Download - Thyroid disease - A medusa of sorts
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In the Name of God, Most Gracious, Most Merciful
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A KALEIDOSCOPIC
PRESENTATION
OF THYROID
DISEASE- Dr.Mohammed Sadiq Azam
Postgraduate MD (Int Med)
Dept Of Internal Medicine, DCMS
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Case 1
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35/F presented with c/o diarrhoea, palpitations and a feeling of restlessness. She has been having increased sweating since 3 months. Complaints of increased appetite and decreased weights over 6 months.
On examination: Irregular pulse, 106pbm, PD 20 bpm.
Thyroid Profile revealed:T3: 210 ng/dl (high)T4: 15 ug/dl (high)TSH: <0.01 (low)
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THE HYPERTHYROID STATE- Diagnosis & Treatment
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EVALUATION THYROTOXICOSISMeasure TSH, unbound T4
TSH ↓unbound T4 ↑
TSH ↓ unbound T4 - N
TSH - N/↑unbound T4 ↑
TSH & unbound T4 - N
No further testsPrimarythryrotoxicosis
F/S/O Graves?
Unbound T3
High Normal
T3 toxicosis
Subclinicalhyperthyroidism
Follow up 6-12 weeks
TSH secreting pituitary adenoma or thyroid hormone resistance syndrome
Yes, Graves
MNG or Toxic adenoma
Yes, Toxic nodularhyperthyroidism
No, Low RNuptake
Yes, Destructive thyroiditisIodine excess or thyroid hormone excess
Rule out other causes including Stimulation by hCG
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THYROTOXICOSIS
MANAGEMENT
3 approaches 1. Antithyroid drugs
2. Radioactive Iodine I131
3. Subtotal thyroidectomy
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THYROTOXICOSIS
MEDICAL MANAGEMENT
1. ANTITHYROID DRUGS: > Carbimazole
> Propyl thiouracil
Dosage of Carbimazole:
0-3 weeks 40-60 mg daily
4-8 weeks 20-40 mg daily
Maintainence 5-20 mg daily for 18-24 months
ADR: Rash, Agranulocytosis
C/I: Lactating Mothers
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MEDICAL MANAGEMENT
2. RADIOACTIVE I131 :
MOA: > Destroys functioning thyroid cells
> Inhibits their ability to replicate
Dose:
180-370 MBq (5-10mCi) orally (Dep. on goitre size)
• 4-6 weeks to be effective (long lag period)
• -blockers control symptoms in lag period.
• Severe cases: Carbimazole within 48 hrs of I131
THYROTOXICOSIS
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MEDICAL MANAGEMENT
3. Role of -blockers: ONLY SYMPTOMATIC RELIEF
(within 12-24 h)
Propronolol: 160 mg/day
Nadolol: 40-80 mg/day
T3 toxicosis : I131(555-110Mbq), Hemithyroidectomy
THYROTOXICOSIS
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MANAGEMENT OF ATRIAL FIBRILLATION
• Ventricular Rate responds little to Digoxin.• Good response to addition of - blockers.• CARDIOVERSION to revert to sinus rhythm.
(Only after TSH/T4 )• Anti coagulation with Warfarin / Aspirin.
• Generally control of serum T4 causes a return to sinus rhythm.• Drugs provide symptomatic relief.
THYROTOXICOSIS
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GRAVES’ OPTHALMOPATHY
• Gritty sensation, Discomfort, lacrymation
• Exopthalmous
• Periorbital oedema, Chemosis, Scleral injection
THYROTOXICOSIS
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MANAGEMENT - GRAVES’ OPTHALMOPATHY
1. Reassurance
2. Methyl cellulose drops grittiness, discomfort
3. Tinted glasses / Side shields excess lacrymation
Complications:1. Corneal Ulcer: Lid lengthening Sx
2. Papilloedema/Loss of acuity/Field defects:
URGENT trt. with PREDNISOLONE 60mg/d
THYROTOXICOSIS
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GRAVES’ OPTHALMOPATHY
EFFECT OF THERAPY
BEFORE AFTER
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Case 2
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32/F come to hospital for routine physical examination and master heath checkup. Healthy. No specific complaints.
Thyroid profile:T3: 124 ng/dl (normal)T4: 9.1ug/dl (normal)TSH: 7.5 uIU/ml (high)
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SUBCLINICAL THYROID DYSFUNCTION- A Tricky situation
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INCLUDES:
Subclinical hypothyroidism
Commonly encountered
Subclinical hyperthyroidism
Rare entity
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SUBCLINICAL HYPOTHYROIDISM Defined as:
“Biochemical evidence of thyroid hormone
deficiency in patients who have few or no
apparent clinical features of hypothyroidism.”
Previously called:
Mild hypothyroidism
Early thyroid failure
Preclinical hypothyroidism
Decreased thyroid reserve
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SUBCLINICAL HYPOTHYROIDISM
Associated with risk of cardiac,
neuropsychiatric and dyslipidemic
abnormalities.
Risk of neonatal hypothyroidism if
encountered in pregnancy.
Risk of progression to overt hypothyroidism
is high when TSH is elevated and Anti TPO
Ab+
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SUBCLINICAL HYPOTHYROIDISM
Recent guidelines do not recommend
routine treatment when TSH levels are
< 10 mU/L. (Har 18th ed, Pg 2922)
Confirm sustained elevation of TSH over a
3 month period prior to initiating therapy.
Start with low dose of 25-50ug/day with
the goal of normalising TSH.
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Case 3
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23/F, Primi Gravida, no past history of thyroid disease. TFT during ANC (12 weeks GA) revealed a normal T3, T4 but raised TSH 6.4uIU/ml.
No treatment done, at term (36 weeks) her TSH increased to 8.2 uIU/ml (T3, T4 Normal).8 months postpartum:T3: <10ng/dlT4: <0.30 ug/dlTSH: >150.00 uIU/ml
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THYROID FUNCTION IN PREGNANCY - An Enigma in its own right!
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FACTORS ALTERING THYROID FUNCTION
Transient increase in hCG during first trimester
stimulates TSH-R
Estrogen induced rise in TBG during Trimester I
sustained throughout pregnancy
Alterations in immune system expression of an
underlying thyroid disease
Increased thyroid hormone metabolism by placenta
Increased urinary excretion of iodide high risk of
deficiency in women taking <50ug of iodide/day
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The hCG phenomenon Rise in hCG in first trimester is accompanied by a
reciprocal fall in TSH that persists upto the middle of
pregnancy.
Weak binding of hCG, which is present at very high
levels to the TSH-R
hCG induced changes in thyroid function can result in:
Transient gestational hyperthyroidism
Hyperemesis gravidarum
Rarely warrants use of antithyroid drugs
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HYPOTHYROIDISM - PREGNANCY
Maternal hypothyroidism occurs in 2-3% of women of
child-bearing age.
All pregnant women & those planning pregnancy
(esp with family history) must be screened for
hypothyroisism in first & third trimester.
Most pregnant women with primary hypothyroidism
require an additional 25-50ug increase to their dose.
Subclinical hypothyroidism must be treated
TSH Target to treat in pregnacy: 2.5-3.0uIU/ml
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HYPERTHYROIDISM - PREGNANCY
Rare
Pregnancy has an attenuating influence
on hyperthyroidism due to associated
immunosuppression
Medical therapy is the trt of choice
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HYPERTHYROIDISM - PREGNANCY
PTU or Carbimazole?
Both cross placenta, can cause low T4 and high TSH in
fetus
Maternal T4 flux across placenta is highly variable
PTU > 200mg / Carbimazole >15mg is undesirable
(esp in III trim)
Serum free T4 should be maintained in upper limit of
normal and no attempt at normalisation must be made.
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HYPERTHYROIDISM - PREGNANCY
In most cases maintainence dose must be 200mg
PTU or less in early pregnancy.
PTU preferred to methimazole due to risk of fetal
aplasia cutis with the latter.
Emerging reports of a “carbimazole
embryopathy” have made PTU the drug of
choice. (LeBeau et al. Thy dis dur preg. Endo
Clin North Am 2006;35:117-136, vii)
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Case 4
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65/M, admitted with c/o severe abdominal pain and vomintings. High grade fever+.On examination, RIF tenderness + with Guarding and rigidiity +. Patient was taken up or emergency laparotomy for perforated appendix.Post op case kept in SICU, Thyroid profile revealed:T3: 43 ng/dl (low)T4: 8.7 ug/dl (normal)TSH: 3.8 uIU/ml (normal)
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SICK EUTHYROID SYNDROME- To treat or not to treat?
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SICK EUTHYROID SYNDROME
Abnormalities of circulating TSH or thyroid
hormone levels as a consequence of any
acute, severe illness.
Major cause of these hormonal changes is the
release of cytokines such as IL-6.
Unless a thyroid disorder is strongly suspected,
the routine testing of thyroid function should
be avoided in acutely ill patients.
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SICK EUTHYROID SYNDROME (SES)
Most common hormone pattern in SES:
Low T3 (total & free)
Normal T4
Normal TSH
Magnitude of fall in T3 correlates with the severity of
the illness.
Decreased peripheral conversion of T4 T3. leading
to increased rT3 (more due to decreased clearance
rather than increased production).
Low T3 also seen in fasting. (Decreased catabolism)
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SICK EUTHYROID SYNDROME (SES)
Very sick patients exhibit a fall in total T4
as well (low T4 syndrome).
Poor prognosis
Fall in T4 is due to altered binding to
TBG. (Normal unbound fraction)
TSH may range from <0.1 to >20 mIU/L.
These alterations maybe due to IL-12 and
IL-18.
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SICK EUTHYROID SYNDROME (SES) Acute liver failure:
Initial rise in total T3 and T4 (but not unbound hormone), due to
TBG release.
Levels become subnormal with progression to liver failure.
Acute psychiatric states (5-30%):
Transient increase in total & unbound T4
Normal T3, Low, normal or high TSH
HIV:
Early disease T3, T4 rise, TSH normal. T3 falls with progression
to AIDS.
Renal disease:
Low T3, normal rT3 (NOT increased rT3) due to increased rT3
uptake by liver.
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SICK EUTHYROID SYNDROME (SES)
Based on history, severity of patient state,
thyroid hormone assays (including rT3)
Diagnosis is frequently presumptive
Treatment is controversial. Most of the
abnormalities recover with recovery from the
acute crisis.
Monitor TFT during recovery. No need of
hormonal replacement unless clinical evidence
of hypothyroidism + or low T4 levels.
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THANK YOU