The thyroid Flashcards

1
Q

where does the thyroid originate from embryologically?

A

the back of the tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what joins the two lobes of the thyroid?

A

a central isthmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how can the thyroid be distinguished from other neck lumps?

A

by its movement from swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what nerve and gland are at risk of damage during thyroid surgery and why?

A

the recurrent laryngeal nerve lies laterally each side

also the parathyroid gland lies posteriorly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the blood supply to the thyroid?

A

inferior and superior thyroid arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what makes up the thyroid tissue?

A

Colloid mades up the thyroid

it contains iodinated thyroglobulin which then converted to thyroxine

thyroid also contains neuroendocrine cells (C cells) which secrete calcitonin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the physiological function of the thyroid?

A

Iodinated tyrosine molecules form thyroxine which is T4 and T3.

T4 is the main circulating hormone which is converted peripherally the more potent and shorter acting T3.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the two main types of thyroid receptor?

A

TRa and TRB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what vertebral level is the thyroid?

A

c5-t1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what hormone levels characterise primary hypothyroidism compared to secondary hypothyroidism?

A

Primary = problem with thyroid itself

so get reduced circulating T4 and high TSH

Secondary = TSH deficiency, usually the result of pituitary disease.

so have low T4 levels and non elevated TSH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what hormone levels characterise primary hyperthyroidism compared to secondary hyperthyroidism?

A

Primary = increased T3/T4 levels with suppressed TSH

secondary = TSH is not suppressed and T3/T4 us high. This suggests a TSHoma, thyroid hormone resistance or assay interference.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what causes hyperthyroidism/thyrotoxicosis?

A
  • Autoimmune (Graves disease) is the commonest cause due to presence of TSH receptor stimulating antibodies
  • usually affects young women and follows a relapse-remitting cause
  • nodular disease presents presents older than auto-immune and is caused by autonomous secretion of T3/T4 from either a solid toxic nodule or numerous nodules.
  • Thyroiditis is inflammation of the thyroid and can occur as a result of infection, medication e.g amidarone or following childbirth and involves the release of thyroxine.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the clinical features of hyperthyroidism?

A
  • weight loss with increased appetite
  • insomnia
  • irritability
  • anxiety
  • heat intolerance
  • palpitations
  • tremor
  • puritis
  • increased bowel frequency and loose motions
  • menstrual disturbance and reduced fertility
  • resting tachycardia
  • lid lag
  • hyperreflexia
  • warm peripheries
  • lid retraction and proptosis in graves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what investigations are done for hyperthyroidism?

A

bloods for elevated fT4 and fT3 with undetectable TSH.

elevated fT3 alone with normal fT4 and suppressed TSH is a T3 taco

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what investigations are done for hyperthyroidism?

A

bloods for elevated fT4 and fT3 with undetectable TSH.

elevated fT3 alone with normal fT4 and suppressed TSH is a T3 toxicosis

the presence of elevated fT4 and fT3 with non suppressed TSH is unusual

normal fT4 and fT3 and suppressed TSH have subclinical hyperthyroidism suggesting autonomous thyroid activity

thyroid peroxidase antibodies are non specific markers of auto immune thyroid disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what imaging can be done of the thyroid in hyperthyroidism ?

A

ultrasound

can help confirm nodular thyroid disease but doesn’t not assess gland activity

can do nuclear imaging e.g iodine uptake isotope scan can help determine functionality

if nodular disease, there is increased uptake only in autonomous nodules, in thyroiditis there is absent uptake and in graves disease there is uniform uptake

17
Q

what is the medical treatment for hyperthyroidism?

A

medication is first line, with thionamides e.g carbimazole and propylthiouracil which reduce T3 and T4 synthesis. Take 4-6 weeks to normalise results.

NB: Thionamides can cause bone marrow suppression, and if unexplained fever or sore throat occurs, urgent FBC is required to exclude pancytopenia and drug should be stopped if neutrophil count is low. Can also get a rash as a side effect.

Also, women of child bearing age should be on contraception with carbamazepine. if they fall pregnant, switch to propylthiouracil.

18
Q

what is the surgical treatment for hyperthyroidism?

A

1) Radioactive iodine

administration of single dose that causes ablation to the thyroid. don’t do in pregnancy and may lead to flare up of eye disease in pre existing ophthalmopathy. Can commonly cause hypothyroidism so will need lifelong thyroxine replacement e.g levothyroxine. Post treatment will emit radiation so must avoid children and pregnant women.

2) Surgery
good for people who can’t take radioactive iodine e.g mothers with young children. Complications of surgery include bleeding, infection, damage to recurrent laryngeal nerve and temporary/permanent hypocalcaemia due to hypoparathyroidism.

19
Q

what are the causes of primary hypothyroidism?

A
  • autoimmune Hashimotos thyroiditis
  • pregnancy, post natally can be misdiagnosed as post partum depression
  • iodine deficiency can cause neonatal hypothyroidism
  • genetic defect
  • drugs e.g amiodarone and lithium
  • iatrogenic e.g surgery/radioiodine
20
Q

what causes secondary hypothyroidism (TSH deficiency)?

A

caused by TSH deficiency due to hypothalamic pituitary disease.

get low fT4 with non elevated TSH.

21
Q

what are the clinical features of hypothyroidism?

A
  • weight gain
  • cold intolerance
  • fatigue
  • constipation
  • bradycardia
  • myxoedema
  • thickening skin
22
Q

what investigation are done hypothyroidism?

A

bloods

low fT4 and elevated TSH

in Hashimotos autoimmune thyroiditis thyroid peroxidase TPO antibodies are strongly positive

23
Q

how is hypothyroidism treated?

A

thyroxine replacement, starting at 50-100ug a day. elderly/IHD patients will be started on a lower dose e.g 25ug.

if persistently elevated, suggests poor compliance or Malabsorption. Suppressed or undetectable TSH suggests over replacement, leading to risk of AF and osteoporosis.

24
Q

what is subclinical hypothyroidism?

A

refers to normal fT4 and elevated TSH.

asymptomatic patient may not need to be treated.

Guidelines recommend starting thyroxine if TSH >10miU/L even if patients are asymptomatic due to likelihood of progression to frank hypothyroidism.

25
Q

what is are the consequence of thionamides?

A

can cause agranulocyotisis (bone marrow suppression) and patients should be warned of this potential rare side-effect before commencing treatment.

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

A more common side-effect is generalised rash, which disappears after cessation of the drug.