Thyroid Flashcards
Thyroid hormones pathway
TRH from hypothalamus stimulates anterior pituitary
Anterior pituitary produces TSH
TSH stimulates T3 and T4 (5x less active), majority produced is T4 as 85% of T3 production is from peripheral T4 conversion
Majority of T4 and T3 bound to thyroxine-binding globulin
Unbound T3 + T4 are active forms, inc cell metabolism + catecholamine effects via nuclear receptors
Factors increasing TBG (and therefore total T3+T4)
Pregnancy
Oestrogen therapy (HRT, oral contraceptives)
Hepatitis
Factors decreasing TBG
Nephrotic syndrome Malnutrition Drugs (Androgens, corticosteroids, phenytoin) Chronic liver disease Acromegaly
Hyperthyroidism test results
Increased T4, only ~1% have increased T3
Decreased TSH, unless rare TSH-secreting pituitary adenoma
Hypothyroidism test results
Ask only for T4 and TSH, T3 adds nothing
TSH varies through day, trough at 2pm and 30% higher during darkness so test at same time
TFTs in systemic disease
Euthyroid but everything low
What is assay interference in TFTs
Abs in serum interfering with test
What is thyroid autoantibody test
Anti-thyroid peroxidase (TPO) increased in Hashimoto’s/ Graves
What TSH receptor antibody test
May be increased in Graves, useful in pregnancy
What is serum thyroglobulin test used for
Monitoring treatment of carcinoma
Detection of self-medicated hyperthyroidism where it is low
What is thyroid US used for
Distinguishing cystic from solid nodules
If solitary/dominant large nodule in multinodal goitre, do fine-needle aspiration looking for thyroid cancer
Thyroid isotope scan use
123-Iodine often used
Useful for determining hyperthyroidism cause + detect retrosternal goitre/ ectopic thyroid tissue/ thyroid metastases (+ whole body CT)
If increased or neutral isotope uptake, unlikely to be malignant, if decreased then 20% chance of malignancy
Thyroid tissue surgery indications
Rapid growth Compression signs Dominant nodule on scintigraphy Nodule ≥3cm Hypo-echogenicity
Which pt to screen for thyroid abnormalities
AF
Hyperlipidaemia
DM (yearly)
Pts with Down’s, Turner’s or Addison’s (yearly)
Women with T1DM during 1st trimester and post delivery
Pts on amiodarone/ lithium 6mthly
What is thyrotoxicosis
Clinical effect of excess thyroid hormone
Thyrotoxicosis presentation
Diarrhoea, weight loss (if very high paradoxical gain in 10%), appetite inc
Over-active, sweats, heat intolerance
Palpitations, tremor, irritability
Fast pulse, moist warm skin
Thyrotoxicosis tests
Decreased TSH, inc T4/T3 May be mild normocytic anaemia + mild neutropenia Raised ESR, Ca and LFT Check thyroid autoAbs Isotope scan if cause unclear
Thyrotoxicosis causes
Graves' (2/3 of cases) Toxic multinodule goitre Toxic adenoma (solitary 'hot' nodule producing T3/4) Ectopic thyroid tissue Exogenous (iodine excess, levothyroxine excess) Subacute de Quervain's Amiodarone, lithium (hypo more common) Postpartum TB (rare)
Graves’ disease pathology
IgG stimulates thyrotropin receptors
Toxic multinodule goitre features
Seen in elderly/iodine deficient areas
Nodules secrete T3/4
Surgery if dysphagia/ dyspnoea
Ectopic thyroid tissue causes
Metastatic follicular thyroid cancer Struma ovarii (ovarian teratoma with thyroid tissue)
What is subacute de Quervain’s thyroiditis
Self-limiting post viral with painful goitre
Subacute de Quervain’s thyroiditis treatment
NSAIDs
Thyrotoxicosis drug treatment
Beta-blockers (propranolol 40mg/6h) for rapid control
Carbimazole 20-40mg/24h PO for 4wks, reduce according to TFTs every 1-2mths
OR Carbimazole + levothyroxine simultaneously
In Graves maintain for 12-18mths then withdraw, 50% relapse
If relapse then radioiodine or excision
Carbimazole SE
Agranulocytosis, can lead to dangerous sepsis
Warn pt to stop and get urgent FBC if infection signs
Thyrotoxicosis further treatment (drugs ineffective)
Radioactive 131-Iodine, most become hypothyroid post treatment, CI in pregnancy/ lactation
Thyroidectomy (usually total), pts become hypo post treatment again, risk of recurrent laryngeal damage + hypoparathyroidism
Thyrotoxicosis complications
Heart failure
Angina
AF
Osteoporosis
Gynaecomastia
Opthalmology
Thyroid storm
Eye problems in Graves
Exopthalmos (proptosis)
Eyelids retracted from iris exposing sclera
Diplopia (can be corrected with Fresnel prism in one lens of spectacle)
Thyroid eye problem treatment
Supportive and underlying cause
If severe, IV methylprednisolone (best) or prednisolone 100mg/day PO, decreasing according to symptoms
Surgical decompression if sight-threatening disease or cosmesis
Causes of goitre
Diffuse: Physiological Graves Hashimoto's Subacute de Quervain's (painful)
Nodular:
Multinodular goitre
Adenoma
Carcinoma
Hypothyroidism signs
BRADYCARDIC Reflexes relax slowly Ataxia Dry hair Yawning Cold hands Ascites ± non-pitting oedema Round puffy face Defeated demeanour Immobile ± ileus CCF
Hypothyroidism diagnosis
TSH ≥4mU/L (unless rare 2˚ hypothyroidism, then decreased) depending on pt
Decreased T4
Cholesterol + triglyceride increased
Macrocytosis (less common is normocytic anaemia)
Causes of 1˚ autoimmune hypothyroidism
Primary atrophic hypothyroidism - common, lymphocytic infiltration causes atrophy of thyroid so no goitre
Hashimoto’s - lymphocytic + plasma cell infiltration so goitre, very high Ab titre
1˚ non-autoimmune hypothyroidism causes
Iodine deficiency
Post-thyroidectomy/ radioiodine treatment
Drug-induced (anti-thyroid drugs, amiodarone, lithium, iodine)
Subacute thyroiditis - temp hypo after hyper phase
Hypothyroidism associations
Autoimmune disease (T1DM, Addison's, pernicious anaemia) Turner's, Down's, CF Genetic conditions (Pendred's if with deafness)
Hypothyroid pregnancy problems
Eclampsia Anaemia Prematurity/ dec birth weight Still birth Post-partum haemorrhage
Hypothyroid treatment
In healthy + young: levothyroxine (T4) 0-100mcg/24h PO, check TSH 6wkly until normal then yearly
Elderly/ischaemic heart disease: 25mcg/24h dose then inc 25mcg/4wks as needed
If diagnosis unsure stop T4 and check TSH in 6wks
Amiodarone thyroid problems
Can cause hypo as is iodine rich, iodine excess inhibits T4 release
Can cause thyrotoxicosis from a destructive thyroiditis
T1/2 of amiodarone is ~80d so symptoms continue after drug stopped
Myxoedema coma
Hypothyroid coma before death
Thyroid receptor processes influenced
Metabolism of substrates, vitamins, minerals
Modulation of all other hormones and target-tissue responses
Stimulation of O2 use and generation of metabolic heat
Protein synthesis + carb/lipid metabolism regulation
Stimulation of co-enzyme + related vitamin demand
Subclinical hypothyroidism clinical features
TSH>4mU/L with normal T4 and T3
No symptoms
Subclinical hypothyroidism management
Confirm raised TSH is persistent in 2-4mths
Recheck history and discuss treatment if non-specific effects affecting pt life
Treat if TSH≥10; +ve thyroid autoAbs; past Graves’; other organ-specific autoimmunity
Subclinical hyperthyroidism clinical features
Low TSH, normal T3 + T4
41% increase in relative mortality from all causes vs euthyroid
Subclinical hyperthyroidism management
Confirm suppressed TSH is persistent
Check for non-thyroid cause (pregnancy, pituitary/ hypothalamic insufficiency, TSH-suppressing medication (thyroxine, steroids))
If no symptoms, recheck 6mthly
Carbimazole or propylthiouracil if symptoms + TSH<0.1
