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Hyperthyroidism
This document discusses hyperthyroidism, its causes, clinical manifestations, diagnosis, and treatment. The main causes discussed are Graves' disease, toxic multinodular goiter, and toxic adenomas. Graves' disease is an autoimmune disorder causing thyroid infiltration. Clinical manifestations include symptoms of hyperthyroidism as well as signs specific to Graves' such as ophthalmopathy. Diagnosis involves thyroid hormone blood tests. Treatment options include antithyroid medications, radioactive iodine therapy, and subtotal thyroidectomy. Congenital hyperthyroidism can occur when mothers pass antibodies to their infants and requires similar treatments.
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Hyperthyroidism
- 1. HYPERTHYROIDISM Soumya Ranjan Parida BasicB.Sc. Nursing 4th year Sum Nursing College
- 2. Hyperthyroidism Etiology :- • Diffusetoxic goiter (Graves disease ) • Mc Cune Albright syndrome • Toxic uninodular goiter (Plummer disease ) • Hyper functioning thyroid Ca • Thyrotoxicosis factitia • Subacute thyroiditis • Acute suppurative thyroiditis
- 3. Graves disease • Incidence:- It occurs in 1: 5000 children. Peak at 11 – 15 years. F :M 5 :1 • Etiology :- Infiltration of thyroid gland with lymphocytes & plasma cells. CD4/Th- predominate in dense lymphoid aggrgate. CD8/Ts - predominate in low dense area.
- 4. Etiology Activated beta lymphocytes,infiltrating the thyroid is higher than in peripheral blood. CD4/Th activated beta cells Plasma cells TRSAb / TRBAb TSH receptor cAmp
- 5. Etiology Ophthalmopathy :- Ab againstthyroid & eye muscle Ag TSH receptor Eye muscle & orbital fibroblast Glycosaminoglycans Cytotoxic effects
- 6. Clinical manifestations Manifestations ofhyperthyroidism :- Symptoms – • Hyperactivity, irritability, • Altered mood, insomnia • Heat intolerance, increased sweating • Palpitations • Fatigue, weakness • Dyspnea • Weight loss with increased appetite • Pruritus • Increased stool frequency • Thirst & polyuria • Amenorrhea, loss of libido
- 7. Clinical manifestations Manifestations ofhyperthyroidism :- Signs- • Sinus tacycardia • Atrial fibrillation • High output heart failure • Fine tremor, hyperkinesis • Hyperreflexia • Warm, moist skin • Pamer erythema, onycholysis • Hair loss • Muscle weakness & wasting • Chorea, periodic paralysis
- 8. Clinical manifestations Manifestations ofGraves disease :- • Diffuse goiter • Ophthalmopathy – • Dalrymples sign • Von Graefe’s sign • Enroth’s sign • Gifford’s sign • Stellwag’s sign
- 9. Clinical manifestations Manifestations ofGraves disease :- • Conjunctival sign • Pupillary sign • Ocular mobility defects • Exophthalmos • Exposure keratitis • Optic neuropathy • Localised dermopathy • Lymphoid hyperplasia • Thyroid acropachy
- 10. Diagnosis Lab findings :- Hyperthyroidism– T3, T4, TG ed ; TSH ed Increased TBG levels – T4 ed, T3 N - ed, FT4,TSH - N Familial dysalbuminemic hyperthyroxinemia – T4 ed, T3 N - ed, FT3,FT4,TSH - N Functional thyroid nodule – T3 - ed,
- 11. Diagnosis Thyroid hormone unresponsiveness– T4, T3, FT4, FT3 ed ; TSH N - ed Pit unresponsiveness toThyroid hormone - TSH N- ed TSH secreting pit tumor – TSH ed alfa chain Exogenous T4 – FT4 ed, TSH ed, TG ed
- 12. Treatment Drugs :- 1. Propylthiouracil- ( PTU ) • Dose to dose less potent. • Highly plasma protein bound. • Less transferred across placenta, milk • Plasma T ½ is 1- 2 hour • Single dose acts for 4-8 hour • No active metabolite • Multiple doses • Inhibit peripheral T4 T3
- 13. Treatment 2. Carbimazole – •3 times more potent • Less bound to plasms proteins • Large amount transferred across placenta • Plasma T ½ is 6 – 8 hour • Acts for 12 - 24 hour • Methimazole is active metabolite • Single dose • Does not inhibit peripheral T4 T3
- 14. Treatment Dose :- • Propylthiouracil- ( PTU ) 5 - 10 mg/kg/day TDS orally • Methimazole – 0.25 – 1.0 mg/kg/day OD orally • Propranolol – 0.5 – 2 mg/kg/day TDS orally Clinical response in 2–3 weeks Adequate control in 1–3 months Duration – 5 years
- 15. Treatment • Subtotal thyroidectomy– ATD is given for 2-3 mo to obtain euthyroid state. 5 drops of saturated solution of KI dailyfor 2 wk • Radioiodine – Safe in more than 10 years age Pretreatment with ATD not necessary ATD should be stopped a week before starting RI Propranolol & low dose ATD for 2-3 mo
- 16. Side effects ATD – Transientleukopenia Transient urticarial rash Hypersensitivity Agranulocytosis Hepatitis Lupus like syndrome Glomerulonephritis vasculitis
- 17. Side effects • Subtotalthyroidectomy – Paralysis of vocal cord Hypoparathyroidism • Radioiodine – Benign adenoma ( 0.6-1.9 % ) Hypothyroidism ( 10-20 % )
- 18. Congenital hyperthyroidism Etiology :– • Transplacental passage of TRSAb • 2 % of infants are born to mothers with graves disease • M : F - 1 : 1 Clinical features : - • PT /IUGR with goiter • Restless, irritable, • Hyperactive,anxious • Microcephaly with ventricular enlargement • Eyes widely open, exophthalmos
- 19. Congenital hyperthyroidism • Tachycardia, •Tachypnea, • Hyperthermia • Weight loss despite revenous appetite • Jaundice, • HSM • Cardiac decompensation, • HT • Advanced bone age, • Frontal bossing with triangular facies, • Craniosynostosis
- 20. Treatment Drugs :- • Propranolol– 1 – 2 mg/kg/day TDS orally • PTU – 5 – 10 mg/kg/day TDS orally • Lugol solution – 1 drop every 8 hr Digitalization Most cases remit in 3–4 mo
- 21.