Presentation on theme: "NES Pharmacy CPD: Thyroid"— Presentation transcript:
1NES Pharmacy CPD: Thyroid Developed and delivered by Dr James BoyleSpR in EndocrinologyGlasgow Royal InfirmaryFebruary 2010Amended by NES 2010
2Glands and HormonesEndocrine Glands: Glands that secrete their products (hormones) directly into the bloodstream rather than through a ductHormone: Chemical substance formed in the body that is carried in the bloodstream to affect another part of the body.
3Thyroid 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.
5TRH Thyrotrophin releasing hormone. Tripeptide produced by hypothalamus.Release is pulsatile.Downregulated by T3.Travels through portal venous system to adenohypophysis.Stimulates TSH synthesis and release.
6TSH Thyroid stimulating hormone. Produced by the pituitary gland Upregulated by TRHDownregulated by T4, T3Travels 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
7Thyroid 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.
8Common diagnostic tools TSHFree T3,Free T4Thyroid autoantiboidesThyroid ultrasoundRadio-isotope uptake and scanFine need aspiration of thyroid
9HypothyroidismClinical syndrome that results in deficiency of the thyroid hormones T4 and T3.Common, prevalence 1-2%F:M preponderance of 10:1Congenital hypothyroidism is 1:4000 live births in the UK.
12Subclinical hypothyroidism Estimated to affect 10% of females > 50yrsNormal FT4/FT3, mildly elevated TSHFew report symptomsHigh risk of developing primary hypothyroidismCan be associated with dyslipidaemia and subtle cardiac abnormalities.Management a matter of clinical judgement
14Diagnosis of hypothyroidism Primary – Low FT4/FT3 and high TSHSecondary – Low FT4/FT3 and low TSHTertiary – Low FT4/FT3 and low TSHSub-clinical – Normal FT4/FT3 and slightly high TSH
15ManagementApart from subacute and postpartum thyroiditis most require long term replacement in form of Levothyroxine.Starting dose usually mcg/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
16ManagementIn 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 % and more monitoring is required. Use TSH to monitor at least every trimester.
17Management of subclinical cases If TSH>10 – treat with thyroxineIf TSH 4-10 and asymptomatic – rpt TFT 6/12If TSH 4-10 and symptomatic or antibodies +ve or dyslipidaemia or history or radioiodine or surgery – treat with thyroxine
18Nurse Led ManagementPatients 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.
20HyperthyroidismClinical 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 yearSecondary hyperthyroidism due to increased TSH secretion is very rare (>1% of all cases) Common, prevalence 1-2%
21Aetiology of hyperthyroidism Grave’s diseaseToxic multinodular goitreToxic adenomaThyroiditis (sub-acute, postpartum)Drug induced (amiodarone)Over treatment of T4TSH secreting adenoma
23Diagnosis of thyrotoxicosis Primary – High FT4 and/or FT3 and low TSHSecondary – High FT4 and/or FT3 and high TSHSub-clinical – Normal FT4/FT3 and low TSH
24Grave’s disease versus Toxic MNG Multinodular GoitreFemale>malePeak age yearsDiffuse and smoothLid lag and retraction, Grave’s eye signs, pretibial mxyoedmaAcropachy, onycholysisAutoantibodies usually presentRAU scan uniform increased uptakeFemale>malePeak age >50 yearsMultinodular goitreLid lag and retractionNo skin, nail or finger changesAutoantibodies usually absentRAU patchy, irregular appearance
25ManagementCarbimazole 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.
26DrugsCarbimazole: 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%).
27Pregnancy 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 pregnancyTSH receptor titres should be determined early in third trimester to assess risk of neonatal thyroid dysfunction.
28ManagementIn 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.
29Radio-iodine therapy 131I 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.
30Nurse Led ManagementPatients often managed in nurse led clinics using questionnaire/algorithms.Very few if any patients discharged to GP on anti-thyroid drugsNurse 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.
33Pharmaceutical Care Issues – Hypothyroidism (examples) Monitoring for signs & symptoms for dosageCompliance can be a problemAdvise on treatment incrementsSlow dose increments in heart diseaseAnaemia can be associated with hypothyroidMacrocytic mild anaemia (responds to thyroxine)Pernicious anaemia common (treatment)
34Pharmaceutical Care Issues – Hyperthyroidism (examples) Explain dosage regime for carbimazoleMonitor for side-effects of carbimazoleskin rashes, sore throat or mouth ulcersMonitor for side-effects of beta blockersBlock & replace – also on thyroxineEye grittiness ->hypromellose eyedrops