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Dr S P Kataria
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
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)
introduction
In 1909 Theodor Kocher
from Switzerland won
the Nobel prize in
medicine for his work on
physiology
pathology, &
surgery
of thyroid gland.
Origin of gland
Development– floor of primitive
pharynx during 3rd week of
gestation.
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
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
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 .
Congenital hypothyroid
Rx.
If treatment is delayed , premanent neurologic damage
results.
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.
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.
Hypothyroidism
Hypothyroidism: Clinical features
Symptoms : 1. dry skin
2. hair loss 3. feeling cold
4. weight gain with poor
appetite
5.constipation 6. poor
memory 7. poor concent.
8.dyspnoea
9. hoarseness of voice
10. paresthesia
12.impared hearing .
13. menorrhagia
Signs : 1. dry coarse skin
2. cool peripheral
extremity
3. diffuse alopecia
4. bradycardia
5. peripheral edema
6. delayed tendon reflex
relaxation
7.carpal tunnel
syndrome
8. serous cavity effusions
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 )
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
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.
Thyroid disorders ---hypo

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Thyroid disorders ---hypo

  • 1. Dr S P Kataria
  • 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.
  • 5. Origin of gland Development– floor of primitive pharynx during 3rd week of gestation.
  • 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 .
  • 9. Congenital hypothyroid Rx. If treatment is delayed , premanent neurologic damage results.
  • 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.
  • 13. Hypothyroidism: Clinical features Symptoms : 1. dry skin 2. hair loss 3. feeling cold 4. weight gain with poor appetite 5.constipation 6. poor memory 7. poor concent. 8.dyspnoea 9. hoarseness of voice 10. paresthesia 12.impared hearing . 13. menorrhagia Signs : 1. dry coarse skin 2. cool peripheral extremity 3. diffuse alopecia 4. bradycardia 5. peripheral edema 6. delayed tendon reflex relaxation 7.carpal tunnel syndrome 8. serous cavity effusions
  • 14.
  • 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.