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Hormones > Endo 5: Hyperthyroidism > Flashcards

Endo 5: Hyperthyroidism Flashcards

1
Q

How does Graves work

A

Antibodies target TSH receptors on the thyroid gland (they’re called TSH receptor autoantibodies or TRAB), which stimulates the thyroid gland, which makes it grow and make more thyroxine

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2
Q

What is the cause of goitre

A

Big, smooth lump in the neck, caused by increased size of the thyroid gland

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3
Q

Why are there eye symptoms

A

Because thyroxine makes your beta receptors more sensitive (which is how it increases BMR).

So if you have more sensitive beta receptors, and you know that the eyelids are sympathetically controlled. So you get eye symptoms relating to the eyelids being more open, and this can lead to lid lag

SEPARATELY, other antibodies to TSH-antibodies attack the eye causing exopthalmos

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4
Q

What is pretibial myxoedema

A

Swelling that occurs in the shins of patients with Grave’s disease because of a third antibody (distinct from the TSH and the antibody causing exopthalmos)

non-pitting

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5
Q

2 causes of hyperthyroidism

A

Grave’s and Plummer’s (nodular goitre)

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6
Q

Cause of tremor and tachycardia in hyperthyroidism?

A

increased sensitivity of beta receptors due to increase thyroxine, so increased contractility of skeletal muscle (=tremor) and heart (=tachycardia)

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7
Q

What test can detect an enlarged thryoid gland

A

Scintigram (using radioactively labelled iodine)

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8
Q

What is plummer’s disease?

A

‘Toxic nodular goitre’= not an immune problem but BENIGN ADENOMA that is over active at making thyroxine

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9
Q

How can you differentiate betweeen plummers adn graves

A

Because the graves patients get eye symptoms due to autoimmune, but plummers is not autoimmune so wont. Also no pre-tibial myxoedema

Secondly, you can do a scan (radioactive) and you get a ‘hot nodule’. a large bulge which is the benign tumour but the rest of the gland shrinks because the high levels of the thyroxine due to the tumour will supress TSH and the rest of the thyroid gland will atrophy (apart from the adenoma which is autonomous)

May have family history of grave’s but not with plummers

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10
Q

What is the effect of beta receptors on the sympathetic NS

A

Sensitises beta adrecnoceptors to ambient levels of E and NE
APPARENT sympathetic acivation
Tachycardia, palpitations, tremor in hands and lid lag (due to levator palpebrae)

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11
Q

What is a thyroid storm

A

Extreme hyperthyroidism= thyroid storm

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12
Q

What are the features of thyroid storm

A 
Hyperpyrexia >41 degrees 
Accelerated tachycardia 
Cardiac failure 
Delirium/frank psychoosis 
Hepatocellular dysfunction or jaundice (cholestatic type)
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13
Q

Treatment options for hyperthyroidism

A

Surgery (thyroidectomy)
Radioiodine
Drugs

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14
Q

Classes of drugs used to treat hyperthyroidism

A
  1. Thionamides/thiolurynenes
  2. Potasssium iodide
  3. Radioiodine
  4. Beta blockers

1st three reduce thyroid hormone synthesis, beta blockers help with symptoms

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15
Q

List 2 drug names for thionamides

A

(propylthiouracil, carbimazole)

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16
Q

When would thionamides be used

A
  1. daily treatment of hyperthyroid conditions (Graves or plummers)
  2. treatment before surgery
  3. reduce symptoms while waiting for radioactive iodine to act
17
Q

How do thianamides work

A
  1. Inhibit thyroid peroxidase, which stops two steps:
    a. Iodination of the tyrosine residues within the thyroglobulin
    b. coupling of iodinated thyroglobulins (MIT and DIT) to make t3 and t4
  2. Suppress antibody production in Grave’s
  3. Reduces conversion of T4 to T3 in peripheral tissues (just PTU) so more of inactive form
18
Q

Why don’t thionamides work immediately

A

In the colloid there is a large store of t3/t4 (long half life of drugs already in the circulation too)
Thus you get biochemical effect of hours and a clinical effect of weeks

19
Q

What would be given while waiting for thionamides to work?

A
  1. Non-cardio selective beta blocker (in cardio diseases we usually use selective ones now) e.g. propanalol which rapidly reduces tachycardia but also (because non cardio selective) tremor of skeletal muscle
20
Q

State the side effects of thionamides drugs

A

You get agranulocytosis (reduction in usually neutrophils)- rare and reversible on withdrawal of drug
Rashes

21
Q

Pharmacokinetics of the thionamides drugs

A

orally active
carbimazole is a PRODRUG which has to be converted to methimazole

it can cross the placenta, and is secreted in breast milk (PTU less than carbimazole)

It is metabolised by the liver and excreted into the urine)

22
Q

How long do you give thionamides for?

A

You give for 18 months, then stop the course and review patient periodically after including thyroid function tests for remission and relapse (50% will relapse)

23
Q

When is potassium iodide (KI) used in hyperthyroidism

A

Preparation of hyperthyroid patients for surgery and severe thyrotoxic crisis

24
Q

Mechanism of KI action

A

Inhibits iodination of thyroglobulin and it inhibits H2O2 generation and thyoperoxidase. WOLFF-CHAIKOFF EFFECT (autoregulatory effect)

25
Q

When will symptoms reduce with KI and what are the other effects?

+

what are the pharmacokinetics of KI

A

Hyperthyroid symptoms go down within 1-2 days, and the vascularity and the size of the gland reduces within 10-14 days (this is good for surgeon)

You might wonder why this drug is not used all the time then, as it is much faster onset….

it is not used all the time because, after a while, the KI will actually cause an increase in thryoid hormone levels (so only used for short term, i.e. before surgery on in storm)

--------------------------------
Given orally (Lugol’s solution; aqueous iodine), maximum effects after 10 days’ continuous administration
26
Q

Mechanism of radioiodine action

A

Taken up by NIS and it accumulates in the colloid and it emits beta particles and destroys the gland

27
Q

Pharmacokinetics of radioiodine

A

Discontinue antithyroid drugs 7-10 days priot to treatment with thise drug. Single oral drug. Radioactive half life of 8 days, radioactivity negligible after 2 months
Can be used to treat thyroid cancer but at a much higher dose (3,000 MBq for cancer, 500MBq for Grave’s)

28
Q

Cautions with radioiodine

A

Avoid close contact with small children for several weeks after taking radioiodine,
contra-indicated in pregnancy and breast feeding
(this is a reminder that thionamides also make it through palcenta and breast milk, but less so with PTU)

29
Q

When else is radioiodine used

A

Test of thyroid gland pathology e.g toxic nodule, thyroiditis vs. graves
You administer i.v. but cytotoxicity is negligible
Can use technetium 99- pertechnetate for scans but not treatment (very low, tracer doses)

30
Q

Reason to give radioiodine

A

If patient has been on anti-thyroid drugs for 18 months or so, couldn’t reduce the dose, they become overactive again after finishing etc.
So it’s like a last resort

31
Q

State the signs of viral (de Quervain’s) thyroiditis

A

Painful dysphagia (virus causes inflamamtion)
Thyroid gland is damaged and releases all of the colloid
Pyrexia (fever)
Raised ESR

32
Q

How would viral thyroiditis appear on a radioiodine scan

A

NO uptake, because thyroid gland just making viruses not thyroxine anymore, so not thyroxine taken up!

33
Q

Outline the thyroxine levels in viral thyroiditis

A

Hyperthyroidism (because all the colloid is released), hypothyroidism once all the stored thyroxine is released, but not more thyroxine being made because the gland is now only making viruses. After a further month, resolution occurs like in all viral diseases and patient becomes euthyroid again

34
Q

If KI acts in 1-2 days and ATDs take weeks, why don’t we give KI all the time

A

Because after a while, the t3/t4 levels will spike again, so it’s only used for SHORT TERM

35
Q

Why do patients stop taking anti-thyroid drugs 7-10 days before radioiodine is given

A

To allow thyroid gland to become very active again so it will take up the radioiodine very well via the NIS

Hormones (23 decks)

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