2. introduction
It is located in neck , anterior to the trachea ,b/w cricoid
cartilage & suprasternal notch opp. C5-T1 vertebra .
50% thyroid glands have pyramidal lobes
largest endocrine gland.
Weight 12-20 gm,
Consistency = soft,
thyroid release 100-125 n mol of T4 daily , small
amount T3.
Half life of T4 =7-10 days.
Half life of TSH =50 min
thyroid gland is highly vascular , supplied by sup. &
inf. thyroid artery
thyroid blood flow rate = 1.2 ml/min/gm
3. introduction
normal thyroid uptake of radio iodine =25 % in 24 hr
Thyroid in grave’s disease radioiodine uptake = 90 %
over 24 hour.
RDA intake of iodine ( recommended daily avg .)
150 mcg (adults) ,
90-120 ( children),
200 mcg (pregnant women)
4. introduction
In 1909 Theodor Kocher
from Switzerland won
the Nobel prize in
medicine for his work on
physiology
pathology, &
surgery
of thyroid gland.
6. Thyroid gland development is controlled by series of
transcription al factors.
1. TTF= thyroid transcription factor--- 1 & 2
2. Paired homeobox-8
they finish proper thyroid development & induce three
imp. thyroid specific genes
a. thyroglobulin
b. thyroid peroxidase
c. TSH-receptor
mutation in above 3 factors / genes :
cause
thyroid agenesis ,
dys-hormogenesis,
cong hypothyroidism
7. Function of thyroid
It secretes two hormones
(a) thyroxin =T4
(b) tri-iodothyronine
it regulates all body functions including
1.metabolism of all 3 :– cabohydrates , fats , protein.
2. growth & reproduction
3. cardiac & neural functions
8. Congenital hypothyroid
is common 1: 3000-4000 newborn ,
underlying cause is unknown in most cases,
early treatment (HRT) is important to prevent
potentially severe developmental abnormalities.
Introduction of iodized salt in early 20th century made
cong. hypothyroidism rare . Untreated case results
potentially severe developmental abnormalities.
C/F : 1. prolong jaundice 2.hypotonia 3. enlarged
tongue 3. delayed bone maturation 4.umbilical hernia
5. feeding problems .
10. Regulation of HPT axis
Thyroid axis is classical
example of endocrine
feedback loop.
1.TRH is major positive
regulator of TSH
synthesis & secretion ,
Exogenous TRH cause
peak TSH after 15 min .
2.TSH is released in
pulsatile manner,
exhibits diurnal rhythm,
highest occur @ night.
11. Regulation of HPT axis
TSH has long plasma half life (50 minutes).
TSH is measured using RIA =radio immuno assay ,
single measurement is adequate to access it’s
circulating level.
Set point of this axis is established by TSH .
Thyroid hormones T3, T4 are dominant regulator of
TSH production , their reduced level increases basal
TSH production also enhance TRH mediated
stimulation of TSH.
High T3 ,T4 rapidly , directly suppress TSH, also
inhibit TRH mediated stimulation.
Thyroid hormones are dominant regulator of TSH.
15. Investigations
1. Screening TSH = if normal , excludes pri. hypothyroidism
if TSH is elevated , then free T4 is required to confirm the
clinical hypothyroidism
2. Thyroid profile
FT3, FT4, TSH ,
circulating FT3 is normal in 25% pt due to adaptive
response .
once clinical or sub clinical hypothyroidism is confirmed
etiology is now established by demonstrating presence
of antibodies by
3. Anti TPO ( 95% pt of auto immune hypothyroidism )
16. investigations
4. TB II = TSH binding inhibiting immunoglobulin
present in 10-20% patients.
5. FNAC-Thyroid biopsy is used to confirm the auto
immune thyroiditis & focal nodule.
6. USG –Thyroid for –solitary or multi nodular goiter
7. Fasting lipid profile----dyslipidemia
8. CBC ---anemia
17. Management
Daily replacement dose = 1.5 mcg /kg body weight of
levo-thyroxine.
Pt may not experience full relief from symptoms until
3 to 6 months.