Hyperthyroidism

Prof. Dr. Hamid Saeed

 What is hyperthyroidism?

• Hyperthyroidism is a disorder that occurs when the thyroid gland makes more thyroid hormone
than the body needs.

• Hyperthyroidism is sometimes called thyrotoxicosis, the technical term for too much thyroid
hormone in the blood.

• Thyroid hormones circulate throughout the body in the bloodstream and act on virtually every
tissue and cell in the body.

• Hyperthyroidism causes many of the body’s functions to speed up.

• About 1 percent of the U.S. population has hyperthyroidism.

Function and Regulation

• The thyroid gland makes two thyroid hormones, triiodothyronine (T3) and thyroxine
(T4).

• T3 is made from T4 and is the more active hormone, directly affecting the tissues.

• Thyroid hormones affect metabolism, brain development, breathing,

• heart and nervous system functions, body temperature, muscle strength, skin
dryness, menstrual cycles, weight, and cholesterol levels.
• Thyroid hormone production is regulated by thyroid-stimulating hormone
(TSH), which is made by the pituitary gland in the brain.

• When thyroid hormone levels in the blood are low, the pituitary releases more
TSH.

• When thyroid hormone levels are high, the pituitary responds by decreasing
TSH production.
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 (retrosternal goiter)

Where to look for Thyroid ?
Clinical Anatomy of Thyroid
Thyromegaly
Hyperthyroidism

• A hyper metabolic biochemical state

• It is a multi system disease with

• Elevated levels of T4 or T3 or both

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 Tumors – excess TSH
6. Molar pregnancy & Choriocarcinoma (↑↑ βHCG)
7. Metastatic thyroid cancers (functioning)
8. Struma Ovarii (Dermoid and Ovarian tumors)
9. Thyrotoxicosis Factitia ; INF, Amiodarone, SSRIs
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
Graves Disease

I 123 or TC 99m Normal v/s Graves – thyroid scan

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 T4 and T3
• Progresses slowly over time
• Clinically multiple firm nodules (called Plummer’s disease)
• Scintigraphy shows - hot and normal areas
Toxic Multinodular Goiter (TMG)
Toxic Multinodular Goiter (TMG)
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

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

Toxic Single Adenoma (TSA)
Radio-Nucleotide
Scintigraphy
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
Radio-Nucleotide Scintigraphy
Common Symptoms
• irritability or nervousness
• anxiety • more frequent stools and/or diarrhea
• bulging eyes
• muscle weakness
• chest pain
• rapid or irregular heartbeat
• difficulty sleeping and/or insomnia
• elevated blood pressure • restlessness
• fatigue • sensitivity to heat
• hand tremors • shortness of breath and/or difficulty
• increased sweating breathing
• irregular menstrual periods
• unexplained weight loss (typically despite
an increase in appetite)
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
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)
Clinical Presentations
MNG and Graves

Huge Toxic MNG Diffuse Graves Thyroid

Higher grades of Goiter

Toxic MNG (Diffuse) Graves

Grade IV Toxic MNG

Huge Toxic MNG Huge Toxic MNG

 Thyroid Ophthalmopathy

Proptosis

Lid lag
Ophthalmopathy in Graves

Periorbital edema and chemosis

Ophthalmopathy in Graves

Occular muscle palsy

Severe Exophthalmia
Thyroid Dermopathy

Pink and skin coloured papules, plaques on the shin

Graves with Acropathy

Graves Goiter Acropathy

Thyroid Acropathy

Clubbing and
Osteoarthropathy
Onycholysis
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

 Nine Square Approach

FREE THYROXINE or FT4

HIGH
PRIMARY
HYPERTHYROID

NORMAL
LOW

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

 Nine Square Approach

FREE THYROXINE or FT4

HIGH
NORMAL
SUB CLINICAL
LOW HYPERTHYROID

LOW NORMAL HIGH

THYROID STIMULATING HORMONE - TSH

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

Diagnosis

• Hormone test – TSH and T4

• Anti-body test – TSI, anti-TPO (thyro-peroxidase)

• Ultrasonography

• Thyroid Scan (radio-nucleotide scintigraphy)

• Biopsy - find needle aspiration (FNA)

 Algorithm for Hyperthyroidism
Measure TSH and FT4

 TSH,  FT4  TSH, FT4 N  TSH,  FT4 N TSH, FT4 N

Primary (T4) Pituitary Adenoma FNAC, N Scan

Thyrotoxicosis Measure FT3

High T3 Toxicosis
Features of Grave’s

Normal Sub-clinical Hyper

Yes No
 RAIU Low RAIU F/u in 6-12 wks
Rx. Grave’s
Single Adenoma, MNG Sub Acute Thyroiditis, I2, ↑ Thyroxine
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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

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

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
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.

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

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

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

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

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.
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

 Algorithm for Thyroid
Nodule
Thyroid Nodule

Low TSH Normal TSH

TC 99 Nuclear Scan
FNAC or US
Hot Nodule Cold Nodule guided biopsy
4% 10% 69% 17%
RAI Ablation,
Non diagnostic –
Surgery or
Malignant Suspicious or Benign Cyst repeat FNAC
ATD
follicular Ca

T4 Surgery or
Surgery
suppression Cytology
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