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    Course presentation[ Course presentation[ Presentation Transcript

    • NES Pharmacy CPD: Thyroid SpR in Endocrinology Glasgow Royal Infirmary February 2010 Amended by NES 2010 Developed and delivered by Dr James Boyle
    • 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.
    • 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.
    • TRH/TSH Feedback Loop
    • 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.
    • 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
    • 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.
    • Common diagnostic tools
      • TSH
      • Free T 3 ,
      • Free T 4
      • Thyroid autoantiboides
      • Thyroid ultrasound
      • Radio-isotope uptake and scan
      • Fine need aspiration of thyroid
    • 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.
    • Types of hypothyroidism
      • Primary – Thyroid gland failure
      • Secondary – Pituitary failure
      • Tertiary – Hypothalamic failure
      • Sub-clinical
    • 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)
    • 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
    • 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.
    • 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
    • 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
    • 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.
    • 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
    • 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.
    •  
    • 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%
    • 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
    • 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 .
    • 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
    • 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
    • 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.
    • 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%).
    • 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.
    • 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.
    • 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.
    • 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.
    •  
    •  
    • 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)
    • 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