The thyroid gland Flashcards

1
Q

Hyperthyroidism

A

Is where there is over-production of the thyroid hormones, triiodothyronine (T3) and thyroxine (T4), by the thyroid gland

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2
Q

Thyrotoxicosis

A

refers to the effects of an abnormal and excessive quantity of thyroid hormones in the body

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3
Q

Primary Hyperthyroidism

A

Is due to thyroid pathology. The thyroid is behaving abnormally and producing excessive thyroid hormone.

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4
Q

Secondary Hyperthyroidism

A

is due to pathology in the hypothalamus or pituitary. The pituitary gland produces too much thyroid-stimulating hormone, stimulating the thyroid gland to produce excessive thyroid hormones.

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5
Q

Subclinical hyperthyroidism

A

is where the thyroid hormones (T3 and T4) are normal and thyroid-stimulating hormone (TSH) is suppressed (low). There may be absent or mild symptoms.

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6
Q

Graves Disease

A

is an autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism. These TSH receptor antibodies, produced by the immune system, stimulate TSH receptors on the thyroid. This is the most common cause of hyperthyroidism.

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7
Q

Toxic multinodular goitre

A

(also known as Plummer’s disease) is a condition where nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones. It is most common in patients over 50 years.

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8
Q

Causes of hyperthyroidism

A

GIST
Graves’ disease
Inflammation (thyroiditis)
Solitary toxic thyroid nodule
Toxic multinodular goitre

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9
Q

Causes of thyroiditis

A

De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis

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10
Q

Hyperthyroidism presentation

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination

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11
Q

Graves disease specific features

A

Diffuse goitre (without nodules)
Graves’ eye disease, including exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)

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12
Q

Solitary toxic thyroid nodule

A

A solitary toxic thyroid nodule is where a single abnormal thyroid nodule acts alone to release excessive thyroid hormone. The nodules are usually benign adenomas. Treatment involves surgical removal of the nodule

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13
Q

Management of hyperthyroidism

A

Carbimazole is the first-line anti-thyroid drug, usually taken for 12 to 18 months. Once the patient has normal thyroid hormone levels (usually within 4-8 weeks), they continue on maintenance carbimazole and either:

The carbimazole dose is titrated to maintain normal levels (known as titration-block)
A higher dose blocks all production, and levothyroxine is added and titrated to effect (known as block and replace)
Propylthiouracil is the second-line anti-thyroid drug. It is used in a similar way to carbimazole. There is a small risk of severe liver reactions, including death, which is why carbimazole is preferred.

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14
Q

MHRA alert carbimazole

A

The MHRA issued a warning in 2019 about the risk of acute pancreatitis in patients taking carbimazole. In your exams, look out for a patient on carbimazole presenting with symptoms of pancreatitis (e.g., severe epigastric pain radiating to the back).

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15
Q

carbimazole and propylthiouracil cautions

A

Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections. A sore throat is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.

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16
Q

Iodine treatment rules

A

Women must not be pregnant or breastfeeding and must not get pregnant within 6 months of treatment
Men must not father children within 4 months of treatment
Limit contact with people after the dose, particularly children and pregnant women

17
Q

Hypothyroidism

A

refers to insufficient thyroid hormones, triiodothyronine (T3) and thyroxine (T4).

18
Q

Primary hypothyroidism

A

is where the thyroid behaves abnormally and produces inadequate thyroid hormones. Negative feedback is absent, resulting in increased production of TSH. TSH is raised, and T3 and T4 are low

19
Q

Secondary hypothyroidism

A

also called central hypothyroidism, is where the pituitary behaves abnormally and produces inadequate TSH, resulting in under-stimulation of the thyroid gland and insufficient thyroid hormones. TSH, T3 and T4 will all be low.

20
Q

causes of primary hypothyroidism

A

Hashimoto’s thyroiditis is the most common cause of hypothyroidism in the developed world. It is an autoimmune condition causing inflammation of the thyroid gland. It is associated with anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies.

Iodine deficiency is the most common cause of hypothyroidism in the developing world. In the UK, iodine is particularly found in dairy products and may be added to non-dairy milk alternatives (e.g., soya milk).

21
Q

Treatments for hyperthyroidism have the potential to cause hypothyroidism:

A

Carbimazole
Propylthiouracil
Radioactive iodine
Thyroid surgery

22
Q

What drugs can cause hypothyroidism

A

Lithium inhibits the production of thyroid hormones in the thyroid gland and can cause a goitre and hypothyroidism.

Amiodarone interferes with thyroid hormone production and metabolism, usually causing hypothyroidism but can also cause thyrotoxicosis.

23
Q

causes of secondary hypothyroidism

A

Secondary hypothyroidism is often associated with a lack of other pituitary hormones, such as ACTH, referred to as hypopituitarism. This is rarer than primary hypothyroidism, and may be caused by:

Tumours (e.g., pituitary adenomas)
Surgery to the pituitary
Radiotherapy
Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
Trauma

24
Q

presentation of hypothyroidism

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation

25
hypothyroidism management
Oral levothyroxine is the mainstay of treatment of hypothyroidism. Levothyroxine is a synthetic version of T4 and metabolises to T3 in the body. The dose is titrated based on the TSH level, initially every 4 weeks. Liothyronine sodium is a synthetic version of T3 and is very rarely used under specialist care where levothyroxine is not tolerated
26
The thyroid axis physiology
The hypothalamus releases thyrotropin-releasing hormone (TRH). TRH stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH). TSH stimulates the thyroid gland to release triiodothyronine (T3) and thyroxine (T4). The hypothalamus and anterior pituitary respond to T3 and T4 by suppressing the release of TRH and TSH, resulting in lower amounts of T3 and T4. The lower T3 and T4 offer less suppression of TRH and TSH, causing more of these hormones to be released, resulting in a rise of T3 and T4. This way, the thyroid hormone level is closely regulated to keep it within normal limits. When the end hormone (e.g., T3 and T4) suppresses the release of the controlling hormones (e.g., TRH and TSH), this is called negative feedback.