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MET3B > Hyper and Hypothyroidism > Flashcards

Hyper and Hypothyroidism Flashcards

1
Q

Which artery supplies the thyroid gland?

A

Superior and Inferior thyroid glands

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2
Q

What is the normal weight of the thyroid gland?

A

10-20g

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3
Q

There are 2 main thyroid cell types, name them

A

Follicular cells around colloid pool

C cells – calcitonin producing

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4
Q

What is the difference between Hyperthyroidism and thyrotoxicosis?

A

Hyperthyroidism: overactive thyroid gland (i.e. increased thyroid hormone production) causing an excess of thyroid hormone and thyrotoxicosis.

Thyrotoxicosis: refers to an excess of thyroid hormone, having an overactive thyroid gland is not a prerequisite (e.g. consumption of thyroid hormone).

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5
Q

Describe the normal physiology of the thyroid hormone

A
  1. TRH is secreted from the paraventricular nucleus of the hypothalamus
  2. It reaches the anterior pituitary via the hypophyseal portal system. Here it causes the release of thyroid stimulating hormone.
  3. TSH, is produced and released by the thyrotrophs of the anterior pituitary
  4. TSH acts upon the thyroid gland promoting the synthesis and release of thyroid hormone.
  5. The thyroid produces two hormones, thyroxine (T4) and triiodothyronine (T3).
  6. These hormones suppress TRH and TSH release
  7. secreted thyroid hormone is 90% T4.
  8. Peripherally much of T4 is converted to T3
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6
Q

Which thyroid hormone is most biologically active?

A

T3

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7
Q

What do inactive thyroid hormones bind to in the blood?

A

thyroxine-binding globulin (TBG) - thyroglobulin

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8
Q

What are the normal physiological effects of T3/T4? 5 main features.

A

BMR: increases the basal metabolic rate.

Metabolism: it has anabolic effects at low serum levels and catabolic effects at higher levels.

Growth: increases release and effect of GH and IGF-1.

Cardiovascular: increases the heart rate and contractility through increasing sensitivity to catecholamines.

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9
Q

Which organs are responsible for the conversation of T4 to T3?

A

Liver (most common)
Skeletal muscle
Kidneys

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10
Q

Name the 8 main causes of hyperthyroidism?

A
  1. Graves’ disease
  2. Toxic multinodular goitre
  3. Solitary toxic adenoma
  4. Amiodarone-induced thyrotoxicosis type 1
  5. Beta-HCG related
  6. Pituitary adenoma
  7. Follicular thyroid cancer
  8. Struma ovarii
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11
Q

Describe graves disease and how it causes hyperthyroidism

A
  • Autoimmune condition
  • Most common cause of hyperthyroidism

Caused by IgG antibodies to the TSH receptors found within the thyroid = TSHR-Ab

Antibodies mimic the action of TSH causing excessive stimulation of the gland.

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12
Q

Which eye pathologies are associated with graves disease?

A

exophthalmos

ophthalmoplegia (weakness of eye muscles),

conjunctival oedema (white part of eye swells)

Papilloedema (oedema of the optic disc)

Keratopathy (abnormal gray band across eye (circumcorneal band))

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13
Q

Which clinical findings are directly associated with Graves disease?

A
  • ophthalmopathy
  • Diffuse moderate enlargement of the thyroid gland which feels firm on palpation
  • pretibial myxoedema
  • lymphoid hyperplasia including splenomegaly and an enlarged thymus
  • Clubbing due to acropachy
  • Patients may be euthyroid or become hypothyroid
  • May be a personal or family history of autoimmune disease.
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14
Q

Describe Toxic nodular goitre and how it causes hyperthyroidism

A

multiple nodules develop that are capable of secreting thyroid hormones.

The presence of a multinodular goitre without the above symptoms (ie specific features of Graves’ disease) suggests toxic nodular goitre

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15
Q

Describe Solitary toxic adenoma and how it causes hyperthyroidism

A

a single adenoma which produces thyroid hormones.

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16
Q

Describe what Amiodarone-induced thyrotoxicosis type 1 is and how it causes hyperthyroidism

A

Amiodarone has a iodine content.
Can cause both hypothyroidism and hyperthyroidism

In type 1 the Jod-Basedow phenomenon, in which excess iodine intake causes excess thyroid hormone synthesis. It is seen in patients with pre-existing thyroid disease.

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17
Q

What is amiodarone?

A 
class III anti-arrhythmic drug
with a high iodine content
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18
Q

Describe Beta-HCG and how it causes hyperthyroidism

A

Beta-HCG is thought to mimic the action of TSH causing thyroid hormone synthesis and release

It occurs in states of elevated Beta-HCG:

  • Pregnancy
  • Hydatidiform mole
  • Choriocarcinoma
  • Testicular germ cell tumour
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19
Q

How does a Pituitary adenoma causes hyperthyroidism?

A

TSH-secreting pituitary adenoma causes excess stimulation of the thyroid gland and resultant hyperthyroidism.

Secondary
hyperthyroidism – raised TSH and FT4

Rare

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20
Q

How does a Follicular thyroid cancer causes hyperthyroidism?

A

In metastatic follicular thyroid cancer, malignant tissue may remain functional. The increased amounts of tissue can lead to an overproduction of thyroid hormone.

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21
Q

Describe Struma ovarii and how it causes hyperthyroidism

A

Hyperthyroidism is caused by thyroid hormone release from ectopic thyroid tissue related to:

  • Ovarian teratomas
  • Dermoid tumours

The majority of these
tumours are benign.

Rare condition

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22
Q

What can cause thyrotoxicosis without a previous case of hyperthyroidism?

A

Levothyroxine
De Quervain’s (subacute granulomatous) thyroiditis
Amiodarone-induced thyrotoxicosis type II

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23
Q

Describe how Levothyroxine can cause thyrotoxicosis without a previous case of hyperthyroidism?

A

When taken at supra-therapeutic doses

Patients may abuse levothyroxine for weight-loss purposes.

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24
Q

Describe how De Quervain’s (subacute granulomatous) thyroiditis can cause thyrotoxicosis without a previous case of hyperthyroidism?

A
  • a self-limiting condition
  • viral in origin
  • results in inflammation of the thyroid gland and release of thyroid hormone.
  • Characteristically causes a painful goitre.
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25
Q

What are the 3 phases of De Quervain’s (subacute granulomatous) thyroiditis?

A

Thyrotoxicosis
Hypothyroidism
Resolution

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26
Q

Describe how Amiodarone-induced thyrotoxicosis type II causes thyrotoxicosis without a previous case of hyperthyroidism?

A

Type 2 is caused by a destructive thyroiditis with resultant release of thyroid hormone.

in which there is excess release of pre-formed T4 and T3 into the circulation. It typically occurs in patients without underlying thyroid disease and is caused by a direct toxic effect of amiodarone on thyroid follicular cells

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27
Q

Which drugs can cause thyrotoxicosis and hyperthyroidism?

A 
amiodarone / lithium
exogenous iodine (Jod-Basedow)
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28
Q

What are the signs and symptoms associated with hyperthyroidism?

A 
Symptoms
Goitre
Palpitations
Heat intolerance
Weight loss
Diarrhoea 
Amenorrhoea 
Reduced libido
Gynaecomastia (in men)
Fatigue
Signs
Goitre
Sinus tachycardia/arrhythmias
Hair loss
Palmar erythema
Tremor
Thyroid bruit (Graves’)
Myxoedema -
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29
Q

What is the cause of Myxoedema?

A

Deposition of mucopolysaccharides in the skin leading to swelling

30
Q

What are the features of Graves’ ophthalmopathy?

A

proptosis, periorbital oedema, lid retraction, eye pain and visual loss.

31
Q

List the 2 main causes of secondary hypothyroidism

A

TSH-secreting pituitary adenoma.

hCG-secreting tumour.

32
Q

What is the most common cause of subclinical hyperthyroidism and how would it be diagnosed on a blood test?

A

toxic nodular goitre,

low TSH with normal thyroid hormone levels

33
Q

What else can cause a low TSH with normal thyroid hormone levels?

A

glucocorticoids, dopaminergic drugs or amiodarone

34
Q

How is hyperthyroidism diagnosed? How do the results relate to each type of hyperthyroidism?

A

Measurement of TSH and fT4/fT3

Primary hyperthyroidism: low TSH, raised fT4 and fT3

Subclinical hyperthyroidism: low TSH, normal fT4 and fT3

Pituitary adenoma: high TSH, raised fT4 and fT3

35
Q

Which imaging techniques are used in the assessment of thyperthyroidism?

A
  • Ultrasonography
  • Thyroid uptake scan:

Thyrotoxicosis with increased uptake: indicative of increased hormone synthesis

Thyrotoxicosis with decreased uptake: indicative of inflammation/destructions of the thyroid gland with release of thyroid hormone

36
Q

How is hyperthyroidism treated?

A

Following diagnosis
Thioamides - carbimazole or propylthiouracil

beta-blocker or calcium channel blocker until thioamides take effect

Radioactive iodine - taken up by the thyroid causing destruction and reduces thyroid hormone release.
offered first-line in Graves and toxic multinodular goitre

Thioamides

  • drugs reduce thyroid synthesis working over a number of weeks
  • May be offered first line in Graves’ disease (mild uncomplicated)
  • Remission may be seen after 18-24 months of treatment
  • UK carbimazole is used first-line. Propylthiouracil may be used first-line if the patient is intolerant to carbimazole, in the first trimester of pregnancy or if in thyroid storm

Thyroidectomy
used as definitive therapy if malignancy is suspected, there is a compressive goitre or RAI/ anti-thyroid medications are unsuitable

solitary toxic nodule = Hemithyroidectomy

37
Q

Which tests must be done before Thioamides therapy and why?

A

Baseline FBC and LFTs are obtained prior to the commencement of thioamides. Neutropaenia or severely deranged transaminases are a contraindication to treatment.

Agranulocytosis is a severe side effect associated with both thioamides.

38
Q

What are the 2 regimes available for Thioamides use?

A

Block and replace: Thioamides given at a level sufficient to block endogenous T3/T4 production alongside levothyroxine. This regime must not be used in pregnancy.

Dose titration: Thioamides are given alone, dose adjusted to give normal levels of T3/T4.

39
Q

Radioactive iodine is contraindicated in who?

A

pregnant women and those breastfeeding

40
Q

Why is surgery or RAI often preferred to Thioamides treatment in those with toxic nodules?

A

treatment is likely life-long if Thioamides is chosen as definitive management

41
Q

What are the complications of thyroidectomy?

A

Hypocalcaemia: affects 10%, typically transient, may be permanent in a minority of cases. Due to the proximity of parathyroid gland to the thyroid gland.

Recurrent laryngeal nerve injury: presents with hoarse voice post-operatively.

Hypothyroid & sometimes hypoparathyroid post op

42
Q

How is Graves’ ophthalmopathy treated?

A

Mild disease-
In mild disease (‘NO’) artificial tears, elevation of the head during sleep and sunglasses may help symptoms. Smoking cessation is always advised.

More sever -
Referral to an ophthalmologist is required if there is evidence of optic nerve compression, corneal opacity or inability to close an eye.

Treatment may include:

Steroids
Irradiation
Surgical decompression

43
Q

What are the symptoms of Thyrotoxic crisis?

A

hyperthermia, tachycardia, arrhythmias, nausea, vomiting, seizures and cognitive decline.

44
Q

How is Thyrotoxic crisis treated?

A

Nonselective Beta-blockers e.g propranolol

Thionamides: typically propylthiouracil, which in addition to its anti-thyroid effect also reduces the conversion of T4 to T3.

Corticosteroids: reduce the conversion of T4 to T3.

Lugol’s iodine

Electrolyte imbalances, heart failure and hyperthermia should be addressed.

Blood sugar must be monitored.

Dialysis or plasma exchange may be required.

45
Q

What is primary hypothyroidism? What are the 2 types it can be divided into?

A

Primary hypothyroidism - where disease is intrinsic to the thyroid gland

Primary hypothyroidism (overt): Elevated thyroid stimulating hormone (TSH) levels (typically > 10 mU/L) with a free T4 (fT4) level below the normal range.

Subclinical hypothyroidism: The subclinical state is characterised by elevated TSH levels but T3/T4 that remains within the normal range.

46
Q

What is secondary hypothyroidism?

A

Disease or damage to the pituitary may reduce the production or release of TSH. Most frequently caused by pituitary adenomas.

There will be low THS and fT3 and fT4

In even rarer cases the TSH level is normal (or high) but the structural abnormalities cause the hormone to have less biological activity.

47
Q

What is tertiary hypothyroidism?

A

Disease or damage to the hypothalamus or the hypophyseal portal system may reduce the production, release or transport of TRH

Reduced levels of thyroid hormone (T3 and T4) accompanied by reduced TSH and TRH.

48
Q

What is thyroid hormone resistance

A

In rare circumstances, individuals may suffer from resistance to thyroid hormone. This genetically inherited disorder is caused by an unresponsive form of one of the T3 receptors.

It is characterised by raised levels of thyroid hormone and TSH (as negative feedback is somewhat inhibited by hormone resistance).

This compensatory increase means most individuals are clinically euthyroid.

49
Q

List the 5 main causes of Primary hypothyroidism

A

Chronic autoimmune (Hashimoto’s) thyroiditis

Iodine deficiency

Postpartum thyroiditis

Amiodarone-induced hypothyroidism

Congenital hypothyroidism

50
Q

Describe what is Hashimoto’s thyroiditis and how it causes hypothyroidism

A

Cell and Antibody mediated destruction of the thyroid gland

2 types
Goitrous: characterised by a firm and rubbery goitre

Atrophic: characterised by an atrophic gland

associated with autoimmune conditions such as type 1 diabetes mellitus and

51
Q

Which genetic conditions are associated with Hashimoto’s thyroiditis

A

Turner’s and Down’s syndrome.

52
Q

Which auto antibodies are found in Hashimoto’s thyroiditis?

A

~90% of patients having positive Thyroid peroxidase antibodies (TPO) antibodies

~50% of patients having positive thyroglobulin antibodies.

Thyroid stimulating hormone receptor (TSHR) antibodies: may be measured if the patient suffers with thyroid eye disease.

53
Q

Describe how is Iodine deficiency causes hypothyroidism

A

Iodine is a key component of thyroxine and its deficiency results in ‘endemic’ goitres.

Rare in developed world as foods are now fortified with iodine

54
Q

Describe what is Postpartum thyroiditis and how it causes hypothyroidism

A

Postpartum thyroiditishappens when a woman’sthyroidgland becomes inflamedafterhaving a baby.

A transient change that occurs in the six months following birth,

Might experience two phases.

Hyperthyroidism phase-
Inflammation and release of thyroid hormone

Hypothyroid phase -
Presents later, as thyroid cells become impaired

Most women will show complete resolution of the condition. Lasts 6- 12 months

55
Q

Describe what is Amiodarone-induced hypothyroidism and how it causes hypothyroidism

A

Pre-existing autoimmune disease: hypothyroidism may occur secondary to the Wolff–Chaikoff effect - a phenomenon in which raised iodine intake results in reduced levels of thyroid hormone.

Normal thyroid gland: those with a normal gland may also develop hypothyroidism, frequently affecting T3.

56
Q

What is Congenital hypothyroidism

A

Congenital hypothyroidism is screened for with the Guthrie screen to prevent cretinism (the syndrome caused by congenital hypothyroidism). It may be due to:

Dyshormonogenesis
Abnormal gland development

57
Q

What are the signs and symptoms of hypothyroidism?

A 
Symptoms
Tiredness
Lethargy
Weight gain
Cold intolerance
Menstrual irregularities (Oligomenorrhoea, amenorrhoea, menorrhagia)
Reduced libido
Goitre

Signs
Hair loss (characteristically the outer third of the eyebrows)
Dry skin
Goitre
Bradycardia
Myxoedema
Delayed relaxation phase of deep tendon reflexes

58
Q

How is hypothyroidism diagnosed?

A

Measurement of TSH and fT4 is usually enough

Primary hypothyroidism: raised TSH and reduced fT4.

Subclinical hypothyroidism: raised TSH and normal fT4.

Secondary or tertiary hypothyroidism: normal (inappropriately normal) or lowered TSH or TRH and a reduced fT4.

59
Q

Which other abnormalities is an untreated hypothyroidism associated with? How are these conditions tested for?

A

CK,
raised cholesterol and triglycerides- Serum lipid

anaemia (normocytic or macrocytic) - FBC, B12 and Folate

Diabetes - HbA1c

Coeliac disease - Coeliac serology

60
Q

How is hypothyroidism treated?

A

Treat with levothyroxine – titrated to target TSH (aim for normal range)

61
Q

If a patient being treated for hypothyroidism has high TSH and normal FT4 what could be the cause?

A

intercurrent illness
• inadequate dose
• malabsorption
• poor concordance with therapy

62
Q

If a patient presents with a potential goitre how is this investiagted and what would the imaging show?

A

Investigations
• Thyroid function test
• Lung function – signs of tracheal compression
• CXR +/- thoracic inlet views
• Ultrasound scan +/- fine needle aspiration
• CT (without contrast)

Chest XR – retrosternal mass and deviated trachea

CT (without contrast as this is iodinated and may exacernate goitre in
this patient) – shows marked goitre compressing trachea

63
Q

In hyperthyroidism Radioactive iodine can exacerbate which pathology in graves disease?

A

ophthalmopathy.

64
Q

If a patient presents with a goitre which symptoms may they have specific to the goitre?

A

dysphagia

• cough / dyspnoea / stridor

65
Q

When a patients presents with a goitre, is it always treated/ operated straight away?

A

Watch and wait – especially if lots of co- morbidities
then maybe
• Surgery vs RadioIodine

66
Q

If a patient has medullary cancer of the thyroid

what would be elevated?

A

calcitonin levels

67
Q

How is Thyroid Neoplasia

investigated and treated?

A

Investigated in a similar way to goitres + Ultrasound scan +/- Fine Needle Aspiration

Treatment - Surgery
• Diagnostic hemithyroidectomy - to confirm histology - papillary / follicular cancer

• Near-total thyroidectomy

Adjunctive therapy - Iodine 131 ablation

Therafter - suppressive thyroid replacement – ie high dose
thyroxine to suppress TSH and reduce chance of recurrence

External beam radiotherapy also given

Serum thyroglobulin is a useful tumour marker – rising levels may
indicate recurrence

Iodine tracer scan may also be useful for monitoring

68
Q

What can be used as a tumour marker for thyroid cancer?

A

Serum thyroglobulin is a useful tumour marker – rising levels may
indicate recurrence

69
Q

What is Myxoedema coma?

A

rare but potentially fatal outcome of untreated/undertreated hypothyroidism.

It is a medical emergency requiring admission to hospital and often results from acute decompensation during an intercurrent illness. Patients are hypotensive, hypothermic, bradycardic and demonstrate cognitive decline.

IV levothyroxine is the mainstay of management. Electrolyte imbalances and hypothermia should be addressed. IV hydrocortisone may be needed unless hypopituitarism is ruled out as a cause.

70
Q

What are the causes of subclinical hypothyroidism (high HTS with normal FT4) and how should the condition be treated?

A

intercurrent illness
• inadequate dose
• malabsorption
• poor concordance with therapy

Initial diagnosis - repeat thyroid function test after 3-6 months. If normal it means condition was transient e.g due to a virus. If still abnormal - treat

Treatment is levothyroxine dose adjusted to ensure TSH is within normal range - if not already on medication

71
Q

How are eye pathologies caused by graves disease treated?

A

Can be sight threatening, so steroids, radiotherapy or surgery may be required

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