Management of thyroid diseases

1. DISEASES OF THE THYROID
GLAND
DR A. O. YUSUF
CONSULTANT PHYSICIAN/ENDOCRINOLOGIST,
ENDOCRINE, DIABETES AND METABOLISM UNIT,
DEPT. OF INTERNAL MEDICINE, LAUTECH
TEACHING HOSPITAL, OSOGBO

2. Anatomy and physiology of the
thyroid
• Anatomy:
• Made up of 2 lobes (lying in front of the lower
half of the thyroid cartilage) joined by an
isthmus (lying at the midline just below the
cricoid cartilage).
• Enclosed in the pretracheal fascia hence
moves with swallowing.
• Weighs about 25g

3. Anatomy and physiology of the
thyroid
• Histologically: consists of follicules (lined by
single layer of cuboidal cells) surrounded by
capillary network and parafollicular C cells
which secrete calcitonin. The lumen of the
follicle contains thyroglobulin.

4. Anatomy and physiology of the
thyroid
• Embryology: develops from endoderm of
pharyngeal floor and lateral pharyngeal pouches
during the 4th wk of IU life. Descends from the
base of the tongue thus giving rise to the
thyroglossal duct. Follicles identifiable by 10th wk
and hormone production begins by 12th wk.

5. Anatomy and physiology of the
thyroid
• Fetal thyroid begins to concentrate and
organify iodine at about 10-12th wk of IU life.
• Maternal THR crosses the placenta but
maternal TSH and T4 do not.
• T4 from the fetal thyroid is the major
hormone available to the fetus and pituiatary-
thyroid axis is active and functionally separate
from the maternal by 18 to 20 weeks.

6. Physiology
Iodine is converted into iodide and then transported
into the thyroid by sodium iodide symporter.
Oxidized iodine under the stimulation of thyroid
peroxidase combines with thyroglobulin to form
monoiodotyrosine (MIT) and diiodotyrosine (DIT).
Coupling of 2 molecules of DIT gives rise to
thyroxine (T4) and 1 molecule of MIT and 2
molecules of DIT gives rise to triiodothyronine T3.
Proteolytic digestion of thyroglobulin leads to the
release of the hormones

7. Physiology
• In the blood they are carried by thyroxine binding
globulin (TBG) 60-70%, transthyretin 15%,
albumin 15-20%, and lipoproteins.
• Deiodinases convert T4 to T3 by
5’monodeiodination and inactive rT3 by 3’
monodeiodination (occurs in illnesses) in the
peripheral tissues: kidneys, muscle and liver, only
5-10% of circulation T3 is secreted directly by the
thyroid.
• Free T3 binds to nuclear receptors α and β1, β2

8. DISEASES OF THE THYROID
• Thyrotoxicosis:
–Graves’ disease
–Toxic multinodular goitre
–Toxic adenoma
–Subclinical hyperthyroidism

9. DISEASES OF THE THYROID
• Thyroiditis;
–Acute thyroiditis
–Subacute (de Quervain’s)
thyroiditis
–Subacute lymphocytic thyroiditis

10. Thyrotoxicosis
Graves’ disease;
• Commonest cause of hyperthyroidism
• Autoimmune
• Serum IgG antibodies TSHR-Ab bind to TSH
receptor stimulating it.
• TSHR-Ab are specific for Graves’ disease

11. Clinical features of hyperthyroidism
• Symptoms;
• Weight loss
• Increased appetite
• Restlessness
• Tremor
• Palpitation
• Heat intolerance
• Hyperdeafecation
• Eye and skin changes.

12. Clinical features of hyperthyroidism
• Signs;
• goitre
• Tremor
• Tachycardia
• Atrial fibrillation
• Systolic hypertension
• Warm extremities
• Eye signs (NO SPECS)
• Graves dermopathy

13. Investigations
• Suppressed TSH
• ↑ free T3 and T4
• TPO and thyroglobulin antibodies are present in
most cases of Graves disease.
• TSHR-Ab: stimulatory IgG.
• Thyroid USS
• FNAC
• Other ancillary investigations: FBC,EUCr,ECG,CXR

14. TREATMENT
• 3 modalties;
• Antithyroid drugs: carbimazole, methimazole
• Radioiodine:200-550MBq
• Surgery; total or subtotal thyroidectomy

15. • Antithyroid medications; 2 regimens exist
• Gradual dose titration or ‘block and replace
regimen.
• Start with carbimazole 20mg-40mg in divided
doses. Review dose after 4-6weeks and
subsequently reduce based on T3/T4 levels.

16. Thyroid storm
• Medical emergency representing severe/life
threatening thyrotoxicosis.
• Precipitated by; infection, surgery,
anaesthezia,
• Presentation; exageration of symptoms
• Rx; IVF., carbimazole 20mg 6-8hrly,
propanolol 40mg 4hrly, potassium iodide 5
drops 6hrly after carbimazole/PTU has been
started, dexameth 2mg 6hrly, antibiotics.

17. I0 Hypothyroidism
• Etiology of I0 Hypothyroidism
• Autoimmune causes;
– Atrophic hypothyroidism: autoantibodies
– Hashimoto’s thyroiditis: late middle age, firm
goitre formation
– Postpartum thyroiditis.

18. Causes of hypothyroidism
• Post surgical/irradiation
• Defects of hormone synthesis;
– Iodine deficiency
– Dyshormonogenesis ; Pendred’s syndrome
– Antithyroid medications
– Other drugs- amiodarone,lithium
• Post surgical/irradiation
– Thyroidectomy
– Radioiodine therapy

19. Clinical features
• Tiredness
• Weight gain
• Cold intolerance
• Dry brittle hair
• Depression
• Poor memory
• Constipation

20. Clinical features
• Signs;
• Mental slowness
• Hypertension hypothermia
• Bradycardia
• Oedema
• Poverty of movement

21. Investigation
• Serum TSH is elevated
• Low T4, low T3
• Thyroid Ab
• FBC-anaemia
• EUCr- low Na
• Fasting lipid-↑TG and chol.

22. Treatment
• Replacement therapy for life with L-thyroxine.
• Consider patient’s age, fitness and cardiovascular
status before commencement starting with low
dose and gradually uptitrating.
• Starting with as low as 25µg in px with ischaemic
heart disease, 100µg in fit individuals as single
dose daily.
• Combination of T3 and T4 may be used in
patients with poor response to T4 alone.

23. Borderline hypothyroidism
• Also called compensated euthyroidism.
• Occurs in the setting of surgery or iodine
radiation. Investigation most times reveal s
low-normal T4 and slightly elevated TSH.
• L- thyroxine is used if TSH is consistently above
10mU/L or ↑Ab levels or lipid abnormalities.

24. Myxoedema coma
• This is severe hypothyroidism. It is a medical
emergency. Tends to be more in elderly.
• Presents with; hypothermia,
hypoventilation,cardiac failure,
hyponatreamia, among others.
• RX;
• T3 orally or i.v. @ 2.5-5µg 8hourly, oxygen,
hydrocortisone 100mg i.v. 8hourly i.v. glucose
to prevent hypoglycaemia