Clinical Case Studies - Thyroid Flashcards

1
Q

What is hyperthyroidism?

A

Too much circulating thyroid hormone in the body.

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2
Q

What are the symptoms of hyperthyroidism?

A
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3
Q

How do you investigate disorders of the thyroid?

A

History

Physical examination

  • Signs of dysfunction
  • The presence and size of a goiter or discrete nodules

Laboratory tests

  • T3 and T4. TSH
  • Thyrotropin receptor antibodies (TRab) - Graves (hyper)
  • Thyroid peroxidase antibodies, Thyroglobulin antibodies, - Hashimotos thyroiditis (hypo)
  • Guthrie test (heel prick on babies)

Imaging

  • USS
  • CT chest - ?retrosternal expansion
  • Isotope scan - hot vs cold nodule

Histopathology/cytology

  • Fine needle aspiration - exclude malignancy
  • Core biopsy

Non-diagnostic for cytological diagnosis – Thy 1

Non-neoplastic – Thy 2

Neoplasm possible – Thy3. Thy3f: samples suggesting follicular neoplasms - unable to reliably test (benign and malignant very similar)

Suspicious of malignancy – Thy4

Malignant – Thy5

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4
Q

What are causes of hyperthyroidism?

A
  • Graves’ disease
  • Toxic adenoma and toxic multinodular goiter
  • De Quervain’s thyroiditis/Subacute thyroiditis
  • Iodine-induced hyperthyroidism
  • Trophoblastic disease and germ cell tumors — hydatidiform mole or choriocarcinoma or in men with testicular germ cell tumors via direct stimulation of the TSH receptor.
  • TSH-mediated hyperthyroidism — Hyperthyroidism caused by increased thyroid-stimulating hormone (TSH) production is rare. Two forms, neoplastic and non-neoplastic, are recognized.
    TSH-producing pituitary adenomas are usually macroadenomas by the time of diagnosis, and some are locally invasive.
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5
Q

What is the pathophysiology of Graves disease?

A
  • Most common cause of hyperthyroidism
  • Autoimmune disorder resulting from thyroid-stimulating hormone (TSH)-receptor antibodies (also called thyroid-stimulating immunoglobulins), which stimulate thyroid gland growth and thyroid hormone synthesis and release.
  • Stressful life events and high iodine intake may be a risk factor for the disease
  • Several drugs have been implicated → lithium, interferon alfa, and alemtuzumab.
  • Exophthalmos, periorbital and conjunctival edema, limitation of eye movement, and infiltrative dermopathy (pretibial myxedema) occur only in patients with Graves’ disease.
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6
Q

What is the pathophysiology of Toxic multinodular goitre and Toxic adenoma?

A

The result of focal and/or diffuse hyperplasia of thyroid follicular cells whose functional capacity is independent of regulation by TSH.

Mutations of the genes for the TSH receptor have been identified in both toxic adenomas and nodules of toxic multinodular goiters.

Toxic multinodular goiter tends to be more common in areas where iodine intake is relatively low.

In comparison, the frequency of thyroid adenomas is not related to iodine intake.

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7
Q

What is the pathophysiology of De Quervain’s thyroiditis/Subacute thyroiditis

A
  • Transient hyperthyroidism often following viral infection.
  • Resulting thyroid inflammation damages thyroid follicles and activates proteolysis of the thyroglobulin stored within the follicles.
  • Unregulated release of large amounts of thyroxine (T4) and triiodothyronine (T3) into the circulation resulting in clinical and biochemical hyperthyroidism.
  • New hormone synthesis also ceases, not only because of damage to the thyroid follicular cells but also because of inhibition of thyroid-stimulating hormone (TSH) secretion by the increased serum T4 and T3 concentrations.
  • Inflammation subsides, the thyroid follicles regenerate and thyroid hormone synthesis and secretion resume
  • There is usually a period of rapid evolution through euthyroidism and then into hypothyroidism.
  • The hypothyroidism lasts until the thyroid gland can generate sufficient thyroid hormone synthesis and secretion so that the patient regains normal homeostasis.
  • Each phase typically lasts two to eight weeks with the possible exception of the initial transition through euthyroidism, which may be shorter.
  • Recovery is nearly always complete.
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8
Q

What are complications of Hyperthyroidism?

A
  • AF
  • High output cardiac failure
  • Cardiomyopathy
  • Osteoporosis
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9
Q

What are the symptoms of hypothyroidism?

A
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10
Q

What types of hypothyroidism are there?

A

Primary - accounts for over 95 percent of cases of hypothyroidism.

  • iodine deficiency
  • Hashimoto’s thyroiditis - autoimmune
  • Post-thyroidectomy

Secondary - insufficient stimulation of the thyroid gland by TSH, caused by pituitary

  • Pituitary adenoma
  • Sheehan’s syndrome (ischaemic necrosis of pituitary gland after childbirth)

Tertiary - hypothalamic damage

  • tumors, trauma, radiation therapy, or infiltrative disease - TB/Haemochromatosis
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11
Q

What are the complications of hypothyroidism?

A
  • Hypercholesterolaemia
  • Myxodema coma
  • Pre-eclampsia
    *
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12
Q

What are the complications of hypothyroidism?

A
  • Hypercholesterolaemia
  • Myxodema coma
  • Pre-eclampsia
    *
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