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MSc Endocrinology > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What is the Thyroid Gland?

A

Essential gland. Secretes Thyroid hormones have wide ranging effects:

  • Metabolic rate
  • Development
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2
Q

What is the anatomical location of the Thyroid Gland?

A
  • Butterfly shaped lobe sitting at the front of the neck with 2 interconnecting lobes connected by the narrow thyroid isthmus.
  • Lies against and around the larynx and trachea.
  • Two parathyroid glands lie on each side in the same capsule, at the back of the thyroid lobes. Weighs 10-20g in adults.
    *
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3
Q

How does the thyroid gland develop?

A

Foetal thyroid gland starts to function from 10-12 weeks gestation, and from second trimester produces thyroid hormones. Thyroid development is detectable in the third week of gestation

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4
Q

What is the blood supply to the thyroid gland?

A

Blood supply from the superior thyroid artery and the inferior thyroid artery, derived from the external carotid arteries and the thyrocervical trunk.

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5
Q

What is the composition of the Thyroid Gland?

A

Thyroid is composed of spherical follicles, each composed of a single layer of follicular cells surroding a lumen filled with colloid (which is mostly thyroglbulin).

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6
Q

What are the cells of Thyroid Gland?

A

Follicular Cells

  • Follicular cells are stimulated to become columnar and the lumen is depleted of colloid
  • Follicular cells secrete T3 and T4

Parafollicular Cells

  • Parafollicular cells secrete calcitonin
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7
Q

What is the Thyroid Function through thyroid hormone?

A

Metabolic – increase catabolism

  • Increase basal metabolic rate, oxygen consumption and heat production
  • Gut motility and absorption
  • Uptake and breakdown of glucose by cells
  • Breakdown of fats

Cardiovascular

  • Increase the rate and strength of heartbeat

Developmental

  • Critical for brain development in infants
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8
Q

What the biologically active thyroid hormones?

A
  • Thyroxine (T4)
  • 3, 5, 3’-triiodothyronine (T3)

Phenyl ring attached via an ether linkage to a tyrosine molecule

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9
Q

What is Reverse T3?

A
  • Formed if an iodine atom is removed from the inner ring of T4 giving 3, 3’, 5’-triiodothyronine
  • Has no biological activity
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10
Q

Where are thyroid hormones molecules produced?

A
  • T4 is only produced by the thyroid gland
  • T3 is produced by the thyroid and in peripheral tissues by deiodination of T4
  • T4 and T3 stored in the thyroid gland incorporated in thyroglobulin as well and can be secreted more quickly as a result if they had to be. Transport proteins provide a store of thyroid hormones.
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11
Q

What is the biological function of Iodine?

A
  • Essential for normal thyroid function
  • Sources include: Seafood, dairy products, vegetables, Sea salt (Iodination)
  • Absorbed as iodide
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12
Q

What is the effect of iodine deficiency and how is it diagnosed?

A
  • Iodine deficiency is diagnosed by urinary iodine excretion
  • Severe iodine deficiency in infants and pregnancy results in severe mental and growth retardation
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13
Q

How is Thyroid Hormone produced?

A
  • Iodide transported into thyroid follicular cells (against a chemical and electrical gradient).
  • Linked to sodium transport in sodium iodine transporter (intrinsic transmembrane proteins found on basolateral membrane of thyroid follicular cells)
  • Iodide rapidly diffuses to the apical surface of the cells where it is transported by pendrin (membrane iodide-chloride transporter) to exocytic vesicles fused with the apical cell surface.
  • In these vesicles iodide is oxidised and covalently bound to tyrosyl residues of thyroglobulin
  • Oxidation of iodide is catalysed by thyroid peroxidase (required H2O2)
  • T4 is formed by coupling of two diiodotyrosine residues and T3 by one monoiodo and one diiodo within the thyroglobulin molecule. Catalysed by thyroid peroxidase
  • Thyroglobuin is 660KDa glycoprotein
  • Coupling process is not random as T4 and T3 are formed in regions of the thyroglobumin molecule which have unqiue amino acid sequences
  • To liberate T4 and T3 thyroglobulin is resorbed into the thyroid follicular cells in the form of colloid droplets which fuse with lysosomes where thyroglobulin is hydrolysed to T4, T3 and other amino acids
  • Hormones are then secreted
  • Iodotyrosine deoiodinase plays a role in recycling iodide (mutations in gene can result in congenital hypothyroidism
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14
Q

How is T3 produced peripherally?

A
  • ~80% of T3 production is formed by 5’-deiodination of T4
  • Catalysed by (iodothyronine) deiodinases expressed in most tissues which remove iodine moieties. Activate to T3 and deacitivate to reverse T3
  • T4 is considered a prohormone as T3 is responsible for most biological effects
  • Essential control points of thyroid activity

Three types (D1, D2, D3)

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15
Q

What are the tissues of high activity of thyroid hormone within the body?

A
  • D1: Liver and Kidney
  • D2: CNS, Pituitary, Brown Adipose Tissue, Placenta
  • D3: Placenta, CNS, Hemangiomas
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16
Q

How are Thyroid Hormone molecules transported in Blood?

A
  • 0.02% of T4 and 0.2% of T3 travel freely in the blood
  • 70% bound to thyroxine binding globulin (TBG)
  • 20% bound to transthyretin
  • 10% bound to albumin
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17
Q

How is Thyroid Hormone excreted?

A

Excreted in bile/urine following sulphation, glucuronidation, deamination, oxidative decarboxylation, ether cleavage or deiodination

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18
Q

What are the types of Thyroid Transport Hormone?

A

Thyroid Binidng Globulin

  • TBG is 54 kDa glycoprotein,
  • Very high affinity for T4 (less so for T3).
  • Only about one third of TBG in serum normally contains T4

Tranthyretin

  • Tranthyretin (55Kda tetramer)
  • Composed of 4 identical subunits.
  • Each molecule has two T4 binding sites but occupying one site decreases affinity for the second etc
  • Affinity of TTR for T4 is less than that of TBG
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19
Q

What is TRH and its molecular activity?

A
  • Tripeptide. Synthesised as a 36kDa protein (proTRH)
  • Plasma half life is about 3 min
  • TRH receptor is a GPCR coupled to the phosphoinositide cascade
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20
Q

What are the effects of Exogenous TRH?

A

Exogenous TRH administration

  • Stimulates TSH release. Increased in hypothyroid and hyperthyroid
  • Stimulates prolactin release in normal subjects and most patients with hyperprolactinemia
  • Stimulates growth hormone secretion in normal elderly subjects and patients with acromegaly, chronic liver disease, and diabetes mellitus.
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21
Q

What is TSH and its molecular activity?

A
  • Glycoprotein synthesised and secreted by thyrotrophs of the anterior pituitary to stimulate thyroid hormone production
  • Composed of non-covalently bound alpha and beta subunits
  • Plasma half life is about half an hour
  • TSH receptor is a GPCR predominantly on the plasma membrane of follicular cells within the thyroid gland coupled to cAMP

α subunit very similar to that of LH, FSH and hCG

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22
Q

What is the Thyroid hormone receptor?

A
  • TRα1, TRα2
  • TR β1, β2: Receptors are concentrated in brain, heart, liver, kidney and in pituitary and hypothalamic tissue

Monocarboxylate transporters MCT8 and MCT10 are involved in the transport of T4 and T3, although other transporters have been identified. Variable tissue response to occupation of nuclear receptors

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23
Q

How is TSH regulated?

A

TSH Inhibition

  • Very small increases in serum T3/T4 inhibit synthesis and release of TSH and TRH. TSH is primarily due to inhibition of transcription of subunits. Maintained within very tight limits
  • Somatostatin, Dopamine and Glucocorticoids also inhibit TSH release
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24
Q

How is Thyroid Function evaluated?

A

Frontline tests:

  • Serum TSH
  • Serum fT4

Serum fT3 may also be useful in certain situations

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25
Q

What is the clinical uses of Thyroid Function tests?

A
  • Screening for thyroid dysfunction
  • Investigating thyroid dysfunction
  • Monitoring therapy
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26
Q

What are the ranges of TSH tests?

A
  • Measuring range ~0.01 – 100 mU/L
  • Reference range ~0.2 – 5 mU/L

Immunoassay measurement. Single most specific and sensitive test to investigate thyroid function. Function sensitivity of an assay should be lower than 0.02 mU/L to be fit for purpose.

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27
Q

What are the ranges for fT4 and fT3?

A

Immunoassay with tightly titrated levels of antibody

  • Reference range fT4 ~9 – 24 pmol/L
  • Reference range fT3 ~3.6 – 6.4 pmol/L

Measures the unbound hormone available. No effect from altered concentrations of binding proteins or interactions due to drugs/illness. Reference method is equilibrium dialysis.

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28
Q

What causes changes in TBG concentration?

A

High TBG

  • Genetic, Physiological (e.g. pregnancy), Hydatiform mole, Oestrogens (inc.OCP), Other drugs (e.g. opiates), Hepatitis, Acute intermittent porphyria

Low TBG

  • Genetic, Androgens, Protein losing states (e.g. nephrotic syndrome), Malnutrition, Malabsorption, Severe illness, Acromegaly, Cushing’s disease
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29
Q

What are factors affecting TFT results?

A

Neonate

  • Rapid transient rise of TSH, T3 and T4 during first 24 hrsafter birth

Pregnancy

  • Large increase in plasma TBG concentration due to oestrogen stimulated increase in synthesis and diminished clearance
  • Marked increase in the requirement for iodine
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30
Q

What are other Thyroid Functions Tests?

A

TRH test

  • TSH response to TRH measured. Only occasionally used in the diagnosis of thyroid hormone resistance or TSH secreting adenoma

Thyroglobulin

  • Normally present in the circulation in very small amounts although maybe raised in many disorders.
  • Measurement generally only used in follow up to thyroid cancer when elevation of previously suppressed levels may indicate tumour recurrence

α subunit of TSH

  • May be raised in patients with pituitary tumours
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31
Q

What are Antibodies found in TFT measurements?

A

Thyroglobulin

  • Found in patients with thyroid autoimmunity but at a lower frequency than TPOAb.

TPO

  • Found in almost all (95%) of patients with autoimmune hypothyroidism secondary to Hashimoto’s thyroiditis and in some patients with other autoimmune thyroid diseases

TSH receptor (TRAb)

  • Classified as stimulating, blocking or neutral.
  • Hyperthyroidisim of Grave’s disease. Blocking and Stimulating is in Grave’s but stimulating causes Grave’s.
    *
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32
Q

Which patient groups should be screened for thyroid disease?

A
  • Measured in patients presenting with: Goitre, Atrial fibrillation, Dyslipidaemia, Osteoporosis, Subfertility
  • Annual check: History of postpartum thyroiditis, Down’s syndrome/Turner’s
  • Women with type I diabetes should have their thyroid function (Including TPO antibodies) established preconception, at booking when pregnant and at 3 months post-partum
33
Q

How are TFT results interperated?

A
  • Normal: Normal TSH and Normal T4
  • Hyperthyroidism: Low TSH and High T4
  • Hypothyroidism (primary): High TSH and Low T4
  • Hypothyroidism (secondary): Low TSH and Low T4
34
Q

What are imaging techniques for Thyroid Pathologies?

A
  • Ultrasound used to demonstrate thyroid size: Ability of the thyroid to concentrate radioisotopes of iodine and other substances has been used for years to identify areas within the gland which are not functionally active
  • Thyroid scintillation scanning
  • CT scan
  • Perchlorate discharge test
  • US guided fine needle aspirate
35
Q

What are some non-thyroidal pathologies that present with abnormal TFTs?

A
  • Acute hepatitis
  • Hepatoma
  • Acute intermittent porphyria
  • Acromegaly
  • Nephrotic syndrome
  • Cushing’s syndrome
  • Acute psychosis
  • Depression
  • Psychiatric illness: Some patients with acute psychiatric illnesses, particularly schizophrenia, have transient elevations in serum T4 concentrations with or without low serum thyroid-stimulating hormone (TSH) concentrations
36
Q

When can TSH results be misleading?

A
  • Assay interference e.g.heterophilic antibodies
  • Pregnancy
  • Situations in which Thyroid Status is Unstable
  • Following an episode of thyroiditis
  • Early weeks of thyroxine therapy
  • Poor compliance
  • Hypopituitarism
  • TSH secreting adenoma (α subunit)
  • End organ resistance
37
Q

What are symptoms of Hypothyroidism?

A
  • Constant stimulation of thyroid gland may lead to enlargement and therefore a goitre
  • A generalized slowing of metabolic processes slow movement and slow speech
  • Weight gain (but not morbid obesity)
  • Coarse hair and skin
  • Puffy facies
  • Enlargement of the tongue
  • Hoarseness.
  • Fatigue
  • Cold intolerance
  • Weight gain
  • Constipation
  • Dry skin
  • Myalgia
  • Menstrual irregularities
  • Bradycardia
  • Hypertension
  • Delayed relaxation phase of the deep tendon reflexes
  • Chronic autoimmune thryoiditis, likely to have raised TPO antibodies
  • Hypercholesterolaemia
  • Macrocytic anaemia
  • Elevated CK
  • Hyponatraemia
38
Q

What is Hypothyroidism?

A
  • Underproduction of thyroid hormones that has insidious development over a number of years

Can be:

  • Primary (95%): Problem is with the thyroid gland
  • Secondary/Central: Problem is with the hypothalamus/pituitary gland
39
Q

What is Primary Hypothyroidism?

A

Overt hypothyroidism

  • TSH ≥ 10 mU/L
  • fT4 below the normal reference range

Subclinical hypothyroidism

  • TSH levels are above the normal reference range but T3 and T4 are within the normal reference range
  • Clinical features of hypothyroidism are usually absent
40
Q

What are causes of Primary Hypothyroidism?

A
  • Iodine deficiency
  • Autoimmune thyroiditis (e.g. Hashimoto’s thyroiditis)
  • Post-ablative therapy or surgery
  • Drugs e.g. lithium
  • Transient thyroiditis: Subacute (de Quervain’s) thyroiditis, Postpartum thyroiditis (PPT)
  • Thyroid infiltrative disorders: Amyloidosis, sarcoidosis, haemochromatosis, tuberculosis, and fibrous thyroiditis (Reidel’sthyroiditis)
  • Congenital hypothyroidism
41
Q

What is Hashimoto’s Thyroiditis?

A
  • Autoimmune-mediated destruction of the thyroid gland involving apoptosis of thyroid epithelial cells
  • Chronic autoimmune thyroiditis.
  • Most common cause of hypothyroidism in iodine-sufficient areas of the world
  • Affects 7 times more women than men and increasing incidence with age
42
Q

What are features of Hashimoto’s Thyroiditis?

A
  • High serum concentrations of Tg/TPO antibodies
  • Diffuse lymphocytic infiltration of the thyroid
  • Follicular destruction
43
Q

What is some evidence regarding genetic susceptibility of Hashimoto’s Thyroiditis?

A
  • The disease clusters in families, sometimes alone and sometimes in combination with Graves’ disease
  • The sibling recurrence risk is >20
  • The concordance rate in monozygotic twins is 30 to 60 percent
  • It occurs with increased frequency in patients with Down’s syndrome and Turner’s syndrome.
  • The thyroglobulin (Tg) gene (TG) has been linked to autoimmune thyroid disease and has been suggested to code for Tgforms with different immune reactivity
44
Q

What are precipitating factors for Hashimoto’s Thyroiditis?

A

Infection, stress, sex steroids, pregnancy, iodine intake, and radiation exposure are the known possible precipitating factors for Hashimoto’s thyroiditis.

45
Q

Describe Congenital Hypothyroidism

A
  • May be detected in neonatal period
  • Agenesis and dysgenesis of the thyroid leading to defects in thyroid hormone biosynthesis
  • More common in mothers who were receiving an anti-thyroid drug for hyperthyroidism
  • Newborn screening programme
  • TSH measured on day 5-8 of life
46
Q

What are some drugs causing Hypothyroidism?

A
  • Inhibition of thyroid hormone synthesis and/or release: Thionamides, lithium, perchlorate, aminoglutethimide, thalidomide, and iodine and iodine-containing drugs including amiodarone, radiographic agents, expectorants (eg, guaifenesin), kelp tablets, potassium iodine solutions (SSKI), Betadine douches, topical antiseptics
  • Decreased absorption of T4: Cholestyramine, colestipol, colesevelam, aluminum hydroxide, calcium carbonate, sucralfate, iron sulfate, raloxifene, omeprazole, lansoprazole, and possibly other medications that impair acid secretion, sevelemer, lanthanum carbonate, and chromium
  • Immune dysregulation: Interferon-alfa, interleukin-2, ipilimumab, alemtuzumab, pembrolizumab, nivolumab
  • Suppression of TSH: Dopamine
  • Possible destructive thyroiditis: Sunitinib
  • Increased type 3 deiodination: Sorafenib
  • Increased T4 clearance and suppression of TSH: Bexarotene
47
Q

What is Secondary Hypothyroidism?

A
  • <1% of hypothyroidism
  • Low or normal serum TSH, low serum fT4 and fT3
  • Pituitary or Hypothalamic

Few patients with TSH deficiency have slightly high serum TSH values because they secrete TSH that is less glycosylated and therefore has less biological activity than normal TSH (but is normally immunoreactive)

48
Q

What causes of Pituitary Dysfunction?

A
  • Tumours
  • Surgery, radiotherapy, or trauma
  • Infarction
  • Sheehan’s syndrome
  • Infiltrative disorders such as tuberculosis, syphilis, sarcoidosis, amyloidosis, and haemochromatosis
  • Isolated thyroid-stimulating hormone (TSH) deficiency or inactivity
49
Q

What is Subclinical Hypothyroidism(compensated hypothyroidism)?

A
  • Generally don’t require treatment
  • Elevated TSH whilst fT4 remains within the reference range
  • May have clinical symptoms
  • Elevated TSH reflects the sensitivity of the HP axis to small decreases in circulating hormone
50
Q

What causes hypothalamic dysfunction?

A
  • Tumours such as gliomas
  • Surgery, radiotherapy, or trauma
  • Infiltrative disorders such as tuberculosis, syphilis, sarcoidosis, and haemochromatosis
  • Idiopathic hypothalamic disease
  • Drugs (such as bexarotene and other retinoids)
51
Q

What is Myxedema?

A
  • Myxedema coma is a rare life-threatening clinical condition that represents severe hypothyroidism with physiological decompensation
  • Precipitated by infection, cerebrovascular disease, heart failure, trauma, or drug therapy
  • Usually occurs in patients with long-standing, undiagnosed hypothyroidism
52
Q

What is Myxedema coma?

A
  • Patients with myxedema coma are generally severely-ill with significant hypothermia and depressed mental status.
  • Medical emergency

If the condition is not promptly diagnosed and treated, the mortality rate can be more than 50%. Even with immediate recognition and timely medical intervention, mortality rates are as high as 25%.

53
Q

How are patient managed based on their results

A
  • Serum TSH > 10 mU/L and fT4 concentration below the reference range is overt hypothyroidism and should be treated
  • High serum TSH and a normal fT4 should have follow up 3-6 months later - Exclude non thyroidal illness and drug interference
  • Serum TSH above reference range but <10 mU/L then serum TPO antibodies should be measured and if they are high then serum TSH should be measured annually or earlier if symptoms develop. Thyroxine should be started if the TSH concentration rises above 10 mU/L. If low TPO then measure TSH every 3 years
54
Q

What is used to manage patient with overt hypothyroidism?

A

Overt primary hypothyroidism is treated with levothyroxine. This is reviewed every 3–4 weeks until:

  • Resolve the symptoms and signs of hypothyroidism
  • Normalise serum TSH and improve thyroid hormone concentrations to the euthyroid state
  • Once a stable TSH is achieved, TSH can be checked 4–6 monthly and then annually
55
Q

How are patient who are being treated managed if their results for the TFTs remain abnormal?

A
  • Compliance with LT4 treatment.
  • Drug interactions with drugs containing calcium carbonate, ferrous sulphate, multivitamins, cholestyramine, and proton pump inhibitors can reduce LT4 absorption.
  • Drug including oral contraceptives, anti-epileptic medication (such as carbamazepine and phenytoin), and some antibiotics (such as rifampicin) can increase LT4 requirements.
  • Several gastrointestinal conditions such as coeliac disease, Helicobacter pylori-related gastritis, atrophic gastritis/pernicious anaemia, and inflammatory bowel disease can reduce absorption of LT4 in the gut.
  • Several foods impair absorption of LT4 including milk, coffee, soya products, and papaya.
  • Drugs including iron salts, calcium salts, antacids (including H2-receptor blockers and proton pump inhibitors), cholestyramine, and raloxifene can interfere with LT4 absorption.

Adjust the dose of LT4 as appropriate if a contributing factor is identified and managed.

56
Q

How is treatment with thyroid replacement therapy guided?

A
  • Thyroxine replacement guided by TFTs. Titrate against TSH concentration
  • Assess clinical well being
  • Target is TSH within the reference range
  • Majority of patients have a dose of 50-100μg thyroxine can be used as the starting dose
  • Alteration of the dose by 25-50μg increments and repeat measurement of TSH 2-3 months after a change in dose.
  • Try to avoid over replacement and have care in the elderly
57
Q

What are symptoms of Hyperthyroidism?

A
  • Thyrotoxicosis
  • Heart problems: Some of the most serious complications of hyperthyroidism involve the heart. These include a rapid heart rate, a heart rhythm disorder called atrial fibrillation and congestive heart failure — a condition in which your heart can’t circulate enough blood to meet your body’s needs. These complications generally are reversible with appropriate treatment.
  • Brittle bones: Untreated hyperthyroidism can also lead to weak, brittle bones (osteoporosis). The strength of your bones depends, in part, on the amount of calcium and other minerals they contain. Too much thyroid hormone interferes with your body’s ability to incorporate calcium into your bones.
  • Eye problems: People with Graves’ ophthalmopathy develop eye problems, including bulging, red or swollen eyes, sensitivity to light, and blurring or double vision. Untreated, severe eye problems can lead to vision loss.
  • Red, swollen skin: In rare cases, people with Graves’ disease develop Graves’ dermopathy, which affects the skin, causing redness and swelling, often on the shins and feet.
  • Thyrotoxic crisis: Hyperthyroidism also places you at risk of thyrotoxic crisis — a sudden intensification of your symptoms, leading to a fever, a rapid pulse and even delirium. If this occurs, seek immediate medical care.
  • Clubbing
  • Tremors
  • Diarrhoea
  • Intolerance to heat
  • Bulging eyes
  • High systolic BP
  • Breast Enlargement
  • Muscle Wasting
58
Q

What are Goitres?

A

Swelling of the neck associated with thyroid gland which has become enlarged. Worldwide 90% cases are due to iodine deficiency

  • Diffuse goitre: Where the entire thyroid gland swells and feels smooth to the touch
  • Nodular goitre: Where solid or fluid-filled lumps called nodules develop within the thyroid. Nodules can be single or multiple and may contain fluid
59
Q

What are causes of Hyperthyroidism?

A
  • Graves’ disease (70% of cases)
  • Hyperfunctioning thyroid nodules: Toxic adenoma. Toxic multinodular goitre, Plummer’s disease
  • Thyroiditis
  • Pituitary adenoma (TSH secreting)
60
Q

What is the cause of Grave’s Disease?

A

Syndrome that may consist of hyperthyroidism, goiter, eye disease (orbitopathy). Hyperthyroidism is the most common feature of Graves’ disease. Caused by

  • Autoantibodies to the TSH receptor (TRAb) which activate receptor stimulating thyroid hormone synthesis and secretion
  • This stimulates thyroid growth (causing a diffuse goiter)
  • Genetic susceptibility
61
Q

What is Subclinical Hyperthyroidism?

A
  • Based exclusively on lab findings
  • Subnormal serum TSH, with normal levels of fT3 and fT4
  • Can be divided into two categories:
    • Grade 1 – low but detectable serum TSH levels (e.g. TSH 0.1–0.39 mU/L)
    • Grade 2 which has suppressed serum TSH levels (<0.1 mIU/L)
62
Q

What is a Thyroid Storm?

A
  • Thyrotoxic crisis which is a medical emergency
  • Symptoms include fever, tachycardia, hypertension, neurological and GI abnormalities
  • Fatal if untreated.

Used to occur during surgery, but now better managed

63
Q

What is used to guide treatment of Hyperthyroidism?

A
  • Serum TSH <0.1 mU/L and fT4 concentration above the reference range is overt hyperthyroidism and should be treated
  • If FT4 is not above the reference range in a patient with low serum TSH, FT3 should be measured - “T3-toxicosis”
  • Typically observed in mild cases of toxic nodular hyperthyroidism and early in the course of Graves’ disease (either primary presentation or relapse)
  • In a few cases the converse is true in that a rise in FT3 is absent despite elevation of FT4 and suppression of TSH in a patient thought clinically to have thyrotoxicosis
  • Lack of rise in FT3 may reflect the presence of“non-thyroidal illness”
64
Q

How is Hyperthyroidism pharmacologically managed?

A

Anti-Thyroid Drugs (Thioamides)

  • Carbimazole and Propylthiouracil (PTU)
  • Occasionally prescribed long-term (e.g. in elderly frail subjects with limited life expectancy)
  • May be used short-term in preparation for definitive treatment with radioiodine or surgery or medium-term in the hope of inducing remission in cases of Graves’ disease
  • Propylthiouracil, but not carbimazole, may induce relative radioresistance determining the need for larger or repeated doses of radioiodine

Beta-Blockers

  • If the patient has marked adrenergic symptoms e.g. tremor, tachycardia e.g. Propranolol
65
Q

What are definitive treatments for Hyperthyroidism?

A
  • Most patients with hyperthyroidism require definitive treatment with 131-Iodine
  • Surgery: All patients proceeding to surgery should be rendered euthyroid (normal FT4 and FT3) with thionamides
66
Q

What is the managment of subclinical hyperthyroidism?

A

Patient with TSH value below the reference range but >0.1mU/L, and is not on thyroxine therapy

  • Repeat the measurement together with FT4 and FT3 within one to two months to exclude overt hyperthyroidism (and also central hypothyroidism)
  • If the repeat serum TSH measurement remains low but >0.1mU/L with normal FT4 and/or FT3, then repeat testing every 6-12 months is required

In those with serum TSH < 0.1 mU/L, fT4 and fT3 should be measured to exclude overt hyperthyroidism

Potential benefits of therapy must be weighed against the substantial morbidity associated with treatment of thyrotoxicosi

67
Q

What is Post partum Thyroiditis?

A
  • Thought to be an autoimmune disease very similar to Hashimoto’s thyroiditis
  • Thyrotoxicosis followed by hypothyroidism
  • Women with positive anti-thyroid antibodies are at a much higher risk of developing postpartum thyroiditis
  • Most women will have return of their thyroid function to normal within 12-18 months of the onset of symptoms
68
Q

What increases risk of Post partum Thyroiditis?

A
  • Autoimmune disorders
  • Positive anti-thyroid antibodies
  • History of previous thyroid dysfunction
  • History of previous postpartum thyroiditis
  • Family history of thyroid dysfunction
69
Q

What are types of Thyroid Cancers?

A
  • Papillary thyroid cancer (70–80%) - Slow growth
  • Follicular thyroid cancer (10–15%) - More likely to spread than papillary thyroid cancer
  • Medullary thyroid cancer (2%) - RET proto-oncogene can lead to an early diagnosis of medullary thyroid cancer
  • Anaplastic thyroid cancer (Very rare) - Most advanced and aggressive thyroid cancer
70
Q

How are people with Thyroid Cancer investigated?

A
  • Usually present with a nodule or goitre
  • TFTs used to check for toxic nodular goitre or goitrous hypothyroidism
  • Patients with thyroid cancer generally euthyroid
71
Q

What happens with Thyroid Cancer patient post surgery?

A
  • After surgery, treatment aims to have long term suppression of TSH with exogenous thyroid hormone
  • Post thyroidectomy, the TSH should be suppressed to and maintained at a level of <0.1 mU/L in a reputable assay
72
Q

What is the purpose of Calcitonin as a marker?

A
  • Calcitonin is a useful tumour marker for medullary thyroid cancer; positive correlation between level and tumour mass
  • Pre-operative diagnosis should include baseline values for calcitonin
73
Q

When is Calcitonin stimulation test indicated?

A

A stimulation test with calcium/pentagastrin may also be indicated in the following situations:

  • To confirm a diagnosis of MTC pre-operatively when calcitonin levels are only mildly elevated (<100ng/L)
  • For pre-surgical assessment of RET positive children
  • For post-operative monitoring for tumour recurrence

Patients with MTC will require lifelong follow-up, including regular measurement of plasma calcitonin

74
Q

How are Thyroid Cancers treated?

A
  • Surgery: Lobectomy, Total thyroidectomy
  • Radioactive iodine therapy
75
Q

What is Sick Euthyroid Syndrome?

A
  • Clinical picture of hypothyroid results in the context of other disease states
  • Difficult to investigate especially those on ICU. Thyroid function should not be assessed in seriously ill patients unless there is a strong suspicion of thyroid dysfunction
  • Many have low concentrations of T4, T3 and TSH. May have transient central hypothyroidism
  • Treatment with thyroxine has little benefit and may even be harmful
  • May be that changes in thyroid function during severe illness are protective as they prevent excessive tissue catabolism
76
Q

How does Amiodorance affect Thyroid?

A

Amiodarone contains 75mg iodine per 200mg tablet. Frequently associated with iodide-induced thyroid dysfunction

  • Amiodarone-induced hyperthyroidism is particularly prevalent (10%) in areas of iodine-deficiency and in patients with underlying thyroid disease
  • Amiodarone-induced hypothyroidism is more common in iodine-replete communities (up to 20%) and related to the presence of thyroid autoimmunity
77
Q

How does Lithium affect Thyroid?

A
  • Lithium, used in the treatment of bipolar depression, is associated with mild and overt hypothyroidism in up to 34% and 15% of patients respectively,
  • Can appear abruptly even after many years of treatment
  • Lithium-associated thyrotoxicosis is rare and occurs mainly after long-term use
78
Q

What is the causes of Non-Thyroidal Dysfunction of the Thyroid Gland?

A

Most hospitalised patients will have low serum T3. 5’-monodeiodination decreases whenever caloric intake is low and in any nonthyroidal illness, even mild illness. Several mechanisms can contribute to the inhibition of 5’-monodeiodination

  • High endogenous serum cortisol concentrations and exogenous glucocorticoid therapy
  • Circulating inhibitors of deiodinase activity, such as free (non-esterified) fatty acids
  • Treatment with drugs that inhibit 5’-monodeiodinase activity (e.g. amiodarone and propranolol)
79
Q

Thyroglobulin

A
  • Specific tumour marker for differentiated thyroid cancer (papillary/follicular)
  • No role in the diagnosis of the condition
  • Thyroglobulin is secreted by both normal and cancerous thyroid cells
  • In patients who have been treated with total thyroidectomy and 131Iodine ablation, detectable serum Tg (>2ug/L) is highly suggestive of residual or recurrent tumour, but could also indicate persistence of a remnant of normal thyroid

therefore in patients who have not had a total thyroidectomy and 131iodine ablation, the interpretation of serum Tgmeasurements is limited by the inability to differentiate between tumour and thyroid remnant

Thyroid function tests should be performed whenever thyroglobulin and

thyroglobulin antibodies are measured The requesting clinician

should indicate on the form whether the patient is on thyroxine or triiodothyronine

therapy.

Thyroglobulin antibodies should be measured at diagnosis and

simultaneously with measurement of thyroglobulin.

Labs should tell users when changing methods

MSc Endocrinology (16 decks)

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