THYROID MANAGEMENT

1. clinical
• History and Physicalexamination.
labs
• Thyroid functiontest.
• Auto antibodies.
imaging
• Iodine uptake.
• ThyroidUSS.

2. Thyroid function test
TSH level
Low TSH
High TSH (rare)
Measure T4
High
Secondary
hyperthyroidism
Image pituitary gland

3. Low TSH
Measure Free T4 Level
Normal High
Measure Free T3 Level
Normal High
-Subclinical
hyperthyroidism
-Resolving
Hyperthyroidism
-Medication
-Pregnancy
T3 Toxicosis
Primary hyperthyroidism
Thyroid uptake
Low High
Measure thyroglobulin
decreased Increased
Exogenous
Thyroiditis
Iodide exposure
Exrtraglandular
production
DIffuse Nodular
hormone
Graves
disease
Multiple
areas
One “hot” area
Toxic multinodular
goiter
Toxic
adenoma

4.  TFT-TSH/FT4FT3
 SecondgenerationAntiTSHab ->95%sensitivity
& specificity for diagnosis
 AntiTBGab/AntiTPOab found in up to 80%of
Graves’disease(also 15%healthy women & 5%
of men)
 Thyroid scintiscanning withT
c99 /I 131in doubt
about the nature of the goiter or thyrotoxicosis
without hyperthyroidismis suspected.
 ANA/dsDNAlevels areelevated without
evidenceof SLEor otherARD’s.

6.  Thethyroid gland is diffusely enlarged, and
often homogeneous.
 parenchymal hypervascularity isobserved.
 Goiter size isvariable,

8.  Carbimazole(CBZ)/methimazole/propylthiour
acil(PTU)
 Inhibits iodine organification by thyroid
peroxidase(TPO),reducingT4&T3
 PTH-inhibitsT4T3
 Also inhibitsTSIlevelsaccounting for
sustainedremission in 40-50%of GD

9.  Titration regimen-initial highdoses
 CBZ(40-60mg/d) orPTU(300-
450mg/d) initially/divided doses/3-4
perday
 Tailoff every 4-8 weeksbasedon FT4
 FT4normalizes-CBZ-once/day with
maintenance dose5-15mg/day& PTU50-
150mg/day
 Treat for 18-24 months/monitor FT4&TSH

10.  Block-replace regimen-CBZ 40mg/d orPTU
300mg/d is maintainedthroughout
 Hypothyroidism is avoidedby givingT4-
addingT4100mic/d, needed3-4wks
after starting.
 T4doseis adjusted basedinT4levels
 Continued for about 6mths with remission
rate similar to titrationregimen!
 Needsfew visits/control is smoother
 Only the doseof T4 is altered to optimizeTFT
 NOT used inpregnancy!

11.  Patients are reveiwedregularly in the year
after stopping drugs-70%of relapses!
 Supervenes 15%of autoimmune
hypothyroidism.
 Other drugs- Betablockers(BB)
 Propanolol 20-40mg/ tds or other non-
selective BBused temporarily in sever
thyrotoxicosis or thyroidcrisis.

13. Minor and major AE
MINOR
Agranulocytosis (<0.1%) –within3/12
Vasculitis(lupus-likesyndrome)
Polyarthritis
Hepatitis
Cholestatic jaundice
Liver failure
Thrombocytopenia
Stevens-Johnson syndrome *
• Papular or urticarial skinrashes(1-
5%)
• Arthralgias
• Nausea/vomiting
• Pruritis
• Hair loss
• Abnormal tastesensation
• Drug fever Lymphandenopathy

14.  I 131concentrates in the thyroid & damageit.
 400-600 MBq, higher dosesfor larger goitres
 C/I–pregnancy& breast feeding
 Pregnancy is safeafter 6 mths/avoid
fathering within4 mths
 Avoid close contacts with children for several
weeks
 A/E- transient thyroiditis/exacerbationof
thyrotoxicosis/sialoadenitis- occasionally
 ATD’sgiven before & or shortly after RAIto
prevent thyroidcrisis

15.  ATD’sstopped before RAI-CBZfor 2
days/PTU for 2weeks
 NO overall risk of malignancy after RAI
 RAIacts slowly- wait 4-6 mths before
repeating forpersisting thyrotoxicosis
 Transient hypothyroidism within3mths/
persistent in about 10%in 1st year
 TFT’scheckedannually
 Poor response- largegoiter/opthalmopathy

16.  Removesufficient thyroid tissue-more than
less, hypothyroidism istreatable!
 Recurrence 2-4% inbest centers
 Complications(1%) areuncommon-
hypoparathyroidism/RLN
palsy/bleeding/laryngeal edema
 Ensure euthyroidism-avoid crisis-lugol’s
iodine 10 days before surgery to reduce
vascularity & inhibit hormone synthesis

17.  <50years- initial courseofATD’svsRAI
 Relapseistreated with RAIor surgery (ATD’s
seldom results inremission!)
 In elderly –indefinite treatment with low dose
ATD’swith risk of recurrence
 >50years- RAIis thechoice!
 RAImay worsens opthalmopathy,specially in
smokers & caution in opthalmopathy
 Try long-termATD’s/surgery/RAIcombined with
tapering regimen ofsteroids

18.  Eyediscomfort-artificial
rears(day)/oinments(night),glasses
 Periorbital edema-elevate head
end/diuretics(co-amilozide)/radiotheraphy(RT
 Eyeprotective measures-eye
tapes(night),severe-RT/surgery/corticosteroids
 Congestive opthalmopathy-mild-selenium 100
mic bd
 Severe-high doseprednesolone(40-60mg/d
with taperingor
 IV methylprednesolon pulse theraphy-
500mg/wk for 6wks & 250mg/wk for 6wks

19.  Other immunosupressives-rituximab
 Progressive/active disease-decompressive
surgery or retrobulbarRT
 Optic nerve compression- high dose
prednesols-80-120mg daily withatapering
regimen.

20.  Lowest possible dose ofATD’susedto maintain
euthyroidism
 Someprefer PTU>CBZ-duetoA/Elike aplasia
cutis 7choanal atresia
 Block-replace regimen isC/I- due to insufficient
T4 crossing the placenta & causing neonatal
hypothyroidism
 <5%sufficient maternalTSHRabcrossing the
placenta causing fetal & neonatal
hyperthyroidism

21.  Inutero- tachycardia(.160/min)& poor growth
 CancheckmaternalTSHRablevelsinT3
 Mx-ATD’sto mother & monitor fetal
response by cordocentesissamples
 Neonatal hyperthyroidism isself limiting, due
to disappearance of maternal Ab’s within
3mths
 BF-possibleduringATD’sprovided low doses
areused

22.  Thyrotoxicosis is asyndrome causedby
excessivethyroid hormone & is commonly
due toGD
 ATD’sare usually initial treatment of GD&
RAIor surgery being for relapses
 TSHRab’saresensitive & specific for GD
 RAIin the presenceof opthalmopathy should
avoid unless prophylacticCSare given
 Careis neededin managingGDin pregnancy
to avoidA/Efor fetus %mother.