Graves' disease is the most common cause of hyperthyroidism. It is an autoimmune disorder where antibodies stimulate the thyroid gland to overproduce thyroid hormones. This causes a rapid heart rate, weight loss, eye changes, and enlarged thyroid gland. Treatment options include anti-thyroid medications to block hormone production, radioactive iodine therapy to destroy thyroid cells, or surgery to remove most of the thyroid gland. Long term treatment is needed to prevent recurrence of hyperthyroidism.

1. GRAVES’ DISEASE
By- Dr. PALLAVIPARBHAT PATHANIA

3. TOXIC GOITRE-
THYROTOXICOSIS
 Complex disorder- occurs due to increased levels of
thyroid hormones (hyperthyroidism)
 Manifests clinically with various signs and symptoms
involving many body systems
 Clinical types are:
> Primary thyrotoxicosis (Graves’ disease)
>Secondary thyrotoxicosis : secondary to multinodular
goitre {occurs due to hypertrophy and hyperplasia of
gland}

4. DIFFERENCES BETWEEN PRIMARY AND
SECONDARY THYROTOXICOSIS
Primary
thyrotoxicosis
Secondary
thyrotoxicosis
1. Age 15-25 years 25-40 years
2. Symptoms and
signs
Appear
simultaneously;
Duration is short
Long duration of a
swelling and short
duration of symptoms
3. Skin over the
swelling
Warm Not warm
4. Consistency Soft or firm Firm or hard
5. Surface Smooth Nodular
6. Eye signs Commonly found Rarely found
7. Predominant
symptoms
CNS CVS

5.  Discovered by Irish Physician Robert J. Graves in 1835.
 Most common form of hyperthyroidism.
 Aetiopathogenesis
*Autoimmune- Occurs when immune system mistakenly attacks the thyroid gland
causing it to overproduce the hormone thyroxine demonstrated by auto-
antibodies (TSH receptor antibodies) in the circulation
High thyroxine level greatly increase body’s metabolic rate
*Familial
*Thyroid stimulating immunoglobulins (TSI)
*Exophthalmous producing substance (EPS)
*Female sex, emotions, stress, young age

6.  Gender
 Age
 Family history
 Smoking
 Pregnancy
 Stress
Gender
Female
Male

7. PHYSIOLOGICAL EFFECTS ON
GRAVES’ DISEASE
TSIs mimics the action
of the TSH
Immune systems produces
autoantibodies called thyroid
stimulating immunoglobulin
(TSI) attach to thyroid cells.
TSI binds to TSH
receptors.
Thyroid gland is stimulated to
produce excess amounts of
thyroid hormone.
B cells Plasma Cells
secrete
antibodies
Antibodies
immobilize
antigens
This is where
autoimmune disorder
occurs.

8. CLINICAL FEATURES
Symptoms
 Fatigue or muscle weakness
 Emotional liability
 Heat Tolerance
 Weight loss
 Excessive appetite
 Palpitations

9. CLINICAL FEATURES
Signs
Tachycardia
Hot, moist palms
Exophthalmos {bulging of eyes}
Lid lag/retraction (von graefe’s sign)
Agitation{emotional disturbances}
Thyroid goitre and bruit

10. SIGNS OF THYROID GLAND IN GRAVES’
DISEASE
 Uniformly enlarged (mild degree)
 Smooth surface-no nodules
 Gland is soft or firm in consistency
 Warm and highly vascular

11. CNS SIGNS
 Tremors of the tongue when the tongue is within the oral
cavity and tremors of the outstretched hand
 Always a moist,warm hand

12. CARDIO VASCULAR S. SIGNS
 Tachycardia- depending upon pulse rate,
thyrotoxicosis can be classified as:
*mild-90-100/min
*moderate-100-110/min
*severe- >110/min
 Palpitations and extra systoles

13. EYE SIGNS
 Exophthalmos is common-caused by infiltration of the
retrobulbar tissues with fluid and round cells,with a
varying degree of retraction or spasm of upper eye lid
 Von graefe’s sign (lid lag sign)-
when patient is asked to look up and down,
upper eyelid cannot cope up with the speed
of movement of the finger because of lid spasm

14. MALIGNANT EXOPHTHALMOUS
 Occurs in untreated cases of Graves’ disease
 If the disease continues, infrequent blinking
secondary to exophthalmous results in constant
exposure of the cornea to the atmosphere. This
results in keratitis, corneal ulcer, conjunctivitis, can
occur, may even lead to blindness
 In late stages optic nerve damage and blindness
can occur.

15. THYROTOXIC MYOPATHY
 Mild weakness of proximal limb muscles is common
 Weakness of extraocular muscles results in double
vision (diplopia)
 Myopathy responds to antithyroid treatment
 Proximal limb muscles, ocular muscles, and
frontalis show weakness

16. PRETIBIAL MYXOEDEMA
 Seen in thyrotoxicosis patients treated with surgery
or antithyroid drugs
 Bilateral symmetrical deposition of myxomatous
tissue in pretibial region
 Skin is dry and coarse
 Non pitting, may be associated with clubbing of
fingers and toes called
Thyroid acropachy

17.  Physical Examination
 Laboratory Test-
1) Complete blood picture, fasting and post prandial blood
sugar estimation, urine examination, chest X-ray including
neck and indirect laryngoscopy
2) Serum T3 and T4 are elevated while TSH is low
3) Thyroid antibodies are elevated
4) Sleeping pulse rate- elevated
 Radioactive iodine uptake

18. TREATMENT
AIM
 To restore the patient
 To reduce the functioning thyroid mass to a very critical level (about
6-8gm of thyroid tissue)
 To minimise complications

19. ANTI THYROID DRUGS
Anti thyroid drugs
• Carbimazole- most commonly used,
dose- 5-10mg 8 hourly, duration- 12-18 months
Mode of action- blocks oxidation of iodide to iodine there by
reducing T3 and T4 levels,
thyroid hormone synthesis is blocked
• Methimazole- 5-20mg daily
• Propylthiouracil-blocks thyroid hormone synthesis
Given in pregnancy and children, dose-200mg 8 hourly
• Propranolol- dose-10-20mg twice or thrice a day
Reduces tachycardia
• Lugol’s iodine-is given to reduce the vascularity of the
Gland makes the gland more firm and hard to handle easily
during surgery. 10-12 drops three times a day for 10 days before
surgery

20. ANTI THYROID DRUGS
Advantages
 Avoids surgery and its complication
 Avoids radiotherapy
 Clinical improvement occurs in 2 weeks and biochemical in 6
weeks
Dis Advantages
 Prolonged course of treatment
 Relapse rate is very high (40%)
 Size of the swelling may not regress
 Other side-effects are very severe- agranulocytosis and
thrombocytopenia, liver damage, hair loss

21. SURGERY
Indications
 Failure of ATD in young patients
 If there is autonomous toxic nodule
 Nodular toxic goitre
 Surgery is subtotal-only 6-8gms is left behind

23. SURGERY
Advantages
 Rapid cure and high cure rate
Disadvantages
 Reoccurence – 5% cases
 Thyroid insufficiency- hypothyroidism in 20-40% cases
 Complications by surgery itself

24. POSTOPERATIVE COMPLICATIONS
 Haemorrhage
 Respiratory obstruction-
 Recurrent laryngeal nerve paralysis-
 Permanent hypothyroidism-
 Permanent hypoparathyroidism-
 Wound infection-

25. RADIOIODINE THERAPY
Indications
 Primary thyrotoxicosis after 45 years of age
 Recurrent thyrotoxicosis
 Autonomous toxic nodule
• Radio iodine destroys thyroid cells
• Given only after the age of 45 as chances of genetic
mutations, leukemia and carcinoma is there
• Dose-5-10 mCi

26. RADIOIODINE THERAPY
Advantages
 No surgery
 No prolonged drug therapy
Disadvantages
 Availability
 Proper follow-up is necessary