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METABOLIC > ENDOCRINOLOGY - HYPERTHYROIDISM > Flashcards

ENDOCRINOLOGY - HYPERTHYROIDISM Flashcards

1
Q

What is thyrotoxicosis?

A

The clinical syndrome of excess circulating thyroid hormones, irrespective of the source.

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2
Q

Outline the basic structure of thyroid anatomy?

A

Comprises 2 lobes connected by an isthmus and they extend from the oblique line on thyroid cartilage to the 5th-6th tracheal rim.

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3
Q

What’s the histology of the thyroid gland?

A

The functional unit is the follicle - this consists of epithelial follicular cells surrounding a colloid
The thyroid also contains parafollicular cells which produce calcitonin

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4
Q

Outline the synthesis and release of thyroid hormones?

A

Follicular epithelial cells secrete thyroglobulin into the colloid. Binding of TSH to its receptors in the follicle cells of the thyroid gland causes the cells to actively transport iodide ions across their cell basolateral membrane from the bloodstream via a sodium iodide cotransporter (2NA+ and I-) - Na+ transported back into blood via Na+K+ ATPase. Iodide ions are then transported across the apical membrane into the colloid space via the pendrin cotranporter (I- in return for Cl-)
In the colloid space, thyroperoxidase oxidises 2 iodide ions to form 1 iodine molecule.
thyroperoxidase enzymes iodinates tyrosine residues in thyroglobulin to form T4, T3 and r-T3
These hormones remain in the colloid centre of the thyroid follicles until TSH stimulates endocytosis of colloid back into the follicle cells. There, lysosomal enzymes break apart the thyroglobulin colloid, releasing T3 and T4 so they can diffuse across the follicle membrane and enter the bloodstream.

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5
Q

How are T3 and T4 transported in the blood?

A

Less than 1% travels unbound and this free T3 and T4 cash cross the lipid bilateral of cell membranes.
The remaining 99% is bound to thyroxine binding globulins, albumin or other plasma proteins. This prevents their free diffusion into body cells. When blood levels of T3 and T4 begin to decline, the bound molecules are released from the plasma cells and can readily cross membranes of target cells

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6
Q

What’s the blood supply to the thyroid gland?

A

Superior (from ECA) and inferior thyroid artery (from thyrocervical trunk)

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7
Q

What’s the venous drainage from the thyroid gland?

A

Superior, middle and inferior thyroid veins which form a venous plexus around the thyroid gland
Superior and middle veins drain into the internal jugular vein
Inferior vein drains into the brachiocephalic vein

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8
Q

Outline the HPA axis for thyroid?

A

Thyrotrophin releasing hormone is secreted in the hypothalamus and travels via the portal system to the anterior pituitary where is stimulates thyroid stimulating hormone
TSh is secreted into the systemic circulation where it stimulates increased iodine uptake by the thyroid, and synthesis and release of T4 and T3
TSH also stimulates the conversion of T4 to T3 (more active hormone) in peripheral tissues
T3 and T4 enter cells where they bind to nuclear receptors and promote increased metabolic and cellular activity
If T3 and T4 rise above normal levels, TRH and TSH production is suppressed so peripheral T3 and T4 levels can fall to normal.

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9
Q

Where peripherally is T3 produced from T4?

A

Liver, kidney and spleen

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10
Q

Why is T4 converted to T3 in peripheral tissues?

A

Because more T4 is produced but T3 is 5x more bio active

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11
Q

What are the main causes of thyrotoxicosis with hyperthyroidism?

A

Graves’ disease
Toxic multinodular goitre
Solitary toxic adenoma
Amiodarone induced thyrotoxicosis
Follicular thyroid cancer
Beta-HCG related e.g. in pregnancy or hydatidiform mole
Secondary hyperthyroidism caused by a TSH-secreting pituitary adenoma

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12
Q

What’s the difference between primary and secondary hyperthyroidism?

A

Primary - when pathology is within the thyroid gland
Secondary - where the thyroid is producing excessive thyroid hormone as a result of overstimulation by thyroid stimulating hormone. The pathology is in the hypothalamus or pituitary.

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13
Q

What are the main causes of secondary hyperthyroidism?

A

TSH secreting pituitary adenoma
Thyroid hormone-resistance syndrome
HCG secreting tumour
Gestational thyrotoxicosis (excessive stimulation of thyroid gland by HCG)

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14
Q

What are the main causes of hyperthyroidism?

A

Graves’ disease - 75%
Toxic modular goitre
Thyroiditis
Drugs

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15
Q

What is Graves’ disease

A

an autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism. Serum IgG antibodies bind to TSH receptors in the thyroid, stimulating thyroid hormone production

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16
Q

What is graves opthalmopathy?

A

Aka thyroid eye disease
Bulging of eyeball out of the socket due to inflammation, swelling and hypertrophy of the tissue behind the eyeball (exophthalmos)
Smoking significantly increases the risk
SEE GP PROMPTLY IF NOTICE PAIN< REDNESS< SWELLING, bulging eyes, blurred or double vision

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17
Q

What is pretibial myxoedema?

A

Dermatological condition where there are deposits of mucin under the skin in the pre-tibial area of the leg; this gives a discoloured, waxy, oedematous appearance to the skin over this area
This is specific to Graves’ disease

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18
Q

What are some unique features of Graves’ disease?

A

Graves eye disease
Pretibial myxoedema
Thyroid acropachy

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19
Q

What are some universal features of hyperthyroidism?

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss despite eating normal/more
Fatigue
Diarrhoea
Sexual dysfunction
Weakness
Tremor
Palpitations
Increased persiration

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20
Q

What are risk factors for hyperthyroidism?

A

Family history
High iodine intake
Smoking (esp for Graves’ disease)
Female
Co-existent autoimmune disease
Trauma to thyroid gland
Childbirth

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21
Q

What are features unique to multinodular goitre?

A

Goitre with firm nodules (nodules are often present years before thyrotoxicosis occurs)
Most patients are aged over 50

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22
Q

What is thyroiditis?

A

Inflammation of the thyroid gland. Destruction of thyroid cells causing release of thyroid hormone into the blood - can be caused by viruses and drugs

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23
Q

What drugs commonly cause hyperthyroidism?

A

Lithium and amiodarone
Overdose of levothyroxine

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24
Q

Outline how amiodarone can affect the thyroid function?

A

Amiodarone-induced thyrotoxicosis. It can cause hypothyroidism and, less commonly, hyperthyroidism
Amiodarone is a heavily iodinated drug that blocked the conversion of T4 to T3. This leads to a decrease in inhibition at pituitary due to low levels of T3 = increase TSH levels. Overtime increased TSH causes increased T4 production and eventually the higher levels of T4 can overcome the blockade of amiodarone and convert to adequate levels of T3. This increases inhibition at pituitary level. After several months, TSH is normal with high T4 and low T3.
Patients should have their thyroid function tested before going on amiodarone
This is more common in areas with low iodine intake

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25
Q

What are the 2 types of amiodarone induced thyrotoxicosis?

A

Type 1 - thyrotoxicosis in a patient who has underlying thyroid dysfunction.
Type 2 - thyrotoxicosis resulting from destructive thyroiditis 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. The thyrotoxic phase may last several weeks to several months and it is often followed by a hypothyroid phase with eventual recovery in most patients

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26
Q

Which demographic does Graves’ disease typically affect?

A

Younger aged women (F:M 10:1)
Often familial

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27
Q

What demographic does nodular thyroid disease typically affect?

A

Older age
Females/males equally
Rarely familial

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28
Q

What does the presence of a multi nodular goitre without Graves’ disease symptoms suggest?

A

Toxic nodular goitre

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29
Q

Why is thyrotoxic crisis?

A

An extreme manifestation of thyrotoxicosis due to overproduction of thyroid hormones

It occurs as a sudden onset of hyperpyrexia (>41 degrees). Tachycardia
Diarrhoea and nausea
Jaundice
Severe agitation and confusion
Loss of consciousness

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30
Q

What are the clinical symptoms and signs of thyrotoxicosis?

A

Anxiety
Emotional lability
Proximal myopathy
Fine tremor
Palpitations
Heat intolerance
Increased perspiration
Weight loss despite normal or increased appetite
Agitation
Lid retraction and lag
Orbital inflammation
Warm and moist skin
Tachycardia or AF
Goitre
Palmar erythema
Hair thinning
Brisk reflexes
oligomenorrhoea or amenorrhoea

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31
Q

What is thyrotoxic periodic paralysis?

A

A serious complication characterised by muscle paralysis and hypokalaemia due to a massive intracellular shift of potassium
Acute proximal symmetrical lower limb weakness

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32
Q

How do you investigate hyperthyroidism?

A

TFTs: serum TSh should be suppressed and T3 and T4 raised
Check for TSH receptor antiboides
Can ultrasound for goitre or MRI of orbits
thyroid uptake scans

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33
Q

What do compression symptoms of breathlessness, hoarse voice, dysphasia and neck pressure suggest with hyperthyroidism?

A

A large enough goitre - typically toxic multi nodular goitre

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34
Q

How does a goitre present in Graves’ disease?

A

Diffusely symmetrically enlarged without nodules and there may be a bruit

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35
Q

How does a goitre present in toxic multinodular goitre?

A

Non-tender thyroid nodules

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36
Q

How does a goitre present in toxic adenoma?

A

Unilateral, non-tender thyroid made

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37
Q

How does a goitre present in subacute thyroiditis?

A

Tender, firm, irregular, diffusely enlarged thyroid gland which may be asymmetrical

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38
Q

How does a goitre present in amiodarone-induced thyroiditis?

A

Small goitre usually present

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39
Q

How to investigate hyperthyroidism?

A

Check serum TSH levels
If TSH level is low then T3 and T4 should be measured
Suspect overt hyperthyroidism if TSH level is low and T4/T3 raised
Suspect SU clinical hyperthyroidism if TSH is below normal and T3 and T4 are normal
Consider checking TSh receptor antibodies if Graves’ disease is suspected
Measure thyroid peroxidase antibodies if woman is postpartum and postpartum thyroiditis is suspected
Check inflammatory markers if a diagnosis of thyroiditis is suspected (CRP and ESR)

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40
Q

How to manage hyperthyroidism?

A

Anti thyroid drugs
Radioactive iodine treatment
Thyroid surgery

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41
Q

What are the 2 anti thyroid drug treatments?

A

Carbimazole and propylthiouracil - act as a preferred substrate for iodisation by thyroid peroxidase

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42
Q

Which anti thyroid drug treatment is used first line and why?

A

Carbimazole because propylthiouracil has a small risk of severe liver injury

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43
Q

How does radioactive iodine treatment work for hyperthyroidism?

A

It gets taken up by the thyroid and then uses beta and alpha rays to induce damage of DNA leading to death of thyroid cells, causing a decrease in thyroid function/reduction in thyroid size

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44
Q

Who is radioactive iodine treatment indicated first line in?

A

First line treatment for adults with Graves’ disease and toxic multinodular goitre

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45
Q

Who is radioactive iodine treatment contraindicated in?

A

in people with Graves’ disease with active or severe orbitopathy as it may cause an exacerbation of orbitopathy or de novo development.
It is also contraindicated in pregnancy or women planning to become pregnant in the next 4–6 months as it crosses the placenta and can cause severe hypothyroidism in the fetus, and it is contraindicated in breastfeeding women.

46
Q

What are thyroid surgery options for hyperthyroidism?

A

Total thyroid to my
Hemithyroidectomy for a single thyroid nodules

47
Q

Which hyperthyroidism patients should you consider referral for urgent admission?

A

Those with AF or cardiac failure
Those with dehydration
Psychosis patients

48
Q

What can you give to hyperthyroidism patients to control symptoms driven by sympathetic nervous system?

A

Beta blockers

49
Q

Outline the course of hyperthyroidism?

A

Relapses and remittances

50
Q

What are some complications of hyperthyroidism?

A

Irregular heartbeat - increased risk of death from CVD and stroke
Graves opthalmopathy
Thinning bones, osteoporosis and muscle problems
Menstrual cycle and fertility issues
Thyroid storm

51
Q

What’s a complication of Carbimazole?

A

Agranulocytosis and neutropenia
Increased risk of congenital malformations when used during pregnancy
Risk of acute pancreatitis

52
Q

What are the symptoms/signs to watch out for for agranulocytosis after taking Carbimazole?

A

Sore throat and fever - suggestive of infection

53
Q

What are the complications of a thyroidectomy?

A

Bleeding - can block airway
Infections
Low parathyroid hormone levels = hypocalcaemia
Permanent hoarse or weak voice due to damage of recurrent laryngeal nerve
Can lead to hypothyroidism

54
Q

How should antithyroid drugs be taken?

A

Used short term to restore euthyroidism in preparation for definitive treatment with radioactive iodine treatment or thyroid surgery
Medium term with the aim of inducing remission of Graves’ disease
Long term if radioactive iodine treatment or surgery is contraindicated

55
Q

What is sub clinical hyperthyroidism?

A

Low TSH but normal thyroid hormone levels
It doesn’t usually cause symptoms

56
Q

When does subclinical hyperthyroidism need to be treated?

A

Those with persistant TSH <0.1

57
Q

How does an HCG secreting tumour cause hyperthyroidism?

A

hCG can bind to the TSH receptors present in thyroid tissue and act like a weak form of TSH to cause the thyroid to produce and release more thyroxine and triiodothyronine.

58
Q

Why can low iodine intake cause hyperthyroidism?

A

Without adequate iodine, the thyroid progressively enlarges (develops a goiter) as it tries to keep up with demand for thyroid hormone production
Toxic goitre can case hyperthyroidism

59
Q

What is thyroid acropachy?

A

Extreme manifestation of autoimmune thyroid disease
Acropachy means thickening of the extremities and it is manifested by a triad of signs:
digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.

60
Q

What are the possible complications for hyperthyroidism?

A

Heart failure (thyrotoxic cardiomyopathy)
Angina
AF
Osteoporosis
Opthalmopathy
Gynaecomastia
Thyroid storm

61
Q

What are the 3 most common reasons for hyperthyroidism?

A

Graves’ disease
Toxic adenoma
Toxic multinodular goitre

62
Q

What autoantibodies are present in Graves’ disease?

A

TSH receptor antibodies

63
Q

What’s the cause of both toxic adenomas and toxic multinodular goitre?

A

TSH receptor mutation = can auto activate itself.

64
Q

What’s the most common cause of secondary hyperthyroidism?

A

Pituitary adenoma - releases a lot of TSH

65
Q

How does molar pregnancy or choriocarcinoma cause hyperthyroidism?

A

They produce lots of beta HCG which can act like TSH and stimulate the thyroid gland to produce more T3 and T4

66
Q

Why does thyroid destruction only cause a transient hyperthyroidism?

A

Destruction leads to release of thyroid hormones into the circulation but eventually when enough follicular cells are damaged you would not get synthesis of thyroid hormones which can lead to hypothyroidism

67
Q

Why can Hashimoto’s disease and post partum thyroiditis cause transient hyperthyroidism?

A

The anti-TPO and anti-TG can damage follicular cells and lead to release of T3 and T4 into the circulation

68
Q

Why can subacute granulpmatois thyroiditis cause transient hyperthyroidism?

A

Virus damaged follicular cells and causes a release of thyroid hormones into circulation

69
Q

How can amiodarone and lithium cause transient hyperthyroidism?

A

Drug damages follicular cells and causes a release of thyroid hormones into the circulation

70
Q

How can excess iodine cause transient hyperthyroidism?

A

In those with iodine deficiency, TNG or Graves’ disease lap up the iodine. They use it to produce lots of thyroid hormones. Too much iodine in cells can cause inflammation and damage thyroid tissue which can release thyroid hormones into the circulation

71
Q

What is the Jod-Basedow syndrome?

A

is a rare cause of thyrotoxicosis typically seen after the administration of exogenous iodine

72
Q

Why does hyperthyroidism cause weight loss ?

A

Increased metabolic activity - breakdown more glycogen, lipids etc

73
Q

Why does hyperthyroidism cause increased body temperate ?

A

Increased metabolic activity causes increased heat production as a byproduct

74
Q

Why does hyperthyroidism cause tachycardia?

A

High thyroid hormone levels increases the sensitivity of beta 1 adrenergic receptors leads to increased HR

75
Q

Why does hyperthyroidism cause hypertension?

A

High thyroid hormone levels increase contractility of the heart which causes increased stroke volume = increased CO

76
Q

Why does hyperthyroidism cause osteoporosis and increased fracture risk?

A

When thyroid hormones are too high osteoclastic activity increases so bone resorption increases

77
Q

Why does hyperthyroidism cause anxiety, insomnia and irritability?

A

High thyroid hormones increase sympathetic nervous system

78
Q

Why does hyperthyroidism cause lid retraction with lid lag?

A

Increased thyroid hormones increases sympathies NS. Lavatory palpabrae superioris is sympathetically innervated

79
Q

Why does hyperthyroidism cause diarrhoea?

A

Increased thyroid hormones increases gut motility and gut secretions

80
Q

Why does hyperthyroidism cause proximal myopathy?

A

High thyroid hormones causes increased contraction and growth of muscles - this causes irritation and pain
(Different to hypothyroidism as no skeletal muscle damage which means no CK release)

81
Q

Why does hyperthyroidism cause increased hair growth, onycholysis?

A

High thyroid hormones = increased cutaneous blood flow

82
Q

Why does hyperthyroidism cause sweating?

A

High thyroid hormones = increase sebaceous and eccrine sweat glands

83
Q

Why does hyperthyroidism cause decreased libido, decreased sperm production, gynaecomastia, infertility, oligomenorrhoea and amenorrhoea?

A

High thyroid levels act on the liver which causes it to produce thyroxine binding globulin. As well as this is produced sex hormone binding globulins which bind oestrogen and testosterone. Lots of this leads to low circulating oestrogen and testosterone

84
Q

Why does Graves’ disease cause exophthalmos?

A

TSH antibodies can activate T cells in the retro-orbital space. They start producing TNF-alpha and INF-gamma which stimulate fibroblasts here. Fibroblasts produce glycosaminoglycans which hold onto lots of water = swelling
GAGs also increase the number of adipocytes
Both lead to bulging of eyes

85
Q

Why can Graves’ disease cause pretibial myxoedema?

A

TSH antibodies can activate T cells in the dermis They start producing TNF-alpha and INF-gamma which stimulate fibroblasts here. Fibroblasts produce glycosaminoglycans which hold onto lots of water = swelling

86
Q

How do we determine if the hyperthyroidism is primary or secondary?

A

Thyroid function test
Primary - high free T4, low TSH
Secondary - high free T4, high TSH

87
Q

How do you determine between pituitary or hypothalamic causes of secondary hyperthyroidism?

A

MRI

88
Q

Why do beta blockers provide symptomatic relief of hyperthyroidism?

A

It prevents conversion of T4 to T3 so metabolism cannot be increased

89
Q

When do we not give methimazole?

A

First trimester of pregnancy

90
Q

What is propylthiouracil moa?

A

Inhibits thyroperoxidase so less production of iodinated thyroglobulin = decreased thyroid hormones
Also inhibits T4 to T3 conversion

91
Q

What is Carbimazole moa?

A

It works by inhibiting the thyroid peroxidases (TPO) that catalyze the iodination of tyrosine residues in thyroglobulin and the oxidative coupling of iodinated tyrosines.

92
Q

How does radioactive iodine 131 treat hyperthyroidism?

A

Enters cells and releases gamma waves which damage follicular tissue which decreases synthesis of thyroid hormone

93
Q

What are the indications for surgery?

A

Goitre with compression symptoms
Graves with opthalmopathy
Refractory hyperthyroid

94
Q

What are the triggers for thyroid storm? Why does this happen?

A

Trauma, infection and surgery (DKA and MI can both also cause it)
Increase the already exaggerate sympathetic nervous system even more than it already is

95
Q

What are the symptoms and signs of thyroid storm?

A

Tachycardia/AF
Hypertension - can cause high output CHF if not treated
Confusion, delirium, altered mental status and coma
Hyperthermia (due to increased metabolic activity of cells)

96
Q

What is the treatment of thyroid storm?

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

97
Q

What are 3 disorders that cause weight loss with preserved appetite?

A

Hyperthyroidism
Diabetes
Malabsorption

98
Q

How does thyroiditis cause thyrotoxicosis?

A

Through leakage of thyroid hormones

99
Q

What will a goitre feel like in thyroiditis?

A

Diffuse goitre which may or may not be painful

100
Q

How can you treat thyroiditis?

A

It’s often self limiting
But you can offer beta blockers for symptomatic relief as they treat adrenergic symptoms

101
Q

What can cause thyrotoxicosis without hyperthyroidism?

A

Thyroiditis
Exogenous ingestion e.g. levothyroxine
Amiodarone induced thyrotoxicosis type 2

102
Q

What are sympotms/signs specific to Graves’ disease?

A

Opthalmopathy - affects 50% but is more commonly seen in smokers
Pretibial myxoedema
Thyroid acropachy

103
Q

What causes pretibial myxoedema in Graves’ disease?

A

Deposition of mucopolysaccharides in the dermis

104
Q

Who should be tested for thyroid dysfunction?

A

Anyone presenting with suggestive features of hyperthyroidism
Those with type 1 diabetes and other autoimmune disease
Those with new onset AF
Those with depression and anxiety

105
Q

Whats the commonest cause of painless goitre?

A
106
Q

What is post partum thyroiditis?

A

the immune system attacks the thyroid within around 6 months of giving birth. This causes a temporary rise in thyroid hormone levels (thyrotoxicosis) and symptoms of an overactive thyroid gland. Then, after a few weeks, the gland becomes depleted of thyroid hormone.

107
Q

When is propylthiouracil considered?

A

If intolerant or allergic to Carbimazole
If pregnant or planning pregnancy in the next 6 months
A history of pancreatitis

108
Q

What are the main side efefcts of Carbimazole?

A

Agranulocytosis - severe risk of infection and sepsis
Bone marrow disorders
Haemolytic anaemias
Thrombocytopenia
All above are rare

109
Q

What are the 2 regimes available for antithyroid drugs?

A

Block and replace: thioamides are 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 TSH.

110
Q

What does raised total T3 and T4 but normal fT3 and fT4 suggest?

A

High concentrations of thyroid binding globulin - seen in pregnancy

111
Q

How can you distinguish toxic multinodular goitre from Graves’ disease?

A

Nuclear scintigraphy reveals patchy uptake in toxic multinodular goitre
In Graves’ disease the uptake is uniform

112
Q

How is toxic multinodular goitre managed?

A

radioiodine therapy.

METABOLIC (43 decks)

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