Short notes on a quick History and investigations of hyperthyroidism including treatment

1. HYPERTHYROIDISM
A Practical Approach to Dx. and Rx.
Courtesy of
Dr. R.V.S.N.Sarma., M.D., M.Sc., (Canada)
Consultant Physician and Chest Specialist
www.drsarma.in

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Clinical Exam. of Thyroid
 Have patient seated on a stool / chair
 Inspect neck before & after swallowing
 Examine with neck in relaxed position
 Palpate from behind the patient
 Remember the rule of finger tips
 Use the tips of fingers for palpation
 Palpate firmly down to trachea
 Pemberton’s sign for RSG

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Where to look for Thyroid ?

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Clinical Anatomy of Thyroid

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Clinical Exam of Thyroid

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Clinical Exam of Thyroid

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Clinical Exam of Thyroid

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Thyromegaly

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Hyperthyroidism
 A hyper metabolic biochemical state
 It is a multi system disease with
 Elevated levels of FT4 or FT3 or both
 What is thyrotoxicosis ?
 What is hyperthyroidism ?
 What are the various causes ?
 How to differentiate the causes ?
 What is the appropriate treatment ?

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Causes of Hyperthyroidism
1. Graves Disease – Diffuse Toxic Goiter
2. Plummer’s Disease – Toxic MNG
3. Toxic phase of Sub Acute Thyroiditis - SAT
4. Toxic Single Adenoma – STA
5. Pituitary Tumours – excess TSH
6. Molar pregnancy & Choriocarcinoma (↑↑ βHCG)
7. Metastatic thyroid cancers (functioning)
8. Struma Ovarii (Dermoid and Ovarian tumours)
9. Thyrotoxicosis Factitia ; INF, Amiodarone, SSRIs

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Graves Disease
 The most common cause of thyrotoxicosis (50-60%).
 Organ specific auto-immune disease
 The most important autoantibody is
 Thyroid Stimulating Immunoglobulin (TSI) or TSA
 TSI acts as proxy to TSH and stimulates T4 and T3
• Anti thyro peroxidase (anti-TPO) antibodies
• Anti thyro globulin (anti-TG) Anti Microsomal and other
• Autoimmune diseases - Pernicious Anemia, T1DM
• RA, Myasthenia Gravis, Vitiligo, Adrenal insufficiency.

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Graves Disease
I 123 or TC 99m Normal v/s Graves

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Graves Disease

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Toxic Multinodular Goiter (TMG)
 TMG is the next most common hyperthyroidism - 20%
 More common in elderly individuals – long standing goiter
 Lumpy bumpy thyroid gland
 Milder manifestations (apathetic hyperthyroidism)
 Mild elevation of FT4 and FT3
 Progresses slowly over time
 Clinically multiple firm nodules (called Plummer’s disease)
 Scintigraphy shows - hot and normal areas

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Toxic Multinodular Goiter (TMG)

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Toxic Multinodular Goiter (TMG)

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Sub Acute Thyroiditis (SAT)
 SAT is the next most common hyperthyroidism – 15%
 T4 and T3 are extremely elevated in this condition
 Immune destruction of thyroid due to viral infection
 Destructive release of preformed thyroid hormone
 Thyroid gland is painful and tender on palpation
 Nuclear Scintigraphy scan - no RIU in the gland
 Treatment is NSAIDs and Corticosteroids

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Toxic Single Adenoma (TSA)
 TSA is a single hyper functioning follicular thyroid adenoma.
 Benign monoclonal tumor that usually is larger than 2.5 cm
 It is the cause in 5% of patients who are thyrotoxic
 Nuclear Scintigraphy scan shows only a single hot nodule
 TSH is suppressed by excess of thyroxines
 So the rest of the thyroid gland is suppressed

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Toxic Single Adenoma (TSA)
Nucleotide
Scintigraphy

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Age and Sex
 Age
 Graves disease 20 to 40
 Toxic MNG > 50 yrs
 Toxic Single Adenoma 35 to 50
 Sub Acute Thyroiditis Any age
 Sex M : F ratio
 Graves Disease 1: 5 to 1:10
 Toxic MNG 1: 2 to 1: 4

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Nucleotide Scintigraphy

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Clinical Features
1. Those that occur with any type of thyrotoxicosis
2. Those that are specific to Graves disease
3. Non specific changes of hyper metabolism

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Common Symptoms
1. Nervousness
2. Anxiety
3. Increased perspiration
4. Heat intolerance
5. Tremor
6. Hyperactivity
7. Palpitations
8. Weight loss despite increased appetite
9. Reduction in menstrual flow or oligo-menorrhea

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Common Signs
1. Hyperactivity, Hyper kinesis
2. Sinus tachycardia or atrial arrhythmia, AF, CHF
3. Systolic hypertension, wide pulse pressure
4. Warm, moist, soft and smooth skin- warm handshake
5. Excessive perspiration, palmar erythema, Onycholysis
6. Lid lag and stare (sympathetic over activity)
7. Fine tremor of out stretched hands – format's sign
8. Large muscle weakness, Diarrhea, Gynecomastia

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Specific to Graves Disease
1. Diffuse painless and firm enlargement of thyroid gland
2. Thyroid bruit is audible with the bell of stethoscope
3. Ophthalmopathy – Eye manifestations – 50% of cases
 Sand in eyes, periorbital edema, conjunctival edema
(chemosis), poor lid closure, extraocular muscle dysfunction,
diplopia, pain on eye movements and proptosis.
4. Dermoacropathy – Skin/limb manifestations – 20% of cases
 Deposition of glycosamino glycans in the dermis of the lower
leg – non pitting edema, associated with erythema and
thickening of the skin, without pain or pruritus - called
(pre tibial myxedema)

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Clinical Presentations

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MNG and Graves
Huge Toxic MNG Diffuse Graves Thyroid

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Higher grades of Goiter
Toxic MNG (Diffuse) Graves

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Grade IV Toxic MNG
Huge Toxic MNG Huge Toxic MNG

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Proptosis
Lid lag
Thyroid Ophthalmopathy

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Ophthalmopathy in Graves
Periorbital edema and chemosis

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Ophthalmopathy in Graves
Occular muscle palsy Laka Laka Laka

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Severe Exophthalmia

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Thyroid Dermopathy
Pink and skin coloured papules, plaques on the shin

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Graves with Acropathy
Graves Goiter Acropathy

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Clubbing and
Osteoarthropathy
Thyroid Acropathy

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Onycholysis

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Non specific changes
1. Hyperglycemia, Glycosuria
2. Osteoporosis and hypercalcemia
3. ↓ LDL and Total Cholesterols
4. Atrial fibrillation, LVH, ↑ LV EF
5. Hyper dynamic circulatory state
6. High output heart failure
7. H/o excess Iodine, amiodarone, contrast dyes

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Diagnosis
1. Typical clinical presentation
2. Markedly suppressed TSH (<0.05 µIU/mL)
3. Elevated FT4 and FT3 (Markedly in Graves)
4. Thyroid antibodies – by Elisa – anti-TPO, TSI
5. ECG to demonstrate cardiac manifestations
6. Nuclear Scintigraphy to differentiate the causes

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Treatment Options
1. Symptom relief medications
2. Anti Thyroid Drugs – ATD
 Methimazole, Carbimazole
 Propylthiouracil (PTU)
3. Radio Active Iodine treatment – RAI Rx.
4. Thyroidectomy – Subtotal or Total
5. NSAIDs and Corticosteroids – for SAT

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Symptom Relief
1. Rehydration is the first step
2. β – blockers to decrease the sympathetic excess
 Propranalol, Atenelol, Metoprolol
3. Rate limiting CCBs if β – blockers contraindicated
4. Treatment of CHF, Arrhythmias
5. Calcium supplementation
6. SSKI or Lugol solution for ↓ vascularity of the gland

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Anti Thyroid Drugs (ATD)
Imp. considerations Methimazole Propylthiouracil
Efficacy Very potent Potent
Duration of action Long acting BID/OD Short acting QID/TID
In pregnancy Contraindicated Safely can be given
Mechanism of action Iodination, Coupling Iodination, Coupling
Conversion of T4 to T3 No action Inhibits conversion
Adverse reactions Rashes, Neutropenia Rashes, ↑Neutropenia
Dosage 20 to 40 mg/ OD PO 100 to 150mg qid PO

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How long to give ATD ?
 Reduction of thyroid hormones takes 2-8 weeks
 Check TSH and FT4 every 4 to 6 weeks
 In Graves, many go into remission after 12-18 months
 In such pts ATD may be discontinued and followed up
 40% experience recurrence in 1 yr. Re treat for 3 yrs.
 Treatment is not life long. Graves seldom needs surgery
 MNG and Toxic Adenoma will not get cured by ATD.
 For them ATD is not the best. Treat with RAI.

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Radio Active Iodine (RAI Rx.)
 In women who are not pregnant
 In cases of Toxic MNG and TSA
 Graves disease not remitting with ATD
 RAI Rx is the best treatment of hyperthyroidism in adults
 The effect is less rapid than ATD or Thyroidectomy
 It is effective, safe, and does not require hospitalization.
 Given orally as a single dose in a capsule or liquid form.
 Very few adverse effects as no other tissue absorbs RAI

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Radio Active Iodine (RAI Rx.)
 I123 is used for Nuclear Scintigraphy (Dx.)
 I131 is given for RAI Rx. (6 to 8 milliCuries)
 Goal is to make the patient hypothyroid
 No effects such as Thyroid Ca or other malignancies
 Never given for children and pregnant/ lactating women
 Not recommended with patients of severe Ophthalmopathy
 Not advisable in chronic smokers

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Surgical Treatment
 Subtotal Thyroidectomy, Total Thyroidectomy
 Hemi Thyroidectomy with contra-lateral subtotal
 ATD and RAI Rx are very efficacious and easy – so
 Surgical treatment is reserved for MNG with
1. Severe hyperthyroidism in children
2. Pregnant women who can’t tolerate ATD
3. Large goiters with severe Ophthalmopathy
4. Large MNGs with pressure symptoms
5. Who require quick normalization of thyroid function

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Preoperative Preparation
 ATD to reduce hyper function before surgery
 βeta blockers to titrate pulse rate to 80/min
 SSKI 1 to 2 drops bid for 14 days
 This will reduce thyroid blood flow
 And there by reduce per operative bleeding
 Recurrent laryngeal nerve damage
 Hypo parathyroidism are complications

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Dietary Advice
 Avoid Iodized salt, Sea foods
 Excess amounts of iodide in some
 Expectorants, x-ray contrast dyes,
 Seaweed tablets, and health food
supplements
 These should be avoided because
 The iodide interferes with or complicates the
management of both ATD and RAI Rx.

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Summary of Hyperthyroidism
Hyperthyroidism Age % Enlarged Pain RAIU Treatment
Graves (TSI Ab
eye, dermo, bruit)
20 - 40 60% Diffuse None ↑↑ ATD – 18 m
Toxic MNG > 50 20% Lumpy Pressure ↑ RAI, Surgery
Single Adenoma 35 - 50 5% Single None ± RAI, ATD
S Acute Thyroiditis Any age 15% None Yes ↓↓ NSAID, Ster.
TSH is markedly low, FT4 is elevated

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Thyrotoxicosis Factitia
 Excessive intake of Thyroxine causing thyrotoxicosis
 Patients usually deny – it is willful ingestion
 This primarily psychiatric disorder
 May lead to wrong diagnosis and wrong treatment
 They are clinically thyrotoxic without eye signs of Graves
 High doses of Thyroxine lead to TSH suppression
 This causes shrinkage of the thyroid
 Stop Thyroxine and give symptom relief drugs

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Case # 1
A patient complains of “sandy” sensation in his eyes,weight
loss, and a tremor. His extraocular muscles are inflammed.
His thyroid is diffusely enlarged and non tender.
The most likely diagnosis is
a. Iodine deficiency
b. Sub-acute thyroiditis
c. Multinodular goiter
d. Graves’ disease
e. Silent thyroiditis

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Case # 2
A 55 year old woman is anxious, irritable, frequent semi
solid stools and she reports weight loss of 5 kgs in the past
six months. She was having a lumpy bumpy painless
swelling in her neck for past 20 years.
The most likely diagnosis is
a. Iodine deficiency goiter
b. Sub-acute thyroiditis
c. Multinodular goiter
d. Graves’ disease
e. Solitary toxic adenoma

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Case # 3
A 60 year patient from a mountain region complains of
constipation. He has a heart rate of 60, dry thick skin,
and a tongue that has scalloped edges from teeth
indentation. He has a goiter.
The most likely diagnosis is
a. Iodine deficiency
b. Subacute thyroiditis
c. Graves’ disease
d. Silent thyroiditis

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Case # 4
A 25 year old woman is three months pregnant. She has
a large goiter. Her exam is otherwise normal. Her thyroid
tests are normal.
You recommend
a. Cassava five times weekly
b. Fish three times weekly
c. Formula milk for the baby when it is born
d. A very low salt diet

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Case # 5
A 72 year old man complains of tremor and inability to
concentrate. On exam, he has a heart rate of 100 beats
per minute. He has a large goiter with many nodules. He
has a fine tremor. His serum T4 is very high and TSH is
very low.
Treatments that are likely to improve his symptoms are
a. Iodine therapy
b. Ethanol injection of his thyroid (PEI)
c. 6 weeks of Methimazole
d. Radio Active Iodine therapy

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Case # 6
In Nuclear Scintigraphy Scan I123 uptake is very high in
the thyroid of patients with
a. Silent thyroiditis
b. Single functional adenoma
c. Sub-acute thyroiditis
d. Acute ingestion of animal thyroid extract
e. Graves’ disease

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