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Endocrine > Thyroid physiology > Flashcards

Thyroid physiology Flashcards

1
Q

Which hormones does the thyroid gland secrete?

A

T3- tri-iodothyronine

T4- thyroxine

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2
Q

Why do surgeons have to be so careful in thyroid gland surgery?

A

The thyroid gland is highly vascular and therefore risk of haemorrhage.
Close to the recurrent laryngeal nerve

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3
Q

Which ligament does the recurrent laryngeal nerve run close too?

A

Berry ligament

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4
Q

What would damage to the Berry ligament cause?

A

Hoarse voice

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5
Q

Blood supply to the thyroid gland

A

Superior and inferior thyroid arteries.

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6
Q

Venous drainage of the thyroid artery

A

Superior and middle thyroid vein which drain to the internal jugular vein.
Then also inferior thyroid vein which drains to the brachiocephallic vein.

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7
Q

Where is the Berry ligament

A

Posterior.

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8
Q

Cells that contain a colloid.

A

Follicular cells

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9
Q

What does a colloid do?

A

All thyroid hormone is stored here (T3, T4)

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10
Q

What makes up a follicle?

A

An inner colloid surrounded by follicular cells.

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11
Q

Function of follicular cells

A

Allow transport of iodine into the colloid and thyroid hormones out of the colloid.

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12
Q

Function of parafollicular cells

A

Neuroendocrine cells that secrete calcitonin- important in calcium regulation.

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13
Q

Where can you get iodine from?

A

The diet

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14
Q

Process of releasing T3 and T4

A

Iodine is transported into the follicular cell from the bloodstream. This is then transported into the colloid. Subsequently through a process of pinocytosis T3 and T4 are released into the follicular cell and then into the bloodstream.

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15
Q

Synthesis of T3 and T4

A

Iodine is taken up by the follicle cell. Iodine attaches to thyroglobulin (tyrosine residues on thyroglobulin). This forms one of the two types of thyroglobulin- either MIT( where one iodine attaches) or DIT (where two iodines are attached).
MIT(1) + DIT(2) forms T3
DIT(2) + DIT(2) forms T4.

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16
Q

How much of each thyroid hormone is present

A

90% T4
10% T3
However T3 is more potent and biologically active.

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17
Q

Where can T4 be converted to T3

A

The liver and the kidneys

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18
Q

Main regulator of thyroid hormone and where it originates from?

A

Thyroid stimulating hormone- from the pituitary.

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19
Q

How does TSH work?

A

Acts on a receptor on the follicular cell wall. triggering release of T3 and T4 into the bloodstream.

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20
Q

How do thyroid hormones travel in the blood?

A

They are hydrophillic therefore travel bound to certain plasma proteins. Some also are transported in the plasma- these are the biologically active ones.

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21
Q

Proteins thyroid hormone can bind too?

A

Thyroxine binding globulin (70%)
Thyroxine binding prealbumin (20%)
Albumin (5%)
The rest travels unbound.

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22
Q

What is required to have a tissue effect?

A

Unbound T3.

Therefore bound T3 has to unbind or T4 has to be converted to T3 to have an effect.

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23
Q

Which thyroid hormone is more readily bound to plasma proteins?

A

T3- has more rapid onset of biological response due to it being more likely to travel unbound.

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24
Q

How does metabolic state correlate with thyroid hormones?

A

More metabollicly active- more unbound thyroid hormone in the plasma.

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25
Q

Alterations in thyroid hormone can effect?

A 
Metabolism
Growth
Development
Reproduction
Behaviour
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26
Q

How does thyroid hormone affect metabolic rate?

A

Causes an increase in number and size of mitochondria
Increase oxygen use and rates of ATP hydrolysis
Increase synthesis of respiratory chain enzymes.

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27
Q

How do thyroid hormones effect thermogenesis?

A

Approximately 30% of temperature regulation is due to thyroid hormone.

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28
Q

Thyroid hormone effects on carbohydrate, lipid and protein metabolism.

A

Causes an increase in blood glucose due to an increase in gluconeogenesis and gluconeolysis
Increase in glucose dependent uptake into cells.

Mobilises fats from adipose tissues
Increase in fatty acid oxidation in tissues.

Increase in protein synthesis.

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29
Q

How can dysfunction in thyroid hormones effect newborn babies?

A

It can cause mental disability in serious cases or low IQ in mild cases.

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30
Q

Over production of thyroid hormones effect on the nervous system?

A

Increase sympathetic effect- e.g. feeling nervous, shaky, sweaty,
Also increase responsiveness to adrenaline by increasing numbers of receptors.
Increase force and rate of heart contraction- can cause a fib.

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31
Q

How are thyroid hormones regulated?

A

Thyrotrophin releasing hormone (TRH) stimulates the pituitary to release TSH. This stimulates T3 and T4 release from the thyroid.
When levels of T3 and T4 become high- they feedback to the hypothalamous and the pituitary to stop or decrease release of TRH and TSH.

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32
Q

Environmental factors that affect thyroid hormone release

A

Lower temperatures- stimulates TRH release
Stress- inhibits TRH and TSH release
Circadian rhythm-thyroid hormone highest late at night. Lowest in the morn.

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33
Q

What are delodinase enzymes

A

They are a family of enzymes (1,2 or 3) which are important in the activation of thyroid hormones (converting T4 to T3)

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34
Q

Delodinase type II

A

Converts T4 to T3 by the removal of an iodine.

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35
Q

Where is delodinase type II found in the body?

A

heart and skeletal muscles, CNS, fat, thyroid and pituitary.

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36
Q

Causes of hypothyroidism

A

Primary- May be associated with enlarged thyroid.

Secondary- could be due to the pituitary gland not releasing stimulating hormones

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37
Q

Causes of hyperthyroidism

A

Could be due to autoimmune disease e.g. Graves

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38
Q

What nerve can be potentially damaged in thyroid surgery?

A

Recurrent laryngeal nerve

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39
Q

What is the most biologically active thyroid hormone

A

T3

40
Q

What is the main regulator of thyroid hormone release

A

TSH

41
Q

Describe the levels in the blood of T3, T4 and TSH in hypothyroidism

A

Low levels of T4 and T3 will be found due to the gland being underactive- therefore the thyroid stimulating hormone is trying to make up for it by being in high quantities.
Low T3, T4. High TSH.

42
Q

Describe the levels in the blood of T3, T4 and TSH in hyperthyroidism

A

High levels of T4 and T3 due to the gland being overactive. The pituitary tries to counteract these high levels by producing low levels of TSH.
High T4, T3. Low TSH

43
Q

Describe the levels in the blood of T3, T4 and TSH in secondary hyperthyroidism

A

Secondary hyperthyroidism could be due to a tumour on the pituitary secreting more TSH. Therefore TSH will be high and so will T3 and T4 due to it stimulating the thyroid gland.

44
Q

Describe the levels in the blood of T3, T4 and TSH in secondary hypothyroidism

A

Secondary hypothyroidism is caused by pituitary gland failure. This means that it will fail to produce much TSH and therefore the thyroid gland will not produce much T3 and T4.

45
Q

What is myxoedema?

A

Either refers to severe hypothyroidism e.g. myxoedema coma or pretibial myxoedema.

46
Q

What is pretibial myxoedema?

A

Accumalation of mucopolysacherides in the dermis and other tissues classicly seen in the shin. Associated with graves disease.

47
Q

Most common cause of hypothyroidism

A

Hashimotors disease.

48
Q

What is hashimotors?

A

Autoimmune destruction of the thyroid gland resulting in reduced hormone release.
Antibodies are produced against the thyroid gland (various thyroid antigens).

49
Q

Goitrous causes of hypothyroidism

A

Enlargement of the thyroid.
Could be due to Hashimotors disease.
Or iodine deficiency (leads to hypothyroidism) caused by environment or drugs e.g. amiodarone being the commonest.

50
Q

Non-goitrous causes of hypothyroidism

A

No enlargement of the thyroid
Congenital developmental defect
Atrophic thyroiditis

51
Q

Which antibodies are associated with Hashimotors disease?

A

Thyroid peroxidase antibodies (anti-tpo)- found in the blood.
Other hormones could be antithyroglobulin (anti-tg)
And to a lesser extent TSH receptor blocking antibody (TBII)

52
Q

On microscopy what would you expect to find in Hashimotors?

A

T cell infiltrate and inflammation.

53
Q

What in a history would suggest that it could be Hashimotors?

A

If the patient was female-more likely.

If there has been a family history of thyroid/autoimmune disease

54
Q

Subclinical hypothyroidism

A

This is when the patient hasn’t fully developed hypothyroidism. The T3 and T4 levels will be within the normal range however will be falling and therefore the TSH will be increased.

55
Q

Hair/skin changes in hypothyroidism

A 
Coarse/sparse hair
Expressionless face
Periorbital puffiness
Pale cool skin that feels doughy to touch
Vitiligo
56
Q

General symptoms of hypothyroidism

A 
Cold intolerance
Pitting oedema
Decreased appetite 
Weight gain
Constipation
57
Q

Cardiac symptoms of hypothyroidism

A

Reduced heart rate
Cardiac dilatation
Pericardial effusion
Worsening of heart failure

58
Q

Respiratory symptoms of hypothyroidism

A

Deep hoarse voice
Macroglossia (unusually large tongue)
Obstructive sleep apneoa

59
Q

Neurological symptoms of hypothyroidism

A 
Decreased intellectual and motor activities. 
Depression, psycosis, 
Muscle stiffness and cramps
Peripheral neuropathy
Carpal tunnel syndrome
60
Q

Gynae and reproductive symptoms of hypothyroidism

A

Menorrhagia
Oligo or ammenorheoa
Hyperprolactinaemia

61
Q

Other lab test findings in hypothyroidism

A

Macrocytosis- enlargement of RBC
Raised creatinine kinase.
Increased LDL cholesterol
Hyponatraemia- reduced tubular water loss in the kidneys
Hyperprolactinaemia- increased TRH means increased prolactin.

62
Q

Management of hypothyroidism

A

Normal metabolic rate should be restored gradually. Rapid metabolic rate restoration may result in cardiac arrhythmia’s.
Treat with thyroxine
In the young- 50-100ug
In the elderly- 25-50ug
Check TSH two months after any dose change.
Once stabilised- check every 12-18months.

63
Q

Why do you use thyroxine (T4) as a therapy but not T3?

A

T4 can be converted by the body to T3 therefore is equally effective and has a longer life.

64
Q

In a stable patient treated with thyroxine- under which circumstances would you increase the dose?

A

When the person is pregnant because the thyroid requirements increase.

65
Q

Why are doctors so keen on upping the dose of thyroxine by so much in pregnancy?

A

Reduces the risk of foetal abnormalities and mental disability of the newborn.

66
Q

In primary hypothyroidism- how can you tell how well a person is doing in managing their disease?

A

Use thyroid stimulating hormone (TSH) because it reflects tissue thyroid hormone actions.

67
Q

In secondary hypothyroidism- how can you tell how well a person is doing in managing their disease?

A

In people with secondary hypothyroidism- the pituitary is not a trustworthy source and therefore you cannot use TSH. In this case you use free T4 in the blood.

68
Q

Severe hypothyroidism can cause

A

myxoedema coma

69
Q

Who does myxoedema coma usually effect?

A

Typically effects elderly women with longstanding or undiagnosed hypothyroid.

70
Q

What is myxoedema coma?

A

Severe hypothyroidism
Investigations will show severe bradycardia, low voltage complexes, varying degrees of heart block, T wave inversion, prolongation of the QT interval.
Respiratory failure- hypoxia, hypercarbia, acidosis

71
Q

Treatment of myxoedema coma?

A 
ABCDE- intensive care
Passively rewarm- slowly increase body temp.
Cardiac monitoring for arrhythmias 
Fluid to maintain electrolyte balance
thyroxine cautious (hydrocortisone)
72
Q

Cardiac symptoms of hyperthyroidism

A 
Palpitations/atrial fibrillation 
Cardiac failure (rare)
73
Q

General symptoms of hyperthyroidism

A 
Tremor
Sweating
Lighter, less frequent periods
Muscle weakness
Weight loss
Intolerance to heat.
74
Q

Neurological symptoms of hyperthyroidism

A

Anxiety, nervousness, irritability, sleep disturbance

75
Q

Gi symptoms of hyperthyroidism

A

Diarrhoea

76
Q

Visual and hair symptoms of hyperthyroidism

A

Visual- lid retraction
Double vision
Eyes that bulge out (in patients with graves disease)

Brittle, thin hair
Rapid nail growth

77
Q

Causes of hyperthyroidism

A

Auto-immune- graves disease
Multi-nodular goitre
Toxic nodule (adenoma)
Thyroiditis- subacute (occurs transiently due to viral infection) or post partum (2-3 months after child birth)

78
Q

Medication that causes hyperthyroidism

A

Amiodarone, thyroxine, lithium

Supplements e.g. kelp

79
Q

Which age group does graves disease effect?

A

Often occurs in younger people (20-50)

80
Q

Risk factors for developing graves disease?

A 
Family history of graves disease. 
High iodine intake. 
More common in female
Smoking 
Could be due to viral infection (however unsure if this is definitely the trigger)
81
Q

Tests for graves and their results

A

High T3 and T4. Low TSH.
Antibody positive- TSH receptor antibodies (TRA)
On examination- smooth symmetrical goitre.

82
Q

Describe the natural progression of graves disease

A

About 18 months down the line- graves disease either burns out because the thyroid stops overproducing the hormones or relapses.

83
Q

Other symptoms associated with graves disease that are not necessarily associated with hyperthyroidism

A

Opthalmopathy- bulging eyes.
Lid retraction
Lid lag- when the patient looks down- takes a while for the lid to follow.
Chemosis- redness of the eye
Proptosis- forward movement of the eye (look side on)

84
Q

Why does the eye bulge in graves disease?

A

The muscles behind the eye become inflamed and therefore cause them to bulge out.

85
Q

Treatment of the eye manifestations in graves disease

A 
Lubrication in mild.
Decompression surgery
Radiotherapy
Corrective surgery
Stopping smoking
86
Q

Multinodular goitre

A

Generally seen in older patients,
They will be antibody negative
Patient will have asymmetrical goitre.

87
Q

On scintagraphy how will multinodular goitre show?

A

Patchy uptake. Areas of lower and higher density.

88
Q

Thyroid storm

A

Medical emergency.
Severe hyperthyroidism. Respiratory and cardiac collapse.
Hyperthermia
Exaggerated reflexes
May require ventilation
May be associated with underlying infection.

89
Q

Treatment of thyroid storm

A

Lugos iodine- stuns the thyroid into stopping while the longer term drugs take hold.
Use beta blockers to control heart.

90
Q

Treatment of hyperthyroidism

A

Carbimazole
Propylthyrouracil (preferred in pregnancy)

In graves- start at a high dose and reduce over 12-18 months.

Symptom control use beta blockers.
Radio-iodine
Surgery

91
Q

Radio-iodine

A

Tends to be used in multinodular goitre or relapsing graves.
Radioactivity destroys part of the thyroid gland reducing its ability to release hormones.

92
Q

Arguments against surgery for hyperthyroidism

A

Against- cosmetically undesirable scar
Anaesthetic risks
Can cause hypothyroidism

93
Q

Name some types of thyroiditis

A 
Technically graves and hashimotors are types of thyroiditis because they cause inflammation to the thyroid gland. 
DeQuervains
Post partum
Drug induced
Acute thyroiditis.
94
Q

What is DeQuervains thyroiditis?

A

Thyroid is initially overactive so the patient gets symptoms of hyperthyroidism. They then completely switch and have an underactive thyroid. After about 6 months it then levels out and normal thyroid function is restored.

95
Q

What is said to cause DeQuervains (subacute thyroiditis)?

A

A viral infection e.g. patient will complain of a sore throat or fever.

96
Q

What will tests show for DeQuervains?

A

Early stage- T4 high, TSH low
Later stage- T4 low, TSH high
Then everything returns to normal.
Also scintagraphy will show low uptake.

Endocrine (20 decks)

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