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MD4001 Pathology > Treatment of thyroid disorders > Flashcards

Treatment of thyroid disorders Flashcards

1
Q

What is the main hormone released by the thyroid gland?

A

T4 (thyroxine)

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2
Q

How can T4 be converted to T3?

A

5’ deiodinase

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3
Q

Where is T4 converted to T3?

A

Kidney and liver

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4
Q

How much more active is T3 than T4?

A

5 - 10 x more active

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5
Q

What does T3 bind to?

A

Nuclear receptor on various different tissues

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6
Q

What does T3 binding to nuclear receptors result in?

A
  • Gene transcription
  • mRNA synthesis
  • Protein synthesis
  • Affects many tissues - increase in BMR
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7
Q

What are the main effects of the thyroid hormones?

A
  • Increased soft tissue growth and bone maturation
  • Increased maturation of CNS
  • Increased Na/K+ ATPase
  • Increased O2 consumption
  • Increased Heat production
  • Increased BMR
  • Increased Glucose absorption
  • Increased Glyogenolysis
  • Increased gluconeogenesis
  • Increased lipolysis
  • Increased protein synthesis and degradation
  • Increased cardiac output (ionotropic and chronotropic affects)
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8
Q

What are the main affects of hyperthyroidism?

A
  • High BMR
  • Increased temperature, sweating
  • Nervousness, tremor, tachycardia, heat sensitivity and loss of weight
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9
Q

What are 2 common manifestations of hyperthyroidism?

A
  • Diffuse toxic goitre

- Toxic nodular goitre

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10
Q

What is diffuse toxic goitre?

A
  • Autoimmune disorder where antibodies to the TSH receptor stimulate thyroxine secretion
  • Toxic nodular goitre is caused by benign neoplasm/adenoma
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11
Q

What are causes which lead to hyperthyroidism?

A
  • Graves disease (LATS/TSI)
  • Overtreatment with thyroxine
  • Thyroid adenoma
  • Transient neonatal thyrotoxicosis (mother with Graves disease)
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12
Q

What cells are affected by graves disease specifically?

A

Thyroid follicular cells

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13
Q

How can hyperthyroidism be diagnosed?

A
  • Measure blood TSH, T3 and T4 levels
  • Test for anti-thyroid antibodies (especially TSH receptor antibodies)
  • Radionucleotide thyroid scan (123I - or 99mTcO4 - uptake) viewed by a gamma camera
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14
Q

What does an overactive part of the thyroid look like on a radionucleotide thyroid scaN?

A

Dark

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15
Q

What does the thyroid look like in thyroiditis on a radionucleotide thyroid scan?

A

Light - maybe nothing (hypothyroidism)

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16
Q

What are the 3 main treatments in thyroid disease?

A
  • Anti-thyroid drugs
  • Radioactive iodine
  • Surgery
    All have drawbacks
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17
Q

What is given to treat hyperthyroidism?

A

Oral radioiodine (131I)

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18
Q

How does radioiodine (131I) work?

A
  • Selectively taken up by thyroid
  • Damages cells - emits a short-range Beta radiation and affects only the follicle cells
  • Hypothyroidism eventually occur which can be treated with replacement therapy
19
Q

How is radioiodine (131I) given?

A
  • Orally
  • Given as single dose
  • Lasts ~ 2 months
  • Not to be given during pregnancy / lactation
20
Q

What drugs are used to treat hyperthyroidism?

A
  • Carbimazole (methimazole), Thioureylenes (thioamides)
  • Iodine
  • Beta blockers (propranolol)
  • Calcium supplements
21
Q

How do thioureylenes and carbimazole affect the thyroid?

A
  • Decrease synthesis of thyroid hormones

- Inhibit thyroperoxidase so reducing the iodination of thyroglobulin. Acts over 3-4 weeks

22
Q

How does iodine affect the thyroid?

A

Given orally in high doses and is converted to iodide and transiently reduces thyroid hormone secretion and vascularity of the gland

23
Q

What is the purpose of prescribing calcium supplements in the treatment of hyperthyroidism?

A

To maintain normal bone density

24
Q

What are the thioamides?

A
  • Propylthiouracil

- Methimazole (Carbimazole is its pro-drug)

25
Q

What group in thioamides is essential for antithyroid activity?

A

Thiocarbamide

26
Q

What does hypothyroidism lead to in children?

A

Cretinism

27
Q

What are the signs / symptoms of hypothyroidism?

A
  • Low BMR
  • Slow speech
  • Deep hoarse voice
  • Lethargy
  • Bradycardia
  • Sensitivity to cold
  • Mental impairment
28
Q

What can severe hypothyroidism be called?

A

Myxedema - can also be used to describe dermatological changes associated with hypothyroid and hyperthyroid conditions

29
Q

What is hypothyroidism due to?

A
  • Reduction removal ofthyroid hormones

- Preduction of antibodies that can break down the thyroid follicular cells

30
Q

What other cells have TSH receptors on them?

A

Fibroblasts - can be stimulated in hypothyroidism

31
Q

What is myxedema caused by?

A
  • Accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesioned and normal skin causing swelling/puffiness to the subcutaneous tissue
32
Q

What % of patients with hyperthyroidism have symptoms limited to pretibial myxedema?

A

1 - 5% of patients (due to high levels of antibody)

33
Q

What is Exophthalmos in Grave’s disease due to?

A

Depositing mucopolysaccaridies in the muscles at the back of the eye (antibody which does this not the high amounts of thyroid hormone)

34
Q

What are the symptoms of hypothyroidism due to?

A
  • Low levels of thyroid hormones and/or increased concentrations of TSH
35
Q

When would TSH not be raised in hypothyroidism?

A

Pituitary problem (test with protirelin, synthetic analogue of TRH)

36
Q

What can congenital hypothyroidism causes be?

A
  • Hypoplasia (agenesis/dysgenesis of gland during development)
  • Familial enzyme defects (dyshormonogenesis)
  • Iodine deficiency (endemic cretinism, perchlorate)
  • Intake of goitrogens during pregnancy
  • Pituitary defects
  • Idiopathic
37
Q

Why is it extremely important to detect hypothyroidism in newborns / babies as quickly as possible?

A
  • Longer the condition goes undetected the lower the IQ (also height)
  • May have few or no clinical manifestations
38
Q

What can be the causes of acquired hypothyroidism be?

A
  • Iodine deficiency
  • Auto-immune thyroiditis
  • Thyroidectomy or RAI therapy
  • TSH or TRH deficiency
  • Medications (iodine and cobalt)
  • Idiopathic
39
Q

What is hashimoto’s disease?

A
  • Enlarged, inflammed hypofunctioning thyroid (goite)
  • Caused by antibodies attacking the thyroid gland causing it to atrophy
  • Autoimmune lymphocytic thyroiditis
40
Q

What are the anti-thyroid antibodies in hashimoto’s disease?

A
  • Thyroglobulin Ab
  • Microsomal Ab/Thyroid peroxidase (TPO) Ab
  • TSH-R Ab (blocking antibodies)
41
Q

Is hashimoto’s disease heritable?

A

Yes - it runs in families

42
Q

What are the treatments for hypothyroidism?

A
  • Levothyroxine - synthetic analogue of thyroxine - has all the actions of endogenous thyroxine. Standard T4 replacement therapy for hypothyroidism
  • Liothyronine - synthetic analogue of tri-iodothyronine - has all the actions of endogenous tri-iodothyronne. Treatment of choice for myxedema coma
43
Q

What is Myxedema coma (an extreme form of hypothyroidism compounded by some stressful state, such as infectio, MI or stroke) treated with?

A

Liothyronine (Synthetic T3)

MD4001 Pathology (18 decks)

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