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Hypothyroidism – A clinical state 
due to underproduction 
of thyroid hormones .PRIMARY HYPO-
( > 95 % )

TSH high
T3 low or normal
T4 low

. Problem is in the gland – ie gland failure due to
♦ damage
♦ inhibition
♦ removal of gland itself. Iodine deficiency- worldwide commonest cause. Autoimmune thyroiditis- most common cause- Hashimoto thyroiditis Atrophic thyroiditis 
( Primary Myxoedema ) May happen with or without goitre Atrophic autoimmune thyroiditis . Post-ablative therapy or surgery- Thyroidoectomy Radioactive Iodine External radiotherapy. drugs – Anti-thyroid drugs- about 15 % people will develop hypothyroidism 10-20 yrs after treatment
♦ Carbimazole
♦ Propylthiouracil Amiodarone Lithium Interferons Thalidomide Rifampicin. Transient 
thyroiditis-  Subacute thyroiditis 
( de Quervain’s ) Postpartum thyroiditis- within 6/12 post partum. Infiltration Thyroid hypoplasia /agenesis – Tumour , amyloidosis , sarcoidosis , haemochromatosis , TB and scleroderma. Congenital -Absence or underdevelopment of the thyroid gland , ectopic hypoplastic gland or enzyme defect

Overt-TSH above normal reference range
♦ usually above 10
♦ FT4 is below the normal reference range May not be symptomatic In Pregnancy- TSH > 10 is overt hypothyroidism
 regardless of T4

Subclinical- Raised TSH but FT4 and FT3 normal Clinical features of hypothyroidism usually absent , but if present -related to degree of TSH elevation TPO antibodies help define the risk of developing overt hypothyroidism Repeat test in 3-6 mts time ( exclude transient causes of ↑ in TSH )

( < 5 % ) 

Low T4
TSH low / normal or slightly raised. Pituitary- Pituitary dysfunction- Tumours ( adenoma ) Surgery , radiotherapy or trauma Infarction Sheehan’s synd Infiltrative disorders Isolated TSH deficiency or inactivity

Hypothamamic dysfunction
Often also mentioned as tertiary hypothyroidism in literature Tumours ( eg glioma ) Surgery , radiotherapy or trauma Infiltrative disorders Idiopathic hypothalamic dis Drugs ( eg retinoids )

How common- Prevalence 1-2 % in the UK More common in women ( up to 10 times ) One of the most common chronic disorders Secondary hypothyroidism is rare A major cause of 1 ary hypothyroidism in the developing world is Iodine deficiency Primary hypothyroidism – management is straightforward → mostly done in primary care with thyroxine replacement

See chart for presentation Symptoms may be vague subtle and non-specific – reputation as mimicker Progressive fatigue and malaise Myalgia arthlagias and paraesthesias Symptoms may be insidious developing over yrs Elderly may be asymptomatic

Myxedema coma -also known as myxedema is the rare but deadly manifestation of severe hypothyroidism high mortality rate presents with hypothermia ( as low as 23° ), coma and seizures

Risk factors- Iodine deficiency Family h/o thyroid or autoimmune disorders Middle age Female sex ↑ common in whites compared to other races and ethnicities Pre-existing other autoimmune illnesses as type 1 diabetes
rheumatoid arthritis
multiple sclerosis
Coeliac disease
Addison’s disease
pernicious anaemia
vitiligo Previous treatment with radioactive iodine or radiation to upper neck/ chest H/O thyroid surgery Down’s and Turner’s syndrome Bi-polar disorder Primary pulmonary hypertension Amiodarone use Lithium use

Complications – Dyslipidemia CAD and stroke Heart failure Impaired fertility Pregnancy- miscarriage , anaemia , pre-eclampsia , placental abruption , PPH , stillbirth Adverse neo-natal outcomes

Clinical symptoms – Slow , dry haired ,thick skinned , deep voiced patient with weight gain , cold intolerance , bradycardia and constipation
( classical presentation ) Diffuse hair loss from scalp and eyebrows Most cases present with non-specific symptoms Poor memory or general intellectual deterioration Usually picked up on biochemical testing Delayed relaxation phase of Achilles’s jerk

Investigations – Dyslipidemia- improves with treatment FBC- mild normocytic anaemia Fasting blood glucose may be elevated Muscle enzymes e.g CK may be elevated Consider cortisol 
(exclude co-existent Addison’s disease ) Hyponatraemia in severe cases Thyroid antibodies – antithyroid peroxidase antibodies elevated in 90 % of patients with autoimmune thyroiditis ECG- bradycardia , low voltage complexes

Treatment -All symptomatic patients with Primary hypothyroidism-Levothyroxine – synthetic compound
 identical to T4 converted to T3 in extrathyroidal tissue 1/2 life of 7 days Single dose 1/2 an hr to an hr before breakfast-Cause of hypothyroidism Age of the patient Co-existing heart disease Usual dose to achieve full replacement is between 100 µg to 150 µg

TSH level is used to assess response
( other than people with pituitary disease ) It take atleast 2 months ( 6-8 weeks ) for the pituitary-thyroid axis to re-set after introducing treatment or a dose adjustment Aim of the treatment is to 
◘ make the patient feel better
◘ normalise serum TSH
◘ avoid over-treatment

Referral –Age less than 16 Pregnant or post-partum Subacute thyroiditis Goitre , Nodule or structural change in thyroid gland Suspected of having associated endocrine disease
♦ Do not start thyroxine replacement if suspected adrenal 
failure → can precipitate adrenal crisis Newborn infant Particular management problems 
♦ IHD or pre-existing cardiac disease
♦ Treatment with amiodarone or Lithium
♦ adverse effects from treatment -If worse after starting Rx → suspect Addison’s disease Female and planning pregnancy Atypical or misleading thyroid functions Persistently raised TSH despite adequate treatment after excluding
♦ poor adherence
♦ drug interactions
♦ malabsorption Persistent symptoms despite treatment e ,g > 200 µcg of treatment and compliant with treatment. 

References CKS NHS hypothyroidism BMJ Best practice Hypothyroidism Clinical Review Management of hypothyroidism in adults BMJ 2008 ; 337 ;a801 Hypothyroidism – Causes , Killers and Life-Saving Treatments Sarah B Dubbs MS et al Emerg Med Clin N Am 32 ( 2014 ) 3030-317 Management of Hypothyroidism in Adults Nikhil Tandon Supplement to JAPI January 2011 Vol 59 Clinical Examination E-Book – Owen Epstein Kumar and Clark’s Clinical Medicine Abnormal TFT Results NHS Guidance Camden Clinical Commissioning 

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