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Year 5 - Pathology > CHEMPATH: Thyroid > Flashcards

CHEMPATH: Thyroid Flashcards

1
Q

A. TSH < 0.01, Free T3 15.6, Free T4 38.0.

    1. Consistent with clinical primary hypothyroidism
  • 2.Consistent with euthyroid status in a patient complaining of tiredness.
  • 3.Consistent with pituitary driven thyrotoxicosis
  • 4.Consistent with secondary or pituitary hypothyroidism.
  • 5.Consistent with sub-clinical hypothyroidism with risk of later clinical hypothyroidism.
  • 6.Consistent with thyrotoxicosis.
  • 7.To screen for medullary thyroid carcinoma
  • 8.To screen for recurrence of differentiated thyroid carcinoma.

Normal ranges TSH 0.33-4.5mU/L Free T3 (3.2-6.5pmol/L) Free T4 (10.2-22.0pmol/L) Thyroglobulin <5 ug/L

A

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2
Q

TSH 8.4, Free T4 11.7, Thyroid peroxidase (thyroid antibodies) positive

    1. Consistent with clinical primary hypothyroidism
  • 2.Consistent with euthyroid status in a patient complaining of tiredness.
  • 3.Consistent with pituitary driven thyrotoxicosis
  • 4.Consistent with secondary or pituitary hypothyroidism.
  • 5.Consistent with sub-clinical hypothyroidism with risk of later clinical hypothyroidism.
  • 6.Consistent with thyrotoxicosis.
  • 7.To screen for medullary thyroid carcinoma
  • 8.To screen for recurrence of differentiated thyroid carcinoma.

Normal ranges TSH 0.33-4.5mU/L Free T3 (3.2-6.5pmol/L) Free T4 (10.2-22.0pmol/L) Thyroglobulin <5 ug/L

A

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3
Q

TSH 1.4, Free T4 12.1.

    1. Consistent with clinical primary hypothyroidism
  • 2.Consistent with euthyroid status in a patient complaining of tiredness.
  • 3.Consistent with pituitary driven thyrotoxicosis
  • 4.Consistent with secondary or pituitary hypothyroidism.
  • 5.Consistent with sub-clinical hypothyroidism with risk of later clinical hypothyroidism.
  • 6.Consistent with thyrotoxicosis.
  • 7.To screen for medullary thyroid carcinoma
  • 8.To screen for recurrence of differentiated thyroid carcinoma.

Normal ranges TSH 0.33-4.5mU/L Free T3 (3.2-6.5pmol/L) Free T4 (10.2-22.0pmol/L) Thyroglobulin <5 ug/L

A

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4
Q

TSH 22. 4, Free T4 6.3.

    1. Consistent with clinical primary hypothyroidism
  • 2.Consistent with euthyroid status in a patient complaining of tiredness.
  • 3.Consistent with pituitary driven thyrotoxicosis
  • 4.Consistent with secondary or pituitary hypothyroidism.
  • 5.Consistent with sub-clinical hypothyroidism with risk of later clinical hypothyroidism.
  • 6.Consistent with thyrotoxicosis.
  • 7.To screen for medullary thyroid carcinoma
  • 8.To screen for recurrence of differentiated thyroid carcinoma.

Normal ranges TSH 0.33-4.5mU/L Free T3 (3.2-6.5pmol/L) Free T4 (10.2-22.0pmol/L) Thyroglobulin <5 ug/L

A

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5
Q

Thyroglobulin 254

    1. Consistent with clinical primary hypothyroidism
  • 2.Consistent with euthyroid status in a patient complaining of tiredness.
  • 3.Consistent with pituitary driven thyrotoxicosis
  • 4.Consistent with secondary or pituitary hypothyroidism.
  • 5.Consistent with sub-clinical hypothyroidism with risk of later clinical hypothyroidism.
  • 6.Consistent with thyrotoxicosis.
  • 7.To screen for medullary thyroid carcinoma
  • 8.To screen for recurrence of differentiated thyroid carcinoma.

Normal ranges TSH 0.33-4.5mU/L Free T3 (3.2-6.5pmol/L) Free T4 (10.2-22.0pmol/L) Thyroglobulin <5 ug/L

A

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6
Q

What naturally occurring compound blocks TSH?

A

Perchlorate

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7
Q

Describe the molecular mechanisms of T3/4 production.

A

This occurs in thyrocytes in thyroid follicles.

  • Iodide goes through the membrane via Na+/K+ ATPase
  • Iodide –> iodine by thyroid peroxidase (TPO)
  • The iodine is then taken up by thyroglobulin(TG) and –> thyroxine through a number of processes involving TPO –>MIT and TIT via iodination of tyrosine residues in thyroglobulin
  • There is coupling of monoiodotyrosine (MIT) and DIT to form T3 and 2 diiodotyrosine (DIT) to form T4
  • Once the thyroxine (T4) is produced, it is stored within the thyroid gland (and taken up by BM again and secreted into the lumen when required)
    • In the periphery, T4 –> T3
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8
Q

Which form is thyroxine most commonly found in the periphery?

A
  • A very small proportion is active thyroxine (fT4)
  • Only 0.03% of thyroxine in the circulation is active
  • Thyroxine can bind to thyroxine-binding pre-albumin (TBPA) & albumin
  • Most of the thyroxine is bound to thyroxine binding globulin (TBG) – 75%
  • NOTE: if lacking albumin in diet, you TBG levels will go down
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9
Q

Describ the axis.

A
  • Hypothalamus produces TRH à stimulates production of TSH from pituitary gland à stimulates T4 production
    • T4 converted to T3 in peripheries (active component of thyroxine)
  • Too much T4 –> feedback to the hypothalamus to prevent it from producing too much TRH
    • So, if you have low T4, you should have high TRH and high TSH

NB: hCG and TSH have similar structures (hCG has 1/10,000 activity of TSH) and so can stimulate same actions I.E. a string around the neck is used as a pregnancy test in Africa (hCG –> goitre)

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10
Q

List the most common causes of hypothyroidism.

A

Most hypothyroidism is PRIMARY

  • Hashimoto’s thyroiditis (autoimmune)
  • Atrophic thyroid (congenital or age)
  • Post-Graves’ disease (radioactive iodine, surgery, natural history or thionamines)
  • Other minor causes:
    • Post-thyroiditis
    • Drugs (amiodarone, lithium)
    • Thyroid agenesis or dysgenesis
    • Iodine deficiency and dyshormonogenesis
    • 2nd hypothyroidism (pituitary disease)
    • Peripheral thyroid hormone resistance
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11
Q

What are the clinical features of hypothyroidism?

A
  • Metabolic rate - reduced –> weight gain
  • Cardiovascular - bradycardia
  • Gastrointestinal - constipation
  • Respiratory- laboured breathing
  • Reproductive - oligomenorrhoea
  • Other:
    • Weight gain (metabolic rate issues) and poor appetite
    • Cold/dry hands/feet
    • Hyponatraemia (thyroxine is involved with Na transport in kidneys)
    • Normocytic anaemia + pernicious anaemia)
    • Myxoedema, goitre
    • Subtle in the elderly
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12
Q

What investigations should be done for primary hypothyroidism? What other conditions should you test for?

A
  • High TSH + Low T4 if primary
  • Thyroid peroxidase autoantibodies (suggests autoimmune hypothyroidism / Hashimoto’s thyroiditis)
  • Remember to consider any other autoimmune conditions that the patient may also have (e.g.
    • pernicious anaemia
    • coeliac disease
    • Addison’s disease
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13
Q

What is the management of primary hypothyroidism?

A
  • Perform an ECG:
    • If there is co-cardiac failure alongside the hypothyroidism, giving levothyroxine will exacerbate any myocardial ischaemia and MAY worsen the heart failure à start at a VERY low dose and titrate
  • Levothyroxine (T4), 50-125-200 mcg/day -
    • Titrated to a normal TSH
    • Titrated by BMI, most patients are on about 100mcg,
  • Liothyronine (T3)
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14
Q

What is the problem with overtreating patients with T4? Is there evidence for T3 rather than T4?

A
  • NO evidence base for over-treating patients with too much T4
    • Some patients prefer to take too much thyroxine because it helps them lose weight
    • Excessive thyroxine can cause osteopaenia and AF
  • There is NO evidence base for giving T3 rather than T4
    • T4 is sometimes converted to T3 in some tissues; patients think that T3 is more natural.
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15
Q

What type of hypothyroidism is associated with normal T4 but high TSH?

A

Subclinical hypothyroidism (SH) / “Compensated Hypothyroidism”

  • T4 level is NORMAL but TSH is HIGH
  • Pituitary gland senses T4 and* thinks the thyroid is NOT producing enough thyroxine so it produces more TSH
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16
Q

Which antibody if positive in subclinical hypothyroidism, may indicate thyroid disease?

A

If TPO antibodies are positive, it suggests that may –> thyroid disease

17
Q

Is there any benefit of treating subclinical hypothyroidism? Does it help with symptoms?

A

Generally asymptomatic

Subclinical hypothyroidism is UNLIKELY to be the cause of their presenting symptoms – no change in symptoms will occur.

But hypothyroidism is associated with hypercholesterolaemia (may be only benefit of treating SH)

18
Q

How soon after radioiodine treatment do patients become hypothyroid?

A

Usually hypothyroid within 1 year of receiving treatment

But may take many years in some patients (up to 15yrs) ( 50% of patients)

19
Q

Describe the changes in thyroid function in pregnancy and why they occur.

A
  1. hCG has a similar structure to TSH - so can bind onto THSr and cause thyroid to produce more thyroxine
    • Can cause thyrotoxicity if malignancy produces hCG
  2. Rise in hCG in the 1st trimester –> increase in free T4 but this is a normal physiological process
    • Normal ranges’ of TSH and T4 in pregnancy are slightly different to non-pregnancy
    • Later in pregnancy, hCG levels will drop –> T4 levels drop and TSH levels will rise slightly
  3. TBG levels increase in pregnancy (as TBG is under the control of oestrogen) – but cannot be measured in serum, only T4

If T4 was low or extremely high at the start of pregnancy then this would be abnormal.

20
Q

What is the most thing to remember when testing for neonatal hypothyroidism?

A

Test must be done at the appropriate time (48-72hrs) after birth otherwise you may be detecting the mother’s TSH and miss the neonatal hypothyroidism (common as occurs in 1 in 3500)

Done using Guthrie test

21
Q

What is sick euthyroid syndorme? How is it managed?

A

Occurs when severe illness affects the HPT axis and thyroid may shut down to reduce the BMR BUT no hypothyroid symptoms occur and no improvement on giving thyroxine

  • Biochemistry
    • Low T4 and T3 (and reduced T3 action)
    • Normal/high TSH (later decreased)
22
Q

What are the causes of hyperthyroidism and how can they be divided?

A

High uptake and low uptake on technetium scan

  • HIGH UPTAKE:
    • Graves’ disease- 40-60%
    • Toxic multinodular goitre - 30-50%
    • Single toxic adenoma - 5%
  • LOW UPTAKE:
    • Sub-acute thyroiditis / viral thyroiditis / de Quervain’s thyroiditis (all the same)
    • Postpartum thyroiditis

Rare causes:

  • Silent thyroiditis (AI, amiodarone)
  • Factitious thyroiditis
  • TSH-induced
  • Thyroid cancer induced
  • Trophoblastic tumour and Struma ovarii (high hCG production)
23
Q

List 2 causes of low and high uptake on technetium scan.

A

Technetium scan can be used to see which parts of the thyroid are producing excessive thyroid hormone. All three of the above conditions that are high uptake will show increased uptake of technetium

  • Graves’ disease
  • Toxic multinodular goitre
  • Single toxic adenoma

In pregnancy, the body may produce antibodies that stimulate the thyroid gland to release excess amounts of thyroxine. These have low uptake in a technetium scan:

  • Postpartum thyroiditis
  • Sub-acute thyroiditis, de Quervain’s
24
Q

What are the clinical features of hyperthyroidism?

A
  • Metabolic rate- increased –> weight loss
  • Cardiovascular - tachycardia
  • Gastrointestinal- diarrhoea
  • Respiratory - tachypnoea
  • Skeletal - osteopaenia & osteoporosis (thyroxine acts on osteoclasts)
  • Reproductive - irregular periods
25
Q

What do investigations show in hyperthyroidism?

A
  • Low TSH, high T3 and T4
  • Technetium scan may show high or low uptake depending on the cause
  • Thyroid autoantibodies (thyroid microsomal)
26
Q

What is the management of hyperthyroidism?

A
  • Keep safe:give beta-blocker if pulse > 100 bpm
  • Radioactive iodine – taken up by the thyroid gland, which then releases radiation to destroy the thyroid gland

Consider other autoimmune conditions (e.g. coeliac disease, Addison’s disease)

ECG - AF

Bone mineral density

27
Q

What are the side effects of using radioiodine treatment?

A

131I is used

  • Can precipitate a thyroid storm and
  • Make the thyroid gland underactive (i.e. hypothyroidism) - good
  • Side effects: ophthalmopathy/tracheal compression

NB: Stop thionamine if using radioactive iodine

28
Q

What are the clinical features of Graves’ disease?

A
  • Diffuse goitre
  • Thyroid associated ophthalmopathy (TSH-R on muscles of eyes) – do not give radioiodine
  • Thyroid associated dermopathy – pretibial myxoedema
  • Thyroid acropachy – bones of fingers affected
  • Other AI
29
Q

How can hyperthyroidism be managed medically?

A

Thionamides (e.g. carbimazole, propylthiouracil / PTU)

  • They work by preventing conversion of iodide –> iodine by thyroid peroxidase

These medications are either:

  1. Titrated to achieve normal T4 levels or they can be…
  2. ‘Block and replaced’ (a high dose of thionamides are used to block the thyroid gland completely, then given thyroxine to maintain normal)
30
Q

What are the side effects of thionamides?

A

Rash

Rare side-effect = agranulocytosis

Patients should STOP treatment if they develop a sore throat or fever + seek medical attention

31
Q

What are the two main drug mechanims for hyperthyroidism treatment?

A
  • Potassium perchlorate can be given to hyperthyroid patients before surgery to block the uptake of iodide by the thyroid cells
  • Thionamides (PTU/carbimazole) inhibit thyroid peroxidase, thereby preventing the conversion of iodide to iodine
32
Q

What are the types of thyroiditis?

A
  • Silent (painless) thyroiditis (most have some pain in the neck)
  • Viral / sub-acute thyroiditis
  • Post-partum thyroiditis (tx for viral or post-partum thyroiditis is different to hyperthyroidism)

In most cases this is painful.

33
Q

What is the most common course of thyroiditis? What is the management?

A
  • Initial inflammation –> release of thyroid hormone –> hypothyroidism long term.
  • Most thyroiditis patients present at the stage where their TSH is high and their T4/T3 is low
  • Long-term treatment of thyroiditis is thyroid hormone replacement

NB: patients can present at different stages e.g. when TSH and T3 are both low, T3 high and TSH low etc.

34
Q

Name 4 types of thyroid cancer. Which are the most common?

A
  1. Papillary thyroid cancer (pathology = Psammoma body)
  2. Follicular thyroid cancer
  3. Medullary carcinoma of the thyroid
  4. Anaplastic thyroid cancer

1 + 2 are most common. Typically slow progressing.

35
Q

Which thyroid cancer is this associated with?

A

Papillary thyroid cancer - Psammoma body

36
Q

What is the treatment of thyroid cancer?

A
  1. Total thyroidectomy ± radioiodine
  2. Supraphysiological doses of thyroxine (to lower the TSH levels so that TSH does NOT stimulate any remaining thyroid cancer cells, as many of these tumours cells are sensitive to TSH and may grow again)
  3. Measure TG (thyroglobulin) to monitor if the cancer ever returns (as everything has been wiped out so no TG should be released)

*TG is a protein produced by RER in thymocytes.

37
Q

What are the causes of medullary thyroid cancer? Which cells are affected?

A
  • Causes:
    • sporadic
    • familial
    • MEN 2

This is RARE but can be devastating

It is a cancer of the C-cells of the thyroid gland (these produce calcitonin so if too much then may be MCC)​

38
Q

What are the tumour markers of medullary thyroid cancer?

A

Tumour markers:

  1. Calcitonin (normally released but at high levels in cancer)
  2. CEA (carcinoembryonic antigen)
39
Q

What are the MEN1 and MEN2a/b cancers?

A

Year 5 - Pathology (89 decks)

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