follicular cells
1. against a chemical and electrical gradient
2. Na+/I– symporter (NIS) -secondary active
transport
3. basolateral membrane of the thyroid
follicular cells
 (2) diffusion of iodide to the apex of the

cells
 (3) transport of iodide into the colloid

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 (4)oxidation of inorganic iodide to
iodine and incorporation of iodine
into tyrosine residues within
thyroglobulin molecules in the colloid
catalyzed by iodinase

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 (5) combination of two diiodotyrosine
(DIT) molecules to form
tetraiodothyronine (thyroxine, T4) or
of monoiodotyrosine (MIT) with DIT to
form triiodothyronine (T3)
 Coupling is catalyzed by thyroid

peroxidase.

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 (6) uptake of thyroglobulin from the
colloid into the follicular cell by
endocytosis, fusion of the thyroglobulin
with a lysosome, and proteolysis and
release of T4, T3, DIT, and MIT
 (7) release of T4 and T3 into the
circulation;
 (8) deiodination of DIT and MIT to yield
tyrosine.
 T3 is also formed from monodeiodination
of T4 in the thyroid and in peripheral
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 Extrathyroidal T3 production —
  80 percent of the T3 produced is

formed by 5'-deiodination of T4 in
extrathyroidal tissue.
 Catalyzed by T4-5'-deiodinases
 Liver and kidney contain abundant

deiodinase activity

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METABOLISM
 Thyroxine-T4 
 Rate of production T4 is 80 to 100 µg
per day
 Degraded at a rate of about 10

percent per day.


 80 percent is deiodinated-
• 40 % form T3
• 40 % to form rT3.
 20 percent conjugated with
glucuronide and sulfate
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 Triiodothyronine 
 80 % is produced by extrathyroidal
deiodination of T4
 The total production rate is 30 to 40

µg per day.
 The extrathyroidal T3 pool contains

about 50 µg, most of which is


intracellular.
 T3 is degraded by deiodination

(about 75 percent per day).


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Reverse triiodothyronine
  The rate of production -30 to 40 µg

daily
 nearly all by extrathyroidal

deiodination of T4

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SERUM BINDING
PROTEINS 
 99.95%-T4 and 99.5 % -T3 in serum
are bound to serum proteins

 T4
• 75 %-TBG
• 10 %TTR
• 12 %albumin
• 3 % lipoproteins.
• 0.02 percent, or 2 ng/dL (25 pmol/L] is free.

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T3
 80 %-TBG
 5 % -TTR
 15 %-albumin and lipoproteins.
 0.3 percent, or 0.4 ng/dL (6 pmol/L),

is free.

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Hormone Property T4 T3
Total hormone 5-12 70-195
µg/dL ng/dL
Fraction of total hormone in the free 0.02% 0.3%
form
Free (unbound) hormone 0.9-2.4 6 × 10–12M 
ng/dl
Serum half-life 7-8 d 3d
Fraction directly from the thyroid 100% 10-20%

Production rate, including peripheral 80-100 30-40 µg/d


conversion µg/d
Intracellular hormone fraction 10% 90%

Relative metabolic potency 1 3-4

Receptor binding 10–10M 10–11M


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Mechanism of Action
 Thyroid hormones enter cells, binds to
thyroid receptors (TR) in the nuclei.
 hormone-receptor complex then binds to

DNA via zinc fingers


 Increases or decreases the expression of a

variety of different genes that code for


enzymes that regulate cell function

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REGULATION OF THYROID HORMONE
PRODUCTION

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 Reduced levels of thyroid hormone increase
basal TSH production and enhance TRH-
mediated stimulation of TSH.
 High thyroid hormone levels rapidly and
directly suppress TSH gene expression
secretion and inhibit TRH stimulation of TSH
 Thyroid hormones are the dominant
regulator of TSH production
 TSH is released in a pulsatile manner and
exhibits a diurnal rhythm; its highest levels
occur at night.

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Target Tissue Effect Mechanism

Heart Chronotropic Increase number of


  -adrenergic receptors.
 
Inotropic Enhance responses to
  circulating catecholamines.
Increase proportion of -myosin
heavy chain (with higher
ATPase activity).

Resp Increase Co2 production, TV, RR

Adipose tissue Catabolic Stimulate lipolysis.

Muscle Catabolic Increase protein breakdown.

Bone Developmental Promote normal growth and


skeletal development.
Nervous system Developmental Promote normal brain
development.
Gut Metabolic Increase rate of carbohydrate
absorption
Lipoprotein Metabolic Stimulate formation of LDL
receptors.
Other Calorigenic Stimulate oxygen consumption
by metabolically active tissues
(exceptions: testes, uterus,
lymph nodes, spleen, anterior
pituitary).
Increase metabolic rate
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Diagnosis
 History:
 Age: simple goiter-puberty
:MNG, SNG & colloid goiter-
women of 20-30yrs
 Cancers
 Toxic goiter
 Sex
 Occupation
 Residence-Endemic goiter

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 Swelling
 Pain
 Pressure effect

 Symptoms of thyrotoxicosis
 Primary thyrotoxicosis- No much

enlargement of gland, loss of wt,


preference for cold, excessive sweating,
nervous excitability, irritability, insomnia,
tremor, muscle weakness.
 Exophthalmos
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 Secondary thyrotoxicosis: long
standing thyroid swelling,
Palpitations, ectopic beats,
arrhythmias, CCF

 Hypothyroidism- increase of wt,


intolerance of cold weather, dry skin,
puffiness of face, loss of hair, muscle
fatigue, lethargy, failing memory,
hoarseness of voice 26-Feb-20 1:37 AM
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 Past history
 Personal history
 Family history-Endemic goiter

Enzyme deficiancy
Primary
thyrotoxicosis
Cancers

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• Physical examination: Build & State of nutrition,
Facies, Mental state & intelligence, Skin

• F/o primary toxic manifestations


1. Eye signs- lid retraction (over activity of
smooth muscle part of levator palpebrae
superioris), Exophthalmos, Ophthalmoplegia,
Chemosis
2. Tachycardia
3. Tremor
4. Moist skin
5. Thyroid bruit

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Exophthalmos
 Sclera become visible below the lower edge of the
iris first followed by the upper edge

1. Von graefe’s sign- upper eye lid lags behind


eyeball
2. Joffroy’s sign- absence of wrinkling on the
forehead
3. Stellwag’s sign- staring look & infrequent
blinking of eye with widening of palpebral fissure
due to contraction of involuntary fibres of levator
palpabrae superioris
4. Moebius sign- inability to converge
5. Dalrympte’s sign- visible upper sclera due to
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retraction of upper eye lid 41
Secondary thyrotoxicosis
1. AF
2. Cardiomegaly
3. CCF
4. Exophthalmos & tremor-are absent

Cancer-metastasis-CLN

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Local examination
• Inspection- Pizzillo’s method
• Moving upward with deglution
• Retrosternal goiter- dilatation of veins
on the upper ant chest
 Lower border
 Pemberton sign- raise the arm
straight up- SVC obstruction - facial
congestion & venous engorgement over
head and neck, inspiratory stridor,
elevated IJV pressure-thoracic inlet-IJV
 Maranon’s sign- distention of rt EJV
on abduction of both UL-90°
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 Palpation- size, shape, extent, consistency,
mobility.
 Lower border- to get below the thyroid gland
 Pressure effect
• Trachea- Kochers test- slight push on the
lateral lobes produce stridor
• Oesophagus
• sympathetic trunk
 Percussion- dullness over manubrium
 Auscultation -bruit

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Assessment of tracheal deviation
 History- breathing difficulty, stridor
 O/E-

1. for deviation: palpation, auscultation over


trachea
2. For compression: kocher’s test
 Inv:

1. x-ray neck AP, lateral,


2. CT neck and upper thorax: to delineate site
and degree of compression, to predict size
of ETT, guide placement
3. Flow-volume loop
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Biochemical investigation
 Thyroid
function is assessed by one
or more of the following tests

 Serum TSH concentration


 Serum total T4 concentration
 Serum total T3 concentration
 Serum free T4 (or T3) concentration

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Serum TSH concentration
 First generation TSH radioimmunoassays:
 detection limits -1 mU/L.
 normal range -0.4 to 5.0 mU/L
 for the diagnosis of primary hypothyroidism
 Second generation TSH- immunometric assays
 detection limits is 0.1 mU/L.
 screening tests to distinguish hyperthyroidism
from euthyroidism
 do not distinguish the degree of hyperthyroidism
 Third generation -chemiluminometric assays
 detection limits of about 0.01 mU/L.
 Detect mild hyperthyroidism

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 Single best test for thyroid action at cellular
level
 Subclinical hyperthyroidism: 0.01-0.4mU/L, FT3,
FT4-N
 Overt hyperthyroidism: <0.03mU/L, elevated T3,
T4
 Thyroid storm: <0.01mU/L

 Subclinical hypothyroidism: 5-10mU/L, FT3, FT4-


N
 Overt hypothyroidism: >20mU/L, reduced T3, T4

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 Elevated TSH level
1. hypothyroidism is the most common cause
2. severe nonthyroidal illness
3. TSH-secreting pituitary tumor
4. thyroid hormone resistance
5. assay artefact.

 Suppressed TSH level


1. thyrotoxicosis
2. first trimester of pregnancy (due to hCG
secretion)
3. after treatment of hyperthyroidism
4. high doses of glucocorticoids, dopamine

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 secondary hypothyroidism-
hypothalamic-pituitary disease,
 variable (low to high-normal) TSH

level
 TSH should not be used as an

isolated laboratory test to assess


thyroid function in patients with
suspected or known pituitary disease.

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Serum total T4
 RIA,chemiluminometric assay
 Serum total T4 assays measure both

bound and unbound ("free") T4.


 Normal ranges -5 to 12 mcg/dL
 Elevated in 90% of patients with

hyperthyroidism
 Reduced in 85% patients with

hypothyroidism

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Serum T3
 RIA, chemiluminometric assay
 normal range -75 to 195 ng/dL
 Active form of the hormone

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Total thyroid hormone
 Elevated with increased TBG
1. OCP, estrogen, Tamoxifen, Pregnancy
2. Infectious hepatitis, Chronic active hepatitis
3. Neonatal state
4. Acute intermittent porphyria
5. Inherited conditions
 Decreased with decreased TBG
1. Testosterone, Androgens, corticosteroids
2. Acromegaly
3. Severe illness, Cirrhosis, Nephrotic syndrome
4. Inherited conditions
 Drugs interfere with thyroid hormone binding:
Phenytoin, Carbamazepine, Salicylates, NSAIDs

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Serum free T4 and free T3
 correspond to the biologically available
hormone pool.
 Represents 0.02 percent of serum total T4
 Normal: 0.9-2.4 ng/dl

 Two direct methods


 unbound thyroid hormone competition with
radiolabeled T4 (or an analogue) for binding
to a solid-phase antibody
 physical separation of the unbound hormone
fraction by ultracentrifugation or equilibrium
dialysis

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 indirectmethod
 THBR x total T3 = FT3 index
 THBR x total T4 = FT4 index: 1.2-4.9
 corrects for anomalous total hormone
values caused by abnormalities in
hormone-protein binding.
 FT4I, FT3I proportional to FT4, FT3
 T3, FT3, FT3I rarely used
 FT4, serum TSH most commonly used

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T3-resin uptake test
 RT3U x T4 = FT4 index.
 Indirect method of unbound T4
 Used less frequently
 Quantitates degree of saturation of

TBG sites by T4 & T3


 Directly proportional to fraction of

free T4
 Inversely proportional to TBG binding

site
 Normal: 24-39%
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 Theunbound T4 is sufficient to
confirm thyrotoxicosis

 2–5%- T3 toxicosis.
 Unbound T levels should be
3
measured in patients with a
suppressed TSH with normal unbound
T4 levels

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Clinical use of TFT
 Toscreen thyroid function,
 Assess the adequacy of

levothyroxine therapy
 Monitor the treatment of

hyperthyroidism

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Screening for thyroid dysfunction
 Serum TSH normal — no further testing
performed
 Serum TSH high — free T4 to determine the
degree of hypothyroidism
 Serum TSH low — free T4 and T3 to determine
the degree of hyperthyroidism
 two amendments to this strategy:
 measure both serum TSH and free T4 if pituitary
or hypothalamic disease is suspected (eg, a
young woman with amenorrhea and fatigue).
 serum free T4 if the patient has convincing
symptoms of hyper- or hypothyroidism despite a
normal TSH result

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 Monitoring levothyroxine therapy: 
1. primary hypothyroidism: monitored by
serum TSH.
2. secondary hypothyroidism: FT4 maintained
in the upper 50% of normal.
 Monitoring treatment of hyperthyroidism:
 serum free T4 and T3 measurements when
assessing the efficacy of antithyroid drugs,
radioiodine, or surgery

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 monitoring suppressive therapy may be
used with a third generation TSH assay:
 Third generation serum TSH value normal
— increase levothyroxine dose
 Third generation serum TSH value 0.06 to
0.5 mU/L — appropriate for suppressive
therapy; adjust dose if indicated
 Third generation serum TSH value <0.05
mU/L — add serum free T4 to assess the
degree of potentially excessive therapy;
adjust dose if indicated

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 Tests for the end-organ effects of
thyroid hormone:
1. estimation of basal metabolic rate-
Roth’s apparatus
2. tendon reflex relaxation rates
3. serum cholesterol

 TRH stimulation test


1. Assess functional status of TSH
secreting mechanism in response to
TRH
2. Used to assess pituitary function

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Tests to determine the etiology of
thyroid dysfunction
 Autoimmune thyroid disease: antibodies against TPO
and Tg, antimicrosomal antibody, antithyroglobulin
antibody, long acting thyroid stimulator, TSI.
 TPO antibodies: Autoimmune hypothyroidism, 80% of
Graves' disease
 TSI stimulate TSH-R in Graves' disease.
 predict neonatal thyrotoxicosis caused by high
maternal levels of TSI in the last trimester of
pregnancy.
 Serum Tg: increased in all types of thyrotoxicosis
except thyrotoxicosis factitia
 increased in thyroiditis

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Radioiodine Uptake and Thyroid
Scanning
 Transports radioisotopes of iodine (123I, I,
125 I)
131
and 99mTc pertechnetate
 Normal uptake 10-25%

 Graves' disease –↑ed tracer uptake distributed


homogeneously.
 Toxic adenomas – focal areas of ↑ed uptake,
with ↓ed tracer uptake in the remainder of the
gland.
 Toxic MNG- Multiple areas of ↑ed or ↓ed tracer
uptake.
 Subacute thyroiditis – very low uptake because
of follicular cell damage and TSH suppression.
 Thyrotoxicosis factitia – low uptake.

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Prognostic significance
 Warm is normal
 cold nodules-
• diminished tracer uptake
• usually benign.
 hot nodules –
• more likely to be malignant
 follow-up of thyroid cancer-
• After thyroidectomy and ablation diminished
uptake
• metastatic thyroid cancer deposits retain the
ability to transport iodine
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Thyroid Ultrasound
 90-95% accurate
 Using 10-MHz instruments, allowing the
detection of nodules and cysts >3 mm.

1. Nodular thyroid disease


2. monitoring nodule size
3. aspiration of nodules or cystic lesions.
4. Ultrasound-guided FNA biopsy.
5. evaluation of recurrent thyroid cancer
6. cervical lymph nodes.

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 Xray neck –position, compression of
trachea, Retrosternal goiter
 Bone scan
 FNAC
 CT & MRI

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Cervical Plexus Blockade
 The cervical plexus is derived from the C1,
C2, C3, and C4 spinal nerves and supplies
branches to the prevertebral muscles, strap
muscles of the neck, and phrenic nerve.
 The deep cervical plexus supplies the
musculature of the neck and skin between
the trigeminally innervated face and the T2
dermatome of the trunk.
 Blockade of the superficial cervical plexus
results in anesthesia of only the cutaneous
nerves.

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Clinical Applications
 Blockade of the cervical plexus provides
anesthesia for surgical procedures in the
distribution of C2 to C4, including lymph
node dissection, plastic repair, and carotid
endarterectomy.
 The ability to monitor the awake patient's

neurologic status continuously is an


advantage of this anesthetic technique
 Bilateral blocks can be used for

tracheostomy and thyroidectomy.

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Superficial Cervical Plexus Block
 The superficial cervical
plexus is blocked at the
midpoint of the posterior
border of the
sternocleidomastoid
muscle.
 A skin wheal is raised at
this point, and a 22-gauge,
4-cm needle is advanced
while injecting 5 mL of
solution along the posterior
border and medial surface
of the sternocleidomastoid
muscle.
 Block the accessory nerve
results in temporary 26-Feb-20 1:37 AM
paralysis of the ipsilateral 70
Deep Cervical Plexus Block
 The deep cervical plexus block is a paravertebral
block of the C2 to C4 spinal nerves as they
emerge from their foramina in the cervical
vertebrae.
 The traditional approach involves the use of three
separate injections at C2, C3, and C4.
 The patient lies supine with the neck slightly
extended and the head turned away from the side
to be blocked.
 A line is drawn connecting the tip of the mastoid
process and the Chassaignac tubercle (i.e.,
transverse process of C6); a second line is drawn
1 cm posterior to the first line.
 The C2 transverse process lies 1 to 2 cm caudad
to the mastoid process, where it can usually be
palpated.
 The C3 and C4 transverse processes lie at 1.5-cm
intervals along the second line.
 After skin wheals are raised over the transverse
processes of C2, C3, and C4, three 22-gauge, 5-
cm needles are advanced perpendicular to the
skin entry site at a slight caudad angulation.
 The transverse process is contacted at a depth of
1.5 to 3 cm.
 If a paresthesia is obtained, 3 to 4 mL of solution
is injected after careful aspiration for blood and
cerebrospinal fluid.
 If no paresthesia is elicited initially, the needle is
walked along the transverse process in the
26-Feb-20 1:37 AM
anteroposterior plane until a paresthesia is 71
obtained.
 This block can also be performed with a
single injection of 10 to 12 mL at the C4
transverse process.
 Cephalad spread of the local anesthetic
usually anesthetizes the C2 and C3
nerves.
 Maintenance of distal pressure and a
horizontal or slightly head-down position
may facilitate the onset of cervical plexus
blockade via the interscalene technique.

26-Feb-20 1:37 AM
72
Side Effects and Complications
 intravascular injection,
 blockade of the phrenic and superior

laryngeal nerve,
 spread of local anesthetic solution

into the epidural and subarachnoid


spaces.

26-Feb-20 1:37 AM
73
Thank you!

26-Feb-20 1:37 AM
74

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