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Medicine Year 2 > Endocrine Topic 6 - Thyroid Gland > Flashcards

Endocrine Topic 6 - Thyroid Gland Flashcards

1
Q

How is hyperthyroidism treated?

A
  • Thionamides - carbizamole, propylthiouracil
    • Carbizamole - drug of choice, absorbed well from gut, converted to methimazole via 1st pass metabolism, half life = 12-15 hours
    • Propylthiouracil - less active, shorter half-life, higher dose needed - 2nd line or in pregancy
  • Beta-blockers e.g. propanolol - reduces sympathetic symptoms, no hormonal effect
  • Potassium iodide - reduced TH released acutely
  • Radioactive iodine
  • Surgery - thyroidectomy (partial or total)
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2
Q

Describe the location of the thyroid gland

A
  • Anterior neck, C5-T1
  • Behind sternohyoid and sternothyroid muscle
  • Visceral compartment of neck (with trachea, oesophagus and pharynx) - bound by the pre-tracheal fascia
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3
Q

What are the risk factors for hypothyroidism?

A
  • Female
  • Age
  • Genetic predisposition (autoimmune)
  • Drugs e.g. lithium
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4
Q

What change occurs in the follicles when they become active?

A

Epithelial cells - Cuboidal/squamous to columnar when active

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5
Q

Describe the pathophysiology of autoimmune hypothyroidism

A
  • Infiltration of CD4+ and CD8+ T cells, autoantibodies blocking TSH receptor/attacking thyroid peroxidase/Tg
  • Progressive destruction of thyroid follicular tissue
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6
Q

How is thyroid hormone release stimulated?

A
  • Thyroid releasing hormone (TRH) secreted by hypothalamus, stimulates thyroid stimulating hormone (TSH) release from the anterior pituitary
  • TSH binds to G protein coupled receptor on follicular cells, activated cAMP and phospholipase C
  • cAMP mediates actions - increased Tg iodination, microvilli number and length, endocyotsis of colloid droplets, TH release, iodine influx, cellular metabolism, protein (including Tg) synthesis and DNA synthesis
  • Increases TH stores, within 1 hours increases TH release
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7
Q

Describe the innervation of the thyroid gland

A

Sympathetic trunk, doesn’t control hormone secretion

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8
Q

Why is propylthiouracil used to treat hyperthyroidism in pregnancy?

A

Carbimazole (usually drug of choice) has adverse effects on newborns - skin conditions

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9
Q

How is hyperthyroidism diagnosed?

A
  • Biochemical proof of suppressed TSH and high free thyroid hormone
  • Anti-TSH receptor/Tg/TPO antibodies
  • ESR - inflammation
  • Ultrasound - increased vascularisation of thyroid (Grave’s)
  • Radioactive iodine uptake test with PET scan
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10
Q

How is hypothyroidism treated?

A
  • Levothyroxine
  • 1.7-2.0 micro g/kg/day on empty stomach
  • Avoid taking with PPI, ferrous sulphate or calcium - chelate, won’t be absorbed (incomplete gastric absorption)
  • Start low in elderly/cardiac disease - increase HR quickly, could have ischaemic heart disease
  • Long half-life
  • Travels bound to protein, metabolised to triiodothyronine (T3)
  • Goal = normalise symptoms and TSH (normal level is disputed)
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11
Q

Describe the action of thyroid hormone

A
  • Nuclear receptors - cytosolic T3 transported to the nucleus, binds to thyroid receptors alpha and beta, proteins synthesised
  • T3 acts as ligan for TR - transcription factor, alters gene expression
  • Determinants of brain and somatic development (foetal)
  • Skeletal (increases in bone tumours), cardiovascular (increases HR), increases metabolic rate
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12
Q

What are the functional units of the thyroid gland?

A
  • Follicles - epithelial structures
    • Single layer of cuboidal epithelium with basement membrane, colloid in centre
    • Store thyroglobulin (iodinated glycoprotein) - storage form of T3/4
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13
Q

What are the risks for hyperthyroidism?

A
  • Autoimmune disease
  • Female
  • Pregnancy
  • Drugs e.g. amidarone
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14
Q

How does thyroglobulin become converted to active hormone?

A
  • Colloid enveloped by microvilli on cell surface (endocytosis) to form colloid vesicles within cells, fuse with lysosomes
  • Enzymes in lysosomes break down iodinated thyroglobulin, releasing T3/4
  • T3/4 pass across basal cell membrane into capillary (T4>T3)
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15
Q

What causes hypothyroidism?

A
  • Primary - high TSH, low T4
    • Autoimmune Hashimoto thyroiditis
    • Iodine deficiency
    • Drugs e.g. lithium
    • Congenital hypothyroidism
    • Post-radioactive iodine
    • Post-thyroiditis
  • Secondary - low TSH, low T4
    • Pituitary or hypothalamic disease
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16
Q

Define goitre

A

Swelling of the neck due to enlargement of the thyroid - hypothyroid, hyperthyroid or euthyroid with nodular disease

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17
Q

Describe dermopathy in Grave’s disease

A
  • Infiltrative dermopathy, waxy discoloured induration of the skin (peau d’orange)
  • Begins in feet/lower legs, spreads upwards in advanced cases
18
Q

Compare hypo- and hyperthyroidism

A
  • Hypothyroidism = low TH
    • More common and more difficult to treat
  • Hyperthyroidism = excess TH
19
Q

List the signs/symptoms of hypothyroidism

A
  • Weight gain
  • Depression
  • Lethargy
  • Constipation
  • Cold intolerance
  • Poor concentration
  • Hoarseness
  • Menorrhagia
  • Bradycardia
  • Dry skin
  • Coarse, thin hair
  • Anaemia
  • Slow relaxing reflexes
  • May have goitre
  • Pale, puffy face
  • Lose lateral 1/3 of eyebrows
20
Q

What causes hyperthyroidism?

A
  • Autoimmune - Grave’s disease
  • Toxic adenoma - benign hormone-producing tumour
  • Multinodular goitre
  • Thyroiditis (transient)
  • Excess administration of thyroxine (? weight loss) - high T4, low TSH
21
Q

How does radioactive iodine function to treat hyperthyroidism?

A
  • Destroys thyroid tissue by beta emission
  • May worsen eye disease
  • Defer conception (at least 4 months), pregnancy = contraindication
  • Hypothyrodism is main side effect - may be transient
22
Q

Describe the arterial supply of the thyroid gland

A
  • Superior and inferior thyroid artery (left and right)
    • Superior is 1st branch of external carotid - supplies superior and anterior parts
    • Inferior is branch of thyrocervical trunk, from subclavian artery - supplies posterior and inferior parts
23
Q

Describe the mechanism of action of thionamides

A
  • Reduce TH synthesis
    • Inhibit iodide oxidation (inhibit thyroid perioxidase)
    • Inhibit iodination of tyrosine
    • Inhibit coupling of DI/MIT
  • Slow effect
  • Propylthiouracil - reduces conversion of T4 to T3, reduces action of T3 acutely
24
Q

What causes Hashimoto’s thyroiditis?

A
  • Autoantibodies against thyroid perioxidase, thyroglobulin and TSH
  • Activation of CD8+ T cells in response to cell mediated immune response affected by CD4+ T cells - thyrocyte destruction
  • Type 4 hypersensitivity
25
Q

Describe the venous drainage of the thyroid gland

A
  • Superior, middle and inferior thyroid veins - form venous plexus
  • Supeior and middle drain to internal jugular vein
  • Inferior drains to brachiocephalic vein
26
Q

How is hypothyroidism diagnosed?

A

Measure - free T4, TSH, thyroid autoantibodies

27
Q

Describe circulating thyroid hormone

A
  • Free 0.5%, bound 99.5%
    • Free is active and regulated
    • Bound is bound to thyroid binding globulin, transthyretin and albumin
  • T4 converted to T3 by deiodination from outer ring in periphery
    • Catalysed by selenodiodinase enzymes (D1 in liver, kidney, muscle, D2 in brain, pituitary)
28
Q

What is Grave’s disease?

A

Autoimmune condition, thyroid stimulating antibody

29
Q

Describe the embryonic origin of the thyroid gland

A
  • Endodermal origin, forms in floor of primitive pharynx near base of tongue (thyroglossal duct)
  • Moves down through neck (and hyoid bone) to adult anatomical position
  • Foramen caecum at back of tongue is embryological remnant
30
Q

What are the potential complications of thyroidectomy?

A
  • Haemorrhage - thyroid is very vascular
  • Recurrent laryngeal palsy (hoarseness)
  • Permanent hypocalcaemia (PTH damage)
  • Hypothyroidism
31
Q

Describe the gross structure of the thyroid gland

A
  • L and R lobes (+ pyramidal lobe sometimes - anatomical variant) - R bigger, joined by isthmus
  • Weight 15-25g - varies with I2 intake, increases during puberty, pregnancy, lactation
  • Very vascularised
32
Q

Compare T3 and T4

A
  • T4 - higher quantity released
    • Less active, like a prohormone
  • T3 - more active form, formed by peripheral deiodination of T4
33
Q

How is colloid produced in thyroid follicles?

A
  • Synthesise glycoprotein
    • Protein from RER, sugar added in Golgi
  • Convert iodide to iodine
  • Iodine + glycoprotein = thyroglobulin
34
Q

Describe the structure of T3/4

A
  • T4 - 2 tyrosine and 4 iodine
  • T3 - 2 tyrosine and 2 iodine
35
Q

What is the function of the thyroid gland in calcium homeostasis?

A
  • Thyroid C/parafollicular C cells - in follicles and between follicles
  • Secrete calcitonin - decreases serum Ca2+
36
Q

What are the complications of Grave’s disease?

A
  • Dysthyroid eye disease
  • Dermopathy
  • Thyroid acropachy
37
Q

Describe Grave’s ophthalmopathy

A
  • Swelling in retrobulbar area due to glycosaminoglycan accumulation
  • Lid retraction/lag and periorbital oedema
  • Proptosis (protrusion), diplopia, nerve compression
  • Potentially sight threatening
38
Q

What are the signs/symptoms of classical thyrotoxicosis?

A
  • Weight loss
  • Tremor
  • Heat imbalance
  • Diarrhoea
  • Tachycardia
  • Hypertension
  • Palpitations
  • Sweating
39
Q

Describe the synthesis of thyroid hormones

A
  • Need iodine - seawater, fruit, vegetables
  • Oral iodine converted to iodide in GI tract and absorbed
  • Iodide transported into follicular cells against chemical gradient on basolateral membrane by sodium iodide transporter (thyroid symporter) - active transport, inhibited by perchlorate
  • Iodide diffuses to apex, prendrine transports into vesicles at apical membrane
  • Oxidation of iodide to iodine in vesicles, catalysed by thyroid peroxidase
  • Binds to tyrosine residues on thyroglobulin = organification
  • Formatioin of di/mono-iodotyrosine (T3/4), endocytosis of thyroglobulin into cell
40
Q

What is thyroid acropachy?

A
  • Rare
  • Digital clubbing, swelling of digits and toes - periosteal reaction of extremity bones
  • Usually with ophthalmopathy and dermopathy

Medicine Year 2 (41 decks)

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