Thyroid Flashcards
Blood supply to thyroid
Branches of superior cerebellar artery + common carotid into the superior and inferior thyroid arteries
Thyroid drainage
Superior + middle thyroid veins –> IJV
Inferior thyroid vein –> brachiocephalic vein
Follicular cells
Produce T3 and T4
Parafollicular cells
Produce calcitonin
Circulating thyroid hormones
T3 and T4 bound by TBG
Increased TBG conditions
Pregnancy
–> oestrogen inhibits hepatic breakdown
Decreased TBG conditions
liver failure
Increased TBG
More T3/4 will be bound, less T3/4 will be free
In pregnancy, even though increased TBG, normal free T3/4 as the T3/4 is also increased
Thyroid hormone potency
T3 more potent
T4–>T3
Increased in obesity
Decreased in pregnancy, fasting, stress, hepatic failure, renal failure, beta blockers
Thyroid hormone control
Hypothalamus –> TRH –> Pituitary –> TSH –> Thyroid –> T3+T4
TSH effect
Increases T4/3
Hypertrophy and hyperplasia of thyroid follicular cells
Increased blood flow to thyroid
T3/4 on BMR
Increased Na/K ATPase activity to increase O2 production and heat
T3/4 on Metabolism
Increased glucose uptake and absorption Increased glycogenolysis Increased gluconeogenesis Increased insulin Increased FA oxidation Decreased cholesterol in plasma Decreased muscle mass
T3/4 on Cardiorespiratory
Increased HR and CO
Increased vasodilation
Increased ventilation
T3/4 on CNS
Increased SNS activity
Affects mental state- hyper, anxious, nervous
T3/4 on skeletal
Increases growth plate chondrocytes + osteoblasts
Increased osteoclast activity (in thyrotoxicosis –> osteoporosis)
T3/4 on reproductive
Thickens endometrium in females
Hypothyroidism associated with infertility
T3/4 on development
Potentiates growth
Potentiates foetal and neonatal brain development
Hypothyroidism
Increased TSH
Decreased T4
Treated hypothyroidism or subclinical hypothyroidism
Increased TSH
Normal/variable T4
TSH secreting tumour or thyroid hormone resistance
Increased TSH
Increased T4
Slow conversion T4–>T3 or thyroid hormone antibody artefact
Low TSH
High T4
Low T3
Hyperthyroidism
Low TSH
Increased T4 or T3
Subclinical hyperthyroidism
Decreased TSH
Normal/variable T4 + T3
Central hypothyroidism
Low TSH
Low T4
Sick euthyroidism or pituitary disease
Low TSH
Low T4 and low T3
Consider changes in TBG, assay interference, amiodarone or pituitary TSH tumour
Variable TSH
Abnormal T4
Thyrotoxicosis
Clinical, physiological + biochemical effects that result from exposure to tissues to excess thyroid hormones
Thyrotoxicosis associated with hyperthyroidism
Excessive thyroid stimulation
Thyroid nodules
Excessive thyroid stimulation
Graves Hashitoxicosis Pituitary TSHoma Trophoblastic disease Germ cell tumours (increased hCG --> thyrotrophic activity) Pituitary thyroid hormone resistance
Thyroid nodules
Autonomous secretion by either toxic solitary nodules or multinodular goitre
Thyrotoxicosis NOT associated with hyperthyroidism
Thyroiditis- drug induced (amiodarone), silent De Quervain’s (tender goiter exclusively), subacute (post-partum), radiation induced
Exogenous thyroid hormones
Ectopic thyroid tissue
Thyrotoxicosis symptoms
Diarrhoea Weight loss Increased appetite Restlessness Sweats Heat intolerance Palpations Tremor Irritability Labile emotions Oligomenorrhoea +/- infertility Loss of libido
Thyrotoxicosis Signs
Fast/irregular pulse Warm moist skin Fine tremor Palmar erythema Thin hair Lid lag Lid retraction Goitre or thyroid nodules Thyroid bruits
Grave’s
Most common cause of hyperthyroidism
Triggered by stress, infection and childbirth
Women 40-60 (mainly)
IgG antibodies that bind to and activate TSH receptors, causing smooth thyroid enlargement + thyroid hormone production
Associated with other autoimmune- vitiligo, T1DM, Addison’s
Patients often hyperthyroid but may be or become hypo or euthyroid
Grave’s Ophthalmopathy
25-50%
Auto-antibody cross- reaction with orbital autoantigens
Grave’s Op symptoms
Eye discomfort Grittiness Increased tear production Photophobia Diplopia Decreased acuity and colour vision
Grave’s Op signs
Exophthalmos Proptosis Ophthalmoplegia Afferent pupillary defect- sign of optic nerve compression Conjunctival oedema Corneal ulceration Papilloedema
Grave’s Op RFs
Smoking
Radioiodine therapy
Grave’s Op Management
Treat underlying cause
Mild- artificial tears, elevation of head at night, sunglasses, avoid dust
Severe- steroids, surgical decompression
Grave’s Dermopathy
Pretibial myxoedema- oedematous swelling above lateral malleoli
Thyroid acropachy- extreme manifestation with clubbing, painful finger and toe swelling, and periosteal reaction in limb bones
Toxic adenoma
Solitary focal, diffuse hyperplasia of follicular cells
Secrete thyroid hormones
Toxic multinodular goitre
Most common cause of thyrotoxicosis in iodine-deficient areas
Also seen in elderly patients
Nodules secrete excess thyroid hormones
Thyroiditis
Hormone synthesis is not increased but there is destruction of thyroid follicular cells, resulting in transient increase in thyroid hormones- once exhausted the patient becomes hypothyroid e.g. Hashimoto
Thyroid cysts
Benign solitary nodule that creates pressure symptoms
May be painful if it bleeds- aspirate or exercise
Hyperthyroidism in pregnancy
Increase in circulating thyroid hormones May trigger grave's 1st half of pregnancy- aggravated 2nd half- ameliorated Postpartum- recurrence
Subclinical hyperthyroidism
Normal T3 + $ Suppressed TSH Increases risk of AG Endogenous causes- toxic adenoma, multinodular goitre Exogenous causes- levothyroxine
Thyroid hormone resistance
Mutation in receptor at pituitary gland
Rise in T3 and T4 fails to suppress TSH
DDHx TSHoma
Medical management Thyrotoxicosis
Beta blockers (control of symptoms)
Carbimazole
Propylthiouracil
Carbimazole- two regimes
Titration- 20-40mg/24hr PO for 4 weeks, reduce according to TFTs every 1-2 months
Block-replace: give carbimazole + levothyroxine simultaneously
Carbimazole side effects
Agranulocytosis
Propylthiouracil
1st trimester of pregnancy
Thyroid storm
Carbimazole CI
Radioactive iodine- thyrotoxicosis
Used for MNG, toxic adenoma, carbimazole-relapsed Graces
CIs- pregnancy, lactation, Graves ophthalmopathy
SEs- hypothyroidism
Thyroidectomy- thyrotoxicosis
Indications- suspected malignancy, compressive symptoms
Complications- recurrent laryngeal nerve damage, hypoparathyroidism, local haemorrhage
Thyrotoxicosis Complications
HF Angina AF Osteoporosis Ophthalmology Gynaecomastia Thyroid storm
Thyroid Storm
Life-threatening health condition that is associated with untreated or undertreated hyperthyroidism. During thyroid storm, an individual’s heart rate, blood pressure, and body temperature can soar to dangerously high levels
Thyroid storm presentation
Severe hyperthyroidism Fever Agitation Confusion Coma Tachycardia AF D+V Goitre Thyroid bruit Acute abdomen HF
Thyroid storm diagnosis
Do TFTs
Don’t wait for test results if urgent treatment needed
Thyroid storm Treatment Aim
1) Counteract peripheral effects of thyroid hormones
2) Inhibit thyroid hormone synthesis
3) Treat systemic complications
Thyroid storm treatment
IV access, fluids, NG tube if vomiting
Take blood for TSH, T3, 4 cultures
Sedate if necessary, monitor BP
Propanolol 60mg/4-6h PO, only if normal CO and no CI
–> if asthma/decreased CO, can cause cardiac arrest
High dose digoxin to slow heart
Anti-thyroid drugs- carbimazole 15-25mg/6h PO + after 4h give Lugol’s (iodine) solution 0.3ml/8h PO to block thyroid
Hydrocortisone 100mg/6h IV or Dexamethasone 15-25mg/6h PO
Treat infection if suspected
Adjust IV fluids
