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NES Pharmacy CPD: Thyroid. Developed and delivered by Dr James Boyle. SpR in Endocrinology Glasgow Royal Infirmary February 2010 Amended by NES 2010. Glands and Hormones.

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nes pharmacy cpd thyroid

NES Pharmacy CPD: Thyroid

Developed and delivered by Dr James Boyle

SpR in Endocrinology

Glasgow Royal Infirmary

February 2010

Amended by NES 2010

glands and hormones
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
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.
  • 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.
  • Thyroid stimulating hormone.
  • Produced by the pituitary gland
  • Upregulated by TRH
  • Downregulated by T4, T3
  • 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
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
Common diagnostic tools
  • TSH
  • Free T3,
  • Free T4
  • Thyroid autoantiboides
  • Thyroid ultrasound
  • Radio-isotope uptake and scan
  • Fine need aspiration of thyroid
  • 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
Types of hypothyroidism
  • Primary – Thyroid gland failure
  • Secondary – Pituitary failure
  • Tertiary – Hypothalamic failure
  • Sub-clinical
aetiology of hypothyroidism
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
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
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
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
  • 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
  • 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
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
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.
  • 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
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 presentation1
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
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 versus Toxic MNG

Grave’s Disease

Multinodular Goitre


Peak age >50 years

Multinodular goitre

Lid lag and retraction

No skin, nail or finger changes

Autoantibodies usually absent

RAU patchy, irregular appearance

  • 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
  • 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.
  • 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
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.
  • 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
Radio-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.
nurse led management1
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
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
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