7. Grave’s disease.

Question 1

Grave’s disease - Definition

Answer 1

Graves’ disease is an autoimmune disease that affects the thyroid gland in which circulating TSH receptor autoantibodies lead to
overstimulation of the thyroid gland and excess thyroid
hormone production

Question 2

Graves disease - Main Points

Answer 2

Includes thyrotoxicosis (hypothyroidism), goiter, exophthalmos, pretibial myxoedema when fully expressed

• Usually in young women with no preceding history of goiter
• Gl is smooth with uniform enlargement

Question 3

Graves disease - Etiopatholgenesis

Answer 3

Auto (detectable in serum) Antibodies bind to + stimulate TSH receptor.

These Ab have prolonged stimulatory effect compared with TSH hence “long-acting” thyroid stimulators

• Hyperactivity of acinar cells. Gl is very vascular with little colloid
• Lymphocyte infiltration is predominant feature

Question 4

Graves disease - Diagnostic Investigations

Answer 4

• Serum increase in T3, T4 – decreased TSH

Question 5

Thyroid storm

Answer 5

• Life-threatening complication of thyrotoxicosis
• Fever, agitation, confusion, increased HR, AF
• Precipitated by infec in a pt with unrecognized/inadequately treated thyrotoxicosis

Question 6

Thyrotoxicosis - definition

Answer 6

Thyrotoxicosis means an excess of thyroid hormone in the body

Question 7

Thyrotoxicosis - Clinical Presentation

Answer 7

• Symptoms: decreased weight, increased appetite, heat intolerance, palpitation, tremor, dyspnoea, emotional inability, irritability, fatigue, sweating
• Signs: decreased weight, tremor, palmar erythema, sinus tachy, lid retraction, lid lag, myedema (raised pink-purple plaques on ant. aspect of leg extending to dorsum of foot. Itchy)

Question 8

Hypothyroidism - Clinical Presentation

Answer 8

Symptoms: weight gain, cold intolerance, fatigue, somnolence, dry skin, dry hair, menorrhagia

• Signs: weight gain

Question 9

Graves ophthalmology – exophthalmos

Answer 9

• Condition immunologically mediated – proliferation of fibroblasts within orbit which secrete glycosaminoglycans
• This increases interstitial fluid combined with chronic inflammatory cell infiltrate  swelling + ultimately fibrosis of extraocular muscles + rise in retrobulbar pressure
• Eye displaced forward + in severe cases optic nerve compression
• May be excessive lacrimation made worse by wind + bright light
• Pain + “gritty” sensation in eye due to conjunctivitis + corneal ulceration

Question 10

Grave’s Disease - Treatment

Answer 10

• Carbimazole: 10mg every 8 hrs + sedation + bed rest in acute phase for 12 mnths if s+s continue 6 mnths more  surgery
  o A.E: drug rash, fever, athropathy, lymphadenopathy
• B-blockers: in pts with severe hyperthyroidism. Propanolol = symptomatic improvement of CVS s+s

Surgery:
Only after relapse = subtotal thyroidectomy – but at a point.
External thyroxine will be needed to be prescribed so total thyroidectomy is becoming op of choice

Question 11

Grave’s Disease - Complications

Answer 11

Hypothyroidism – too much thyroid tissue removed, damage surrounding anatomical structures

 Haemorrhage, sepsis, post op infection, hypertrophic scarring (keloid)