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Y3M - Diabetes & Endocrinology > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Remnant tissue of thyroid.

A

Lingual thyroid

Thyroglossal cyst

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2
Q

What is thyroid tissue made up of?

A

Colloid which contains iodinated thyroglobulin.

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3
Q

What is thyroglobulin synthesised by?

A

Surrounding follicular cells.

Thyroglobulin will then form thyroxine and be stored in colloid.

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4
Q

What secretes calcitonin?

A

Neuroendocrine cells also called parafollicular cells or C-cells.

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5
Q

When might calcitonin levels be elevated pathologically?

A

Medullary thyroid cancer - a rare form of thyroid cancer with a genetic basis.

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6
Q

Main circulating thyroid hormone?

A

T4 which can then be converted peripherally to the more potent and shorter-acting T3.

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7
Q

What are thyroid hormones bound to?

A

Thyroxine binding globulin (TBG)

and to a lesser extent:

Transthyretin

Albumin

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8
Q

What does the free thyroid hormones act on?

A

Intracellular thyroid receptors such as TRalpha and TRbeta.

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9
Q

Actions of thyroid hormones.

A

Increase basal metabolic rate

Affect growth in children.

Increase HR

CNS effects such as growth

Reproductive system effects

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10
Q

Reproductive system effects of thyroid hormones.

A

Metabolism and development of ovarian, uterine and placental tissue.

Hypo or Hyperthyroidism can therefore cause sub/infertility in women.

Can also lead to menstrual irregularities.

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11
Q

Pathology of primary hypothyroidism.

A

Problem with thyroid gland itself - most commonly autoimmune.

Such as Hashimoto’s and primary atrophic hypothyroidism.

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12
Q

Pathology of secondary hypothyroidism.

A

TSH deficiency usually due to pituitary disease.

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13
Q

T3, T4 and TSH levels in primary hypothyroidism.

A

T3 and T4 will be low.

TSH will be high.

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14
Q

T3, T4 and TSH levels in secondary hypothyroidism.

A

T3 and T4 will be low.

TSH will be non-elevated.

This is mainly due to hypopituitarism

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15
Q

T3, T4 and TSH levels in primary hyperthyroidism.

A

T3 and T4 will be high.

TSH will be low.

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16
Q

If TSH is not surpressed along with concurrent high T4 and T3 levels…

What is this suggestive of?

A

TSHoma

Thyroid hormone resistance

Assay interference

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17
Q

Give factors that affect thyroid function results.

A

May be affected by non-thyroidal illnesses so try to test when the patients are relatively well.

Lithium and amiodarone.

Pregnancy.

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18
Q

Thyroid hormone levels in subclinical hyperthyroidism.

A

T4 and T3 normal.

TSH is low

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19
Q

Thyroid hormone levels in subclinical hypothyroidism.

A

T4 and T3 normal

TSH elevated

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20
Q

Causes of subclinical hyperthyroidism

A

Recent treatment for hyperthyroidism.

Drugs such as steroids or dopamine

Non-thyroidal illness

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21
Q

Causes of subclinical hypothyroidism.

A

Poor compliance with thyroxine

Malabsorption of thyroxine

Drugs like amiodarone or lithium

Assay interference

Non-thyroidal illness recovery phase

TSH resistance

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22
Q

Hyperthyroidism: Women vs. Men.

A

Most common in young women.

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23
Q

Give causes of hyperthyroidism

A

Grave’s disease (most common)

Nodular thyroid disease (can lead to toxic multi-nodular goitre)

Thyroiditis

De Quervain’s thyroiditis

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24
Q

Course of Graves disease.

A

Relapsing-remitting course.

Typically affects young women.

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25
Q

Age of presentation of nodular thyroid disease compared to Graves.

A

Typically present at an older age than auto-immune does.

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26
Q

Pathology of nodular hyperthyroidism.

A

Caused by autonomous secretion of T3 and T4 either from a solitary toxic nodule, or numerous nodules situated with a toxic multinodular goitre.

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27
Q

Pathology of thyroiditis.

A

Inflammation of thyroid gland causing a release of thyroxine.

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28
Q

Causes of thyroiditis.

A

Viral infection (Subacute de Quervain’s thyroiditis)

Medication such as amiodarone

Following childbirth also called post-partum thyroiditis.

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29
Q

Phases of thyroiditis.

A

Initial toxic hyperthyroidal phase followed by a hypothyroid phase.

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30
Q

What is De Quervain’s thyroiditis?

A

Subacute thyroiditis triggered by a viral infection such as mumps or the flu.

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31
Q

Common clinical features of hyperthyroidism.

A

Increased sympathetic function.

Weight loss

Increased appetite

Insomnia

Irritability

Anxiety

Heat intolerance

Palpitations

Tremors.

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32
Q

Less common clinical features of hyperthyroidism.

A

Pruritus

Increased bowel frequency

Loose motions

Menstrual disturbances

Reduced fertility

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33
Q

What is apathetic thyrotoxicosis?

A

A case of hyperthyroidism where elderly patients might present with atypical features such as reduced energy levels.

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34
Q

Hyperthyroidism is less common in children than adults.

Clinical features of hyperthyroidsm in children.

A

Classical symptoms

Accelerated growth

Behavioural disturbances.

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35
Q

General signs of hyperthyroidism.

A

Resting tachycardia

Warm peripheries

Resting tremors

Hyper-reflexia

Lid lag

Hypertension

Flow murmur

Aggitation

Hyperkinesia

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36
Q

Specific clinical signs of Graves.

A

Lid retraction - Graves ophthalmopathy

Dermopathy

Pre-tibial myxoedema

Nail changes similar to clubbing called thyroid acropachy.

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37
Q

Why do the specific clinical signs of Graves occur?

A

Cross-reactivity with TSH receptors in the back of the orbit and the skin.

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38
Q

Hallmark of hyperthyroidism.

A

Elevated free fT4 and free fT3 with undetectable levels of TSH.

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39
Q

What is an elevated fT3 alone with normal fT4 and suppressed TSH called?

A

T3-toxicosis

40
Q

What is T3-toxicosis?

A

It is caused by iodine deficiency or the earliest stages of disease caused by an autonomously functioning thyroid nodule, multinodular goitre or Graves’ disease

41
Q

What is normal FT4/FT3 and suppressed TSH indicative of?

A

Subclinical hyperthyroidism and suggests autonomous thyroid activity.

42
Q

TPO and TSHrAb differences in regards of specificity.

A

TPO is a non-specific marker for auto-immune thyroid disease (Hashimoto’s)

TSHrAb (Grave’s) is more sepcific and may be helpful in particular clinical situations such as pregnancy.

43
Q

Investigation to confirm nodular thyroid disease.

A

Ultrasound. It will not assess gland activity.

44
Q

What imaging can be used to determine functionality of the thyroid?

A

Nuclear imaging such as technetium-99 or iodine uptake isotope scan.

It can determine functionality and therefore the cause of hyperthyroidism.

45
Q

Explain the iodine uptake isotope scan differences in Graves, nodular disease and thyroiditis.

A

Graves will have a uniform increase uptake

Nodular disease will only have increased uptake in the autonomous nodule/s

Thyroiditis will see an absent of uptake

46
Q

Different treatments of hyperthyroidism.

A

Medication

Surgery

Radioactive iodine

47
Q

What is the first line approach of hyperthyroidism?

A

Medical treatment.

48
Q

Give examples of medical treatment of hyperthyroidism.

A

Thionamides such as carbimazole and propylthiouracil.

Reduces synthesis of T3 and T4 and will take around 4-6 weeks to normalise.

Titration regimen:

Carbimazole for 4 weeks and reduce according to TFTs every 1-2 months

Block replace:

Carbimazole + Levothyroxine simultaneously to reduce risk of iatrogenic hypothyroidism.

In Grave’s you should maintain one of the regimen for at least 12-18mo and then withdraw.

Around 50% will relapse leading to requirement of radioiodine or surgery.

49
Q

What might be used to control symptoms of hyperthyroidism until the thyroid function has returned to normal?

A

Beta-blockers.

50
Q

Important rare side effect of Thionamides?

A

Agranulocytosis

If an unexplained fever or sore throat occurs an urgent full blood count is required to exclude pancytopaenia and drugs should be stopped if the neutrophil count is low.

51
Q

More common side effect of thionamides.

A

Generaled rash which disappears after cessation.

52
Q

Explain why radioactive iodine (131 I) might not be the go-to option for definitive treatment of hyperthyroidism.

A

Contra-indicated in pregnancy.

May lead to flare up of eye disease in patients with pre-existing opthalmopathy.

Can cause hypothyroidism.

Patients will emit a small amount of radiation meaning that they are advised to avoid close contact with young children and pregnant women.

53
Q

What might be given during anaesthetic induction during thyroid surgery to prevent peri-operative atrial fibrillation?

A

Beta-blockade.

This is if thyroid function is not optimal.

54
Q

Complications of thyroid surgery.

A

Bleeding

Infection

Damage to RLN

Temporary or permanent hypocalcaemia due to hypoparathyroidism.

55
Q

Primary hypothyroidism in men vs women.

A

6 times as common in women.

56
Q

Most common cause of primary hypothyroidism.

A

Autoimmune.

If there is enlargement of the gland with hypothyroidism it is sometimes termed Hashimotos thyroiditis.

57
Q

Give other causes of primary hypothyroidism.

A

Pregnancy may lead to transient or permanent.

Iodine deficiency leading to neonatal hypothyroidism and severe mental retardation.

Familial thyroid dyshormonogenesis.

Drugs

Iatrogenic

58
Q

What might pregancy hypothyroidism/post-partum thyroiditis be misdiagnosed as?

A

Post-natal depression

59
Q

Give examples of drugs that can cause hypothyroidism.

A

Amiodarone

Lithium

60
Q

Give examples of iatrogenic causes of hypothyroidism.

A

Thyroid surgery

Radioiodine

Radiation to head and neck

61
Q

Cause of secondary hypothyroidism.

A

TSH deficiency characterised by low fT4 and non-elevated TSH. Means a problem with the pituitary gland.

62
Q

Clinical features of hypothyroidism.

A

Weight gain

Cold intolerance

Fatigue

Constipation

Bradycardia

Thickening of the skin

Puffiness around the eyes (myxoedema)

63
Q

Why might hypothyroidism be diagnosed incidentally?

A

Because the symptoms are most commonly very subtle.

Means during a routine blood test it might be picked up.

64
Q

Why might slightly abnormal thyroid results not always be the cause of the patient’s symptoms?

A

There are symptoms such as fatigue, weight gain etc… that are very similar to depression or chronic fatigue.

Sine this is experienced by up to 40% of the normal population they might not be due to illness, but other factors.

65
Q

Hallmarks of hypothyroidism

A

Usually low fT4 and elevated TSH. TSH alone is commonly used to diagnose hypothyroidism. This is the case of primary hypothyroidism.

In case of secondary since TSH will be low, fT4 also needs to be measured.

Autoimmune is also confirmed by thyroid antibodies such as TPO.

66
Q

Treatment of hypothyroidism.

A

Thyroxine replacement to improve symptoms and normalise thyroid function.

Levothyroxine (T4) 0-100 mcg/24h PO.
Review this at 12 weeks.

Adjust 6-weekly by clinical state and to normalise but not suppress TSH.

Once normal check TSH yearly.

Treat the patient not the blood levels

67
Q

Typical starting dose of thyroxine.

A

50-100 microgram/day

68
Q

Why might elderly patients not be given a dose of 50-100 ug/day?

And instead 25ug/day?

A

If you have ischaemic heart disease an increased sympathetic drive might not be favourable.

69
Q

What does persistently elevated TSH suggest when a patient is on medication?

A

Under-replacement

Poor compliance

Malabsorption (e.g. coeliac disease, concurrent medication)

70
Q

Give examples of which concurrent medications might cause malabsorption of thyroxine.

A

Iron

Calcium

PPis

71
Q

What does a suppressed or undetectable TSH suggest when treating with thyroxine?

A

Over-replacement.

72
Q

What is the risk of overtreating hypothyroidism?

A

Atrial fibrillation

Osteoporosis

73
Q

Give other treatment (not recommended).

A

T3 (liothyronine)

Dessicated thyroid extract (armour thyroid)

74
Q

Option for patients who remain symptomatic despite normalisation of thyroid function.

A

Investigated for non-thyroid pathology.

75
Q

What is the aim of treatment of secondary hypothyroidism (in terms of fT4 levels)?

A

Should be replaced to the upper part of the normal range of fT4.

76
Q

Why should fT4 be replaced to the upper part of the normal range in seconary hypothyroidism?

A

Because TSH cannot be relied upon as a measure of optimal replacement.

This means that doses should not be mistakenly reduced on the basis of a suppressed TSH level

77
Q

Thyroid levels in subclinical hypothyroidism.

A

Normal fT4 with elevated TSH.

78
Q

Treatment of asymptomatic patients with subclinical hypothyroidism.

A

Usually not needed.

Thyroid function spontaneously reverts to normal during repeat testing in 10-15% of patients.

79
Q

When should treatment of thyroxine be commenced if patient has subclinical hypothyroidism but remains asymptomatic?

A

If TSH is >10 miU/L

80
Q

Why is treatment commenced if TSH >10 miU/L?

A

Due to the high likelihood of progressing to frank hypothyroidism.

81
Q

When else should treatment be considered at lower levels of TSH elevation (such as 5-10 miU/L) in subclinical hypothyroidism?

A

In women planning pregnancy

Trial basis in symptomatic patients

Patients with significant dyslipidaemia

82
Q

Follow-up of patients with positive thyroid antibodies.

A

Annual thyroid function test to ensure they do not progress to overt hypothyroidism.

83
Q

Treatment of De Quervain’s Thyroiditis

A

Self-limiting

May have a painful goitre so you can give NSAIDs

84
Q

Treatment of thyroid eye disease.

A

Treat hyper or hypothyroidism.

In severe disease try high dose steroids (IV methylprednisolone is preferred).

Surgical decompression can be done.

Eyelid surgery can be done

Infliximab

85
Q

When to screen for abnormalities in thyroid function.

A

Patients with AF

Patients with hyperlipidaemia (around 4-14% will have hypothyroidism)

DM

Women with T1DM during 1st trimester and post delivery

Patients on amiodarone or lithium (6monthly)

Patients with Down Syndrome, Turner’s syndrome or Addison’s disease (yearly)

86
Q

Causes of diffuse goitre

A

Physiological

Grave’s disease

Hashimoto’s

De Quervain’s (painful)

Iodine def

87
Q

Causes of nodular goitre

A

Multinodular goitre

Adenoma

Carcinoma

88
Q

What is myxoedema coma?

A

The ultimate hypothyroid state before death.

89
Q

Signs and symptoms of myxoedema coma.

A

Looks hypothyroid

Often >65yrs

Hypothermia

Hyporeflexia

Glucose is down

Bradycardia

Coma

Seizures

May have a history of radioiodine or thyroidectomy.

90
Q

Precipitants of myxoedema coma.

A

Infection

MI

Stroke

Trauma

91
Q

Examination of myxoedema coma.

A

Goitre

Cyanosis

Decreased BP

Heart failure

Signs of precipitants

92
Q

Treatment of myxoedema coma.

A

In ICU

Bloods => T3, T4, TSH, FBC, U&Es, cultures, cortisol and glucose

ABG

Correct hypoglycaemia

Give T3 (liothyronine) 5-20 mcg/12h IV slowly

Give hydrocortisone 100mg/8h IV

If infection is suspected give abx IV

Caution with fluid (can cause cardiac dysfunction)

Active warming to treat hypothermia

93
Q

Signs and symptoms of thyrotoxic storm.

A

More common in women

Severe hyperthyroidism.

Fever

Agitation

Confusion

Coma

Tachycardia

AF

D+V

Goitre

Thyroid bruit

Acute abdomen

Heart failure

94
Q

Precipitants to thyroid storm.

A

Recent thyroid surgery or radioiodine

Infection

MI

Trauma

95
Q

Diagnosis of thyrotoxic storm.

A

Do not wait for test results to come back

Do TSH, fT4 and fT3.

Confirm with technetium uptake if possible.

96
Q

Treatment of thyrotoxic storm.

A

Seek endocrinology advice

Counteract peripheral effects of thyroid hormones

Inhibit thyroid hormone synthesis

Treat systemic complications

If no improvement in 24h thyroidectomy may be an option.

Y3M - Diabetes & Endocrinology (17 decks)

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