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  • 1. NES Pharmacy CPD: Thyroid SpR in Endocrinology Glasgow Royal Infirmary February 2010 Amended by NES 2010 Developed and delivered by Dr James Boyle
  • 2. Glands and Hormones
    • Endocrine Glands: Glands that secrete their products (hormones) directly into the bloodstream rather than through a duct
    • Hormone: Chemical substance formed in the body that is carried in the bloodstream to affect another part of the body.
  • 3. Thyroid gland
    • Secrets two iodinated hormones T3 and T4.
    • Responsible for optimal growth, development and function of body tissues.
    • The synthesis of T3 and T4 requires iodine.
    • Release of T3 and T4 controlled by negative feedback.
  • 4. TRH/TSH Feedback Loop
  • 5. TRH
    • Thyrotrophin releasing hormone.
    • Tripeptide produced by hypothalamus.
    • Release is pulsatile.
    • Downregulated by T 3.
    • Travels through portal venous system to adenohypophysis.
    • Stimulates TSH synthesis and release.
  • 6. TSH
    • Thyroid stimulating hormone.
    • Produced by the pituitary gland
    • Upregulated by TRH
    • Downregulated by T 4 , T 3
    • Travels through portal venous system to cavernous sinus and body.
    • Stimulates several processes synthesis and release of hormones from the gland as well as gland growth
  • 7. Thyroid hormones (T4, T3)
    • T3/T4 enter circulation transported to plasma proteins (99%).
    • Thyroid only contributes 20% of the free circulating T3 with the rest produced by peripheral conversion of T4 to T3. T4 may be deiodinated to inactive reverse T3.
    • Regulation is based on the free component of thyroid hormone.
    • Action not understood but thought to involve high affinity binding sites in plasma membrane, mitochondria and nucleus resulting in protein synthesis and increased energy metabolism.
  • 8. Common diagnostic tools
    • TSH
    • Free T 3 ,
    • Free T 4
    • Thyroid autoantiboides
    • Thyroid ultrasound
    • Radio-isotope uptake and scan
    • Fine need aspiration of thyroid
  • 9. Hypothyroidism
    • Clinical syndrome that results in deficiency of the thyroid hormones T4 and T3.
    • Common, prevalence 1-2%
    • F:M preponderance of 10:1
    • Congenital hypothyroidism is 1:4000 live births in the UK.
  • 10. Types of hypothyroidism
    • Primary – Thyroid gland failure
    • Secondary – Pituitary failure
    • Tertiary – Hypothalamic failure
    • Sub-clinical
  • 11. Aetiology of hypothyroidism
    • Agenesis
    • Thyroid destruction
      • Hashimoto’s thyroiditis
      • Surgery
      • Radio-iodine ablation
      • Infiltration (tumour, sarcoidosis)
    • Inhibition of function
      • Iodine deficiency
      • Anti-thyroid medications (Carbimazole, PTU, lithium, amiodarone)
      • Inherited defects
    • Transient
      • Postpartum
      • Sub-acute thyroiditis
    • Secondary/Tertiary (pituitary, hypothalamic)
  • 12. Subclinical hypothyroidism
    • Estimated to affect 10% of females > 50yrs
    • Normal FT4/FT3, mildly elevated TSH
    • Few report symptoms
    • High risk of developing primary hypothyroidism
    • Can be associated with dyslipidaemia and subtle cardiac abnormalities.
    • Management a matter of clinical judgement
  • 13. Clinical Presentation
    • Symptoms – Tiredness, cold intolerance, weight gain, constipation, aches and pains, depression, psychosis, angina and menorrhagia.
    • Signs – Hair loss, hoarseness, goitre, bradycardia, dry skin, slow relaxing reflexes, anaemia, heart failure, effusions, carpal tunnel syndrome, mxyoedema coma.
  • 14. Diagnosis of hypothyroidism
    • Primary – Low FT4/FT3 and high TSH
    • Secondary – Low FT4/FT3 and low TSH
    • Tertiary – Low FT4/FT3 and low TSH
    • Sub-clinical – Normal FT4/FT3 and slightly high TSH
  • 15. Management
    • Apart from subacute and postpartum thyroiditis most require long term replacement in form of Levothyroxine.
    • Starting dose usually 50 -100mcg/daily.
    • Increased in steps of 25-50mcg every 4-6 weeks until FT4 is above middle of normal range and TSH normal/low normal.
    • Usual maintenance is 100mcg-200mcg/daily.
    • Suppressed TSH acceptable in certain cases
  • 16. Management
    • In cardiac disease cautious replacement is required to decompensation ie. Thyroxine 25mcg with steps of 25mcg only.
    • In secondary/tertiary cases ensure good adrenal reserve before commencing thyroxine replacement and dont use TSH to assess response.
    • In pregnancy requirements go up 50-100% and more monitoring is required. Use TSH to monitor at least every trimester.
  • 17. Management of subclinical cases
    • If TSH>10 – treat with thyroxine
    • If TSH 4-10 and asymptomatic – rpt TFT 6/12
    • If TSH 4-10 and symptomatic or antibodies +ve or dyslipidaemia or history or radioiodine or surgery – treat with thyroxine
  • 18. Nurse Led Management
    • Patients often managed in nurse led clinics using questionnaire/algorithms.
    • Once patients with primary hypothyroidism are stable for 6 months (12 months for post radioiodine) they are discharged to GP for annual check.
    • Majority of patients unlikely to need to change dose of levothyroxine in the community.
  • 19.  
  • 20. Hyperthyroidism
    • Clinical syndrome associated with raised levels of the thyroid hormones T4 and/or T3.
    • Can be increased production, release from damaged gland or exogenous T4.
    • Prevalence 1-2%
    • Incidence 3 per 1000 per year
    • Secondary hyperthyroidism due to increased TSH secretion is very rare (>1% of all cases) Common, prevalence 1-2%
  • 21. Aetiology of hyperthyroidism
    • Grave’s disease
    • Toxic multinodular goitre
    • Toxic adenoma
    • Thyroiditis (sub-acute, postpartum)
    • Drug induced (amiodarone)
    • Over treatment of T4
    • TSH secreting adenoma
  • 22. Clinical Presentation
    • Symptoms – Heat intolerance, weight loss, loose motions, tremor, increased appetite, amenorrhoea, fatigue, anxiety, itch, angina.
    • Signs – Goitre, tachycardia, AF, tremor, warm hands, proximal myopathy, lid lag/retraction, Grave’s opthalmopathy, cardiac failure, hypertension, onycholysis, acropachy, pretibial myxoedema, thyroid storm .
  • 23. Diagnosis of thyrotoxicosis
    • Primary – High FT4 and/or FT3 and low TSH
    • Secondary – High FT4 and/or FT3 and high TSH
    • Sub-clinical – Normal FT4/FT3 and low TSH
  • 24. Grave’s disease versus Toxic MNG
    • Grave’s Disease
    • Female>male
    • Peak age 20-40 years
    • Diffuse and smooth
    • Lid lag and retraction, Grave’s eye signs, pretibial mxyoedma
    • Acropachy, onycholysis
    • Autoantibodies usually present
    • RAU scan uniform increased uptake
    • Multinodular Goitre
    • Female>male
    • Peak age >50 years
    • Multinodular goitre
    • Lid lag and retraction
    • No skin, nail or finger changes
    • Autoantibodies usually absent
    • RAU patchy, irregular appearance
  • 25. Management
    • Carbimazole 20-40mg daily to render euthyroid (alternatively PTU).
    • Propanolol 40mg bd/tds to control symptoms in the short term.
    • Dose titration or “block and replace” regimen depending on individual practice.
    • Decision of definitive therapy needs to be made.
  • 26. Drugs
    • Carbimazole: Inhibits hormone production, side effects include rash and agranulocytosis (0.1%).
    • Propythiouracil: Inhibits hormone production as well as blocking T4 to T3 conversion, side effects include rash and agranulocytosis (0.4%).
  • 27. Pregnancy and lactation
    • Increased risk of fetal and neonatal thyrotoxicosis.
    • PTU preferred to Carbimazole due to less found in breast milk and less crossing placenta.
    • Carbimazole has been associated with aplasia cutis.
    • Requirements fall in Grave’s.
    • Lowest dose possible should be used.
    • Radio-iodine contra-indicated during pregnancy
    • TSH receptor titres should be determined early in third trimester to assess risk of neonatal thyroid dysfunction.
  • 28. Management
    • In Grave’s disease option to treat with drugs for 18 months and stop (50% chance of remission). Can also opt for radioiodine or surgery.
    • In toxic multinodular goitre/toxic adenoma need to use radioiodine or surgery to cure. Small number opt for long term drug therapy.
  • 29. Radio-iodine therapy
    • 131 I is a safe and effective means of treatment.
    • Emits locally destructive beta particles to lead to cell damage and death over months.
    • Render euthyroid with drugs first and stop before to allow uptake of isotope.
    • In Glasgow, antithyroid drugs are not restarted afterwards unless thyrotoxicosis confirmed.
    • High risk of subsequent hypothyroidism.
  • 30. Nurse Led Management
    • Patients often managed in nurse led clinics using questionnaire/algorithms.
    • Very few if any patients discharged to GP on anti-thyroid drugs
    • Nurse led management appropriate if diagnosis made, decision of definitive therapy made and no complications.
    • Majority of patients unlikely to need to change dose of anti-thyroid drug in the long term.
  • 31.  
  • 32.  
  • 33. Pharmaceutical Care Issues – Hypothyroidism (examples)
    • Monitoring for signs & symptoms for dosage
      • Compliance can be a problem
    • Advise on treatment increments
    • Slow dose increments in heart disease
    • Anaemia can be associated with hypothyroid
      • Macrocytic mild anaemia (responds to thyroxine)
      • Pernicious anaemia common (treatment)
  • 34. Pharmaceutical Care Issues – Hyperthyroidism (examples)
    • Explain dosage regime for carbimazole
    • Monitor for side-effects of carbimazole
      • skin rashes, sore throat or mouth ulcers
    • Monitor for side-effects of beta blockers
    • Block & replace – also on thyroxine
    • Eye grittiness ->hypromellose eyedrops